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Following collection in appropriate containers, clinical specimens undergo a rapid examination in the laboratory.
Learning Objectives
• Describe how immediate direct examination of a specimen is useful to determine microscopic and macroscopic morphology
Key Points
• Immediate direct examination methods depend on the nature of the specimen.
• Diagnostic laboratory techniques include direct testing using a microscope, and immunological or genetic methods that provide immediate clues as to the identity of the microbe or microbes in the sample.
• Phenotypic methods include the examination of microscopic, macroscopic, and biochemical characteristics of a pathogen.
Key Terms
• biopsied: to remove and examine a sample of tissue from a living body for diagnostic purposes.
Immediate Direct Examination of Specimen
For specimen collection at sites that normally contain resident microflora, care should be taken to sample only the infected site and not the surrounding areas. For example, throat and nasopharyngeal swabs should not touch the tongue, cheek, or saliva. Saliva is an especially undesirable contaminant because it contains millions of bacteria, of which are normal flora. Sputum, the mucous secretion that coats the lower respiratory surfaces, especially the lungs, is discharged by coughing or taken by a catheterization to avoid contamination with saliva. Also the mucous lining of the vagina, cervix, or urethra can be sampled with a swabbed or applicator stick.
Additional sources of specimens are the vagina, eye, ear canal, nasal cavity (all by swab), and diseased tissue that has been surgically removed (biopsied). Urine is taken aseptically from the bladder with a catheter. Another method called the “clean catch” is taken by washing the external urethra and collecting the urine in midstream. Some diagnostic techniques require first-voided “dirty catch” urine. Sterile materials such as blood, cerebrospinal fluid, and tissue fluid must be taken by sterile needle aspiration.
Diagnostic laboratory techniques include direct testing using a microscope, immunological, or genetic methods that provide immediate clues as to the identity of the microbe or microbes in the sample, and cultivation, isolation, and identification of pathogens using a wide variety of general and specific tests (such as blood or other fluids).
Most tests fall into two categories: presumptive data, which place the isolated microbe in a preliminary category such as genus, and more specific, confirmatory data, which provide more definitive evidence of a species. Some diseases are diagnosed without the need to identify microbes from specimens. Serological tests on a patient’s serum can detect signs of an antibody response. One method that clarifies whether a positive test indicates current or prior infection is to take two samples several days apart and see if the antibody titer is raising. Skin testing can pinpoint a delayed allergic reaction to a microorganism. These tests are important in screening the general population for exposure to an infectious agent such as rubella or tuberculosis.
The main phenotypic methods include the direct examination of specimens, observing the growth of specimen cultures on special media, and biochemical testing of specimen cultures.
MICROSCOPIC MORPHOLOGY
Traits that can be valuable aids to identification of cell shape and size, Gram-stain reaction, acid-fast reaction and special structures, including endospores, granules, and capsules. Electron microscopes can pinpoint additional features such as cell wall flagella, pili, and fimbriae.
MACROSCOPIC MORPHOLOGY
Traits that can be assessed with the naked eye are also useful in diagnosis. These include the appearance of colonies, including texture, shape, size, pigment, speed of growth, and patterns of growth in broth and gelatin.
PHYSIOLOGICAL AND BIOCHEMICAL CHARACTERISTICS
Enzymes and other biochemical properties of bacteria are reliable and stable expressions of the chemical identity of each species. Diagnostic tests exist for determining the presence of specific enzymes and assessing nutritional and metabolic activities.
Test examples include: fermentation of sugars, capacity to digest or metabolize complex polymers such as proteins and ploysaccharides; production of gas; presence of enzymes such as catalase, oxidase, and decarboxylase; and sensitivity to antimicrobial drugs.
CHEMICAL ANALYSIS
This involves analyzing the types of specific structural substances that the microorganism contains, such as the chemical composition of peptides in the cell wall and lipids in the membrane. | textbooks/bio/Microbiology/Microbiology_(Boundless)/12%3A_Immunology_Applications/12.03%3A_Preparations_for_Diagnosing_Infection/12.3B%3A__Immediate_Direct_Examination_of_Specimen.txt |
Following direct examination, clinical specimens are cultivated to generate more confirmatory data.
Learning Objectives
• Describe how direct microscope observation of a fresh or stained specimen is one of the most rapid methods of determining its characteristics
Key Points
• The success of pathogen identification and treatment depends on how the specimen is collected, handled, and stored.
• Diagnostic laboratory techniques include direct testing using a microscope, and immunological or genetic methods that provide immediate clues as to the identity of the microbe or microbes in the sample.
• Following direct testing, cultivation, isolation, and identification of pathogens using a wide variety of general and specific tests is required.
Key Terms
• mannitol: A polyhydroxy alcohol, an isomer of sorbitol, used as an artificial sweetener.
• MacConkey agar: A culture medium designed to grow Gram-negative bacteria and differentiate them from lactose fermentation.
Cultivation of Specimen
The success of pathogen identification and treatment depends on how the specimen is collected, handled, and stored. It is also critical that the pathogen is isolated in a pure culture first. Direct microscope observation of a fresh or stained specimen is one of the most rapid methods of determining characteristics. Stains most often employed for bacteria are the gram stain, though they do not work on some organisms.
The direct florescence antibody (DFA) test can highlight the presence of the microbe in patient specimens by means of labeled antibodies. This test is useful for bacteria such as syphilis spirochete, which are not readily cultivated in a laboratory, or if a rapid diagnosis is essential for the survival of a patient.
In most cases, specimens are also inoculated into differential media that define such characteristics as fermentation patters (mannitol salt and MacConkey agar) and as reactions in blood (blood agar). A patient’s blood is usually cultured in a special bottle of broth that can be periodically sampled for growth. Work must be done from isolated colonies or pure cultures, as working with mixed or contaminated cultures gives misleading and inaccurate results. From such isolates, clinical microbiologists obtain information about a pathogen’s microscopic morphology and staining reactions, culture appearance, motility, oxygen requirements, and biochemical characteristics.
Serological testing uses in-vitro diagnostic testing of serum, has a high degree of specificity and sensitivity, and is based on the specificity an antibody has for its antigen. These techniques do not necessitate a cultivation step. Serum can be directly used in agglutination, precipitation, complement fixation, fluorescent microscopy, and enzyme-linked assays. Results of specimen analysis are entered in the patient’s summary chart.
12.3D: DNA Analysis Using Genetic Probes and PCR
Genotyping of pathogenic isolates provides valuable support during investigations of suspected outbreaks and when tracing infectious diseases.
Learning Objectives
• Describe how genetic probes can be used to detect unique nucleotide sequences within the DNA or RNA or a microorganism
Key Points
• Hybridization can identify a bacterial species by analyzing segments of its DNA.
• Genetic probes are small fragments of DNA or RNA that are complementary to the specific sequences of DNA from a particular microbe.
• This approach is most useful in the detection of infections due to microorganisms that are difficult to culture.
Key Terms
• polymerase chain reaction: A technique in molecular biology for creating multiple copies of DNA from a sample; used in genetic fingerprinting etc.
Genetic probes are based on the detection of unique nucleotide sequences with the DNA or RNA of a microorganism. Once such a unique nucleotide sequence, which may represent a portion of a virulence gene or of chromosomal DNA, is found, it is isolated and inserted into a cloning vector ( plasmid ), which is then transformed into Escherichia coli to produce multiple copies of the probe. The sequence is then reisolated from plasmids and labeled with an isotope or substrate for diagnostic use. Hybridization of the sequence with a complementary sequence of DNA or RNA, follows cleavage of the double-stranded DNA of the microorganism in the specimen. The use of molecular technology in the diagnoses of infectious diseases has been further enhanced by the introduction of gene amplication techniques, such as the polymerase chain reaction (PCR) in which DNA polymerase is able to copy a strand of DNA by elongating complementary strands of DNA that have been initiated from a pair of closely spaced oligonucleotide primers. This approach has had major applications in the detection of infections due to microorganisms that are difficult to culture (e.g., the human immunodeficiency virus), or that have not as yet been successfully cultured (e.g., the Whipple’s disease bacillus).
It is well established that genotyping of pathogenic isolates provides valuable support for the investigation of suspected outbreaks, the detection of unsuspected transmission, the tracing of infectious agents within a community, and the identification of possible sources of infection for newly diagnosed cases. At the national or international level, fingerprinting allows strains from different geographic areas to be compared, and the movement of individual strains to be tracked. Fingerprinting technique requires high-quality genomic DNA, which is not only difficult to prepare but also requires culturing of the organism, resulting in a long turnaround time. In addition, fingerprint interpretation and matching can be complicated and require sophisticated computer software for large-scale analysis.
In contrast, nucleic acid amplification-based assays do not require culturing of the organisms, allowing the analysis of samples in real time. In many PCR-based typing assays, the target DNA of interest is amplified and labeled by PCR, and the labeled products are hybridized to an array of immobilized diagnostic probes. This method has been successfully used for the detection of mutations in drug resistance genes of Mycobacterium tuberculosis, and for Mycobacterium species identification. Spoligotyping, a reverse dot blot assay that detects the presence of a series of unique spacers in the direct repeat (DR) locus, meets the need for a simple and rapid method by which to distinguish M. tuberculosis complex strains. However, spoligotyping has significantly less discriminatory power than fingerprinting. | textbooks/bio/Microbiology/Microbiology_(Boundless)/12%3A_Immunology_Applications/12.03%3A_Preparations_for_Diagnosing_Infection/12.3C%3A_Cultivation_of_Specimen.txt |
Nucleic acid sequencing and rRNA analysis consist of comparing nitrogen bases in rRNA.
Learning Objectives
• Describe how the 16SrRNA gene can be used for phylogenetic studies and in medical microbiology for bacterial identification
Key Points
• This method is effective in identifying general group differences of pathogens.
• 16S rRNA gene sequences contain hypervariable regions that can provide species -specific signature sequences useful for bacterial identification.
• This method can also be fine-tuned to identify pathogens at the species level.
Key Terms
• ribosomes: Large and complex molecular machine, found within all living cells, that serves as the primary site of biological protein synthesis.
Sixteen S ribosomal RNA (or 16S rRNA) is a component of the 30S small subunit of prokaryotic ribosomes. It is approximately 1.5kb (or 1500 nucleotides) in length. The genes coding for it are referred to as 16S rDNA, and are used in reconstructing phylogenies. Multiple sequences of 16S rRNA can exist within a single bacterium.
The 16SrRNA gene is used for phylogenetic studies, as it is highly conserved between different species of bacteria and archaea. Carl Woese pioneered this use of 16S rRNA. In addition, mitochondrial and chloroplastic rRNA are also amplified. Unfortunately, while primers can be defined to amplify this gene from single genomes, this method is not accurate enough to estimate the diversity of microbial communities from their environments. Principal limits are the lack of real universal primers; DNA amplification biases and reference database selection impact the annotation of reads.
Paradoxically, methodological denial is now a rule in published articles that use 16S rRNA gene amplicon surveys to study unknown microbial communities. In these articles, one pair of primers (although many of them are designed, and provide different results) is used to amplify a region of the 16S rRNA gene. In addition to highly conserved primer binding sites, 16S rRNA gene sequences contain hypervariable regions that can provide species-specific signature sequences useful for bacterial identification. As a result, 16S rRNA gene sequencing has become prevalent in medical microbiology as a rapid and cheap (while inaccurate) alternative to phenotypic methods of bacterial identification. Although it was originally used to identify bacteria, 16S sequencing was subsequently found to be capable of reclassifying bacteria into completely new species, or even genera. It has also been used to describe new species that have never been successfully cultured.
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Type I (or immediate/anaphylactic) hypersensitivity can be caused by the body’s response to a foreign substance.
Learning Objectives
• Describe Type I hypersensitivity reactions
Key Points
• Common triggers for anaphylaxis include venom from insect bites or stings, foods, and medication.
• People with atopic diseases such as asthma, eczema, or allergic rhinitis have a high risk of anaphylaxis from food, latex, and radiocontrast agents.
• Anaphylaxis is a severe allergic reaction that starts suddenly and affects many body systems due to the release of inflammatory mediators and cytokines from mast cells and basophils.
Key Terms
• anaphylaxis: A severe and rapid systemic allergic reaction to an allergen, causing a constriction of the trachea, preventing breathing; anaphylactic shock.
• hives: Itchy, swollen, red areas of the skin which can appear quickly in response to an allergen or due to other conditions.
• mast cells: A mast cell is a resident cell of several types of tissues and contains many granules rich in histamine and heparin. Mat cells play a role in allergy, anaphylaxis, wound healing and defense against pathogens.
Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity. Anaphylaxis typically produces many different symptoms over minutes or hours. Symptoms typically include raised bumps on the skin (; hives), itchiness, red face or skin (flushing), or swollen lips.
Anaphylaxis can be caused by the body’s response to almost any foreign substance. Common triggers include venom from insect bites or stings, foods, and medication. Foods are the most common trigger in children and young adults. Medications and insect bites and stings are more common triggers in older adults. Less common causes include physical factors, biological agents (such as semen), latex, hormonal changes, food additives (e.g. monosodium glutamate (MSG) and food coloring), and medications that are applied to the skin (topical medications). Exercise or temperature (either hot or cold) may also trigger anaphylaxis by causing tissue cells known as mast cells to release chemicals that start the allergic reaction.
Anaphylaxis caused by exercise is often also linked to eating certain foods. If anaphylaxis occurs while a person is receiving anesthesia, the most common causes are certain medications that are given to produce paralysis (neuromuscular blocking agents), antibiotics, and latex. Many foods can trigger anaphylaxis, even when the food is eaten for the first time. In Western cultures, the most common causes are eating or being in contact with peanuts, wheat, tree nuts, shellfish, fish, milk, and eggs.
People with atopic diseases such as asthma, eczema, or allergic rhinitis have a high risk of anaphylaxis from food, latex, and radiocontrast agents. These people do not have a higher risk from injectable medications or stings. People who have disorders caused by too many mast cells in their tissues (mastocytosis) or who are wealthier are at increased risk. The longer the time since the last exposure to an agent that caused anaphylaxis, the lower the risk of a new reaction.
Anaphylaxis is a severe allergic reaction that starts suddenly and affects many body systems. It results from the release of inflammatory mediators and cytokines from mast cells and basophils. This release is typically associated with an immune system reaction, but may also be caused by damage to cells that are not related to an immune reaction. When anaphylaxis is caused by an immune response, immunoglobulin E (IgE) binds to the foreign material that starts the allergic reaction (the antigen ). The combination of IgE bound to the antigen activates FcεRI receptors on mast cells and basophils. The mast cells and basophils react by releasing inflammatory mediators such as histamine. These mediators increase the contraction of bronchial smooth muscles, cause blood vessels to widen (vasodilation), increase the leakage of fluid from blood vessels, and depress the actions of the heart muscle. There is also an immunologic mechanism that does not rely on IgE, but it is not known if this occurs in humans. When anaphylaxis is not caused by in immune response, the reaction is due to an agent that directly damages mast cells and basophils, causing them to release histamine and other substances that are usually associated with an allergic reaction (degranulation). Agents that can damage these cells include contrast medium for X-rays, opioids, temperature (hot or cold), and vibration. | textbooks/bio/Microbiology/Microbiology_(Boundless)/12%3A_Immunology_Applications/12.04%3A_Immunity_Disorders-_Hypersensitivity/12.4A%3A_Type_I_%28Anaphylactic%29_Reactions.txt |
Allergy testing can help confirm or rule out allergies, reducing adverse reactions and limiting unnecessary avoidance and medications.
Learning Objectives
• Describe how the skin prick test and the allergy blood test work to assess the presence of allergen specific antibodies in an individual
Key Points
• To assess the presence of allergen -specific IgE antibodies, you can use one of two methods: a skin-prick test or an allergy blood test.
• Challenge testing is when small amounts of a suspected allergen are introduced to the body orally, through inhalation, or via other routes.
• Patch testing is used to help ascertain the cause of skin contact allergy (contact dermatitis).
• Traditional treatment and management of allergies consisted of simply avoiding the allergen in question.
• Several antagonistic drugs are used to block the action of allergic mediators or to prevent activation of cells and degranulation processes.
Key Terms
• allergen: a substance that causes an allergic reaction
• antihistamine: a drug or substance that counteracts the effects of a histamine. Commonly used to alleviate the symptoms of hay fever and other allergies
• skin prick test: Skin-prick testing is also known as “puncture testing” and “prick testing” because of the series of tiny punctures or pricks made in the patient’s skin. Small amounts of suspected allergens or their extracts (pollen, grass, mite proteins, peanut extract, etc.) are introduced to sites on the skin marked with pen or dye.
Allergy testing can help confirm or rule out allergies, reducing adverse reactions and limiting unnecessary avoidance and medications. Correct diagnosis, counseling, and avoidance advice based on valid allergy test results will help reduce the incidence of symptoms and medications and will improve quality of life. Earlier and more accurate diagnoses save costs due to a reduction in consultations, referrals to secondary care, misdiagnoses, and emergency admissions.
For assessing the presence of allergen-specific IgE antibodies, you can use two different methods: a skin prick test or an allergy blood test. Both methods are recommended by the NIH guidelines, are equally cost-effective, and have similar diagnostic value in terms of sensitivity and specificity. A healthcare provider can use the test results to identify the specific allergic triggers that may be contributing to symptoms.
Allergies undergo dynamic changes over time. Regular allergy testing for relevant allergens provides information on if and how patient management can be changed in order to improve health and quality of life. Annual testing is often the practice for determining whether allergies to milk, eggs, soy, and wheat have been outgrown. The testing interval is extended to two to three years for allergies to peanuts, tree nuts, fish, and crustacean shellfish. Results of followup testing can guide decision-making regarding whether and when it is safe to introduce or re-introduce allergenic food into the diet.
Skin testing is also known as “puncture testing” and “prick testing” because of the series of tiny punctures or pricks made in the patient’s skin. Small amounts of suspected allergens or their extracts are introduced to sites on the skin marked with pen or dye (the dye should be carefully selected, lest it cause an allergic response itself). Sometimes, the allergens are injected “intradermally” into the patient’s skin with a needle and syringe. Common areas for testing include the inside forearm and the back. If the patient is allergic to the substance, then a visible inflammatory reaction will usually occur within 30 minutes. This response will range from a slight reddening of the skin to a full-blown hive (called “wheal and flare”) similar to a mosquito bite in more sensitive patients. Interpretation of the results of the skin-prick test is normally done by allergists on a scale of severity, with +/- meaning borderline reactivity and 4+ indicating a severe reaction.
In contrast, an allergy blood test is quick and simple and can be performed irrespective of age, skin condition, medication, symptom, disease activity, and pregnancy. In addition, multiple allergens can be detected with a single blood sample. Allergy blood tests are very safe, since the patient is not exposed to any allergens during the testing procedure. The test measures the concentration of specific IgE antibodies in the blood.
Challenge testing is when small amounts of a suspected allergen are introduced to the body orally, through inhalation, or via other routes. Challenge tests are utilized most often with foods or medicines. If the patient experiences significant improvement while avoiding a suspected allergen, she may then be “challenged” by reintroducing it to see if symptoms can be reproduced.
Patch testing is used to help ascertain the cause of skin contact allergy (contact dermatitis). Adhesive patches, usually treated with a number of different commonly allergenic chemicals or skin sensitizers, are applied to the back. The skin is then examined for possible local reactions at least twice, usually 48 hours after application and then again two or three days later.
Traditional treatment and management of allergies consisted of simply avoiding the allergen in question. However, while avoidance of allergens may reduce symptoms and avoid life-threatening anaphylaxis, it is difficult to do for those with allergies to pollen or other airborne allergens. Several antagonistic drugs are used to block the action of allergic mediators or to prevent activation of cells and degranulation processes. These include antihistamines, glucocorticoids, epinephrine (adrenaline), theophylline, and cromolyn sodium.
Desensitization or hyposensitization is a treatment in which the patient is gradually vaccinated with progressively larger doses of the allergen in question. This can either reduce the severity or eliminate hypersensitivity altogether. It relies on the progressive skewing of IgG antibody production to block excessive IgE production seen in atopys. In effect, the person builds up immunity to increasing amounts of the allergen. Studies have demonstrated the long-term efficacy and the preventive effect of immunotherapy in reducing the development of new allergies. A second form of immunotherapy involves the intravenous injection of monoclonal anti-IgE antibodies. These bind to free- and B cell-associated IgE, signaling their destruction. | textbooks/bio/Microbiology/Microbiology_(Boundless)/12%3A_Immunology_Applications/12.04%3A_Immunity_Disorders-_Hypersensitivity/12.4B%3A_Diagnosis_and_Treatment_of_Allergy.txt |
In type II (cytotoxic) hypersensitivity, the antibodies produced by the immune response bind to antigens on the patient’s own cell surfaces.
Learning Objectives
• Describe Type II hypersensitivity reactions
Key Points
• The antigens recognized in this way may either be intrinsic (“self” antigen, innately part of the patient’s cells) or extrinsic (adsorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen).
• Mediators of acute inflammation are generated at the site where a foreign antigen is recognized and membrane attack complexes cause cell lysis and death.
• In antibody -dependent cell-mediated cytotoxicity (ADCC), cells exhibiting the foreign antigen are tagged with antibodies ( IgG or IgM) and they are then recognised by natural killer (NK) cells and macrophages which in turn kill these tagged cells.
Key Terms
• macrophages: A type of white blood cell that targets foreign material, including bacteria and viruses.
• dendritic cells: Dendritic cells are immune cells that function to process antigen material and present it on the surface of other cells of the immune system. They act as messengers between innate and adaptive immunity.
• cytotoxic hypersensitivity: In type II hypersensitivity, the antibodies produced by the immune response bind to antigens on the patient’s own cell surfaces.
In type II hypersensitivity (or cytotoxic hypersensitivity), the antibodies produced by the immune response bind to antigens on the patient’s own cell surfaces. The antigens recognized in this way may either be intrinsic (“self” antigen, innately part of the patient’s cells) or extrinsic (adsorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen). These cells are recognized by macrophages or dendritic cells, which act as antigen-presenting cells. This causes a B cell response, wherein antibodies are produced against the foreign antigen.
An example of type II hypersensitivity is the reaction to penicillin wherein the drug can bind to red blood cells, causing them to be recognized as different; B cell proliferation will take place and antibodies to the drug are produced. IgG and IgM antibodies bind to these antigens to form complexes that activate the classical pathway of complement activation to eliminate cells presenting foreign antigens (which are usually, but not in this case, pathogens). That is, mediators of acute inflammation are generated at the site and membrane attack complexes cause cell lysis and death. The reaction takes hours to a day. The membrane attack complex (MAC; ) is typically formed on the surface of pathogenic bacterial cells as a result of the activation of the alternative pathway and the classical pathway of the complement system, and it is one of the effector proteins of the immune system. The membrane-attack complex (MAC) forms transmembrane channels. These channels disrupt the phospholipid bilayer of target cells, leading to cell lysis and death.
Another form of type II hypersensitivity is called antibody-dependent cell-mediated cytotoxicity (ADCC). Here, cells exhibiting the foreign antigen are tagged with antibodies (IgG or IgM). These tagged cells are then recognised by natural killer (NK) cells and macrophages (recognised via IgG bound (via the Fc region) to the effector cell surface receptor, CD16 (FcγRIII)), which in turn kill these tagged cells.
Autoimmune diseases resemble type II-IV hypersensitivity reactions. They differ from hypersensitivity reactions in that the antigens driving the immune process are self-antigens rather than non-self as in hypersensitivity reactions. Below are some examples of Type II hypersensitivity-like autoimmunity. | textbooks/bio/Microbiology/Microbiology_(Boundless)/12%3A_Immunology_Applications/12.04%3A_Immunity_Disorders-_Hypersensitivity/12.4C%3A_Type_II_%28Cytotoxic%29_Reactions.txt |
Type III hypersensitivity occurs when there is little antibody and an excess of antigen, leading to the formation of small immune complexes.
Learning Objectives
• Describe Type III hypersensitivity reactions
Key Points
• It is characterized by solvent antigens that are not bound to cell surfaces (which is the case in type II hypersensitivity) but bind antibodies to form immune complexes of different sizes.
• Large complexes can be cleared by macrophages but small immune complexes cannot be cleared and they insert themselves into small blood vessels, joints, and glomeruli, causing symptoms.
• The cause of damage is as a result of the action of cleaved complement anaphylotoxins C3a and C5a, which, mediate the onset of the inflammatory response and eventual tissue damage.
Key Terms
• glomerulonephritis: A form of nephritis characterized by inflammation of the glomeruli
• immune complex: An immune complex is formed from the integral binding of an antibody to a soluble antigen. The bound antigen acting as a specific epitope, bound to an antibody is referred to as a singular immune complex.
• Arthus reaction: The Arthus reaction is a type of local type III hypersensitivity reaction which involves the deposition of antigen/antibody complexes mainly in the vascular walls, serosa (pleura, pericardium, synovium) and glomeruli.
Type III hypersensitivity occurs when there is little antibody and an excess of antigen, leading to small immune complexes being formed that do not fix complement and are not cleared from the circulation. It is characterized by solvent antigens that are not bound to cell surfaces (which is the case in type II hypersensitivity). When these antigens bind antibodies, immune complexes of different sizes form. Large complexes can be cleared by macrophages but macrophages have difficulty in the disposal of small immune complexes. These immune complexes insert themselves into small blood vessels, joints, and glomeruli, causing symptoms. Unlike the free variant, small immune complex bound to sites of deposition (like blood vessel walls) are far more capable of interacting with complement. These medium-sized complexes, formed in the slight excess of antigen, are viewed as being highly pathogenic.
Such depositions in tissues often induce an inflammatory response, and can cause damage wherever they precipitate. The cause of damage is as a result of the action of cleaved complement anaphylotoxins C3a and C5a, which, respectively, mediate the induction of granule release from mast cells (from which histamine can cause urticaria), and recruitment of inflammatory cells into the tissue (mainly those with lysosomal action, leading to tissue damage through frustrated phagocytosis by polymorphonuclear neutrophils and macrophages).
Immune complex glomerulonephritis, as seen in Henoch-Schönlein purpura is an example of IgA involvement in a nephropathy. The reaction can take hours, days, or even weeks to develop, depending on whether or not there is immunlogic memory of the precipitating antigen. Typically, clinical features emerge a week following initial antigen challenge, when the deposited immune complexes can precipitate an inflammatory response. Because of the nature of the antibody aggregation, tissues that are associated with blood filtration at considerable osmotic and hydrostatic gradient (e.g. sites of urinary and synovial fluid formation, kidney glomeruli and joint tissues respectively) bear the brunt of the damage. Hence, vasculitis, glomerulonephritis and arthritis are commonly-associated conditions as a result of type III hypersensitivity responses. As observed under methods of histopathology, acute necrotizing vasculitis within the affected tissues is observed concomitant to neutrophilic infiltration, along with notable eosinophilic deposition (fibrinoid necrosis).
Often, immunofluorescence microscopy can be used to visualize the immune complexes. Skin response to a hypersensitivity of this type is referred to as an Arthus reaction, and is characterized by local erythema and some induration. Platelet aggregation, especially in microvasculature, can cause localized clot formation, leading to blotchy hemorrhages. This typifies the response to injection of foreign antigen sufficient to lead to the condition of serum sickness. An immune complex is formed from the integral binding of an antibody to a soluble antigen. The bound antigen acting as a specific epitope, bound to an antibody, is referred to as a singular immune complex. After an antigen-antibody reaction, the immune complexes can be subject to any of a number of responses, including complement deposition, opsonization, phagocytosis, or processing by proteases.
Red blood cells carrying CR1-receptors on their surface may bind C3b-decorated immune complexes and transport them to phagocytes, mostly in liver and spleen, and return back to the general circulation. Immune complexes may themselves cause disease when they are deposited in organs, e.g. in certain forms of vasculitis. This is the third form of hypersensitivity in the Gell-Coombs classification, called Type III hypersensitivity. Immune complex deposition is a prominent feature of several autoimmune diseases, including systemic lupus erythematosus, cryoglobulinemia, rheumatoid arthritis, scleroderma and Sjögren’s syndrome. | textbooks/bio/Microbiology/Microbiology_(Boundless)/12%3A_Immunology_Applications/12.04%3A_Immunity_Disorders-_Hypersensitivity/12.4D%3A_Type_III_%28Immune_Complex%29_Reactions.txt |
Type IV hypersensitivity reactions are cell-mediated and take 2 to 3 days to develop.
Learning Objectives
• Describe Type IV cell-mediated reactions and explain why they take two to three days to develop
Key Points
• Cell-mediated immunity is an immune response that does not involve antibodies but rather involves the activation of phagocytes, natural killer cells (NK), antigen -specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen.
• In type IV hypersensitivity reactions, CD4+ helper T cells recognize antigen in a complex with Class 2 major histocompatibility complex on macrophages (the antigen-presenting cells).
• A classic example of delayed type IV hypersensitivity is the Mantoux tuberculin test in which skin induration indicates exposure to tuberculosis.
Key Terms
• cellular immunity: Cellular immunity protects the body by: activating antigen-specific cytotoxic T-lymphocytes, activating macrophages and natural killer cells and stimulating cytokine secretion to stimulate other cells involved in adaptive immune responses and innate immune responses.
• type IV hypersensitivity: A cell-mediated immune response that takes two to three days to develop.
Cell-mediated immunity is an immune response that does not involve antibodies, but rather involves the activation of phagocytes, natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen. Historically, the immune system was separated into two branches: humoral immunity, for which the protective function of immunization could be found in the humor (cell-free bodily fluid or serum) and cellular immunity, for which the protective function of immunization was associated with cells. CD4 cells or helper T cells provide protection against different pathogens. Cytotoxic T cells cause death by apoptosis without using cytokines. Therefore in cell mediated immunity cytokines are not always present.
Cellular immunity protects the body by:
1. activating antigen-specific cytotoxic T-lymphocytes that are able to induce apoptosis in body cells displaying epitopes of foreign antigen on their surface, such as virus-infected cells, cells with intracellular bacteria, and cancer cells displaying tumor antigens
2. activating macrophages and natural killer cells, enabling them to destroy pathogens
3. stimulating cells to secrete a variety of cytokines that influence the function of other cells involved in adaptive immune responses and innate immune responses
Cell-mediated immunity is directed primarily at microbes that survive in phagocytes and microbes that infect non-phagocytic cells. It is most effective in removing virus-infected cells, but also participates in defending against fungi, protozoans, cancers, and intracellular bacteria. It also plays a major role in transplant rejection.
Type IV hypersensitivity is often called delayed type hypersensitivity as the reaction takes two to three days to develop. Unlike the other types, it is not antibody mediated but rather is a type of cell-mediated response. CD4+ helper T cells recognize antigen in a complex with Class 2 major histocompatibility complex. The antigen-presenting cells in this case are macrophages that secrete IL-12, which stimulates the proliferation of further CD4+ Th1 cells. CD4+ T cells secrete IL-2 and interferon gamma, further inducing the release of other Th1 cytokines, thus mediating the immune response. Activated CD8+ T cells destroy target cells on contact, whereas activated macrophages produce hydrolytic enzymes and, on presentation with certain intracellular pathogens, transform into multinucleated giant cells.
A classic example of delayed type IV hypersensitivity is the Mantoux tuberculin test in which skin induration indicates exposure to tuberculosis. Other examples include: temporal arteritis, Hashimoto’s thyroiditis, symptoms of leprosy, symptoms of tuberculosis, coeliac disease, graft-versus-host disease and chronic transplant rejection.
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Immunodeficiency occurs when the immune system cannot appropriately respond to infections.
Learning Objectives
• Explain the problems associated with immunodeficiency
Key Points
• If a pathogen is allowed to proliferate to certain levels, the immune system can become overwhelmed; immunodeficiency occurs when the immune system fails to respond sufficiently to a pathogen.
• Immunodeficiency can be caused by many factors, including certain pathogens, malnutrition, chemical exposure, radiation exposure, or even extreme stress.
• HIV is a virus that causes immunodeficiency by infecting helper T cells, causing cytotoxic T cells to destroy them.
Key Terms
• phagocyte: a cell of the immune system, such as a neutrophil, macrophage or dendritic cell, that engulfs and destroys viruses, bacteria, and waste materials
• lysis: the disintegration or destruction of cells
• immunodeficiency: a depletion in the body’s natural immune system, or in some component of it
Immunodeficiency
Failures, insufficiencies, or delays at any level of the immune response can allow pathogens or tumor cells to gain a foothold to replicate or proliferate to high enough levels that the immune system becomes overwhelmed, leading to immunodeficiency; it may be acquired or inherited. Immunodeficiency can be acquired as a result of infection with certain pathogens (such as HIV), chemical exposure (including certain medical treatments), malnutrition, or, possibly, by extreme stress. For instance, radiation exposure can destroy populations of lymphocytes, elevating an individual’s susceptibility to infections and cancer. Dozens of genetic disorders result in immunodeficiencies, including Severe Combined Immunodeficiency (SCID), bare lymphocyte syndrome, and MHC II deficiencies. Rarely, primary immunodeficiencies that are present from birth may occur. Neutropenia is one form in which the immune system produces a below-average number of neutrophils, the body’s most abundant phagocytes. As a result, bacterial infections may go unrestricted in the blood, causing serious complications.
HIV/AIDS
Human immunodeficiency virus infection / acquired immunodeficiency syndrome (HIV/AIDS), is a disease of the human immune system caused by infection with human immunodeficiency virus (HIV). During the initial infection, a person may experience a brief period of influenza-like illness. This is typically followed by a prolonged period without symptoms. As the illness progresses, it interferes more and more with the immune system. The person has a high probability of becoming infected, including from opportunistic infections and tumors that do not usually affect people who have working immune systems.
After the virus enters the body, there is a period of rapid viral replication, leading to an abundance of virus in the peripheral blood. During primary infection, the level of HIV may reach several million virus particles per milliliter of blood. This response is accompanied by a marked drop in the number of circulating CD4+ T cells, cells that are or will become helper T cells. The acute viremia, or spreading of the virus, is almost invariably associated with activation of CD8+ T cells (which kill HIV-infected cells) and, subsequently, with antibody production. The CD8+ T cell response is thought to be important in controlling virus levels, which peak and then decline, as the CD4+ T cell counts recover.
Ultimately, HIV causes AIDS by depleting CD4+ T cells (helper T cells). This weakens the immune system, allowing opportunistic infections. T cells are essential to the immune response; without them, the body cannot fight infections or kill cancerous cells. The mechanism of CD4+ T cell depletion differs in the acute and chronic phases. During the acute phase, HIV-induced cell lysis and killing of infected cells by cytotoxic T cells accounts for CD4+ T cell depletion, although apoptosis (programmed cell death) may also be a factor. During the chronic phase, the consequences of generalized immune activation coupled with the gradual loss of the ability of the immune system to generate new T cells appear to account for the slow decline in CD4+ T cell numbers. | textbooks/bio/Microbiology/Microbiology_(Boundless)/12%3A_Immunology_Applications/12.05%3A_Immunity_Disorders-_Autoimmune_Diseases/12.5A%3A_Immunodeficiency.txt |
Autoimmunity is the failure of an organism in recognizing “self” which results in an immune response against its own cells and tissues.
Learning Objectives
• Define autoimmunity and explain how it gives rise to autoimmune disease
Key Points
• Autoimmune diseases are very often treated with steroids which will dampen the immune response.
• Certain individuals are genetically susceptible to developing autoimmune diseases and susceptibility is linked to immunoglobulin, T-cell receptor, and MHC complex genes.
• Women are more likely than men to develop an autoimmune disease, but the severity of the disease is more accentuated in men.
Key Terms
• autoimmunity: The condition where one’s immune system attacks one’s own tissues, i.e., an autoimmune disorder.
• alloimmunity: Immunity, obtained from another, against one’s own cells.
Autoimmunity is the failure of an organism in recognizing its own constituent parts as self, which allows an immune response against its own cells and tissues. Any disease that results from such an aberrant immune response is termed an autoimmune disease. Autoimmunity is often caused by a lack of germ development of a target body and as such the immune response acts against its own cells and tissues. Prominent examples include Coeliac disease, diabetes mellitus type 1 (IDDM), Sarcoidosis, systemic lupus erythematosus (SLE), Sjögren’s syndrome, Churg-Strauss Syndrome, Hashimoto’s thyroiditis, Graves’ disease, idiopathic thrombocytopenic purpura, Addison’s Disease, rheumatoid arthritis (RA), and allergies.
Autoimmune diseases are very often treated with steroids. The misconception that an individual’s immune system is totally incapable of recognizing self antigens is not new. Paul Ehrlich, at the beginning of the 20th century, proposed the concept of horror autotoxicus, wherein a ‘normal’ body does not mount an immune response against its own tissues. Therefore, any autoimmune response was perceived to be abnormal and postulated to be connected with human disease. Now, it is accepted that autoimmune responses are an integral part of vertebrate immune systems (sometimes termed ‘natural autoimmunity’), normally prevented from causing disease by the phenomenon of immunological tolerance to self-antigens.
Autoimmunity should not be confused with alloimmunity. While a high level of autoimmunity is unhealthy, a low level of autoimmunity may actually be beneficial. First, low-level autoimmunity might aid in the recognition of neoplastic cells by CD8+ T cells, and thus reduce the incidence of cancer. Second, autoimmunity may have a role in allowing a rapid immune response in the early stages of an infection when the availability of foreign antigens limits the response (i.e., when there are few pathogens present).
Certain individuals are genetically susceptible to developing autoimmune diseases. This susceptibility is associated with multiple genes plus other risk factors. However, genetically predisposed individuals do not always develop autoimmune diseases. Three main sets of genes are suspected in many autoimmune diseases. These genes are related to immunoglobulins, T-cell receptors, and the major histocompatibility complexes (MHC). Immunoglobulins and T-cell receptors are involved in the recognition of antigens and they are inherently variable and susceptible to recombination. These variations enable the immune system to respond to a very wide variety of invaders, but may also give rise to lymphocytes capable of self-reactivity. Scientists such as H. McDevitt, G. Nepom, J. Bell, and J. Todd have also provided strong evidence to suggest that certain MHC class II allotypes are strongly correlated with disease. For example:
1. HLA DR2 is strongly positively correlated with Systemic Lupus Erythematosus, narcolepsy and multiple sclerosis, and negatively correlated with DM Type 1.
2. HLA DR3 is correlated strongly with Sjögren’s syndrome, myasthenia gravis, SLE, and DM Type 1.
3. HLA DR4 is correlated with the genesis of rheumatoid arthritis, Type 1 diabetes mellitus, and pemphigus vulgaris.
Fewer correlations exist with MHC class I molecules. The most notable and consistent is the association between HLA B27 and ankylosing spondylitis. Correlations may exist between polymorphisms within class II MHC promoters and autoimmune disease. The contributions of genes outside the MHC complex remain the subject of research, in animal models of disease (Linda Wicker’s extensive genetic studies of diabetes in the NOD mouse), and in patients (Brian Kotzin’s linkage analysis of susceptibility to SLE).
A person’s sex also seems to have some role in the development of autoimmunity, classifying most autoimmune diseases as sex-related diseases. Nearly 75% of the more than 23.5 million Americans who suffer from autoimmune disease are women, although it is less-frequently acknowledged that millions of men also suffer from these diseases. However, autoimmune diseases that develop in men tend to be more severe. A few autoimmune diseases that men are just as or more likely to develop as women, include: ankylosing spondylitis, type 1 diabetes mellitus, Wegener’s granulomatosis, and Crohn’s disease. The reasons for the sex role in autoimmunity are unclear. However, women appear to generally mount larger inflammatory responses than men when their immune systems are triggered, increasing the risk of autoimmunity. In addition, involvement of sex steroids is indicated by the fact that many autoimmune diseases tend to fluctuate in accordance with hormonal changes, for example, during pregnancy. Interestingly, a history of pregnancy also appears to leave a persistent increased risk for autoimmune disease. Indeed, it has been suggested that the slight exchange of cells between mothers and their children during pregnancy may induce autoimmunity. This would tip the gender balance in the direction of the female. Another theory suggests the female high tendency to get autoimmunity is due to an imbalanced X chromosome inactivation. | textbooks/bio/Microbiology/Microbiology_(Boundless)/12%3A_Immunology_Applications/12.05%3A_Immunity_Disorders-_Autoimmune_Diseases/12.5B%3A__The_Roles_of_Genetics_and_Gender_in_Autoimmune_Disease.txt |
Autoimmunity is a result of the failure of an organism’s immune system to recognize “self”.
Learning Objectives
• Define autoimmunity and describe how it can lead to disease
Key Points
• Autoimmunity is often caused by a lack of germ development of a target body and, as such, the immune response acts against its own cells and tissues.
• Certain individuals are genetically susceptible to developing autoimmune diseases but genetically predisposed individuals do not always develop an autoimmune disease.
• Three main sets of genes are suspected in many autoimmune diseases: immunoglobulins, T-cell receptors and the major histocompatibility complexes (MHC).
• Women are more likely to develop an autoimmune disease.
Key Terms
• alloimmunity: Immunity, obtained from another, against one’s own cells.
• autoimmunity: The condition where one’s immune system attacks one’s own tissues, i.e., an autoimmune disorder.
Autoimmunity is the failure of an organism in recognizing its own constituent parts as self, creating an immune response against its own cells and tissues. Any disease that results from such an aberrant immune response is termed an autoimmune disease.
Autoimmunity is often caused by a lack of germ development of a target body and, as such, the immune response acts against its own cells and tissues. Prominent examples include Coeliac disease, diabetes mellitus type 1 (IDDM), Sarcoidosis, systemic lupus erythematosus (SLE), Sjögren’s syndrome, Churg-Strauss Syndrome, Hashimoto’s thyroiditis, Graves’ disease, idiopathic thrombocytopenic purpura, Addison’s Disease, rheumatoid arthritis (RA) and allergies.
Autoimmune diseases are very often treated with steroids. The misconception that an individual’s immune system is totally incapable of recognizing self antigens is not new. Paul Ehrlich, at the beginning of the twentieth century, proposed the concept of horror autotoxicus, wherein a ‘normal’ body does not mount an immune response against its own tissues. Thus, any autoimmune response was perceived to be abnormal and postulated to be connected with human disease. Now, it is accepted that autoimmune responses are an integral part of vertebrate immune systems (sometimes termed ‘natural autoimmunity’), normally prevented from causing disease by the phenomenon of immunological tolerance to self-antigens.
Autoimmunity should not be confused with alloimmunity. Certain individuals are genetically susceptible to developing autoimmune diseases. This susceptibility is associated with multiple genes plus other risk factors. Genetically predisposed individuals do not always develop autoimmune diseases. Three main sets of genes are suspected in many autoimmune diseases: immunoglobulins, T-cell receptors and the major histocompatibility complexes (MHC).
Immunoglobulins and the T-cell receptors are involved in the recognition of antigens and they are inherently variable and susceptible to recombination. These variations enable the immune system to respond to a very wide variety of invaders, but may also give rise to lymphocytes capable of self-reactivity. Scientists such as H. McDevitt, G. Nepom, J. Bell and J. Todd have also provided strong evidence to suggest that certain MHC class II allotypes are strongly correlated with autoimmunity.
For example:
1. HLA DR2 is strongly positively correlated with Systemic Lupus Erythematosus, narcolepsy and multiple sclerosis, and negatively correlated with DM Type 1.
2. HLA DR3 is correlated strongly with Sjögren’s syndrome, myasthenia gravis, SLE, and DM Type 1.
3. HLA DR4 is correlated with the genesis of rheumatoid arthritis, Type 1 diabetes mellitus, and pemphigus vulgaris.
Fewer correlations exist with MHC class I molecules. The most notable and consistent is the association between HLA B27 and ankylosing spondylitis. Correlations may exist between polymorphisms within class II MHC promoters and autoimmune disease. The contributions of genes outside the MHC complex remain the subject of research both in animal models of disease (Linda Wicker’s extensive genetic studies of diabetes in the NOD mouse), and in patients (Brian Kotzin’s linkage analysis of susceptibility to SLE).
A person’s sex also seems to have some role in the development of autoimmunity, classifying most autoimmune diseases as sex-related diseases. Nearly 75% of the more than 23.5 million Americans who suffer from autoimmune disease are women, although it is less-frequently acknowledged that millions of men also suffer from these diseases.
According to the American Autoimmune Related Diseases Association (AARDA), autoimmune diseases that develop in men tend to be more severe. A few autoimmune diseases that men are just as or more likely to develop as women, include: ankylosing spondylitis, type 1 diabetes mellitus, Wegener’s granulomatosis, Crohn’s disease, Primary sclerosing cholangitis and psoriasis.
The reasons for the sex role in autoimmunity are unclear. Women appear to generally mount larger inflammatory responses than men when their immune systems are triggered, increasing the risk of autoimmunity. Similarly, involvement of sex steroids is indicated by the fact that many autoimmune diseases tend to fluctuate in accordance with hormonal changes. Interestingly, a history of pregnancy also appears to leave a persistent increased risk for autoimmune disease. Indeed, it has been suggested that the slight exchange of cells between mothers and their children during pregnancy may induce autoimmunity. This would tip the gender balance in the direction of the female.
Another theory suggests the female-high tendency to get autoimmunity is due to an imbalanced X chromosome inactivation. The X-inactivation skew theory, proposed by Princeton University’s Jeff Stewart, has recently been confirmed experimentally in scleroderma and autoimmune thyroiditis.
12.5D: Immune Complex Autoimmune Reactions
An immune complex is formed from the integral binding of an antibody to a soluble antigen and can function as an epitope.
Learning Objectives
• Describe how immune complex autoimmune reactions arise
Key Points
• After an antigen – antibody reaction, the immune complexes can be subject to any of a number of responses including complement deposition, opsonization, phagocytosis, or processing by proteases.
• Immune complexes may cause disease when they are deposited in organs.
• The Arthus reaction involves the in situ formation of antigen/antibody complexes after the intradermal injection of an antigen (as seen in passive immunity).
Key Terms
• epitope: That part of a biomolecule (such as a protein) that is the target of an immune response.
• immune complex: An immune complex is formed from the integral binding of an antibody to a soluble antigen. The bound antigen acting as a specific epitope, bound to an antibody is referred to as a singular immune complex.
An immune complex is formed from the integral binding of an antibody to a soluble antigen. The bound antigen acting as a specific epitope, bound to an antibody is referred to as a singular immune complex. After an antigen-antibody reaction, the immune complexes can be subject to any of a number of responses, including complement deposition, opsonization, phagocytosis, or processing by proteases. Red blood cells carrying CR1-receptors on their surface may bind C3b-decorated immune complexes and transport them to phagocytes, mostly in liver and spleen, and return back to the general circulation. Immune complexes may cause disease when they are deposited in organs, e.g. in certain forms of vasculitis. This is the third form of hypersensitivity in the Gell-Coombs classification, called Type III hypersensitivity. Immune complex deposition is a prominent feature of several autoimmune diseases, including systemic lupus erythematosus, cryoglobulinemia, rheumatoid arthritis, scleroderma, and Sjögren’s syndrome.
In immunology, the Arthus reaction is a type of local type III hypersensitivity reaction. Type III hypersensitivity reactions are immune complex-mediated. They involve the deposition of antigen/antibody complexes mainly in the vascular walls, serosa (pleura, pericardium, synovium), and glomeruli. The Arthus reaction involves the in situformation of antigen/antibody complexes after the intradermal injection of an antigen (as seen in passive immunity). If the animal/patient was previously sensitized (has circulating antibody), an Arthus reaction occurs. Typical of most mechanisms of the type III hypersensitivity, Arthus manifests as local vasculitis due to deposition of IgG-based immune complexes in dermal blood vessels. Activation of complement primarily results in cleavage of soluble complement proteins forming C5a and C3a, which activate recruitment of PMNs and local mast cell degranulation (requiring the binding of the immune complex onto FcγRIII), resulting in an inflammatory response. Further aggregation of immune complex-related processes induces a local fibrinoid necrosis with ischemia-aggravating thrombosis in the tissue vessel walls. The end result is a localized area of redness and induration that typically lasts a day or so. Arthus reactions have been infrequently reported after vaccination against diphtheria and tetanus. | textbooks/bio/Microbiology/Microbiology_(Boundless)/12%3A_Immunology_Applications/12.05%3A_Immunity_Disorders-_Autoimmune_Diseases/12.5C%3A__Cytotoxic_Autoimmune_Reactions.txt |
Cell-mediated autoimmunity can happen by several mechanisms involving cells of the immune system and their receptors.
Learning Objectives
• Define cell-mediated autoimmunity and describe the mechanisms that are thought to operate in the pathogenesis of autoimmune disease
Key Points
• Superantigens can bypass the T-cell requirement for B cell activation.
• In some instances such as celiac disease, B cells can be activated to produce antibodies to epitope A by T cells activated by epitope B.
• Autoreactive B cells in spontaneous autoimmunity survive due to subversion both of the T cell help pathway and of the feedback signal through B cell receptor, leading to loss of the negative signals responsible for B cell self- tolerance without necessarily requiring loss of T cell self-tolerance.
• DQ therefore is involved in recognizing common self- antigens and presenting those antigens to the immune system in order to develop tolerance from a very young age.
Key Terms
• autoimmunity: The condition where one’s immune system attacks one’s own tissues, i.e., an autoimmune disorder.
• tolerance: The process by which the immune system does not attack an antigen
Several mechanisms are thought to be operative in the pathogenesis of autoimmune diseases, against a backdrop of genetic predisposition and environmental modulation. Four of the important mechanisms are described below.
T Cell Bypass
A normal immune system requires the activation of B cells by T cells before the former can produce antibodies in large quantities. This requirement of a T cell can be bypassed in rare instances, such as infection by organisms producing super-antigens, which are capable of initiating polyclonal activation of B cells, or even of T cells, by directly binding to the β-subunit of T cell receptors in a non-specific fashion.
T Cell to B Cell Discordance
A normal immune response is assumed to involve B and T cell responses to the same antigen, where B cells recognize conformations on the surface of a molecule for B cells, and T cells recognize pre-processed peptide fragments of proteins for T cells. However, there is no evidence that this response is required. All that is required is that a B cell that recognizes antigen X endocytoses processes a protein Y (normally =X) and presents it to a T cell. Roosnek and Lanzavecchia showed that B cells recognizing IgGFc could get help from any T cell that responds to an antigen co-endocytosed with IgG by the B cell as part of an immune complex. In coeliac disease it seems likely that B cells that recognize transglutamine tissue are helped by T cells that recognize gliadin.
Aberrant B Cell Receptor-Mediated Feedback
A feature of human autoimmune disease is that it is largely restricted to a small group of antigens, several of which have known signaling roles in the immune response (for example DNA, C1q, IgGFc, Ro, Con. A receptor, Peanut agglutinin receptor(PNAR)). This fact gave rise to the idea that spontaneous autoimmunity may result when the binding of antibody to certain antigens leads to aberrant signals being fed back to parent B cells through membrane bound ligands. These ligands include B cell receptor (for antigen), IgG Fc receptors, CD21 (which binds complement C3d), Toll-like receptors 9 and 7 (which can bind DNA and nucleoproteins) and PNAR. More indirect aberrant activation of B cells can also be envisaged with autoantibodies to acetyl choline receptor (on thymic myoid cells) and hormone binding proteins. Together with the concept of T cell-B cell discordance, this idea forms the basis of the hypothesis of self-perpetuating autoreactive B cells. Autoreactive B cells in spontaneous autoimmunity are seen as surviving because of subversion both of the T cell help pathway and of the feedback signal through the B cell receptor. This reaction thereby overcomes the negative signals responsible for B cell self-tolerance without necessarily requiring loss of T cell self-tolerance.
Dendritic Cell Apoptosis
Immune system cells called dendritic cells present antigens to active lymphocytes. Dendritic cells that are defective in apoptosis can lead to inappropriate systemic lymphocyte activation and consequent decline in self-tolerance.
HLA-DQ (DQ) is a cell surface receptor type protein found on antigen presenting cells. DQ is an α heterodimer of the MHC Class II type. The α and β chains are encoded by HLA-DQA1 and HLA-DQB1, respectively. These two loci are adjacent to each other on chromosome 6p21.3. Both the α-chain and β-chain vary greatly. A person often produces two α-chain and two β-chain variants and thus four DQ isoforms.
DQ isoforms can bind to and present foreign and self antigens to T-cells. In this process T-cells are stimulated to grow and can signal B-cells to produce antibodies. DQ therefore is involved in recognizing common self-antigens and presenting those antigens to the immune system in order to develop tolerance from a very young age. When tolerance to self proteins is lost, DQ may become involved in autoimmune disease. Two autoimmune diseases in which HLA-DQ is involved are celiac disease and diabetes mellitus type 1. DQ is one of several antigens involved in rejection of organ transplants. As a variable cell surface receptor on immune cells, these D antigens, originally HL-A4 antigens, are involved in graft versus host disease when lymphoid tissues are transplanted between people.
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Primary immunodeficiencies are disorders in which part of the body’s immune system is missing, or does not function properly.
Learning Objectives
• Describe primary immunodeficiency disorders and explain what treatment options are available
Key Points
• To be considered a primary immunodeficiency, the cause of the immune deficiency must not be secondary in nature (caused by other disease, drug treatment, or environmental exposure to toxins).
• Most primary immunodeficiencies are genetic disorders; the majority are diagnosed in children under the age of one, although milder forms may not be recognized until adulthood.
• The precise symptoms of a primary immunodeficiency depend on the type of defect but generally include recurrent or persistent infections or developmental delay as a result of infection.
Key Terms
• genetic disorder: An illness caused by abnormalities in genes or chromosomes, especially a condition that is present prior to birth. Most genetic disorders are quite rare and affect one person in every several thousands or millions.
• immunodeficiency: A depletion in the body’s natural immune system, or in some component of it.
Primary immunodeficiencies are disorders in which a part of the body’s immune system is missing or does not function properly. To be considered a primary immunodeficiency, the cause of the immune deficiency must not be secondary in nature (caused by another disease, drug treatment, or environmental exposure to toxins). Most primary immunodeficiencies are genetic disorders; the majority are diagnosed in children under the age of one, although milder forms may not be recognized until adulthood.
Symptoms
The precise symptoms of a primary immunodeficiency depend on the type of defect. Generally, the symptoms and signs that lead to the diagnosis of an immunodeficiency include recurrent or persistent infections, or developmental delay as a result of infection. Particular organ problems; such as diseases involving the skin, heart, facial development and skeletal system; may be present in certain conditions. Others predispose to autoimmune disease, where the immune system attacks the body’s own tissues, or tumors (sometimes specific forms of cancer, such as lymphoma). The nature of the infections, as well as the additional features, may provide clues as to the exact nature of the immune defect.
Diagnostic Tests
The basic tests performed when an immunodeficiency is suspected should include a full blood count ( including accurate lymphocyte and granulocyte counts) and immunoglobulin levels. Tthe three most important types of antibodies are IgG, IgA and IgM.
Other tests are performed depending on the suspected disorder:
• Quantification of the different types of mononuclear cells in the blood (lymphocytes and monocytes): different groups of T lymphocytes (dependent on their cell surface markers, e.g. CD4+, CD8+, CD3+, TCRα and TCRγ); groups of B lymphocytes (CD19, CD20, CD21 and Immunoglobulin); natural killer cells and monocytes (CD15+); as well as activation markers (HLA-DR, CD25, CD80 ( B cells )
• Tests for T cell function: skin tests for delayed-type hypersensitivity, cell responses to mitogens and allogeneic cells, cytokine production by cells
• Tests for B cell function: antibodies to routine immunizations and commonly acquired infections, quantification of IgG subclasses
• Tests for phagocyte function: reduction of nitro blue tetrazolium chloride, assays of chemotaxis, bactericidal activity
Due to the rarity of many primary immunodeficiencies, many of the above tests are highly specialized and tend to be performed in research laboratories.
Immunodeficiency Disorders
In genetic immunodeficiency disorders, both T lymphocytes and often B lymphocytes—regulators of adaptive immunity—are dysfunctional or decreased in number. The main members are various types of severe combined immunodeficiency (SCID).
In primary antibody deficiencies, one or more isotypes of immunoglobulin are decreased or don’t function properly. These proteins, generated by plasma cells, normally bind to pathogens, targeting them for destruction.
A number of syndromes, including the following, escape formal classification but are otherwise recognisable by particular clinical or immunological features:
• Wiskott-Aldrich syndrome
• DNA repair defects not causing isolated SCID; for example ataxia telangiectasia and ataxia-like syndrome
• DiGeorge syndrome (when associated with thymic defects)
• Various immuno-osseous dysplasias (abnormal development of the skeleton with immune problems);for example, cartilage-hair hypoplasia, Schimke syndrome
In certain conditions, including the following, the regulation rather than the intrinsic activity of parts of the immune system is the predominant problem:
• Immunodeficiency with hypopigmentation or albinism; for example, Chediak-Higashi syndrome, Griscelli syndrome type two
• Familial hemophagocytic lymphohistiocytosis; for example, perforin deficiency, MUNC13D deficiency, syntaxin 11 deficiency
• X-linked lymphoproliferative syndrome
Phagocytes are the cells that engulf and ingest pathogens (phagocytosis), and destroy them with chemicals. Monocytes/macrophages as well as granulocytes are capable of this process. In certain conditions, either the number of phagocytes is reduced or their functional capacity is impaired. Several rare conditions are due to defects in the innate immune system, which is a basic line of defense independent of the more advanced lymphocyte-related systems. Many of these conditions are associated with skin problems.
Rather than predisposing for infections, most of the autoinflammatory disorders lead to excessive inflammation. Many manifest themselves as periodic fever syndromes. They may involve various organs directly, as well as predisposing for long-term damage by leading to amyloid deposition.
The complement system is part of the innate as well as the adaptive immune system; it is a group of circulating proteins that can bind pathogens and form a membrane attack complex. Complement deficiencies are the result of a lack of any of these proteins. They may predispose to infections but also to autoimmune conditions.
Treatment
The treatment of primary immunodeficiencies depends foremost on the nature of the abnormality. This may range from immunoglobulin replacement therapy in antibody deficiencies—in the form of intravenous immunoglobulin (IVIG) or subcutaneous immunoglobulin (SCIG)—to hematopoietic stem cell transplantation for SCID and other severe immunodeficiences. SCID can now be treated with a bone marrow transplant. Reduction of exposure to pathogens may be recommended, and in many situations prophylactic antibiotics may be advised. | textbooks/bio/Microbiology/Microbiology_(Boundless)/12%3A_Immunology_Applications/12.06%3A_Immunity_Disorders-_Immunodeficiencies/12.6A%3A_Primary_Immunodeficiency_Diseases.txt |
Secondary immunodeficiencies refer to acquired immune system disorders.
Learning Objectives
• Define immunodeficiency and list the types that occur
Key Points
• A deficit in the immune system can lead to unusually severe or uncommon recurrent infections.
• Secondary immune deficiencies or acquired deficiencies, more frequent than primary immune deficiencies, are problems of the immune system that are not genetic and which are caused by external factors.
• Secondary immunodeficiency disorders can occur in, for example, malnutrition, aging, many types of cancer (such as leukemia, lymphoma, multiple myeloma), and certain chronic infections such as acquired immunodeficiency syndrome (AIDS).
• Immunosuppression is one form of secondary immunodeficiency performed to prevent the body from rejecting an organ transplant, treating graft-versus-host disease after a bone marrow transplant, or for the treatment of auto-immune diseases, such as rheumatoid arthritis or Crohn’s disease.
• A person who is undergoing immunosuppression or whose immune system is weak for other reasons (for example, chemotherapy, HIV, and Lupus), is said to be immunocompromised.
Key Terms
• immunodeficiency: A depletion in the body’s natural immune system, or in some component of it.
• immunocompromised: Having an immune system that has been impaired by disease or treatment.
• immunosuppressive: Having the capability to suppress the immune system, capable of immunosuppression.
• secondary infection: any infection that arises subsequent to a pre-existing infection; but especially a nosocomial infection
Immunodeficiency (or immune deficiency) is a state in which the immune system’s ability to fight infectious disease is compromised or entirely absent. Immunodeficiency may also decrease cancer immunosurveillance. Most cases of immunodeficiency are acquired (“secondary”) but some people are born with defects in their immune system, or primary immunodeficiency. Transplant patients take medications to suppress their immune system as an anti-rejection measure, as do some patients suffering from an over-active immune system. A person who has an immunodeficiency of any kind is said to be immunocompromised. An immunocompromised person may be particularly vulnerable to opportunistic infections, in addition to normal infections that could affect everyone. Distinction between primary versus secondary immunodeficiencies are based on, respectively, whether the cause originates in the immune system itself or is, in turn, due to insufficiency of a supporting component of it or an external decreasing factor of it.
Primary Immunodeficiency (PID)
A number of rare diseases feature a heightened susceptibility to infections from childhood onward. Primary Immunodeficiency is also known as “congenital immunodeficiencies. ” Many of these disorders are hereditary and are autosomal recessive or X-linked. There are over 80 recognized primary immunodeficiency syndromes; they are generally grouped by the part of the immune system that is malfunctioning, such as lymphocytes or granulocytes. The treatment of primary immunodeficiencies depends on the nature of the defect and may involve antibody infusions, long-term antibiotics, and (in some cases) stem cell transplantation.
Secondary Immunodeficiencies
Secondary immunodeficiencies, also known as acquired immunodeficiencies, can result from various immunosuppressive agents, for example, malnutrition, aging and particular medications (e.g., chemotherapy, disease-modifying antirheumatic drugs, immunosuppressive drugs after organ transplants, glucocorticoids). For medications, the term immunosuppression generally refers to both beneficial and potential adverse effects of decreasing the function of the immune system, while the term immunodeficiency generally refers solely to the adverse effect of increased risk for infection. Many specific diseases directly or indirectly cause immunosuppression. This includes many types of cancer, particularly those of the bone marrow and blood cells (leukemia, lymphoma, multiple myeloma), and certain chronic infections. Immunodeficiency is also the hallmark of acquired immunodeficiency syndrome (AIDS), caused by the human immunodeficiency virus (HIV). HIV directly infects a small number of T helper cells and also impairs other immune system responses indirectly. | textbooks/bio/Microbiology/Microbiology_(Boundless)/12%3A_Immunology_Applications/12.06%3A_Immunity_Disorders-_Immunodeficiencies/12.6B%3A_Secondary_Immunodeficiency_Diseases.txt |
Cancer immunotherapy is the use of the body’s own immune system to reject cancer.
Learning Objectives
• Describe the use of immunotherapy in cancer treatment
Key Points
• Cancer immunotherapy can involve immunization of the patient with a cancer vaccine, administration of therapeutic antibodies as drugs, or cell-based immunotherapy.
• Vaccines can be raised against antigens that are inappropriate either for the cell type or for its environment.
• Adoptive cell-based immunotherapy involves isolating either allogenic or autologous immune cells, enriching them outside the body, and transfusing them back into the patient.
• Monoclonal antibodies can be raised against unusual antigens that are presented on the surfaces of tumors.
Key Terms
• immunotherapy: the treatment of cancer by improving the ability of the host to reject a tumor immunologically
• allogenic: genetically distinct, but of the same species
• autologous: derived from part of the same individual (i.e., from the recipient rather than the donor)
Cancer immunotherapy is the use of the body’s own immune system to reject cancer. The main idea is stimulating the patient’s immune system to attack the malignant tumor cells that are responsible for the disease. This can be either through immunization of the patient (e.g., by administering a cancer vaccine such as Dendreon’s Provenge), in which case the patient’s own immune system is trained to recognize tumor cells as targets to be destroyed, or through the administration of therapeutic antibodies as drugs, in which case the patient’s immune system is recruited to destroy tumor cells by the therapeutic antibodies. Cell-based immunotherapy is another major entity of cancer immunotherapy. This involves immune cells such as the natural killer cells (NK cells), lymphokine-activated killer cells (LAK cells), cytotoxic T lymphocytes (CTLs), and dendritic cells (DC). These immune cells are either activated in vivo by administering certain cytokines such as interleukins, or they are isolated, enriched, and transfused back into the patient to fight against cancer.
Since the immune system responds to the environmental factors it encounters on the basis of discrimination between self and non-self, many kinds of tumor cells that arise as a result of the onset of cancer are more or less tolerated by the patient’s own immune system since the tumor cells are essentially the patient’s own cells that are growing, dividing, and spreading without proper regulatory control. In spite of this fact, however, many kinds of tumor cells display unusual antigens that are inappropriate for either the cell type or its environment or that are only normally present during the organism ‘s development (e.g. fetal antigens). Examples of such antigens include the glycosphingolipid GD2, a disialoganglioside that is normally only expressed at a significant level on the outer surface membranes of neuronal cells, where its exposure to the immune system is limited by the blood-brain barrier.
GD2 is expressed on the surfaces of a wide range of tumor cells, including neuroblastomas, medulloblastomas, astrocytomas, melanomas, small-cell lung cancer, osteosarcomas, and other soft tissue sarcomas. GD2 is thus a convenient tumor-specific target for immunotherapies.
Adoptive cell-based immunotherapy involves isolating either allogenic or autologous immune cells, enriching them outside the body, and transfusing them back to the patient. The injected immune cells are highly cytotoxic to the cancer cells and so help to fight them.
Antibodies are a key component of the adaptive immune response. They play a central role in both the recognition of foreign antigens and the stimulation of an immune response to them. It is not surprising, therefore, that many immunotherapeutic approaches involve the use of antibodies. The advent of monoclonal antibody technology has made it possible to raise antibodies against specific antigens, such as the unusual antigens that are presented on the surfaces of tumors. A number of therapeutic monoclonal antibodies have been approved for use in humans, such as alemtuzumab, an anti-CD52 humanized IgG1 monoclonal antibody indicated for the treatment of chronic lymphocytic leukemia (CLL). Radioimmunotherapy in turn involves the use of radioactively conjugated murine antibodies against cellular antigens, mostly for treatment of lymphomas.
The development and testing of second-generation immunotherapies is already under way. While antibodies targeted to disease-causing antigens can be effective under certain circumstances, in many cases their efficacy may be limited by other factors. In the case of cancer tumors, the microenvironment is immunosuppressive, allowing even those tumors that present unusual antigens to survive and flourish in spite of the immune response generated by the cancer patient against his own tumor tissue. Certain members of a group of molecules known as cytokines, such as interleukin-2, also play a key role in modulating the immune response. Cytokines have been tested in conjunction with antibodies in order to generate an even more devastating immune response against the tumor. While the therapeutic administration of such cytokines may cause systemic inflammation, resulting in serious side effects and toxicity, there is a new generation of chimeric molecules consisting of an immune-stimulatory cytokine attached to an antibody that targets a tumor. These chimeric molecules are able to generate a very effective yet localized immune response against the tumor tissue, destroying the cancer-causing cells without the unwanted side effects.
Dermatologists use new creams and injections in the management of benign and malignant skin tumors. Topical immunotherapy utilizes an immune enhancement cream (imiquimod), which is an interferon producer, causing the patient’s own killer T cells to destroy warts, actinic keratoses, basal cell carcinoma, squamous cell carcinoma, cutaneous T cell lymphoma, and superficial spreading melanoma. Injection immunotherapy uses mumps, candida, or trichophytin antigen injections to treat warts (HPV-induced tumors).
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An antimicrobial is an agent that kills microorganisms or stops their growth. Antimicrobial medicines can be grouped according to the microorganisms they act primarily against. For example, antibiotics are used against bacteria and antifungals are used against fungi
Thumbnail: Staphylococcus aureus - Antibiotics Test plate. (Public Domain; CDC / Provider: Don Stalons).
13: Antimicrobial Drugs
The era of antimicrobials begins when Pasteur and Joubert discover that one type of bacteria could prevent the growth of another.
Learning Objectives
• Recall the technical defintion of antibiotics
Key Points
• Antibiotics are only those substances that are produced by one microorganism that kill, or prevent the growth, of another microorganism.
• In today’s common usage, the term antibiotic is used to refer to almost any drug that attempts to rid your body of a bacterial infection.
• The discovery of antimicrobials like penicillin and tetracycline paved the way for better health for millions around the world.
Key Terms
• antimicrobial: An agent that destroys microbes, inhibits their growth, or prevents or counteracts their pathogenic action.
• penicillin: Any of a group of broad-spectrum antibiotics obtained from Penicillium molds or synthesized; they have a beta-lactam structure; most are active against gram-positive bacteria and used in the treatment of various infections and diseases.
The history of antimicrobials begins with the observations of Pasteur and Koch, who discovered that one type of bacteria could prevent the growth of another. They did not know at that time that the reason one bacterium failed to grow was that the other bacterium was producing an antibiotic. Technically, antibiotics are only those substances that are produced by one microorganism that kill, or prevent the growth, of another microorganism.
The discovery of antimicrobials like penicillin by Alexander Fleming and tetracycline paved the way for better health for millions around the world. Before penicillin became a viable medical treatment in the early 1940s, no true cure for gonorrhea, strep throat, or pneumonia existed. Patients with infected wounds often had to have a wounded limb removed, or face death from infection. Now, most of these infections can be cured easily with a short course of antimicrobials.
The term antibiotic was first used in 1942 by Selman Waksman and his collaborators in journal articles to describe any substance produced by a microorganism that is antagonistic to the growth of other microorganisms in high dilution. This definition excluded substances that kill bacteria, but are not produced by microorganisms (such as gastric juices and hydrogen peroxide). It also excluded synthetic antibacterial compounds such as the sulfonamides. Many antibacterial compounds are relatively small molecules with a molecular weight of less than 2000 atomic mass units. With advances in medicinal chemistry, most of today’s antibacterials chemically are semisynthetic modifications of various natural compounds.
13.1B: Antibiotic Discovery
Observations of antibiosis between micro-organisms led to the discovery of natural antibacterials produced by microorganisms.
Learning Objectives
• Describe the concept of ‘antibiosis’ and the contributions of the different scientists who discovered it
Key Points
• Before the early 20th century, treatments for infections were based primarily on medicinal folklore.
• Louis Pasteur observed, “if we could intervene in the antagonism observed between some bacteria, it would offer perhaps the greatest hopes for therapeutics”.
• The term ‘antibiosis’, meaning “against life,” was introduced by the French bacteriologist Vuillemin as a descriptive name of the phenomenon exhibited by these early antibacterial drugs.
Key Terms
• micro-organism: A microorganism (from the Greek: μ, mikrós, “small” and ὀ, organismós, “organism”; also spelled micro-organism, micro organism or microörganism) or microbe is a microscopic organism that comprises either a single cell (unicellular), cell clusters, or multicellular relatively complex organisms.
• chemotherapy: Any chemical treatment intended to be therapeutic with respect to a disease state.
• infection: An uncontrolled growth of harmful microorganisms in a host.
Before the early 20th century, treatments for infections were based primarily on medicinal folklore. Mixtures with antimicrobial properties that were used in treatments of infections were described over 2000 years ago. Many ancient cultures, including the ancient Egyptians and ancient Greeks, used specially selected mold and plant materials and extracts to treat infections. More recent observations made in the laboratory of antibiosis between micro- organisms led to the discovery of natural antibacterials produced by microorganisms.
Louis Pasteur observed, “if we could intervene in the antagonism observed between some bacteria, it would offer perhaps the greatest hopes for therapeutics”. The term ‘antibiosis’, meaning “against life,” was introduced by the French bacteriologist Vuillemin as a descriptive name of the phenomenon exhibited by these early antibacterial drugs. Antibiosis was first described in 1877 in bacteria when Louis Pasteur and Robert Koch observed that an airborne bacillus could inhibit the growth of Bacillus anthracis. These drugs were later renamed antibiotics by Selman Waksman, an American microbiologist, in 1942.
John Tyndall first described antagonistic activities by fungi against bacteria in England in 1875. Synthetic antibiotic chemotherapy as a science and development of antibacterials began in Germany with Paul Ehrlich in the late 1880s. Ehrlich noted certain dyes would color human, animal, or bacterial cells, while others did not. He then proposed the idea that it might be possible to create chemicals that would act as a selective drug that would bind to and kill bacteria without harming the human host. After screening hundreds of dyes against various organisms, he discovered a medicinally useful drug, the synthetic antibacterial Salvarsan now called arsphenamine. In 1895, Vincenzo Tiberio, physician of the University of Naples discovered that a mold (Penicillium) in a water well has an antibacterial action. After this initial chemotherapeutic compound proved effective, others pursued similar lines of inquiry, but it was not until in 1928 that Alexander Fleming observed antibiosis against bacteria by a fungus of the genus Penicillium. Fleming postulated the effect was mediated by an antibacterial compound named penicillin, and that its antibacterial properties could be exploited for chemotherapy. He initially characterized some of its biological properties, but he did not pursue its further development. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.01%3A_Overview_of_Antimicrobial_Therapy/13.1A%3A_Origins_of_Antimicrobial_Drugs.txt |
Antibiotics are able to selectively target specific types of bacteria without harming the infected host.
Learning Objectives
• Describe selective toxicity
Key Points
• Their mechanism of action, chemical structure, or spectrum of activity are ways in which antibiotics are classified.
• Broad spectrum antibiotics affect a wide range of bacteria, while narrow spectrum antibiotics are able to target specific types.
• Antibiotics must go through a screening process, where they are isolated, cultured, and then tested for production of diffusible products that inhibit the growth of specific test organisms.
• Due to potential adverse side effects, antibiotics must also be tested for their selective toxicities.
Key Terms
• antibacterial: A drug having the effect of killing or inhibiting bacteria.
• bactericidal: An agent that kills bacteria.
• bacteriostatic: A drug that prevents bacterial growth and reproduction but does not necessarily kill them. When it is removed from the environment the bacteria start growing again.
Selective Toxicity in Antibiotics
Synthetic antibiotic chemotherapy as a science and development of antibacterials began in Germany with Paul Ehrlich in the late 1880s. Ehrlich noted that certain dyes would color human, animal, or bacterial cells, while others did not. He then proposed the idea that it might be possible to create chemicals that would act as a selective drug that would bind to and kill bacteria without harming the human host. After screening hundreds of dyes against various organisms, he discovered a medicinally useful drug, the synthetic antibacterial Salvarsan now called arsphenamine.
Antibiotics are commonly classified based on their mechanism of action, chemical structure, or spectrum of activity. More specifically, narrow spectrum antibiotics target specific types of bacteria, such as Gram-negative or Gram-positive bacteria, whereas broad spectrum antibiotics affect a wide range of bacteria. Following a 40-year hiatus in discovering new classes of antibacterial compounds, three new classes of antibacterial antibiotics have been brought into clinical use: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), and oxazolidinones (such as linezolid).
Some antibacterials have been associated with a range of adverse effects. Side-effects range from mild to very serious depending on the antibiotics used, the microbial organisms targeted, and the individual patient. Safety profiles of newer drugs are often not as well established as for those that have a long history of use. Adverse effects range from fever and nausea to major allergic reactions, including photodermatitis and anaphylaxis. Common side-effects include diarrhea, resulting from disruption of the species composition in the intestinal flora, resulting, for example, in overgrowth of pathogenic bacteria, such as Clostridium difficile. Antibacterials can also affect the vaginal flora, and may lead to overgrowth of yeast species of the genus Candida in the vulvo-vaginal area. Additional side-effects can result from interaction with other drugs, such as elevated risk of tendon damage from administration of a quinolone antibiotic with a systemic corticosteroid.
Antibacterial Production
Despite the wide variety of known antibiotics, less than 1% of antimicrobial agents have medical or commercial value. For example, whereas penicillin has a high therapeutic index as it does not generally affect human cells, this is not so for many antibiotics. Other antibiotics simply lack advantage over those already in use, or have no other practical applications. Useful antibiotics are often discovered using a screening process. To conduct such a screen, isolates of many different microorganisms are cultured and then tested for production of diffusible products that inhibit the growth of test organisms. Most antibiotics identified in such a screen are already known and must therefore be disregarded. The remainder must be tested for their selective toxicities and therapeutic activities, and the best candidates can be examined and possibly modified. A more modern version of this approach is a rational design program. This involves screening directed towards finding new natural products that inhibit a specific target, such as an enzyme only found in the target pathogen, rather than tests to show general inhibition of a culture.
13.1D: Spectrum of Antimicrobial Activity
An antibiotic’s spectrum can be broad or narrow.
Learning Objectives
• Compare narrow and broad spectrum antibiotics
Key Points
• Broad spectrum antibiotics act against a larger group of bacteria.
• Narrow spectrum antibiotis target specific bacteria such as Gram positive or Gram negative.
• Three new classes of antibacterial antibiotics have been brought into clinical use: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), and oxazolidinones (such as linezolid).
Key Terms
• Gram stain: A method of differentiating bacterial species into two large groups (Gram-positive and Gram-negative).
• narrow spectrum antibiotic: A type of antibiotic that targets specific types of Gram positive or Gram negative bacteria.
• broad spectrum antibiotic: A type of antibiotic that can affect a wide range of bacteria.
The range of bacteria that an antibiotic affects can be divided into narrow spectrum and broad spectrum. Narrow spectrum antibiotics act against a limited group of bacteria, either gram positive or gram negative, for example sodium fusidate only acts against staphylococcal bacteria. Broad spectrum—antibiotics act against gram positive and gram negative bacteria, for example amoxicillin.
Gram staining (or Gram’s method; is a method of differentiating bacterial species into two large groups (Gram-positive and Gram-negative ). It is based on the chemical and physical properties of their cell walls. Primarily, it detects peptidoglycan, which is present in a thick layer in Gram positive bacteria. A Gram positive results in a purple/blue color while a Gram negative results in a pink/red color. The Gram stain is almost always the first step in the identification of a bacterial organism, and is the default stain performed by laboratories over a sample when no specific culture is referred. While Gram staining is a valuable diagnostic tool in both clinical and research settings, not all bacteria can be definitively classified by this technique, thus forming Gram-variable and Gram-indeterminate groups as well.
A broad spectrum antibiotic acts against both Gram-positive and Gram-negative bacteria, in contrast to a narrow spectrum antibiotic, which is effective against specific families of bacteria. An example of a commonly used broad-spectrum antibiotic is ampicillin. Broad spectrum antibiotics are properly used in the following medical situations: empirically (i.e., based on the experience of the practitioner), prior to the formal identification of the causative bacteria and when there is a wide range of possible illnesses and a potentially serious illness would result if treatment is delayed. This occurs, for example, in meningitis, where the patient can become fatally ill within hours if broad-spectrum antibiotics are not initiated. Broad spectrum antibiotics are also used for drug resistant bacteria that do not respond to other, more narrow spectrum antibiotics and in the case of superinfections, where there are multiple types of bacteria causing illness, thus warranting either a broad-spectrum antibiotic or combination antibiotic therapy.
Following a 40-year hiatus in discovering new classes of antibacterial compounds, three new classes of antibacterial antibiotics have been brought into clinical use: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), and oxazolidinones (such as linezolid). | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.01%3A_Overview_of_Antimicrobial_Therapy/13.1C%3A_Antibiotics_and_Selective_Toxicity.txt |
Learning Objectives
Compare the two classes of antibiotics: bactericidal and bacteriostatic antibiotic
Antibiotics can be divided into two classes based on their mechanism of action. Bactericidal antibiotics kill bacteria; bacteriostatic antibiotics inhibit their growth or reproduction.
One way that bactericidal antibodies kill bacteria is by inhibiting cell wall synthesis. Examples include the Beta-lactam antibiotics (penicillin derivatives (penams) ), cephalosporins (cephems), monobactams, and carbapenems) and vancomycin. Other ways that bactericidal antibiotics kill bacteria include inhibiting bacterial enzymes or protein translation. Other batericidal agents include daptomycin, fluoroquinolones, metronidazole, nitrofurantoin, co-trimoxazole and telithromycin. Aminoglycosidic antibiotics are usually considered bactericidal, although they may be bacteriostatic with some organisms. The MBC (minimum bactericidal concentration) is the minimum concentration of drug which can kill 99.99% of the population.
Bacteriostatic antibiotics limit the growth of bacteria by interfering with bacterial protein production, DNA replication, or other aspects of bacterial cellular metabolism. This group includes: tetracyclines, sulfonamides, spectinomycin, trimethoprim, chloramphenicol, macrolides and lincosamides. They must work together with the immune system to remove the microorganisms from the body. However, there is not always a precise distinction between them and bactericidal antibiotics. High concentrations of some bacteriostatic agents are also bactericidal. The MIC (minimum inhibitory concentration) is the minimum concentration of drug which can inhibit the growth of the microorganism.
Further categorization is based on their target specificity. “Narrow-spectrum” antibacterial antibiotics target specific types of bacteria, such as Gram-negative or Gram-positive bacteria, whereas broad-spectrum antibiotics affect a wide range of bacteria, usually both gram positive and gram negative cells. Following a 40-year hiatus in discovering new classes of antibacterial compounds, three new classes of antibacterial antibiotics have been brought into clinical use: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), and oxazolidinones (such as linezolid).
Key Points
• Bactericidal antibodies inhibit cell wall synthesis.
• Bacteriostatic antibiotics limit the growth of bacteria by interfering with bacterial protein production, DNA replication, or other aspects of bacterial cellular metabolism.
• Bacteriostatic antibiotics must work together with the immune system to remove the microorganisms from the body.
Key Terms
• bactericidal: An agent that kills bacteria.
• bacteriostatic: A drug that prevents bacterial growth and reproduction but does not necessarily kill them. When it is removed from the environment the bacteria start growing again.
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β-Lactam (beta-lactam) and glycopeptide antibiotics work by inhibiting or interfering with cell wall synthesis of the target bacteria.
Learning Objectives
• Describe the two types of antimicrobial drugs that inhibit cell wall synthesis: beta-lactam and glycopeptide antibiotics
Key Points
• The peptidoglycan layer is important for cell wall structural integrity, being the outermost and primary component of the wall.
• β-Lactam antibiotics are a broad class of antibiotics that includes penicillin derivatives (penams), cephalosporins (cephems), monobactams, and carbapenems.
• β-Lactam antibiotics are bacteriocidal and act by inhibiting the synthesis of the peptidoglycan layer of bacterial cell walls.
• Glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin.
• Glycopeptide antibiotics inhibit the synthesis of cell walls in susceptible microbes by inhibiting peptidoglycan synthesis.
Key Terms
• beta-lactam antibiotic: A broad class of antibiotics that inhibit cell wall synthesis, consisting of all antibiotic agents that contains a β-lactam nucleus in their molecular structures. This includes penicillin derivatives (penams), cephalosporins (cephems), monobactams, and carbapenems.
• Glycopeptide antibiotic: Glycopeptide antibiotics are composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin. This class of drugs inhibit the synthesis of cell walls in susceptible microbes by inhibiting peptidoglycan synthesis.
• peptidoglycan: A polymer of glycan and peptides found in bacterial cell walls.
Two types of antimicrobial drugs work by inhibiting or interfering with cell wall synthesis of the target bacteria. Antibiotics commonly target bacterial cell wall formation (of which peptidoglycan is an important component) because animal cells do not have cell walls. The peptidoglycan layer is important for cell wall structural integrity, being the outermost and primary component of the wall.
The first class of antimicrobial drugs that interfere with cell wall synthesis are the β-Lactam antibiotics (beta-lactam antibiotics), consisting of all antibiotic agents that contains a β-lactam nucleus in their molecular structures. This includes penicillin derivatives (penams), cephalosporins (cephems), monobactams, and carbapenems. β-Lactam antibiotics are bacteriocidal and act by inhibiting the synthesis of the peptidoglycan layer of bacterial cell walls. The final step in the synthesis of the peptidoglycan is facilitated by penicillin-binding proteins (PBPs). PBPs vary in their affinity for binding penicillin or other β-lactam antibiotics.
Bacteria often develop resistance to β-lactam antibiotics by synthesizing a β-lactamase, an enzyme that attacks the β-lactam ring. To overcome this resistance, β-lactam antibiotics are often given with β-lactamase inhibitors such as clavulanic acid.
The second class of antimicrobial drugs that interfere with cell wall synthesis are the glycopeptide antibiotics, which are composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin. This class of drugs inhibit the synthesis of cell walls in susceptible microbes by inhibiting peptidoglycan synthesis. They bind to the amino acids within the cell wall preventing the addition of new units to the peptidoglycan.
13.2B: Injuring the Plasma Membrane
Several types of antimicrobial drugs function by disrupting or injuring the plasma membrane.
Learning Objectives
• Discuss the function of the plasma membrane and how antimicrobial drugs target it
Key Points
• The plasma membrane or cell membrane is a biological membrane that separates the interior of all cells from the outside environment.
• Plasma membranes are involved in a variety of cellular processes such as cell adhesion, ion conductivity, and cell signaling. They serve as the attachment surface for several extracellular structures, including the cell wall, glycocalyx, and intracellular cytoskeleton.
• Disrupting the plasma membrane causes rapid depolarization, resulting in a loss of membrane potential leading to inhibition of protein, DNA and RNA synthesis, which results in bacterial cell death.
Key Terms
• plasma membrane: The semipermeable membrane that surrounds the cytoplasm of a cell.
• cell wall: A thick, fairly rigid layer formed around individual cells of bacteria, Archaea, fungi, plants, and algae, the cell wall is external to the cell membrane and helps the cell maintain its shape and avoid damage.
• plasma cell: a form of lymphocyte that produces antibodies when reacted with a specific antigen; a plasmacyte
The plasma membrane or cell membrane is a biological membrane that separates the interior of all cells from the outside environment. The plasma membrane is selectively permeable to ions and organic molecules. It controls the movement of substances in and out of cells. The membrane basically protects the cell from outside forces. It consists of the lipid bilayer with embedded proteins. Plasma membranes are involved in a variety of cellular processes such as cell adhesion, ion conductivity, and cell signaling. It serves as the attachment surface for several extracellular structures, including the cell wall, glycocalyx, and intracellular cytoskeleton. Fungi, bacteria, and plants also have the cell wall which provides a mechanical support for the cell and precludes the passage of larger molecules. The plasma membrane also plays a role in anchoring the cytoskeleton to provide shape to the cell and in attaching to the extracellular matrix and other cells to help group cells together to form tissues.
There are several types of antimicrobial drugs that function by disrupting or injuring the plasma membrane. One example is daptomycin, a lipopeptide which has a distinct mechanism of action, disrupting multiple aspects of bacterial cell membrane function. It appears to bind to the membrane causes rapid depolarization, resulting in a loss of membrane potential leading to inhibition of protein, DNA and RNA synthesis, which results in bacterial cell death. Another example is polymyxins antibiotics which have a general structure consisting of a cyclic peptide with a long hydrophobic tail. They disrupt the structure of the bacterial cell membrane by interacting with its phospholipids.
13.2C: Inhibiting Nucleic Acid Synthesis
Antimicrobial drugs inhibit nucleic acid synthesis through differences in prokaryotic and eukaryotic enzymes.
Learning Objectives
• State the steps where inhibitors of nucleic acid synthesis can exert their function
Key Points
• Some antimicrobial drugs interfere with the initiation, elongation or termination of RNA transcription.
• Some antimicrobial drugs interfere with various aspects of DNA replication.
• The antimicrobial actions of these drugs are a result of differences in the prokaryotic and eukaryotic enzymes involved in nucleic acid synthesis.
Key Terms
• transcription: The synthesis of RNA under the direction of DNA.
• replication: Process by which an object, person, place or idea may be copied mimicked or reproduced.
Antimicrobial drugs can target nucleic acid (either RNA or DNA) synthesis. The antimicrobial actions of these agents are a result of differences in prokaryotic and eukaryotic enzymes involved in nucleic acid synthesis.
Prokaryotic transcription is the process in which messenger RNA transcripts of genetic material are produced for later translation into proteins. The transcription process includes the following steps: initiation, elongation and termination. Antimicrobial drugs have been developed to target each of these steps. For example, the antimicrobial rifampin binds to DNA-dependent RNA polymerase, thereby inhibiting the initiation of RNA transcription.
Other antimicrobial drugs interfere with DNA replication, the biological process that occurs in all living organisms and copies their DNA and is the basis for biological inheritance. The process starts when one double-stranded DNA molecule produces two identical copies of the molecule. In a cell, DNA replication begins at specific locations in the genome, called “origins. ” Uncoiling of DNA at the origin, and synthesis of new strands, forms a replication fork. In addition to DNA polymerase, the enzyme that synthesizes the new DNA by adding nucleotides matched to the template strand, a number of other proteins are associated with the fork and assist in the initiation and continuation of DNA synthesis. DNA replication, like all biological polymerization processes, proceeds in three enzymatically catalyzed and coordinated steps: initiation, elongation and termination. Any of the steps in the process of DNA replication can be targeted by antimicrobial drugs. For instance, quinolones inhibit DNA synthesis by interfering with the coiling of DNA strands. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.02%3A_Functions_of_Antimicrobial_Drugs/13.2A%3A_Inhibiting_Cell_Wall_Synthesis.txt |
Protein synthesis inhibitors are substances that disrupt the processes that lead directly to the generation of new proteins in cells.
Learning Objectives
• Paraphrase the general mechanism of action of protein synthesis inhibitors
Key Points
• Protein synthesis inhibitors usually act at the ribosome level, taking advantage of the major differences between prokaryotic and eukaryotic ribosome structures.
• Protein synthesis inhibitors work at different stages of prokaryotic mRNA translation into proteins like initiation, elongation (including aminoacyl tRNA entry, proofreading, peptidyl transfer, and ribosomal translocation), and termination.
• By targeting different stages of the mRNA translation, antimicrobial drugs can be changed if resistance develops.
Key Terms
• translation: A process occurring in the ribosome, in which a strand of messenger RNA (mRNA) guides assembly of a sequence of amino acids to make a protein.
A protein synthesis inhibitor is a substance that stops or slows the growth or proliferation of cells by disrupting the processes that lead directly to the generation of new proteins. It usually refers to substances, such as antimicrobial drugs, that act at the ribosome level. The substances take advantage of the major differences between prokaryotic and eukaryotic ribosome structures which differ in their size, sequence, structure, and the ratio of protein to RNA. The differences in structure allow some antibiotics to kill bacteria by inhibiting their ribosomes, while leaving human ribosomes unaffected.
Translation in prokaryotes involves the assembly of the components of the translation system which are: the two ribosomal subunits (the large 50S & small 30S subunits), the mRNA to be translated, the first aminoacyl tRNA, GTP (as a source of energy), and three initiation factors that help the assembly of the initiation complex. The ribosome has three sites: the A site, the P site, and the E site (not shown in ). The A site is the point of entry for the aminoacyl tRNA. The P site is where the peptidyl tRNA is formed in the ribosome. The E site which is the exit site of the now uncharged tRNA after it gives its amino acid to the growing peptide chain.
In general, protein synthesis inhibitors work at different stages of prokaryotic mRNA translation into proteins like initiation, elongation (including aminoacyl tRNA entry, proofreading, peptidyl transfer, and ribosomal translocation), and termination. The following is a list of common antibacterial drugs and the stages which they target.
• Linezolid acts at the initiation stage, probably by preventing the formation of the initiation complex, although the mechanism is not fully understood.
• Tetracyclines and Tigecycline (a glycylcycline related to tetracyclines) block the A site on the ribosome, preventing the binding of aminoacyl tRNAs.
• Aminoglycosides, among other potential mechanisms of action, interfere with the proofreading process, causing an increased rate of error in synthesis with premature termination.
• Chloramphenicol blocks the peptidyl transfer step of elongation on the 50S ribosomal subunit in both bacteria and mitochondria.
• Macrolides, clindamycin, and aminoglycosides have evidence of inhibition of ribosomal translocation.
• Streptogramins also cause premature release of the peptide chain.
By targeting different stages of the mRNA translation, antimicrobial drugs can be changed if resistance develops to one or many of the drugs. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.02%3A_Functions_of_Antimicrobial_Drugs/13.2D%3A_Inhibiting_Protein_Synthesis.txt |
An antimetabolite is a chemical that inhibits the use of a metabolite, a chemical that is part of normal metabolism.
Learning Objectives
• Distinguish between the three main types of antimetabolite antibiotics (antifolates, pyrimidine and purine analogues)
Key Points
• The presence of antimetabolites can have toxic effects on cells, such as halting cell growth or cell division.
• Antimetabolites are also used as antibiotics.
• The three main types of antimetabolite antibiotics are antifolates, pyrimidine analogues and purine analogues.
Key Terms
• antimetabolite: Any substance that competes with or inhibits the normal metabolic process, often by acting as an analogue of an essential metabolite
An antimetabolite is a chemical that inhibits the use of a metabolite, a chemical that is part of normal metabolism. Such substances are often similar in structure to the metabolite that they interfere with, such as antifolates that interfere with the use of folic acid. The presence of antimetabolites can have toxic effects on cells, such as halting cell growth or cell division.
Antimetabolites are also used as antibiotics. There are three main types of antimetabolite antibiotics. The first, antifolates impair the function of folic acid leading to disruption in the production of DNA and RNA. For example, methotrexate is a folic acid analogue, and owing to structural similarity with folic acid, methotrexate binds and inhibits the enzyme dihydrofolate reductase, and thus prevents the formation of tetrahydrofolate. Because tetrahydrofolate is essential for purine and pyrimidine synthesis, its deficiency can lead to inhibited production of DNA, RNA and proteins.
The second type of antimetabolite antibiotics consist of pyrimidine analogues which mimic the structure of metabolic pyrimidines. Three nucleobases found in nucleic acids, cytosine (C), thymine (T), and uracil (U), are pyrimidine derivatives and the pyrimidine analogues disrupt their formation and consequently disrupt DNA and RNA synthesis.
The purine analogues are the third type of antimetabolite antibiotics and they mimic the structure of metabolic purines. Two of the four bases in nucleic acids, adenine and guanine, are purines. Purine analogues disrupt nucleic acid production. For example, azathioprine is the main immunosuppressive cytotoxic substance that is widely used in transplants to control rejection reactions by inhibiting DNA synthesis in lymphocytes.
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• Pyrimidine chemical structure. Provided by: Wikipedia. Located at: en.Wikipedia.org/wiki/File:Pyrimidine_chemical_structure.png. License: CC BY-SA: Attribution-ShareAlike | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.02%3A_Functions_of_Antimicrobial_Drugs/13.2E%3A_Inhibiting_Essential_Metabolite_Synthesis.txt |
An antimicrobial is a substance that kills or inhibits the growth of microorganisms such as bacteria, fungi, or protozoans.
Learning Objectives
• Recall the synthetic antimicrobial drugs that are sulfonamide and sulphonamide based
Key Points
• The discovery of antimicrobials like penicillin and tetracycline paved the way for better health for millions around the world.
• With the development of antimicrobials, microorganisms have adapted and become resistant to previous antimicrobial agents.
• Synthetic agents include: sulphonamides, cotrimoxazole, quinolones, anti-virals, anti-fungals, anti-cancer drugs, anti-malarials, anti-tuberculosis drugs, anti-leprotics, and anti-protozoals.
Key Terms
• antimicrobial: An agent that destroys microbes, inhibits their growth, or prevents or counteracts their pathogenic action.
• microorganism: An organism that is too small to be seen by the unaided eye, especially a single-celled organism, such as a bacterium.
• bacteria: A type, species, or strain of bacterium.
An antimicrobial is a substance that kills or inhibits the growth of microorganisms such as bacteria, fungi, or protozoans. Antimicrobial drugs either kill microbes (microbiocidal) or prevent the growth of microbes (microbiostatic). Disinfectants are antimicrobial substances used on non-living objects or outside the body.
The history of antimicrobials begins with the observations of Pasteur and Joubert, who discovered that one type of bacteria could prevent the growth of another. They did not know at that time that the reason one bacterium failed to grow was that the other bacterium was producing an antibiotic. Technically, antibiotics are only those substances that are produced by one microorganism that kill, or prevent the growth, of another microorganism. Of course, in today’s common usage, the term antibiotic is used to refer to almost any drug that attempts to rid your body of a bacterial infection. Antimicrobials include not just antibiotics, but synthetically formed compounds as well.
The discovery of antimicrobials like penicillin and tetracycline paved the way for better health for millions around the world. Before penicillin became a viable medical treatment in the early 1940s, no true cure for gonorrhea, strep throat, or pneumonia existed. Patients with infected wounds often had to have a wounded limb removed, or face death from infection. Now, most of these infections can be cured easily with a short course of antimicrobials.
However, with the development of antimicrobials, microorganisms have adapted and become resistant to previous antimicrobial agents. The old antimicrobial technology was based either on poisons or heavy metals, which may not have killed the microbe completely, allowing the microbe to survive, change, and become resistant to the poisons and/or heavy metals.
Antimicrobial nanotechnology is a recent addition to the fight against disease-causing organisms, replacing heavy metals and toxins, and may some day be used as a viable alternative.
Infections that are acquired during a hospital visit are called “hospital acquired infections” or nosocomial infections. Similarly, when the infectious disease is picked up in the non-hospital setting, it is considered “community acquired”.
Synthetic agents include: sulphonamides, cotrimoxazole, quinolones, anti-virals, anti-fungals, anti-cancer drugs, anti-malarials, anti-tuberculosis drugs, anti-leprotics, and anti-protozoals.
Sulfonamide or sulphonamide is the basis of several groups of drugs. The original antibacterial sulfonamides (sometimes called sulfa drugs or sulpha drugs) are synthetic antimicrobial agents that contain the sulfonamide group. Some sulfonamides are also devoid of antibacterial activity, e.g., the anticonvulsant sultiame. The sulfonylureas and thiazide diuretics are newer drug groups based on the antibacterial sulfonamides.
Sulfa allergies are common, and medications containing sulfonamides are prescribed carefully. It is important to make a distinction between sulfa drugs and other sulfur-containing drugs and additives, such as sulfates and sulfites, which are chemically unrelated to the sulfonamide group and do not cause the same hypersensitivity reactions seen in the sulfonamides.
In bacteria, antibacterial sulfonamides act as competitive inhibitors of the enzyme dihydropteroate synthetase (DHPS), an enzyme involved in folate synthesis. As such, the microorganism will be “starved” of folate and die.
The sulfonamide chemical moiety is also present in other medications that are not antimicrobials, including thiazide diuretics (including hydrochlorothiazide, metolazone, and indapamide, among others), loop diuretics (including furosemide, bumetanide, and torsemide), sulfonylureas (including glipizide, glyburide, among others), and some COX-2 inhibitors (e.g., celecoxib), and acetazolamide. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.03%3A_Commonly_Used_Antimicrobial_Drugs/13.3A%3A_Synthetic_Antimicrobial_Drugs.txt |
An antimicrobial is a substance that kills or inhibits the growth of microorganisms such as bacteria, fungi, or protozoans.
Learning Objectives
• Discuss the mechanism of action for protein synthesis inhibitors used as antimicrobial drugs, and recognize various naturally occuring antimicrobial drugs
Key Points
• There are mainly two classes of antimicrobial drugs: those obtained from natural sources (i.e. beta-lactam antibiotic (such as penicillins, cephalosporins) or protein synthesis inhibitors (such as aminoglycosides, macrolides, tetracyclines, chloramphenicol, polypeptides); and synthetic agents.
• A β-lactam (beta-lactam) ring is a four-membered lactam. A lactam is a cyclic amide. It is named as such because the nitrogen atom is attached to the β-carbon relative to the carbonyl.
• A protein synthesis inhibitor is a substance that stops or slows the growth or proliferation of cells by disrupting the processes that lead directly to the generation of new proteins.
Key Terms
• β-lactam: A β-lactam (beta-lactam) ring is a four-membered lactam. A lactam is a cyclic amide. It is named as such, because the nitrogen atom is attached to the β-carbon relative to the carbonyl. The simplest β-lactam possible is 2-azetidinone.
• antimicrobial: An agent that destroys microbes, inhibits their growth, or prevents or counteracts their pathogenic action.
• microorganism: An organism that is too small to be seen by the unaided eye, especially a single-celled organism, such as a bacterium.
An antimicrobial is a substance that kills or inhibits the growth of microorganisms bacteria, fungi, or protozoans. Antimicrobial drugs either kill microbes (microbiocidal) or prevent the growth of microbes (microbiostatic). Disinfectants are antimicrobial substances used on non-living objects or outside the body.
The discovery of antimicrobials, like penicillin and tetracycline, paved the way for better health for millions of people around the world. Before penicillin became a viable medical treatment in the early 1940’s, no true cure for gonorrhea, strep throat, or pneumonia existed. Patients with infected wounds often had to have a wounded limb removed or face death from infection. Now, most of these infections can be cured easily with a short course of antimicrobials.
However, with the development of antimicrobials, microorganisms have adapted and become resistant to previous antimicrobial agents. The old antimicrobial technology was based either on poisons or heavy metals, which may not have killed the microbe completely. This allowed the microbe to survive, change, and become resistant to the poisons and/or heavy metals.
Antimicrobial nanotechnology is a recent addition to the fight against disease causing organisms. It replaces heavy metals and toxins and may someday be a viable alternative.
Infections that are acquired during a hospital visit are called “hospital acquired infections” or nosocomial infections. Similarly, when the infectious disease is picked up in the non-hospital setting it is considered “community acquired. ”
There are mainly two classes of antimicrobial drugs: those obtained from natural sources (i.e. beta-lactam) antibiotic (such as penicillins, cephalosporins) or protein synthesis inhibitors (such as aminoglycosides, macrolides, tetracyclines, chloramphenicol, polypeptides); and synthetic agents.
A β-lactam (beta-lactam) ring is a four-membered lactam. A lactam is a cyclic amide. It is named as such, because the nitrogen atom is attached to the β-carbon relative to the carbonyl. The simplest β-lactam possible is 2-azetidinone.
A protein synthesis inhibitor is a substance that stops or slows the growth or proliferation of cells by disrupting the processes that lead directly to the generation of new proteins. While a broad interpretation of this definition could be used to describe nearly any antibiotic, in practice, it usually refers to substances that act at the ribosome level (either the ribosome itself or the translation factor), taking advantage of the major differences between prokaryotic and eukaryotic ribosome structures. Toxins such as ricin also function via protein synthesis inhibition. Ricin acts at the eukaryotic 60S.
In general, protein synthesis inhibitors work at different stages of prokaryotic mRNA translation into proteins, like initiation, elongation (including aminoacyl tRNA entry, proofreading, peptidyl transfer, and ribosomal translocation), and termination. Rifamycin inhibits prokaryotic DNA transcription into mRNA by inhibiting DNA-dependent RNA polymerase by binding its beta-subunit. Linezolid acts at the initiation stage probably by preventing the formation of the initiation complex, although the mechanism is not fully understood.
Tetracyclines and Tigecycline (a glycylcycline related to tetracyclines) block the A site on the ribosome, preventing the binding of aminoacyl tRNAs. Aminoglycosides, among other potential mechanisms of action, interfere with the proofreading process, causing increased rate of error in synthesis with premature termination. Chloramphenicol blocks the peptidyl transfer step of elongation on the 50S ribosomal subunit in both bacteria and mitochondria. Macrolides (as well as inhibiting ribosomal translocation and other potential mechanisms) bind to the 50s ribosomal subunits, inhibiting peptidyl transfer. Quinupristin/dalfopristin act synergistically, with dalfopristin, enhancing the binding of quinupristin as well as inhibiting peptidyl transfer. Quinupristin binds to a nearby site on the 50S ribosomal subunit and prevents elongation of the polypeptide. It also causes incomplete chains to be released. Macrolides, clindamycin, and aminoglycosides (with all these three having other potential mechanisms of action as well) have evidence of inhibition of ribosomal translocation. Fusidic acid prevents the turnover of elongation factor G (EF-G) from the ribosome. Macrolides and clindamycin (both also having other potential mechanisms) cause premature dissociation of the peptidyl-tRNA from the ribosome. Puromycin has a structure similar to that of the tyrosinyl aminoacyl-tRNA. Therefore, it binds to the ribosomal A site and participates in peptide bond formation, producing peptidyl-puromycin. However, it does not engage in translocation and quickly dissociates from the ribosome, causing a premature termination of polypeptide synthesis. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.03%3A_Commonly_Used_Antimicrobial_Drugs/13.3B%3A_Naturally_Occurring_Antimicrobial_Drugs-_Antibiotics.txt |
The β-lactam ring is part of the core structure of several antibiotic families.
Learning Objectives
• Recognize the classes of beta-lactams and their mechanisms of action
Key Points
• The principal antibiotic families of which the β-lactam ring is part of the core structure are the penicillins, cephalosporins, carbapenems, and monobactams, which are also called β-lactam antibiotics.
• A β-lactam (beta-lactam) ring is a four-membered lactam (cyclic amide). -Lactams are classified according to their core ring structures.
• The cephalosporins are a class of β-lactam antibiotics originally derived from the fungus Acremonium, which was previously known as “Cephalosporium”.
Key Terms
• cephalosporins: The cephalosporins are a class of β-lactam antibiotics originally derived from the fungus Acremonium, which was previously known as “Cephalosporium”.
• antibiotic: Any substance that can destroy or inhibit the growth of bacteria and similar microorganisms.
• β-lactam: A β-lactam (beta-lactam) ring is a four-membered lactam. A lactam is a cyclic amide. It is named as such, because the nitrogen atom is attached to the β-carbon relative to the carbonyl. The simplest β-lactam possible is 2-azetidinone.
• β-lactam: Any of a class of cyclic amides, that are the nitrogen analogs of lactones, formed by heating amino acids; the tautomeric enol forms are known as lactims.
A β-lactam (beta-lactam) ring, is a four-membered lactam. It is named as such, because the nitrogen atom is attached to the β-carbon relative to the carbonyl. The simplest β-lactam possible is 2-azetidinone.
The β-lactam ring is part of the core structure of several antibiotic families, the principal ones being the penicillins, cephalosporins, carbapenems, and monobactams, which are, therefore, also called β-lactam antibiotics. Nearly all of these antibiotics work by inhibiting bacterial cell wall biosynthesis. This has a lethal effect on bacteria. Bacteria do, however, contain within their populations, in smaller quantities, bacteria that are resistant against β-lactam antibiotics. They do this by expressing the β-lactamase gene. When bacterial populations have these resistant subgroups, treatment with β-lactam can result in the resistant strain becoming more prevalent and so, more virulent.
β-Lactams are classified according to their core ring structures:
• β-Lactams fused to saturated five-membered rings;
• β-Lactams containing thiazolidine rings are named penams;
• β-Lactams containing pyrrolidine rings are named carbapenams;
• β-Lactams fused to oxazolidine rings are named oxapenams or clavams;
• β-Lactams fused to unsaturated five-membered rings;
• β-Lactams containing 2,3-dihydrothiazole rings are named penems;
• β-Lactams containing 2,3-dihydro-1H-pyrrole rings are named carbapenems;
• β-Lactams fused to unsaturated, six-membered rings;
• β-Lactams containing 3,6-dihydro-2H-1,3-thiazine rings are named cephems;
• β-Lactams containing 1,2,3,4-tetrahydropyridine rings are named carbacephems;
• β-Lactams containing 3,6-dihydro-2H-1,3-oxazine rings are named oxacephems; and
• β-Lactams not fused to any other ring are named monobactams.
Penicillin (sometimes abbreviated PCN or pen) is a group of antibiotics derived from Penicillium fungi. They include penicillin G, procaine penicillin, benzathine penicillin, and penicillin V. Penicillin antibiotics are historically significant because they are the first drugs that were effective against many previously serious diseases, such as syphilis, and infections caused by staphylococci and streptococci. Penicillins are still widely used today, though many types of bacteria are now resistant. All penicillins are β-lactam antibiotics and are used in the treatment of bacterial infections caused by susceptible, usually Gram-positive, organisms.
The cephalosporins (sg. /ˌsɛfəlɵspɔrɨn/) are a class of β-lactam antibiotics originally derived from the fungus Acremonium, which was previously known as “Cephalosporium”. Together with cephamycins, they constitute a subgroup of β-lactam antibiotics called cephems. Cephalosporins are indicated for the prophylaxis and treatment of infections caused by bacteria susceptible to this particular form of antibiotic. First-generation cephalosporins are active predominantly against Gram-positive bacteria, and successive generations have increased activity against Gram-negative bacteria (albeit often with reduced activity against Gram-positive organisms). | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.03%3A_Commonly_Used_Antimicrobial_Drugs/13.3C%3A__Beta-Lactam_Antibiotics-_Penicillins_and_Cephalosporins.txt |
Most of the currently available antibiotics are produced by prokaryotes mainly by bacteria from the genus Streptomyces.
Learning Objectives
• Explain the role of Streptomyces and other prokaryotes in antibiotic production
Key Points
• Gramicidin is one of the first antibiotics to be manufactured commercially. It is a heterogeneous mixture of six antibiotic compounds, all of which are obtained from the soil bacterial species Bacillus brevis.
• Streptomyces is the largest antibiotic-producing genus, producing antibacterial, antifungal, and antiparasitic drugs, and also a wide range of other bioactive compounds, such as immunosuppressants. They produce over two-thirds of the clinically useful antibiotics of natural origin.
• Members of the Streptomyces genus are the source for numerous antibacterial pharmaceutical agents; among the most important of these are: Chloramphenicol (from S. venezuelae), Lincomycin (from S. lincolnensis), Neomycin (from S. fradiae), Tetracycline (from S. rimosus and S. aureofaciens).
• Some Pseudomonas spp. might produce compounds antagonistic to other soil microbes, such as phenazine-type antibiotics or hydrogen cyanide.
Key Terms
• antibiotic: Any substance that can destroy or inhibit the growth of bacteria and similar microorganisms.
• beta-lactamase: An enzyme produced by certain bacteria, responsible for their resistance to beta-lactam antibiotics such as penicillin.
Even though penicillin drugs, antibiotics produced by molds, were the first antibiotics successfully used to treat many serious infections, most of the naturally produced antibiotics are synthesized by bacteria. In 1939 the French microbiologist René Dubos isolated the substance tyrothricin and later showed that it was composed of two substances, gramicidin (20%) and tyrocidine (80%). These were the first antibiotics to be manufactured commercially. Gramicidin is a heterogeneous mixture of six antibiotic compounds, all of which are obtained from the soil bacterial species Bacillus brevis and called collectively gramicidin D.
Streptomyces is the largest antibiotic-producing genus, producing antibacterial, antifungal, and antiparasitic drugs, and also a wide range of other bioactive compounds, such as immunosuppressants. They produce over two-thirds of the clinically useful antibiotics of natural origin. The now uncommonly-used streptomycin takes its name directly from Streptomyces. Aminoglycosides, class of antibiotics, that are derived from bacteria of the Streptomyces genus are named with the suffix -mycin, whereas those that are derived from Micromonospora are named with the suffix -micin. However, this nomenclature system is not specific for aminoglycosides.
Streptomycetes are characterised by a complex secondary metabolism. Almost all of the bioactive compounds produced by Streptomyces are initiated during the time coinciding with the aerial hyphal formation from the substrate mycelium.
Streptomycetes produce numerous antifungal compounds of medicinal importance, including nystatin (from S. noursei), amphotericin B (from S. nodosus), and natamycin (from S. natalensis).
Members of the Streptomyces genus are the source for numerous antibacterial pharmaceutical agents; among the most important of these are: Chloramphenicol (from S. venezuelae), Daptomycin (from S. roseosporus), Fosfomycin (from S. fradiae), Lincomycin (from S. lincolnensis), Neomycin (from S. fradiae), Puromycin (from S. alboniger), Streptomycin (from S. griseus), Tetracycline (from S. rimosus and S. aureofaciens).
Clavulanic acid (from S. clavuligerus) is a drug used in combination with some antibiotics (like amoxicillin) to block and/or weaken some bacterial-resistance mechanisms by irreversible beta-lactamase inhibition.
Other bacterial species produce antibiotics as well. Such an example are some Pseudomonas species which produce antimicrobial compounds. P. aurantiaca produces di-2,4-diacetylfluoroglucylmethane, a compound antibiotically active against Gram-positive organisms. Other Pseudomonas spp. might produce compounds antagonistic to other soil microbes, such as phenazine-type antibiotics or hydrogen cyanide. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.03%3A_Commonly_Used_Antimicrobial_Drugs/13.3D%3A_Antibiotics_from_Prokaryotes.txt |
Antimycobacterial antibiotics target microbes classified as mycobacterium.
Learning Objectives
• Compare and contrast the drugs used for treatment of Mycobacterium tuberculosis and Mycobacterium leprae
Key Points
• The standard “short” course treatment for TB is isoniazid, rifampicin, pyrazinamide, and ethambutol for two months, then isoniazid and rifampicin alone for another four months.
• The standard treatment for leprosy is a multidrug therapy that includes dapsone, clofazimine and rifampicin.
• Mycobacterium are defined by their ability to grow in a mold-like fashion on the surface of liquids when cultured.
Key Terms
• tuberculosis: Tuberculosis, MTB, or TB (short for tubercle bacillus) is a common, and in many cases lethal, infectious disease caused by various strains of mycobacteria, usually Mycobacterium tuberculosis.
• infectious disease: Infectious diseases, also known as transmissible diseases or communicable diseases comprise of clinically evident illness (i.e., characteristic medical signs and/or symptoms of disease) resulting from the infection, presence and growth of pathogenic biological agents in an individual host organism. In certain cases, infectious diseases may be asymptomatic for much or even all of their course in a given host. In the latter case, the disease may only be defined as a “disease” (which by definition means an illness) in hosts who secondarily become ill after contact with an asymptomatic carrier. An infection is not synonymous with an infectious disease, as some infections do not cause illness in a host.
• leprosy: Leprosy, also known as Hansen’s disease (HD), is a chronic disease caused by the bacteria Mycobacterium leprae and Mycobacterium lepromatosis.
• isoniazid: a medication used in the prevention and treatment of tuberculosis, having the chemical formula C6H7N3O
Antimycobacterial antibiotics are a class of antimicrobial drugs that target mycobacterium. Mycobacterium is a genus of Actinobacteria that includes pathogens known to cause serious and infectious disease. The types of pathogens considered to be mycobacterium include Mycobacterium tuberculosis (tuberculosis) and Mycobacterium leprae (leprosy). Mycobacterium grow in a mold-like manner on the surface of liquids when cultured. Antiomycobacterial antibiotics specifically target these types of microbes.
A type of antimycobacterial antibiotic includes the class of drugs used for tuberculosis (TB) treatment. The standard “short” course treatment for TB is isoniazid, rifampicin (also known as rifampin in the United States), pyrazinamide and ethambutol for two months, then isoniazid and rifampicin alone for another four months. The patient is considered cured at six months (although there is still a relapse rate of 2 to 3%). For latent tuberculosis, the standard treatment is six to nine months of isoniazid alone.
If the organism is known to be fully sensitive, then it is treated with isoniazid, rifampicin and pyrazinamide for two months, followed by isoniazid and rifampicin for four months. Ethambutol need not be used. Most regimens have an initial high-intensity phase, followed by a continuation phase (also called a consolidation phase or eradication phase) – the high-intensity phase is given first, then the continuation phase.
There are six classes of second-line drugs (SLDs) used for the treatment of TB. A drug may be classed as second-line instead of first-line for one of three possible reasons: it may be less effective than the first-line drugs (e.g., p-aminosalicylic acid); or, it may have toxic side-effects (e.g., cycloserine); or it may be unavailable in many developing countries (e.g., fluoroquinolones): aminoglycosides: e.g., amikacin (AMK), kanamycin (KM); polypeptides: e.g., capreomycin, viomycin, enviomycin; Fluoroquinolones: e.g., ciprofloxacin (CIP), levofloxacin, moxifloxacin (MXF); thioamides: e.g. ethionamide, prothionamide.
For treatment of leprosy, caused by Mycobacterium leprae, the traditional antimycobacterial drugs include promin (the first treatment introduced to fight leprosy) and dapsone (which eventually become obsolete as Mycobacterium leprae quickly evolved resistance). Modern drugs which were developed in response to the resistance was clofazimine and rifampicin. The use of multidrug therapies including dapsone, clofazimine and rifampicin were advantageous due to the low risk of antibiotic resistance. However, the use of these multidrug treatments was costly and only adopted in endemic countries when the World Health Assembly passed a resolution to eliminate leprosy in 1991.
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The accumulation of antimicrobial drugs and their metabolic byproducts in organs can be toxic, leading to organ damage.
Learning Objectives
• Outline the two major types of organ toxicity and their effects, recognizing additional types of toxicity
Key Points
• Antimicrobial drugs can have unintended side effects, including being toxic to organs.
• The liver and kidney are particularly susceptible to organ toxicity as they are the sites of toxin filtration and toxin metabolic breakdown.
• Almost any organ or tissue in the human body can be affected by antimicrobial toxicity.
• The toxic effects of antimicrobial drugs, while potentially harmful are very rare.
Key Terms
• antimicrobrial drugs: A drug administered to a patient, with the purpose of killing or slowing the growth of a microorganism, including protozoans, fungi and bacteria.
• antibiotics: A chemical that slows the growth of, or kills a bacteria.
The use of antimicrobial drugs can have many unintended side-effects. The use, particularly when repeated, of many drugs can lead to an accumulation of a drug, or harmful byproducts from the metabolism of a drug, in tissues or organs. This accumulation of toxic chemicals can lead to organ damage, and in extreme cases, even organ failure and death. Two severe types of organ toxicity associated with antimicrobial drugs are nephrotoxicity and hepatotoxicity, toxicity of the kidneys and liver respectively.
The liver and kidneys are common organs affected by chemical toxicity. The kidneys are responsible for the filtration of the blood, so it is not surprising that deleterious agents in the blood may accumulate there. The liver is an important site for the breakdown of most metabolites in the body, and is referred to as the “metabolic clearing house” of the body. As drugs are quite often broken down in the liver, they can accumulate there and cause damage, or the byproducts of a drug’s metabolism can be toxic. In addition to direct damage to the liver by an antimicrobial drug, antimicrobial drugs can lead to the formation of dangerous toxins through the breakdown of microbes or due to interaction with other tissues in the body. These secondary toxins from drug metabolism then accumulate in the liver, potentially causing damage. Drug damage to the liver or kidneys can be particularly catastrophic as these organs are needed for the proper “cleaning” of the body. If they are compromised, this leads to further accumulation of potentially toxic metabolites further damaging organs in the body.
Some of the toxic effects can be more benign, as is the case with ototoxicity, or damage to the ear. Use of some antibiotics, such as gentamicin, can cause a lose of hearing, or tinnitus (“ringing in the ears”). Ototoxicity is usually temporary with antibiotics, but permanent hearing damage, while rare, has been reported. Some antibiotics such as Tetracycline can cause phototoxicity, also known as sun poisoning; the result of which is that very short exposures to direct sunlight can cause severe skin irritation, with the appearance being quite similar to a rash or sunburn. The Tetracycline in a patient’s skin becomes toxic when exposed to sunlight, which causes an allergic reaction and leads to rash on the affected area. Broad-spectrum antibiotics in the family of fluoroquinolones can cause neurotoxicity by directly damaging neuronal receptors. This can lead to any number of psychological effects from mild cognitive dysfunction (brain fog) to more severe effects, such as hallucinations and suicidal thoughts.
While a few specific examples have been outlined here, toxic effects are not limited to the organs mentioned. In fact, almost any tissue or organ can be affected by antimicrobial drugs. However, it should be noted that the side-effects due to broad-spectrum antibiotics are actually quite rare, with organ damage being even more rare.The potential side-effects of antibiotics or other antimicrobial drugs are offset by the benefits of combating the microbial infection. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.04%3A_Interactions_Between_Drug_and_Host/13.4A%3A_Organ_Toxicity.txt |
Antimicrobrial drugs can cause immune responses which can be fatal.
Learning Objectives
• Explain the physiology of an immune response responsible for an allergic reaction to drugs
Key Points
• Antimicrobial drugs, can like almost any other substance, act as an allergen.
• Using a drug may not induce an allergic response the first time it is taken, however, subsequent use of the antimicrobial drugs may lead to allergic reactions.
• The most common antimicrobial drug allergy is penicillin. 1-5% of people who have taken it have suspected penicillin allergies.
Key Terms
• allergen: A substance, known as an antigen, which stimulates an immune response from a sensitive individual.
• anaphylaxis: A rapid and severe allergic reaction which can lead to death
• Beta-lactam antibiotics: A broad class of antibiotics of which penicillin is a member.
Virtually any substance, when exposed internally or externally to the body, can act as an allergen and illicit an immune system response, such is the case with antimicrobial drugs. While the drug acts as an allergen, the drug itself is not causing direct damage to the individual, but rather it is the response of an individual’s immune system which is deleterious. An allergic reaction is the body’s response to clear a foreign substance. Once the body recognizes a substance as foreign (in this case an antimicrobial drug), it starts producing antibodies, specifically immunoglobulin E (IgE) against the drug. The IgE binds directly to the drug and sets off a cascade of events, including the activation of receptors on immune system cells. This results in the production of histamines. The worst allergic reactions can be very severe and result in anaphylaxis. Anaphylaxis is an extremely severe allergic reaction caused when histamines are overproduced leading to severe contraction of bronchial muscles. In the most extreme cases, the airways close, which can lead to death. Other less severe symptoms of an allergic reaction can include, hives, angioedema (tissue swelling under the skin, often on the face), tight throat, coughing, wheezing, or watery eyes.
The exposure to a drug may not elicit an allergic reaction during the first exposure, but after the first exposure, the body creates antibodies and memory lymphocyte cells against the drug, therefore later exposures to the drug will illicit an immune response. There are many factors that can determine if an individual is sensitive to an antimicrobial drug, as with other allergens. Some factors include genetics and past exposures to other allergens, typically a person who has allergies to other things, such as various foods, is more prone to have or develop drug allergies. The most reported drug allergy is to Beta-lactam antibiotics, of which penicillin is the most well-known type, affecting 1-5% of people who take penicillin. While the most severe cases can result in anaphylaxis, most reactions are not severe. Additionally the allergic reaction may not even be due to the penicillin, as dyes and other chemicals added to antimicrobial drugs may in fact cause the allergic response instead. Taken together, recent studies show that perhaps only 1/5 people who suspect they have an allergy to penicillin do indeed have such an allergy. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.04%3A_Interactions_Between_Drug_and_Host/13.4B%3A_Allergic_Responses_to_Drugs.txt |
Our bodies depend upon, and host, a vast number of complex microbial flora that can be affected negatively by antimicrobial treatments.
Learning Objectives
• Describe the role and function of the microbiota
Key Points
• The intestinal system has many different species of microbes and huge numbers of individual microbes; we rely on these microbes for proper metabolism of food.
• The use of antimicrobial agents to slow down or kill pathogenic microbes can often kill beneficial bacteria, causing deleterious health effects.
• Our body hosts some microbes that inhibit the growth of pathogenic microbes; using antimicrobial agents can alter the flora allowing pathogenic microbes to overgrow and cause diseases.
Key Terms
• Candidal vulvovaginitis: Candidal vulvovaginitis or vaginal thrush, or yeast infection, is an infection of the vagina’s mucous membranes by Candida albicans.
• microbiota: The microbial flora harbored by normal, healthy individuals.
• pathogenic bacteria: Bacteria which infect and cause deleterious health effects.
The human body hosts thousands of different species of microbial organisms, known as the microbial flora or microbiota. Microbiota serve many functions in our body; most notable is the gut flora, crucial for the proper digestion of food, carbohydrate fermentation, and nutrient absorption. The gut flora in the human intestinal system has hundreds of species of microbes and over 100 trillion individual microbes; in comparison, the human body has around 10 trillion cells. Most of these microbes are bacterial and fungal. This is especially a problem when broad-spectrum antimicrobial agents are used, as antimicrobial treatments while helping to clear up pathogenic microbes from the body will often kill symbiotic bacteria. In addition, some microbial infections are due to translocation, the movement of advantageous bacteria to parts of the body where they might be harmful. An example is gut flora getting into the body’s blood stream. The treatment of translocated or pathogenic bacteria may necessitate the use of antibiotics that will kill symbiotic bacteria. Antimicrobial agents which can kill beneficial gut flora can reduce the numbers of individual microbes or reduce the species of beneficial bacteria. In the case of the gut flora, this may impair the ability of a patient to properly metabolize food. If advantageous bacteria do not repopulate the intestine, this can lead to serious malnutrition problems.
In addition to serving a necessary function as gut flora due in metabolism of food, some microbiota in our bodies serve the function of keeping pathogenic microbes from inhabiting or dominating other flora at locations in our body. This is exemplified by Candida albicans, a yeast which is often found on humans. C. albicans is normally harmless, but when women take some antibiotics this can kill beneficial bacteria, specifically lactobacilli, in the vulvo-vaginal area. Without lactobacilli, C. albicans growth is not suppressed and can thus overgrow. This causes candidal vulvovaginitis, or yeast infections, a potentially painful infection of the vaginal mucous membranes by overgrown C. albicans. Yeast infections can be caused by antibiotics, as well as using aggressive topical cleaning agents such as detergents which again kill off beneficial lactobacilli allowing C. albicans to overgrow.
Fortunately there are antimicrobial agents that specifically target pathogenic bacterial species, which opposed to broad-spectrum treatments can reduce harmful effects on beneficial microbes. Sometimes the use of broad-spectrum antimicrobial agents is unavoidable; in these situations, consuming foods such as yogurt which contains beneficial bacteria can replenish the body’s symbiotic microbes. In extreme cases microbes can be transplanted from a healthy individual to someone with whose symbiotic microbes have been compromised. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.04%3A_Interactions_Between_Drug_and_Host/13.4C%3A_Suppression_and_Alteration_of_Microbiota_by_Antimicrobials.txt |
Antimicrobial drugs can interact with other drugs in deleterious ways or can be used in combination to combat microbial infections.
Learning Objectives
• Give examples of interactions that can render an antimicrobial ineffective
Key Points
• The interaction between one antimicrobial agent and another is very complex, along with the way they target microbes and the organism.
• While it is not certain that a drug may interact with antibiotics, it is considered wise to err on the side that there are potentially unknown and harmful interactions from mixing drugs.
• The use of more than one antimicrobial agent is an effective and widely used practice to reduce the chance that microbes will resist a treatment.
Key Terms
• contraindication: In medicine, a contraindication is a condition or factor that serves as a reason to withhold a certain medical treatment.
• tuberculosis: An infectious disease of humans and animals caused by a species of mycobacterium mainly infecting the lungs where it causes tubercles characterized by the expectoration of mucus and sputum, fever, weight loss, and chest pain, and transmitted through inhalation or ingestion of bacteria.
• combination therapy: Combination therapy is the use of more than one medication or other therapy. Most often, these terms refer to the simultaneous administration of two or more medications to treat a single disease.
Pharmacodynamics is the field that attempts to understand the unintended effects of the use of two or more drugs. Pharmacodynamics is the study of the biochemical and physiological effects of drugs on the body or on microorganisms or parasites within or on the body. It also looks at the mechanisms of drug action and the relationship between drug concentration and effect. These changes are extraordinarily difficult to classify given the wide variety of modes of action that exist and the fact that many drugs can cause their effect through a number of different mechanisms. This wide diversity also means that, in all but the most obvious cases, it is important to investigate and understand these mechanisms. The well-founded suspicion exists that there are more unknown interactions than known ones.
Two well described interactions between antimicrobial drugs and other drugs are between antibiotics and alcohol and antibiotics and the birth control pill. Interactions between alcohol and certain antibacterials may occur, cause side-effects, and decrease effectiveness of antibacterial therapy. Potential risks of side-effects and effectiveness depend on the type of antibacterial administered. Despite the lack of a categorical contraindication, the belief that alcohol and antibacterials should never be mixed is widespread. Some antibacterials may inhibit the breakdown of alcohol, which may result in alcohol-induced vomiting, nausea, and shortness of breath. Other effects of alcohol on antibacterial activity include altered activity of the liver enzymes that break down the antibacterial compound. In addition, serum levels bacteriostatic antibacterials may be reduced by alcohol consumption, resulting in reduced efficacy and diminished pharmacotherapeutic effect.
Another well studied interaction is between antibiotics and the contraceptive pill. The majority of studies indicate that antibiotics do not interfere with contraceptive pills. In cases where antibacterials have been suggested to affect the efficiency of birth control pills may be due to an increase in the activities of hepatic liver enzymes causing increased breakdown of the pill’s active ingredients. Effects on the intestinal flora, which might result in reduced absorption of estrogens in the colon, have also been suggested, but such suggestions have been inconclusive and controversial. Clinicians have recommended that extra contraceptive measures be applied during therapies using antibacterials that are suspected to interact with oral contraceptives.
Additionally, when dealing with a microbial infection, sometimes the use of two or more antibiotics can effectively combat the infection while each drug individually has little or no effect. This method is called combination therapy and is used when the nature of a microbial infection is unknown, as typified by the combination of the antibiotics ampicillin and sulbactam. The use of two antibiotics with different modes of microbial inhibition increases the chance that the treatment will combat the microbial infection. Further, tuberculosis has been treated with combination therapy for over fifty years. This is due to the phenomenon of resistance, whereby a micro-organism gains the ability to resist an antimicrobial drug, while initially the drug effectively slowed the growth of or even killed the target micro-organism. Treating tuberculosis, or other pathogenic microbes with more than one antibiotic reduces the chance that the microbe will adapt and survive the treatment, especially if the two drugs have different methods of reducing the microbe’s normal functions.
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Minimum Inhibitory Concentration is the lowest drug concentration that prevents visible microorganism growth after overnight incubation.
Learning Objectives
• Analyze data to interpret minimal inhibitory concentration values
Key Points
• Minimum inhibitory concentration (MIC) can be determined by culturing microorganisms in liquid media or on plates of solid growth medium.
• A lower MIC value indicates that less drug is required for inhibiting growth of the organism; therefore, drugs with lower MIC scores are more effective antimicrobial agents.
• By identifying appropriate drugs and their effective concentrations, MIC scores aid in improving outcomes for patients and preventing evolution of drug-resistant microbial strains.
Key Terms
• culture: The process of growing a bacterial or other biological entity in an artificial medium.
• minimum inhibitory concentration: This is the lowest concentration of an antimicrobial drug that prevents visible growth of a microorganism after overnight incubation with media.
• bacteriostatic: A drug that prevents bacterial growth and reproduction but does not necessarily kill them. When it is removed from the environment the bacteria start growing again.
Definition and Measurement
In microbiology, minimum inhibitory concentration (MIC) is the lowest concentration of an antimicrobial (like an antifungal, antibiotic or bacteriostatic) drug that will inhibit the visible growth of a microorganism after overnight incubation. MICs can be determined on plates of solid growth medium (called agar, shown in the “Kirby-Bauer Disk Susceptibility Test” atom) or broth dilution methods (in liquid growth media, shown in ) after a pure culture is isolated. For example, to identify the MIC via broth dilution, identical doses of bacteria are cultured in wells of liquid media containing progressively lower concentrations of the drug. The minimum inhibitory concentration of the antibiotic is between the concentrations of the last well in which no bacteria grew and the next lower dose, which allowed bacterial growth. There are also several commercial methods available to experimentally measure MIC values.
Significance and Applications
An MIC is generally regarded as the most basic laboratory measurement of the activity of an antimicrobial agent against an organism. Because a lower MIC value indicates that less of the drug is required in order to inhibit growth of the organism, drugs with lower MIC scores are more effective antimicrobial agents. Currently, there are a few web-based, freely accessible MIC databases. MIC scores are important in diagnostic laboratories to confirm resistance of microorganisms to an antimicrobial agent and also to monitor the activity of new antimicrobial agents. Clinicians use MIC scores to choose which antibiotics to administer to patients with specific infections and to identify an effective dose of antibiotic. This is important because populations of bacteria exposed to an insufficient concentration of a particular drug or to a broad-spectrum antibiotic (one designed to inhibit many strains of bacteria) can evolve resistance to these drugs. Therefore, MIC scores aid in improving outcomes for patients and preventing evolution of drug-resistant microbial strains.
13.5B: Kirby-Bauer Disk Susceptibility Test
Learning Objectives
• Review the procedure for the Kirby-Bauer antibiotic tes
Kirby-Bauer antibiotic testing (also called KB testing or disk diffusion antibiotic sensitivity testing) uses antibiotic-containing wafers or disks to test whether particular bacteria are susceptible to specific antibiotics. First, a pure culture of bacteria is isolated from the patient. Then, a known quantity of bacteria are grown overnight on agar ( solid growth media) plates in the presence of a thin wafer that contains a known amount of a relevant antibiotic. If the bacteria are susceptible to the particular antibiotic from a wafer, an area of clear media where bacteria are not able to grow surrounds the wafer, which is known as the zone of inhibition. A larger zone of inhibition around an antibiotic-containing disk indicates that the bacteria are more sensitive to the antibiotic in the disk.
KB tests are performed under standardized conditions and standard-sized zones of inhibition have been established for each antibiotic. KB test results are usually reported as sensitive, intermediate, or resistant, based on the size of the zone of inhibition. If the observed zone of inhibition is greater than or equal to the size of the standard zone, the microorganism is considered to be sensitive to the antibiotic. Conversely, if the observed zone of inhibition is smaller than the standard size, the microorganism is considered to be resistant. The size of a zone of inhibition in a KB test is inversely related to the minimum inhibitory concentration (MIC), which is the amount of antibiotic required to prevent bacterial growth in an overnight culture. The MIC (in µg/ml) can be calculated from known standard-curve (linear regression) graphs based on the diameter of the observed inhibition zone diameter (in millimeters).
Clinicians can use KB test results to choose appropriate antibiotics to combat a particular infection in a patient. Administering antibiotics that specifically target the particular bacteria that are causing the infection can avoid using broad-spectrum antibiotics, which target many types of bacteria. Thus, clinical application of KB testing results can decrease the frequency with which antibiotic-resistant bacteria evolve.
Key Points
• KB tests are performed under standard conditions, so the minimum inhibitory concentration for a given antibiotic can be calculated by comparing the observed zone of inhibition ‘s size to known values.
• Clinicians use KB test results to choose antibiotics effective against the specific bacteria causing a patient’s infection. Using specifically-targeted antibiotics helps decrease the frequency of drug-resistant bacteria evolving.
Key Terms
• Kirby-Bauer antibiotic testing: This is a method to determine the sensitivity of microorganisms to specific antimicrobial drugs; greater drug efficacy yields larger microbe-free zones surrounding drug-containing disks after overnight growth on solid media.
• zone of inhibition: This is an area of media where bacteria are unable to grow, due to presence of a drug that impedes their growth.
• minimum inhibitory concentration: This is the lowest concentration of an antimicrobial drug that prevents visible growth of a microorganism after overnight incubation with media. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.05%3A_Measuring_Drug_Susceptibility/13.5A%3A_Minimal_Inhibitory_Concentration_%28MIC%29.txt |
Development of microbial resistance to antimicrobial agents requires alterations in the microbe’s cell physiology and structure.
Learning Objectives
• Describe the mechanisms bacteria use to develop antimicrobial resistance and the factors that can lead to it
Key Points
• Antimicrobial resistance can be mediated by the environment or the microorganism itself.
• Environmentally-mediated antimicrobial resistance results from physical or chemical characteristics of the environment that can affect the antimicrobial agent or the microorganism.
• Microorganism-mediated antimicrobial resistance can be intrinsic or acquired.
Key Terms
• intrinsic: innate, inherent, inseparable from the thing itself, essential.
Development of microbial resistance to antimicrobial agents requires alterations in the microbe ‘s cell physiology and structure. Antimicrobial resistance is defined as the loss of susceptibility to an extent that the drug is no longer effective for clinical use against an organism. Resistance can be mediated by the environment or the microorganism itself.
Environmentally-mediated antimicrobial resistance is affected by the environment’s chemical and physical properties such as pH, anaerobic conditions, cation concentrations (calcium, magnesium), and thymine-thymidine content (available metabolites and nutrients).
Microorganism-mediated antimicrobial resistance is due to genetically-encoded traits of the microorganism and can be divided into intrinsic or acquired. Intrinsic resistance is considered to be a natural and inherited property with high predictability. Once the identity of the organism is known, the aspects of its anti-microbial resistance are also recognized. On the other hand, acquired resistance results from a change in the organism’s genetic makeup. This trait is associated with only some strains of an organism’s group but not the others. It is also an unpredictable trait and necessitates the development of laboratory methods to detect it. Microorganism-mediated antimicrobial resistance is acquired by gene change or exchange such as genetic mutations, acquisition of genes from other organisms via gene transfer mechanisms, or a combination of mutational and gene transfer events. Some common pathways bacteria use to effect antimicrobial resistance include: enzymatic degradation or modification of the antimicrobial agent, decreased uptake or accumulation of the antimicrobial agent, altered antimicrobial target, circumvention of consequences of antimicrobial actions, uncoupling of antimicrobial agent-target interaction, or any combination of these mechanisms.
13.6B: Antibiotic Misuse
Learning Objectives
• Explain the effects of antibiotic misuse
With the introduction of antibiotics into medical practice, clinically-relevant bacteria have had to adopt resistance mechanisms as part of their survival strategy. Antibiotic resistance occurs when antibiotics no longer work against disease-causing bacteria. These infections are difficult to treat and can mean longer-lasting illnesses, more doctor visits or extended hospital stays, and the need for more expensive and toxic medications. Some resistant infections can even cause death. Developing new antibiotics and other treatments to keep pace with antibiotic-resistant strains of bacteria is necessary. However, using antibiotics wisely is equally important for preventing the spread of resistant strains.
Antibiotic misuse has contributed largely to the emergence of new resistant strains. It is caused by taking an antibiotic too often for a condition it cannot treat such as viral infections and the common cold or in the wrong doses. It can also be manifested by not finishing a course of antibiotics as prescribed (stopping the antibiotic before the infection is fully cleared from the body). Overuse of antibiotics affects the bodsy’s normal flora and disrupts the balance between beneficial bacteria that help digestion for example, and harmful bacteria. Excessive use of antibiotics in intensive farming units, particularly pig and poultry farms, is also seen as a growing threat. Scientists say antimicrobial resistance may be passing between animals and humans through food consumption, making the need to cut unnecessary use of antibiotics in farming even more urgent. Responsible antibiotic use in industry, and good practice for patients and physicians, are essential to keep resistant bacterial strains curable, and antibiotic treatment affordable to patients.
Key Points
• Antimicrobial resistance is a major public health concern.
• Antimicrobial resistance is brought about by antibiotic misuse, such as overuse, misuse, or interrupted treatment.
• Food industries, physicians, and patients play a role in minimizing the spread of resistance by adhering to good antibiotic practice.
Key Terms
• course of antibiotics: a period of continuous treatment with a drug. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.06%3A_Drug_Resistance/13.6A%3A_Mechanisms_of_Resistance.txt |
Learning Objectives
• Examine the causes and effects of multidrug-resistant organisms on healthcare
Prevention and control of microbial-resistant organisms is one of the most complex management issues that health care professionals face. The clinical and financial burden to patients and health care providers is staggering. Patients who are infected with bacterial strains resistant to more than one type or class of drugs (multidrug-resistant organisms, MDRO) often have an increased risk of prolonged illness, extended hospital stay, and mortality.
The cost of care for these patients can be more than double compared to those without an MDRO infection. The alternative medication they are prescribed to overcome the infection is often substantially more costly. Multidrug resistance forces healthcare providers to use antibiotics that are more expensive or more toxic to the patient.
When no antibiotic is effective, healthcare providers may be limited to providing supportive care rather than directly treating an infection. In a 2008 study of attributable medical costs for antibiotic resistant infections, it was estimated that infections in 188 patients from a single healthcare institution cost between \$13.35 and \$18.75 million dollars.
Research and development of new drugs effective against resistant bacterial strains also comes at a cost. To prevent antimicrobial resistance, the patient and the healthcare provider should discuss the appropriate medicine for the illness. Patients should follow prescription directions and should not share or take medicine that was prescribed for someone else; these virtues should be strictly practiced. Healthy lifestyle habits, including proper diet, exercise, and sleeping patterns, as well as good hygiene such as frequent hand washing, can help prevent illness. These practices, therefore, also help prevent the overuse or misuse of antibiotics and the emergence of problematic resistant strains.
Key Points
• Antimicrobial resistance to available drugs requires the development of new drugs to effectively treat resistant strains and reduce mortality from bacterial infections.
• Antimicrobial resistance can be prevented by practicing good hygiene, and being responsible with antibiotic use.
• Treating antibiotic-resistant bacterial strains is expensive for both the patient and the healthcare provider. The treatment requires extended hospital stay and costly medications.
Key Terms
• multidrug resistance: A condition enabling a disease-causing organism to resist distinct drugs or chemicals of a wide variety of structure and function targeted at eradicating the organism.
13.6D: Biofilms Persisters and Antibiotic Tolerance
Biofilms and persisters are bacterial communities responsible for chronic diseases and antibiotic tolerance.
Learning Objectives
• Explain the role of biofilms and persisters in multidrug tolerance, distinguishing this from multidrug resistance
Key Points
• Biofilms are aggregates of microbial cells that form to avoid antimicrobial agents or attack by the immune system.
• Persisters are slow-growing, dormant microbial cells that can tolerate antibiotic treatment.
• Biofilms and persisters are responsible for chronic bacterial infections and recurrent disease.
• Antibiotic tolerance is different from antibiotic resistance but equally important as a public health burden for eradication of serious bacterial diseases.
Key Terms
• gingivitis: inflammation of the gums or gingivae
• extracellular matrix: All the connective tissues and fibers that are not part of a cell, but rather provide support.
Biofilms are bacteria that have formed a gated community. Biofilms are composed of an aggregate of bacterial cells and are essentially considered a multi-cellular organism. They are characterized by structural heterogeneity, genetic diversity, complex community interactions, and an extracellular matrix of polymeric substances. They live on solid surfaces (e.g., catheters, ) and the extracellular material they produce protects them from external threats, such as attacks by the body’s immune cells. The property of biofilms constitute a penetration barrier for most antibiotics therefore preventing the drug from reaching the microbes. It is being widely recognized that bacterial biofilms are responsible for several chronic diseases that are difficult to treat, hence hard to eradicate (e.g., cystitis, endocarditis, urinary tract infections, gingivitis, dental plaque, and other yet to be identified conditions). They differ from free-floating or planktonic bacteria that cause acute infections and are managed by antimicrobial drugs.
Persisters are multidrug tolerant cells present in all bacterial populations. Bacterial populations that produce persister cells that neither grow nor die in the presence of microbicidal antibiotics are largely responsible for high levels of biofilm tolerance to antimicrobials. Persisters are not mutants, but rather phenotypic variants of the wild-type that upon inoculation produce a culture with similar levels of tolerance. Elimination of persisters remains an obstacle for the eradication of some tenacious and highly recurrent bacterial infections. Biofilms and persisters are the cause of multidrug tolerance. Multidrug tolerance differs from multidrug resistance in that it is not caused by mutant microbes but rather by microbial cells that exist in a transient, dormant state. These non-dividing cells often survive antibiotic exposure targeted to kill highly proliferating bacteria. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.06%3A_Drug_Resistance/13.6C%3A_Cost_and_Prevention_of_Resistance.txt |
Antimicrobial resistance has created a public health crisis in the treatment of infectious diseases and necessitates the discovery of new drugs.
Learning Objectives
• Explain the reasons for low production of new antibiotics and discuss the proposed mechanisms to evade antimicrobial resistance
Key Points
• Finding new antimicrobial drugs requires researchers, pharmaceutical, and biotech companies to invest in new technology and discover new sources for antibiotic development.
• Proposed mechanisms to circumvent antimicrobial resistance range from exploring the list of resistance genes to antibody-based therapy and vaccines.
• Finding new candidates to target is essential but it needs to be accompanied by awareness on antibiotic misuse with the prospect to eliminate the root of the problem.
Key Terms
• mimetic: A substance with similar pharmacological effects to another substance.
Antimicrobial resistance: the problem
Antibiotics, more than any other medicines, have improved the life expectancy of mankind, however, multi-drug resistance has become common in pathogenic bacteria and multiple drugs are losing efficacy. Recent reports on the occurrence of panresistant gram-negative strains, i.e. strains resistant to every registered antibacterial drug, indicate that we are on the verge to lose the battle, taking us back to the pre-antibiotic era. There is world-wide consensus that the medical need for novel antiinfective drugs is enormous and that we are running out of time. Many achievements of modern medicine, not only treatment of infectious diseases, depend on the availability of efficacious antibiotics, still, the antibacterial development pipeline is slow and the number of new drugs reaching the market is alarmingly low. There are many reasons for this at all levels of the discovery and development process. Investments into antibiotic research and technologies is minimal; socioeconomic considerations together with regulatory hurdles have prompted pharmaceutical companies to exit the field and innovative biotech companies were confronted with problems beyond their control. Answers are needed as to where and how we can find new lead compounds with unprecedented activities?
Finding new antimicrobial drugs: the solution
Research on new antimicrobial compounds is geared towards innovative targets to circumvent resistance. Some of the proposed areas to investigate include: collecting and examining the list of antimicrobial resistance genes (e.g. exploring the resistome), targeting teichoic acid biosynthesis as a new method to compromise the bacterial wall integrity, producing ribosomal inhibitors to target protein synthesis, targeting outer-membrane transporters with protein epitope mimetics (e.g. mimetics of the cationic antimicrobial peptides that form part of the immune response to microbes), and developing antibody-based strategies and vaccines. The initiative to develop new antimicrobial agents is urgently needed but is a long process from invention, to development, to actual clinical application. It is also necessary to initiate a worldwide awareness on antibiotic misuse and overuse as a mean to address the root of the problem for antimicrobial resistance.
13.6F: Antimicrobial Peptides
Antimicrobial peptides exhibit cytotoxic activity against all microbes.
Learning Objectives
• Discuss the structure, mechanism, and targets of antimicrobial peptides
Key Points
• Antimicrobial peptides (AMPs) are a unique and assorted group of molecules produced by living organisms of all types, considered to be part of the innate immunity of a host.
• These peptides demonstrate potent antimicrobial activity and are rapidly mobilized to neutralize a broad range of microbes, such as viruses, bacteria, protozoa, and fungi.
• The ability of these natural molecules to kill multidrug-resistant microorganisms has gained them considerable attention and clinical interest.
Key Terms
• neutropenia: A hematological disorder characterized by an abnormally low neutrophil count.
• atopic dermatitis: An atopic, hereditary, and non-contagious skin disease characterized by chronic inflammation of the skin.
A first line of defense against pathogenic insult is called the innate immune system, which is followed by acquired immune responses associated with the activation of T and B cells aimed against specific antigens. In contrast to the clonal, acquired adaptive immunity, endogenous peptide antibiotics or antimicrobial peptides provide a fast and energy-effective mechanism as front-line defense.
Antimicrobial peptides (AMPs) are small molecular weight proteins with broad spectrum antimicrobial activity against bacteria, viruses, and fungi. They are classified on the basis of their structure and amino acid motifs. Peptides of the defensin, cathelicidin, and histatin classes are found in humans. These evolutionarily conserved peptides are usually positively charged and have both a hydrophobic and hydrophilic side that enables the molecule to be soluble in aqueous environments yet also enter lipid-rich membranes. Once in a target microbial membrane, the peptide kills target cells through diverse mechanisms. AMPs secrete lytic enzymes, nutrient-binding proteins or contain sites that target specific microbial macromolecules.
Cathelicidins and defensins are major groups of epidermal AMPs. Decreased levels of these peptides have been noted for patients with atopic dermatitis and Kostmann’s syndrome, a congenital neutropenia. AMPs have proven effective against multidrug-resistant microbes. In addition to important antimicrobial properties, growing evidence indicates that AMPs alter the host immune response through receptor-dependent interactions. AMPs have been shown to be important in such diverse functions as angiogenesis, wound healing, cytokine release, chemotaxis, and regulation of the adaptive immune system. These peptides qualify as innovative drugs that might be used as antibiotics, anti-lipopolysaccharide drugs, or modifiers of inflammation reactions.
13.6G: Antisense Agents
Learning Objectives
• Discuss the mechanism of antisense agents and the advantages and disadvantages of antisense therapy.
Antisense agents are synthetic, single-stranded short sequences of DNA bases designed to hybridize to specific sequences of messenger RNA (mRNA) forming a duplex. This DNA-RNA coupling attracts an endogenous nuclease, RNase H that destroys the bound RNA and frees the DNA antisense to rehybridize with another copy of mRNA. In this way, the effect is not only highly specific but prolonged because of the recycling of the antisense DNA sequence. When this agent binds to the pathogen DNA or messenger RNA, the biosynthesis of target proteins is disrupted. Therefore, there are at least two ways in which antisense agents act to effectively reduce the amount of pathogenic protein being synthesized – RNase H based degradation of RNA and prevention of ribosomal assembly and translation. This approach has a great advantage. It prevents a pathogenic protein from being produced, rather than trying to selectively neutralize it once it is made.
Antisense agents can be specifically targeted to genes that control expression of antibiotic resistance mechanisms, thereby potentially restoring an antibiotic-sensitive phenotype to the cell. A limiting factor in their potential application as therapeutic agents for bacterial infections is their poor uptake by bacterial cells. These agents have been successfully developed for the treatment of viral infections such as cytomegalovirus, hepatitis C, and HIV infections. The advantage of antisense therapy is that they can be manufactured fairly fast, they produce a lasting clinical effect, and they are highly specific to the target. Antisense agents also exhibit efficacy in broader clinical applications such as cancer therapy.
Key Points
• Antisense agents have broad applications in several diseases. Their use for treating microbial infections is promising.
• They are synthetic oligonucleotides that can be manufactured quickly and their biological effect is long-lasting.
• Their use for the treatment of antibiotic resistant bacterial infections is possible but limited by their poor uptake by the bacterial cell. Studies are being developed to improve their penetration into the cell.
Key Terms
• messenger RNA: RNA that encodes and carries information from DNA during transcription to sites of protein synthesis to undergo translation in order to yield a protein
• nuclease: Any of several enzymes capable of cleaving the phosphodiester bonds between the nucleotide subunits of nucleic acids.
• hybridize: To combine complementary subunits of multiple biological macromolecules. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.06%3A_Drug_Resistance/13.6E%3A_Finding_New_Antimicrobial_Drugs.txt |
Different approches are used to target the initial and final steps of a virus life cycle.
Learning Objectives
• Compare the mechanisms of the discussed antiviral drugs
Key Points
• The attachment step is targeted by molecules that will block the receptor on the host cell surface, or on the viral capsid region responsible for binding to the host receptor.
• Drugs that target the uncoating step bind to, and inactivate, proteins on the capsid surface responsible for the uncoating.
• The release step is targeted by drugs that inhibit the activity of neuraminidase, an enzyme on the viral surface.
Key Terms
• sialic acid: A derivative of neuraminic acid (a nine-carbon monosaccharide) that is often the sugar part of glycoproteins.
A viral infection starts with entry of the virus into the cell. The entry mechanism is complex, consists of multiple steps and involves host cell structures.
Targeting the Attachment Step
Virus infection starts with a virus attaching to the host cell by binding to a receptor molecule. There are two main strategies used to design antiviral drugs at this step:
• Using molecules that will bind to the cell receptor and inactivate it; thus preventing the virus from attachment. Examples include anti-receptor antibodies or natural ligands that can bind to the receptor.
• Using receptor-like molecules to bind to the virus and inactivate it before it meets the cell. These include anti-virus antibodies (with specificity against the viral structure that binds to the receptor) or synthetic molecules that mimic the receptor.
The search for such drugs, however, is very expensive and time-consuming.
Targeting the Uncoating Step
Another drug target is the uncoating step during viral infection. Uncoating is the process of capsid disintegration, which leads to the release of the genomic material. This step is performed by viral or host enzymes, or by capsid dissociation alone. Drugs that can perform such functions are used against the influenza virus, rhinoviruses (the cause of the common cold), and enteroviruses (gastrointestinal infections, meningitis, etc.). It is believed that such drugs prevent the virus from uncoating by blocking the proteins on the capsid responsible for uncoating, such as ion channel proteins. An example of such a drug is Rimantadine, which blocks the ion channel in the influenza virus. The ion channel has an important role in disintegrating the viral capsid.
Targeting the Release of the Newly Formed Viral Particles
The last step in the virus life cycle—release from the cell—has been targeted by drugs as well. Neuraminidase is an enzyme on the capsid of influenza virus. It cleaves sialic acid from glycoproteins on the surface of the host cell and allows the viral particles to leave the cell. Tamiflu and Relenza are trend names of two drugs used to treat influenza infections by targeting neuraminidase.
Since viruses use many structures in the host cells to replicate, designing or discovering good antiviral drugs that will not affect the eukaryotic cells is a challenging task. Serious side effects are often observed with the use of antiviral drugs, as is resistance against the drugs. Developing drugs that inhibit different steps in the virus life cycle is of critical importance.
13.7B: Antiviral DNA Synthesis Inhibitors
Inhibiting DNA synthesis during viral replication is another key approach in battling viral infections.
Learning Objectives
• Review the mechanism of action for antiviral DNA synthesis inhibitors and recognize the types of these inhibitors
Key Points
• Drugs such as acyclovir, are nucleoside analogues that lack a free 3′ group that is needed for the addition of the next nucleotide. When added into a growing DNA chain they stop its synthesis.
• Another drug, foscarnet, mimics pyrophosphates and inactivates the activity of the viral DNA polymerase.
• Resistance can develop against both of these groups of drugs.
Key Terms
• CMV retinitis: An inflammation of the eye’s retina caused by CMV. It can lead to blindness.
Inhibiting DNA synthesis during viral replication is another approach to battle viral infections.
The most common strategy used for this approach is to use molecules that mimic the structure of a nucleoside. The similarity is good enough to ensure its incorporation into the newly synthesized DNA chain. However, the nucleoside analogue lacks free 3′ end needed for the addition of the next nucleotide. This prevents the incorporation of the next nucleotide and terminates the elongation of the DNA chain.
One of the most often used antiviral drugs that works with the described mechanism is acyclovir (aciclovir), a guanosine analogue. It is used to treat herpes simplex virus infections (type 1 and type 2) as well as chicken pox and shingles. It was designed based on nucleosides isolated from a Caribbean sponge. After administration, the molecule gets activated by phosphorylation both by viral and host cell kinases and the resulting nucleotide incorporated into the newly synthesized DNA resulting in premature chain termination. The drug has very low cytotoxicity and there is low resistance to it.
Other drugs that are also nucleoside analogues and have the same mode of actions are ganciclovir (a synthetic analogue of 2′-deoxy-guanosine) and vidarabine(an adenosine analog). However, both drugs are more toxic and have more serious side effects than acyclovir.
Another type of drug that is a DNA synthesis inhibitor is foscarnet. It mimics pyrophosphate and inactivates the activity of the DNA polymerase. This inhibitor is active against the viral DNA polymerases at doses much lower than the ones needed to inhibit the human polymerases. This drug is used in cases of resistance against acyclovir and ganciclovir nucleoside analogue chemicals. It is also used to treat cytomegalovirus infection (CMV) and specifically CMV retinitis.
Another antiviral drug that targets DNA synthesis is hydroxycarbamide, commonly referred to as a hydroxyurea. Hydroxycarbamide can be used an antiretroviral drug against HIV/AIDS. The mechanism of hydroxycarbamide is thought to be based on the reduction of production of deoxyribonucleotides; therefore, inhibiting DNA synthesis. Hydroxycarbamide is thought to inhibit the enzyme ribonucleotide reductase. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.07%3A_Antiviral_Drugs/13.7A%3A_Antiviral_Agents_that_Prevent_Virus_Uncoating_or_Release.txt |
Reverse transcriptase in viruses is inhibited by nucleoside (nucleotide) analogues or drugs that change the conformation of the enzyme.
Learning Objectives
• Summarize the mechanism of action for reverse transcriptase inhibitors
Key Points
• Nucleoside and nucleotide inhibitors are competitive substrate inhibitors that mimic the structure of a normal nucleotide but lack the 3′ hydroxyl group needed for the addition of the next nucleotide for DNA elongation.
• Non-nucleotide inhibitors bind to a site different than the active one and cause rearrangements of the protein domains needed for DNA polymerization.
• Mutations in the reverse transcriptase gene can cause resistance to both types of drugs.
Key Terms
• competitive substrate inhibitors: Molecules that bind to the active site of an enzyme and prevent the real substrate from binding to it.
• non-competitive inhibitors: Molecules that bind to sites other than the active site of an enzyme while still being able to indirectly inhibit its function.
• nucleotide: the monomer comprising DNA or RNA biopolymer molecules, consisting of a nitrogenous heterocyclic base; a five-carbon pentose sugar; and a phosphate group
Reverse transcriptase is an enzyme that has the ability to transcribe single-stranded DNA from a single-stranded RNA chain. This is the reverse of the usual flow of information when RNA is synthesized from DNA. Viruses that use reverse transcriptase to convert their genetic material (RNA) into DNA are called retroviruses. One of the most prominent representative of a retrovirus is HIV. Due to the high prevalence of HIV/AIDS in the world, it is important to have drugs that will prevent or cure the infection. This enzyme is also found in tumors and cancer cells.
Drugs that inhibit the function of this enzyme are divided into three groups:
• nucleoside analog reverse transcriptase inhibitors
• nucleotide analog reverse transcriptase inhibitors
• non-nucleoside reverse transcriptase inhibitors
The first two inhibitors act on the same principle. They mimic, respectively, nucleosides or nucleotides but lack a free hydroxyl group at the 3′ end. The major difference between them is that the nucleosides need to be phosphorylated by cellular kinases. The enzyme reverse transcriptase recognizes them as regular nucleotides and inserts them into the newly synthesized DNA chain. But once inserted the elongation stops at them because no more nucleotides can be added due to the lack of the 3′ hydroxyl group and the inability of the formation of 5′-3′ phosphodiester bond. This process is called chain termination. Nucleoside and nucleotide inhibitors are also called competitive substrate inhibitors. Examples of such drugs are Zidovudine (AZT) and Lamivudine. AZT was the first FDA approved drug for the treatment of HIV. Lamivudine is used for the treatment of both HIV and hepatitis B. Since some viruses, such as hepatitis B, carry RNA-dependent DNA polymerases reverse transcriptase inhibitors can be used to treat these infections as well.
Non-nucleotide reverse transcriptase inhibitors bind to a different site, not the active one, of the reverse transcriptase enzyme. That leads to conformational changes that distort the position of the DNA binding sites in the enzyme and lead to halt in DNA polymerization. Non-nucleotide inhibitors are non-competitive inhibitorsof reverse transcriptase. Such drugs are Efavirenz and Nevirapine.
Resistance occurs to all drug groups. The mechanisms for resistance against the nucleoside (nucleotide) inhibitors are two. The first one is due to mutations in the N-terminal polymerase domain of the reverse transcriptase that makes it less likely to incorporate the analogues. The second mechanism is caused by mutations in the transcriptase that allow the removal of the incorporated inhibitor and hence restart of DNA replication.
Resistance to the non-nucleotide inhibitors is caused by mutations in the inhibitor binding site of the enzyme. Such mutations prevent the binding of the inhibitor to the enzyme. | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.07%3A_Antiviral_Drugs/13.7C%3A_Nucleotide_and_Nonnucleotide_Reverse_Transcriptase_Inhibitors.txt |
Protease inhibitors target viral proteases which are key enzymes for the completion of viral maturation.
Learning Objectives
• Describe the mechanism of action for protease inhibitors
Key Points
• Protease inhibitors mimic peptides or are chemicals that can be inserted in the active site of a protease. They prevent it from binding the viral polyproteins.
• Such drugs were one of the first to be used against HIV. They are an inseparable part of the HIV/AIDS therapy.
• Mutations in the enzyme active site and other sites, which cause conformational changes, can cause resistance.
Key Terms
• cross-resistance: Bacterial or viral resistance to a chemical which causes resistance to other chemicals of the same group.
Proteases are enzymes that have the ability to cut proteins into peptides. They are used by some viruses (e.g., HIV) to cleave precursor long protein chains into individual proteins. This allows the completion of the assembly step in the viral life cycle where the proteins and the viral RNA come together to form virion particles ready to exit the cell.
The design of protease inhibitors, that could be used to battle HIV, started soon after the discovery of the virus. The first approved protease inhibitor drug was released on the market in 1995, only 10 years after the discovery of HIV. These drugs are an inseparable part of an HIV therapy. Natural protease inhibitors are found in Shiitake mushrooms. The experimental protease inhibitor drugs Zmapp and Brincidofovir are currently being tested to treat the ebola virus disease.
Protease inhibitors are short peptide-like molecules that are competitive inhibitors of the enzyme. Instead of -NH-CO- peptide link, they contain -(CH2-CH(OH)-). When such a peptide gets into the enzyme active site, the protease is unable to cut the linkage and gets inactivated. This leads to a lack of cleavage of the polypeptide chains of two crucial viral proteins, Gag and Pol, which are essential structural and enzymatic proteins of HIV. Their absence blocks the formation of mature virion particles.
Saquinavir is the first clinically used peptide-like inhibitor. Some protease inhibitors do not mimic peptides in their structure. One such drug is Nelfinavir. In general, protease inhibitors exhibit the unusual side effect of fat storage in non-typical organs and tissues. The reasons for this are still unclear.
Mutations in the enzyme active site and other sites, which cause conformational changes, can cause resistance. Quite often one mutation can lead to resistance to many different drugs simultaneously since they all share the same mode of action. This is called cross-resistance. It is one of the major drawbacks of protease inhibitors therapy.
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Learning Objectives
• Compare and contrast the mechanisms of action for: polyene, azole,allylamine and echinocandin antifungals
The field of mycology deals with the study of fungi and has resulted in the identification of over 60,000 species of fungi. Fungi are classified as eukaryotic organisms which are primarily classified based on spore production. The classification and identification of a species of fungi by spore class, in combination with the basic biological mechanism(s) it uses to sustain life, is key in developing anti-fungal drugs.
The development of antifungal drugs focuses on the classes of mycotic diseases for which fungi are responsible. These classes include hypersensitivity—allergic reactions based on the presence of mold and spores; mycotoxicoses—diseases based on the presence of fungi that produce toxins in animal feed and human food products; mycetismus—mushroom poisoning; and lastly, mycoses—characterized by infection.
Disease-causing fungi are targeted and then drug classes are classified based on drug structure or mechanism. Some of the major classes of antifungal medication include polyene antifungals, azole antifungals, allylamines, and echinocandins. It is important to note that antifungal drugs are not limited to these classes, as there are additional drugs capable of targeting fungi that do not fall into these categories.
Polyene Antifungals
Polyene antifungals are characterized by the presence of multiple conjugated double bonds in the drug structure. This specific antifungal drug class targets the fungal cell membrane. The target sterol is ergosterol, which is specific to fungi cell membranes; in animal cell membranes cholesterol is the key sterol. The fungal cell membrane becomes leaky, resulting in movement of essential cellular contents, such as organic molecules and ions, out of the cell. Amphotericin B is an example of a polyene antifungal; it is selective for ergosterol and can be used as a broad spectrum drug administered intravenously.
Azole Antifungals
Azole antifungals are characterized by the ability to inhibit ergosterol synthesis in fungal membranes. The biosynthesis of ergosterol requires the enzyme lanosterol 14 α-demethylase. This enzyme is needed to convert lanosterol to ergosterol. Targeting this enzyme prevents ergosterol production. Thus, the fungal membrane structure is depleted of ergosterol and the fungus dies. The various types of azole classified drugs include imidazole, triazole and thiazole antifungals. Azole drugs are broad-spectrum drugs and treat fungal infections of the skin or mouth. An example of an azole drug is Clotrimazole, commonly used to treat athlete’s foot, ringworm, vaginal yeast infections, and oral thrush.
Allylamine Antifungals
Allylamine antifungals are characterized by the ability to inhibit fungal squalene metabolism. The biosynthesis of ergosterol requires an enzyme called squalene peroxidase. Squalene peroxidase is responsible for catalyzing the first step in ergosterol biosynthesis; inhibition of this enzyme results in disruption of ergosterol synthesis. The inhibition of squalene metabolism is toxic to the fungi because of the buildup of squalene and the inhibition of ergosterol synthesis. An example of an allylamine drug is Terbinafine, which is commonly used to treat fungal skin infections.
Echinocandin Antifungals
Echinocandins are characterized by their ability to inhibit synthesis of a key component of the fungal cell wall, while previously discussed drugs target the fungal cell membrane. Cell wall synthesis requires the production of glucan by the enzyme 1,3-β glucan synthase. Echinocandins specifically inhibit glucan synthesis by targeting that enzyme. This class of drug is most effective when administered by injection, as it is poorly absorbed when administered orally. Echinocandin injection allows the drug to treat a systemic infection of the sort typically seen in immunocompromised patients. An example of an echinocandin based drug is Caspofungin. Caspofungin blocks cell-wall synthesis by disrupting glucan synthesis; it can target invasive candidiasis and aspergillus.
Additional Antifungal Drugs
The major classes of antifungal drugs are discussed above are not the only drugs capable of effectively targeting fungi. The emergence of alternative medicine as a hot field of research has also increased the list of available antifungal compounds. For example, numerous compounds and essential oils found in nature have been found to have antifungal properties that could be utilized for treatment. Examples of these include coconut oil, orange oil, olive leaf, and zinc.
The identification of additional antifungal compounds is key to the development of drugs that can replace existing drugs to which fungi have developed resistance. The discovery process for effective and fungi-specific drugs is enduring and laborious, as the drugs must be specific for fungi cells. However, with the expansion of molecular studies in fungal organisms, the opportunity to identify novel and fungal specific mechanisms will allow for the development of new drugs.
Key Points
• The various classes of antifungal drugs exploit the unique fungal structure.
• The synthesis of both cell membrane and cell wall components are key targets for antifungal drugs.
• Classes of antifungal medications include: polyene antifungals, azole drugs, allylamines and echinocandins.
Key Terms
• ergosterol: major component of fungal cell membranes.
• mycology: the study of fungi | textbooks/bio/Microbiology/Microbiology_(Boundless)/13%3A_Antimicrobial_Drugs/13.08%3A_Other_Antimicrobial_Drugs/13.8A%3A_Antifungal_Drugs.txt |
Antiprotozoan and antihelminthic drugs are characterized based on structure and the mechanism of action by which they target the organism.
Learning Objectives
• Describe the objective of drugs against helminths anf the disadvantages to developing drugs against protozoa
Key Points
• Antiprotozoan drugs are typically species specific.
• It is essential that antiprotozoan drugs target pathways and mechanisms specific to protozoa as overlap in the basic biology can result in inaccurate targeting of the drug to both the host and protozoa.
• Antihelminthic drugs typically focus on the disruption of structural mechanisms that maintain body structure resulting in paralysis of the helminth which promotes expulsion.
Key Terms
• helminth: A parasitic roundworm or flatworm.
• protozoa: Protozoa are a diverse group of unicellular eukaryotic organisms, many of which are motile. Originally, protozoa had been defined as unicellular protists with animal-like behavior, e.g., movement. Protozoa were regarded as the partner group of protists to protophyta, which have plant-like behavior, e.g., photosynthesis.
• Parasite: Parasitism is a non-mutual relationship between organisms of different species where one organism, the parasite, benefits at the expense of the other, the host.
Parasites are organisms that live on or in a host organism to obtain food. Two major classes of parasitic organisms include protozoa and helminths.
Protozoa are unicellular eukaryotic organisms that are classified as either free-living or parasitic organisms. Protozoa are further classified based on their mode of locomotion and include: Sarcodina (amoeba); Mastigophora (flagellates); Ciliophora (ciliates); and Sporozoa (non motile in adult form). Some examples of diseases caused by protozoa include: Malaria, Giardia, Trichomoniasis, and Leishmaniasis.
Helminths are multicellular eukaryotic organisms that are also classified as either free-living or parasitic chemoheterotrophic organisms. Helminths are parasitic worms and are divided into three major groups including: flatworms (platyhelminths); thorny-headed worms (acanthocephalins); and roundworms (nematodes and hookworms).
The variation that exists between protozoa contributes to complications associated with developing effective drugs. The lack of similarities between protozoans demands the need for highly specific drugs and medications against individual pathogens. In addition, protozoa are eukaryotic and exhibit similar properties and metabolic pathways as human cells. Therefore, the drugs that are developed to target protozoans are classified by either their mechanism of action or the organism for which they target. In terms of mechanism of actions, most antiprotozoan drugs specifically target the organism to prevent its growth and reproduction.
Protozoal diseases can also be prevented by targeting the route of transmission and/or targeting vector organisms. For example, Malaria is caused by the protozoan Plasmodia. This parasite is injected into humans via mosquitoes. The development of antimalarial drugs are based on the life cycle of Plasmodiain both the mosquito and human host.
Other types of antiprotozan drugs specifically target metabolic mechanisms utilized by the parasite. For example, African sleeping sickness is caused by trypanosomes. The drug Eflornithine attacks this parasite by targeting an enzyme responsible for regulating cell division.
Helminths are characterized as various types of parasitic worms, which are effectively targeted by promoting expulsion from the body. Parasitic helminths worms include: tapeworms, flukes, leeches and hookworms. The drugs utilized to target helminths are characterized based on chemical structure and mechanism of action. A few examples of the major drug classes include: piperazine, benzimidazole, levamisole, pyrantel, morantel and emodepside.
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Pathogenicity refers to the ability of an organism to cause disease (ie, harm the host). This ability represents a genetic component of the pathogen and the overt damage done to the host is a property of the host-pathogen interactions. Commensals and opportunistic pathogens lack this inherent ability to cause disease.
Thumbnail: The biohazard symbol was developed by the Dow Chemical Company in 1966 for their containment products. It is used in the labeling of biological materials that carry a significant health risk. (Public Domain; Silsor).
14: Pathogenicity
Microbes gain access to human tissues via mucosal surfaces within the body or epithelial surfaces on the outside of the body.
Learning Objectives
• Recognize the various methods and types of microorganism transmission: vectors, hosts, horizontal, vertical transmissions
Key Points
• Transmission can be direct (vertically or horizontally) or indirect.
• Infectious agents are generally specialized for a particular method of transmission.
• A locus is the point on the body where a pathogen enters.
Key Terms
• infectious: Infectious diseases, also known as transmissible diseases or communicable diseases, comprise clinically evident illness (i.e., characteristic medical signs and/or symptoms of disease) resulting from the infection, presence, and growth of pathogenic biological agents in an individual host organism.
• pathogen: Any organism or substance, especially a microorganism, capable of causing disease, such as bacteria, viruses, protozoa, or fungi. Microorganisms are not considered to be pathogenic until they have reached a population size that is large enough to cause disease.
• contagious: Of a person, having a disease that can be transmitted to another person by touch.
Microbes gain access to human tissues via two main types of routes: mucosal surfaces within the body (linings of the respiratory, digestive, reproductive, or urinary tracts) or epithelial surfaces on the outside of the body (areas of skin that are either undamaged or compromised due to insect bites, cuts/scrapes, or other wounds).
Transmission of Microorganisms
Transmission of microorganisms occurs directly from one person to another by one or more of the following means:
• droplet contact by coughing or sneezing on another person
• direct physical contact by touching an infected person
• direct physical contact (usually by touching soil contamination or a contaminated surface)
• airborne transmission (if the microorganism can remain in the air for long periods)
• fecal-oral transmission (usually from contaminated food or water sources)
• contamination via intravenous drug us
• contamination from blood given via transfusion or organ transplants
Transmission can also be indirect via another organism, either a vector (like a mosquito) or an intermediate host (like how a tapeworm from a pig can be transmitted to humans who ingest improperly cooked pork).
Horizontal or Vertical Transmission
Disease can also be directly transmitted in two ways: horizontally or vertically. Horizontal disease transmission occurs from one individual to another in the same generation (peers in the same age group), and can occur by either direct contact (licking, touching, biting), or indirect contact. Vertical disease transmission involves passing a disease causing agent vertically from parent to offspring.
Pathogens must have a way to be transmitted from one host to another to ensure their species ‘ survival. Infectious agents are generally specialized for a particular method of transmission. Taking an example from the respiratory route, from an evolutionary perspective a virus or bacteria that causes its host to develop coughing and sneezing symptoms has a great survival advantage: it is much more likely to be ejected from one host and carried to another.
A locus is the point on the body where a pathogen enters. In droplet contact and other airborne transmission it is generally the respiratory system through the nose, mouth, or eye surfaces. In direct physical and indirect contact it is generally through a wound in the skin or through a mucous membrane. In fecal-oral transmission, it is through the mouth. In vector-borne transmission, it is at the bite or sting of the vector. Other common indirect routes include contaminated food or water.
Sexual Transmission
In sexual transmission, infection originates directly between surfaces in contact during intercourse (the usual route for bacterial infections and those infections causing sores) or from secretions (semen or the fluid secreted by the excited female). Sexually transmitted diseases such as HIV and Hepatitis B are thought to be transmitted through unprotected sexual intercourse (including anal and oral routes), contaminated blood transfusions, sharing hypodermic needles, and from mother to child during pregnancy, delivery, or breastfeeding. Bodily fluids such as saliva and tears do not transmit HIV. Oral sexual practices have increased the incidence of herpes simplex virus 1 (which is usually responsible for oral infections) in genital infections and the increased incidence of the type 2 virus (more common genitally) in oral infections. Herpes diseases that are transmitted primarily by oral means may be caught through direct contact with an infectious area of the skin.
Direct Contact: Contagious Diseases
Diseases that can be transmitted by direct contact are called contagious (contagious is not the same as infectious). Although all contagious diseases are infectious, not all infectious diseases are contagious. Interestingly, some contagious diseases like tuberculosis were not classically considered to be contagious even though they are transmissible from person to person. Direct transmission can also occur by sharing a towel (where the towel is rubbed vigorously on both bodies) or items of clothing in close contact with the body (socks, for example) if they are not washed thoroughly between uses. Some diseases that are transmissible by direct contact include Athlete’s foot and impetigo. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.01%3A_Entry_into_the_Host/14.1A%3A_Portals_of_Microbe_Entry.txt |
Infection begins when an organism successfully colonizes a host by entering the host’s body, growing and multiplying from there.
Learning Objectives
• Distinguish between colonization and infection
Key Points
• Some virulent bacteria produce special proteins that allow them to colonize parts of the host body.
• Wound colonization refers to nonreplicating microorganisms within the wound, while in infected wounds replicating organisms exist and tissue is injured.
• While a few organisms can grow at the initial site of entry, many migrate and cause systemic infection in different organs.
Key Terms
• infection: An uncontrolled growth of harmful microorganisms in a host.
Infection begins when an organism successfully colonizes by entering the body, growing and multiplying from there. Most humans are not easily infected. Those who are weak, sick, malnourished, have cancer or are diabetic possess an increased susceptibility to chronic or persistent infections. Individuals who have a suppressed immune system are particularly susceptible to opportunistic infections.
Entrance to the host generally occurs through the mucosa in orifices like the oral cavity, nose, eyes, genitalia, anus, or open wounds. While a few organisms can grow at the initial site of entry, many migrate and cause systemic infection in different organs. Some pathogens grow within the host cells (intracellular) whereas others grow freely in bodily fluids. Some virulent bacteria produce special proteins that allow them to colonize parts of the host body. Helicobacter pylori is able to survive in the acidic environment of the human stomach by producing the enzyme urease. Colonization of the stomach lining by this bacterium can lead to gastric ulcer and cancer. The virulence of various strains of Helicobacter pylori tends to correlate with the level of production of urease.
Wound colonization refers to nonreplicating microorganisms within the wound, while in infected wounds replicating organisms exist and tissue is injured. All multicellular organisms are colonized to some degree by extrinsic organisms and the vast majority of these exist in either a mutualistic or commensal relationship with the host. An example of the former is the anaerobic bacteria species, which colonizes the mammalian colon, and an example of the latter is various species of staphylococcus that exist on human skin. Neither of these colonizations are considered infections.
The difference between an infection and a colonization is often only a matter of circumstance. Non-pathogenic organisms can become pathogenic given specific conditions and even the most virulent organism requires certain circumstances to cause a compromising infection. Some colonizing bacteria, such as Corynebacteria sp. and viridans streptococci, prevent the adhesion and colonization of pathogenic bacteria. They thus have a symbiotic relationship with the host, preventing infection and speeding wound healing.
The variables involved in the outcome of a host becoming inoculated by a pathogen and the ultimate outcome include: the route of entry of the pathogen and the access to host regions that it gains, the intrinsic virulence of the particular organism, the quantity or load of the initial inoculant, and the immune status of the host being colonized. As an example, the Staphylococcus species remains harmless on the skin. But when present in a normally sterile space, such as in the capsule of a joint or the peritoneum the Staphylococcus species multiplies without resistance and creates a burden on the host. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.01%3A_Entry_into_the_Host/14.1B%3A_Colonization_and_Growth.txt |
Pathogenicity islands (PAIs) are a distinct class of genomic islands acquired by microorganisms through horizontal gene transfer.
Learning Objectives
• Describe the traits characterizing a pathogenicity island and its advantages
Key Points
• Pathogenicity islands are discrete genetic units flanked by direct repeats, insertion sequences or tRNA genes, which act as sites for recombination into the DNA.
• PAIs are incorporated in the genome of pathogenic organisms, but are usually absent from those nonpathogenic organisms of the same or closely related species.
• PAIs carry genes encoding one or more virulence factors, including, but not limited to, adhesins, toxins, or invasins.
Key Terms
• pathogenicity island: A distinct class of genomic islands acquired by microorganisms through horizontal gene transfer.
• virulence factor: Molecules expressed and secreted by pathogens (bacteria, viruses, fungi and protozoa) that enable them to achieve colonization of a niche in the host, immunoevasion, immunosuppression, entry into and out of the cells, and obtaining nutrition from the host.
Pathogenicity Islands and Virulence Factors
Pathogenicity islands (PAIs) are a distinct class of genomic islands acquired by microorganisms through horizontal gene transfer. They are incorporated in the genome of pathogenic organisms, but are usually absent from those nonpathogenic organisms of the same or closely related species. These mobile genetic elements may range from 10-200 kb, and may encode genes contributing to the virulence of the respective pathogen. Typical examples are adherence factors, toxins, iron uptake systems, invasion factors and secretion systems.
Pathogenicity islands are discrete genetic units flanked by direct repeats, insertion sequences or tRNA genes, which act as sites for recombination into the DNA. Cryptic mobility genes may also be present, indicating the provenance as transduction.
One species of bacteria may have more than one PAI (i.e. salmonella has at least five). PAIs are transferred through horizontal gene transfer events such as transfer by a plasmid, phage, or conjugative transposon. PAIs carry genes encoding one or more virulence factors, including, but not limited to, adhesins, toxins, or invasins. They may be located on a bacterial chromosome or may be transferred within a plasmid. The GC-content of pathogenicity islands often differs from that of the rest of the genome, potentially aiding in their detection within a given DNA sequence.
PAIs are flanked by direct repeats; the sequence of bases at two ends of the inserted sequence are the same. They carry functional genes such as integrases, transposases, or part of insertion sequences, to enable insertion into host DNA. PAIs are often associated with tRNA genes, which target sites for this integration event. They can be transferred as a single unit to new bacterial cells, thus conferring virulence to formerly benign strains.
14.1D: Adherence
Adhesins are cell-surface components or appendages of bacteria that facilitate bacterial adhesion to other cells or to inanimate surfaces.
Learning Objectives
• Review the role of adhesins, including fimbriae and the Dr family, in pathogenic bacteria
Key Points
• Adhesins are a type of virulence factor.
• Adherence is an essential step in bacterial pathogenesis or infection, required for colonizing a new host.
• Fimbriae are believed to be involved in attachment to solid surfaces or to other cells and are essential for the virulence of some bacterial pathogens.
Key Terms
• adhesin: Any of several factors that enable bacteria to adhere to epithelial surfaces as a step towards infection.
• fimbriae: Fine filaments of protein distributed over the surface of bacteria that are believed to be involved in attachment to solid surfaces or to other cells, and are essential for the virulence of some bacterial pathogens.
Adhesins are cell-surface components or appendages of bacteria that facilitate bacterial adhesion or adherence to other cells or to inanimate surfaces. Adhesins are a type of virulence factor. Adherence is an essential step in bacterial pathogenesis or infection, required for colonizing a new host. For example, nontypeable Haemophilus influenzae expresses the adhesins Hia, Hap, Oap, and a hemagglutinating pili.
Fimbriae are fine filaments of protein, just 3–10 nanometers in diameter and up to several micrometers in length. They are distributed over the surface of the cell, and resemble fine hairs when seen under the electron microscope. Fimbriae are believed to be involved in attachment to solid surfaces or to other cells, and are essential for the virulence of some bacterial pathogens. Most fimbriae of Gram-negative bacteria function as adhesins, but in many cases the actual adhesin is a minor subunit protein at the tip of the fimbriae. In Gram-positive bacteria, a protein or polysaccharide surface layer serves as the specific adhesin. To effectively achieve adherence to host surfaces, many bacteria produce multiple adherence factors called adhesins.
The Dr family of adhesins bind to the Dr blood group antigen component of decay-accelerating factor (DAF). These proteins contain both fimbriated and afimbriated adherence structures and mediate adherence of uropathogenic Escherichia coli to the urinary tract. They do so by inducing the development of long cellular extensions that wrap around the bacteria. They also confer the mannose-resistant hemagglutination phenotype, which can be inhibited by chloramphenicol. The N-terminal portion of the mature protein is thought to be responsible for chloramphenicol sensitivity. Also, they induce activation of several signal transduction cascades, including activation of PI-3 kinase. The Dr family of adhesins are particularly associated with cystitis and pregnancy-associated pyelonephritis.
Adhesins are attractive vaccine candidates because they are often essential to infection and are surface-located, making them readily accessible to antibodies. The effectiveness of anti-adhesin antibodies is illustrated by studies with FimH, the adhesin of uropathogenic Escherichia coli (UPEC). In animal models, passive immunization with anti FimH-antibodies and vaccination with the protein significantly reduced colonization by UPEC. Moreover, the Bordetella pertussis adhesins FHA and pertactin are components of 3 of the 4 acellular pertussis vaccines currently licensed for use in the U.S.
14.1E: Host Risk Factors
Individuals who are weak, sick, malnourished, have cancer, or are diabetic have increased susceptibility to chronic or persistent infections.
Learning Objectives
• Recognize the risk factors that increase chance of disease
Key Points
• Risk of infection is a nursing diagnosis; “the state in which an individual is at risk to be invaded by an opportunistic or pathogenic agent (virus, fungus, bacteria, protozoa, or other parasite) from endogenous or exogenous sources” is the diagnostic definition of risk.
• Examples of risk factors includes decreased immune system secondary to disease, compromised circulation secondary to peripheral vascular disease, compromised skin integrity secondary to surgery, or repeated contact with contagious agents.
• Techniques like hand washing, wearing gowns, and wearing face masks can help prevent infections from being passed from the surgeon to the patient or vice versa.
Key Terms
• opportunistic infection: Any infection that causes disease and occurs only when the host’s immune system is impaired.
• colitis: inflammation of the colon.
• vaccination: inoculation with a vaccine in order to protect a particular disease or strain of disease.
Most humans are not easily infected. Those who are weak, sick, malnourished, have cancer, or are diabetic have increased susceptibility to chronic or persistent infections. Individuals who have a suppressed immune system or who are on immunosuppressive drugs are particularly susceptible to opportunistic infections.
Risk of infection is a nursing diagnosis which is defined as “the state in which an individual is at risk to be invaded by an opportunistic or pathogenic agent (virus, fungus, bacteria, protozoa, or other parasite) from endogenous or exogenous sources. ” The risk of infection depends on a number of endogenous sources. Skin damage from incision can increase a patient’s risk of infection, as can very young or old age, due to a naive or compromised immune system respectively. Examples of risk factors include decreased immune system resulting from disease, compromised circulation caused by peripheral vascular disease, compromised skin integrity as a result of surgery, or repeated contact with contagious agents.
Risk Reduction
Techniques like hand washing, wearing gowns, and wearing face masks can help prevent infections from being passed between the surgeon and the patient. Frequent hand washing remains the most important defense against the spread of unwanted organisms. Good nutrition is necessary to reduce risk. So is a healthy lifestyle. By avoiding illicit drugs, using a condom, and entering an exercise program one can improve one’s risk factors. Foods should be cooked to recommended temperatures; avoid foods that have been left outside for long. One should not take antibiotics for longer than needed or when they are not needed—long term use of antibiotics leads to resistance and increased the chance of developing opportunistic infections like clostridium difficile colitis. Vaccination is another vital means of preventing infections by encouraging the development of immune resistance in vaccinated hosts. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.01%3A_Entry_into_the_Host/14.1C%3A_Pathogenicity_Islands_and_Virulence_Factors.txt |
Several barriers protect organisms from infection including mechanical, chemical, and biological barriers.
Learning Objectives
• Discuss the various innate barriers within humans that provide protection from infection
Key Points
• The flushing action of tears and urine also mechanically expels pathogens, while mucus secreted by the respiratory and gastrointestinal tract serves to trap and entangle microorganisms.
• The human microbiome (or human microbiota ) is the aggregate of microorganisms that reside on the surface and in deep layers of skin, in the saliva and oral mucosa, in the conjunctiva, and in the gastrointestinal tracts.
• Some of these organisms perform tasks that are useful for the human host, but the majority have no known beneficial or harmful effect.
Key Terms
• lysozyme: A bacteriolytic (or antibiotic) enzyme found in many animal secretions and in egg white.
• microbiota: The microbial flora harbored by normal, healthy individuals.
• flora: the microorganisms that inhabit some part of the body, such as intestinal flora
Several barriers protect organisms from infection, including mechanical, chemical, and biological barriers. However, as organisms cannot be completely sealed against their environments, other systems act to protect body openings such as the lungs, intestines, and the genitourinary tract. In the lungs, coughing and sneezing mechanically eject pathogens and other irritants from the respiratory tract. The flushing action of tears and urine also mechanically expels pathogens, while mucus secreted by the respiratory and gastrointestinal tract serves to trap and entangle microorganisms.
Chemical barriers also protect against infection. The skin and respiratory tract secrete antimicrobial peptides such as the β-defensins. Enzymes such as lysozyme and phospholipase A2 in saliva, tears, and breast milk are also antibacterials. Vaginal secretions serve as a chemical barrier following menarche, when they become slightly acidic, while semen contains defensins and zinc to kill pathogens. In the stomach, gastric acid and proteases serve as powerful chemical defenses against ingested pathogens. Within the genitourinary and gastrointestinal tracts, commensal flora serve as biological barriers by competing with pathogenic bacteria for food and space and, in some cases, by changing the conditions in their environment, such as pH or available iron. This reduces the probability that pathogens will reach sufficient numbers to cause illness. However, since most antibiotics non-specifically target bacteria and do not affect fungi, oral antibiotics can lead to an “overgrowth” of fungi and cause conditions such as a vaginal candidiasis (a yeast infection). There is good evidence that re-introduction of probiotic flora, such as pure cultures of the lactobacilli normally found in unpasteurized yogurt, helps restore a healthy balance of microbial populations in intestinal infections in children and encouraging preliminary data in studies on bacterial gastroenteritis and inflammatory bowel diseases. Inflammation is one of the first responses of the immune system to infection.
The human microbiome (or human microbiota) is the aggregate of microorganisms that reside on the surface and in deep layers of skin, in the saliva and oral mucosa, in the conjunctiva, and in the gastrointestinal tracts. They include bacteria, fungi, and archaea. Some of these organisms perform tasks that are useful for the human host. However, the majority have no known beneficial or harmful effect. Those that are expected to be present, and that under normal circumstances do not cause disease, but instead participate in maintaining health, are deemed members of the normal flora.
Populations of microbes (such as bacteria and yeasts) inhabit the skin and mucosa. Their role forms part of normal, healthy human physiology. However, if microbe numbers grow beyond their typical ranges (often due to a compromised immune system) or if microbes populate atypical areas of the body (such as through poor hygiene or injury), disease can result.
Many of the bacteria in the digestive tract are collectively referred to as the gut flora. In this context, gut is synonymous with intestinal, and flora with microbiota and microflora, the word microbiome is also in use. They are able to break down certain nutrients such as carbohydrates that humans otherwise could not digest. The majority of these commensal bacteria are anaerobes, meaning they survive in an environment with no oxygen. Normal flora bacteria can act as opportunistic pathogens at times of lowered immunity.
Archaea are present in the human gut, but, in contrast to the enormous variety of bacteria in this organ, the numbers of archaeal species are much more limited. Fungi, in particular yeasts, are present in the human gut. The best-studied of these are Candida species. This is because of their ability to become pathogenic in immune compromised hosts. Yeasts are also present on the skin, particularly Malassezia species, where they consume oils secreted from the sebaceous glands.
A small number of bacteria are normally present in the conjunctiva. Staphylococcus epidermidis and certain coryneforms such as Propionibacterium acnes are dominant. The lachrymal glands continuously secrete, keeping the conjunctiva moist, while intermittent blinking lubricates the conjunctiva and washes away foreign material. Tears contain bactericides such as lysozyme, so that microorganisms have difficulty in surviving the lysozyme and settling on the epithelial surfaces.
The gut flora is the human flora of microorganisms that normally live in the digestive tract and can perform a number of useful functions for their hosts. Though people can survive with no gut flora, the microorganisms perform a host of useful functions such as fermenting unused energy substrates, training the immune system, preventing growth of harmful species, regulating the development of the gut, producing vitamins for the host (such as biotin and vitamin K), and producing hormones to direct the host to store fats. However, in certain conditions, some species are thought to be capable of causing disease by causing infection or increasing cancer risk for the host.
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Normal microbiota are the microorganisms that reside in the bodies of all humans.
Learning Objectives
• Explain the relationship between the normal microbiota and the host upon infection of a pathogen
Key Points
• The phrase “normal microbiota ” refers to the microorganisms that reside on the surface and deep layers of skin, in the saliva and oral mucosa, in the conjunctiva, and in the gastrointestinal tracts of every human being.
• These microbiota are not harmful to humans; some are even beneficial and most help maintain our health.
• Our normal microbiota consists of various bacteria, fungi, and archaea.
• While our bodies are happy to host the array of microbiota that are considered “normal,” the human body does not take a back seat when infection tries to use it as a host.
• Resistance to and recovery from viral infections depends on the interactions that occur between virus and host. The host has a variety of barriers that it uses to prevent infection. One of the first lines of defense is mucus, which has a range of normal microbiota.
• There are a number of other humoral components of the nonspecific immune system as well.
Key Terms
• host: A cell or organism which harbors another organism or biological entity, usually a parasite.
• microorganism: An organism that is too small to be seen by the unaided eye, especially a single-celled organism, such as a bacterium.
• interferon: Any of a group of glycoproteins, produced by the immune system, that prevent viral replication in infected cells.
Normal Microbiota
The phrase “normal microbiota” refers to the microorganisms that reside on the surface and deep layers of skin, in the saliva and oral mucosa, in the conjunctiva, and in the gastrointestinal tracts of every human being. These microorganisms are not harmful to humans; in fact, some are even beneficial and all help maintain our health. Our normal microbiota consists of various bacteria, fungi, and archaea. An example of our bacterial microbiota is E. coli . Many people think of E. coli as the bacteria that makes you sick; however while it has that capacity, it can also remain dormant and benign in your gastrointestinal tract for your entire life. All humans actually acquire E. colishortly after birth with the intake of food or water. Other forms of bacteria present in the human gut are necessary for proper digestion of carbohydrates.
Host Relationships
While our bodies are happy to host the array of microbiota that are considered “normal,” the human body does not take a back seat when infection tries to use it as a host. Interestingly, normal microbiota can be key players helping the body fight off infection. Resistance to and recovery from viral infections depends on the interactions that occur between the virus and its host. The host has a variety of defenses that it uses to prevent infection. One of the first lines of defense is mucus, which has a range of normal microbiota that compete with and may even attack invading bacteria and virae.
Once a virus or bacteria makes its way past the skin and mucosa, there may be changes that occur in the host to diminish the invader’s effectiveness. An example of such a change is a fever. There are a number of other humoral components of the nonspecific immune system as well. Specific immune responses are produced by antibodies. Different interferons (IgA, IgG, IgM, etc. ) play roles in defeating viruses located in our membranes. The body does not easily become a host to infection; it has a line up of defenses to try to protect you from harm.
14.2B: Opportunistic Microorganisms
Learning Objectives
• Describe the traits of an opportunistic microorganism
In the general realm of biology, an opportunist is an organism that is able sustain its life from a number of different sources, but when favorable conditions arise, the organism immediately takes advantage of the opportunity to thrive. When the focus is turned more specifically to microbiology, scientists call organisms that behave this way opportunistic microorganisms. A microorganism is a microscopic organism that can either be a single cell, cell cluster, or multicellular. Microorganisms are very diverse and include bacteria, fungi, algae, and protozoa. Opportunistic microorganisms are typically non-pathogenic microorganisms that act as a pathogen in certain circumstances. They lay dormant for long periods of time until the hosts’ immune system is suppressed and then they seize the opportunity to attack.
Patients with Human Immunodeficiency Virus (HIV) are particularly susceptible to opportunistic infections. HIV can develop into Acquired Immune Deficiency Syndrome ( AIDS ), which infects and destroys helper T cells (specifically CD4+ T cells). When the number of CD4+ T cell numbers fall below a critical level, cell-mediated immunity is lost. When immunity is lost, the opportunistic microorganisms can easily infect the AIDS patient without being destroyed by the immune system. These opportunistic pathogens thrive while the human body slowly deteriorates.
An example of an opportunistic microorganism is Haemophilus ducreyi. This microorganism infects its host through broken skin or epidermis. In other words, without an open wound, this sexually transmitted disease would be unable to use the human body as a host. It takes advantage of the opportunity to infect the lymphocytes, macrophages and granulocytes as soon as it enters the area of broken skin.
Key Points
• A microorganism is a microscopic organism that can either be a single cell, cell cluster, or multicellular. Microorganisms are very diverse and include bacteria, fungi, algae, and protozoa.
• Opportunistic microorganisms are typically non-pathogenic microorganisms that act as a pathogen in certain circumstances. They lay dormant for long periods of time until the host ‘s immune system is suppressed and then they take that opportunity to attack.
• Haemophilus ducreyi, a microorganism, infects its host through broken skin or epidermis. Without the open wound, this sexually transmitted disease would be unable to use the human body as a host.
Key Terms
• microorganism: An organism that is too small to be seen by the unaided eye, especially a single-celled organism, such as a bacterium.
• Opportunistic: Taking advantage of situations that arise.
• immunodeficiency: A depletion in the body’s natural immune system, or in some component of it. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.02%3A_Overview_of_Microbe-Host_Interactions/14.2A%3A_Normal_Microbiota_and_Host_Relationships.txt |
Cooperative behavior, includes mutualism and altruism, benefits one party while the other performs a certain behavior.
Learning Objectives
• Compare and contrast the following cooperative behavior: mutalism and altruism
Key Points
• In microbial systems, there are two main types of cooperation, altruism and mutualism.
• Mutualism is a relationship between microorganisms that is mutually beneficial (+/+). This means that both parties are receiving positive things from their interaction.
• Altruism is a relationship between microorganisms that is beneficial to one party, but harmful to the the (+/-). Scientists believe that the individual that is at a loss performs the action because they believe it will ultimately benefit others whom they share a relationship with (like family).
Key Terms
• Cooperation: Association for mutual benefit.
• mutualism: A relationship between individuals of different species in which both individuals benefit
• altruism: Regard for others, both natural and moral; devotion to the interests of others; brotherly kindness; – opposed to egoism or selfishness.
Microbial Cooperation
A cooperative behavior benefits one party while the other performs a certain behavior or takes a particular action. In microbial systems, there are two main types of cooperation, altruism and mutualism. It is important to remember that microorganisms include bacteria, archaea, fungi, and protists. They are too small to be seen with the naked eye, but they play a huge role in the world as we know it and have a great deal of biological diversity.
Mutualism
Mutualism is a relationship between microorganisms that is mutually beneficial (+/+). This means that both parties benefit from their interaction. A microbial example is the interaction between protozoa and archaea in the digestive tracts of some animals. These animals eat cellulose which is broken down by the protozoa to obtain energy. This process releases hydrogen as a waste product, which in turn reduces energy production. Specialized archaea convert the hydrogen (which they need) to methane, which allows energy production to increase. Both the protozoa and archaea benefit from this relationship.
Altruism
Altruism is a relationship between microorganisms that is beneficial to one party, but harmful to the the (+/-). Most scientists believe that the individual that is harmed, or at a loss, performs the action because they believe it will ultimately benefit others whom it is close to or share a relationship with (like family). On a microscopic level, this happens with programmed cell death, or apoptosis. Although it does not seem like it would be beneficial for the cell to die, it has been suggested that the resources it was using could be better utilized by other cells for growth and survival.
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Learning Objectives
• Recognize the ways a host can be infected by, and resist, pathogens
The human microbiome (or human microbiota) is the aggregate of microorganisms that reside on the surface and in deep layers of skin, in the saliva and oral mucosa, in the conjunctiva, and in the gastrointestinal tracts. They include bacteria, fungi, and archaea. Some of these organisms perform tasks that are useful for the human host. However, the majority have no known beneficial or harmful effect. Organisms that are expected to be present, and that under normal circumstances do not cause disease, but participate in maintaining health, are deemed members of the normal flora.
Many of the bacteria in the digestive tract, collectively referred to as the gut flora, are able to break down certain nutrients such as carbohydrates that humans otherwise could not digest. The majority of these commensal bacteria are anaerobes, meaning they survive in an environment with no oxygen. Normal flora bacteria can act as opportunistic pathogens at times of lowered immunity. Escherichia coli (E. coli) is a bacterium that lives in the colon. It is an extensively studied model organism. Certain mutated strains of these gut bacteria do cause disease. An example is E. coli O157:H7.
Infection is the invasion of a host organism’s bodily tissues by disease-causing organisms, their multiplication, and the host’s reaction to these organisms and the toxins they produce. Infections are caused by pathogens such as viruses, prions, bacteria, and viroids, and larger organisms like macroparasites and fungi.
It is important to keep in mind that although the immune system has evolved to be able to control many pathogens, pathogens themselves have evolved ways to evade the immune response. An example already mentioned is in Mycobactrium tuberculosis, which has evolved a complex cell wall that is resistant to the digestive enzymes of the macrophages that ingest them, and thus persists in the host, causing the chronic disease tuberculosis. This section briefly summarizes other ways in which pathogens can “outwit” immune responses. But keep in mind, although it seems as if pathogens have a will of their own, they do not. All of these evasive “strategies” arose strictly by evolution, driven by selection.
Bacteria sometimes evade immune responses because they exist in multiple strains, such as different groups of Staphylococcus aureus. S. aureus is commonly found in minor skin infections, such as boils, and some healthy people harbor it in their nose. One small group of strains of this bacterium, however, called methicillin-resistant Staphylococcus aureus, has become resistant to multiple antibiotics and is essentially untreatable. Different bacterial strains differ in the antigens on their surfaces. The immune response against one strain (antigen) does not affect the other; thus, the species survives.
Another method of immune evasion is mutation. Because viruses’ surface molecules mutate continuously, viruses like influenza change enough each year that the flu vaccine for one year may not protect against the flu common to the next. New vaccine formulations must be derived for each flu season.
Genetic recombination—the combining of gene segments from two different pathogens—is an efficient form of immune evasion. For example, the influenza virus contains gene segments that can recombine when two different viruses infect the same cell. Recombination between human and pig influenza viruses led to the 2010 H1N1 swine flu outbreak.
Pathogens can produce immunosuppressive molecules that impair immune function, and there are several different types. Viruses are especially good at evading the immune response in this way, and many types of viruses have been shown to suppress the host immune response in ways much more subtle than the wholesale destruction caused by HIV.
Key Points
• Infections are caused by pathogens such as viruses, prions, bacteria, and viroids, and larger organisms like macroparasites and fungi.
• Mammalian hosts react to infections with an innate response, often involving inflammation, followed by an adaptive response.
• Pathogens can evade the body’s immune responses through means that include specialized adaptations, mutation, evolved resistance to treatments, genetic recombination, and the production of immunosuppressive molecules that impair immune function.
Key Terms
• Human microbiome: The aggregate of microorganisms that reside on the surface and in deep layers of skin, in the saliva and oral mucosa, in the conjunctiva, and in the gastrointestinal tracts. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.03%3A_Penetrating_Host_Defenses/14.3A%3A_Penetrating_Host_Defenses.txt |
Learning Objectives
• Describe the function of the pili in regards to pathogenecity
A pilus (Latin for “hair;” plural: pili) is a hairlike appendage found on the surface of many bacteria. The terms pilus and fimbria (Latin for “thread” or “fiber,” plural: fimbriae ) can be used interchangeably, although some researchers reserve the term pilus for the appendage required for bacterial conjugation. All pili are primarily composed of oligomeric pilin proteins.
Dozens of these structures can exist on the bacteria. Some bacterial viruses or bacteriophages attach to receptors on pili at the start of their reproductive cycle. Pili are antigenic. They are also fragile and constantly replaced, sometimes with pili of different composition, resulting in altered antigenicity. Specific host responses to old pili structure are not effective on the new structure. Recombination genes of pili code for variable (V) and constant (C) regions of the pili (similar to immunoglobulin diversity).
Conjugative pili allow the transfer of DNA between bacteria, in the process of bacterial conjugation. They are sometimes called “sex pili”, in analogy to sexual reproduction, because they allow for the exchange of genes via the formation of “mating pairs”. Perhaps the most well-studied is the F pilus of Escherichia coli, encoded by the F plasmid or fertility factor.
A pilus is typically 6 to 7 nm in diameter. During conjugation, a pilus emerging from donor bacterium ensnares the recipient bacterium, draws it in close, and eventually triggers the formation of a mating bridge, which establishes direct contact and the formation of a controlled pore that allows transfer of DNA from the donor to the recipient. Typically, the DNA transferred consists of the genes required to make and transfer pili (often encoded on a plasmid), and is a kind of selfish DNA; however, other pieces of DNA often are co-transferred, and this can result in dissemination of genetic traits, such as antibiotic resistance, among a bacterial population. Not all bacteria can make conjugative pili, but conjugation can occur between bacteria of different species.
Some pili, called “type IV pili,” generate motile forces. The external ends of the pili adhere to a solid substrate, either the surface to which the bacteria are attached or to other bacteria, and when the pilus contracts, it pulls the bacteria forward, like a grappling hook. Movement produced by type IV pili is typically jerky, and so it is called “twitching motility,” as distinct from other forms of bacterial motility, such as motility produced by flagella. However, some bacteria, for example Myxococcus xanthus, exhibit gliding motility. Bacterial type IV pilins are similar in structure to the component flagellins of Archaeal flagella.
Attachment of bacteria to host surfaces is required for colonization during infection or to initiate formation of a biofilm. A fimbria is a short pilus that is used to attach the bacterium to a surface. Fimbriae are either located at the poles of a cell or are evenly spread over its entire surface. Mutant bacteria that lack fimbriae cannot adhere to their usual target surfaces and, thus, cannot cause diseases. Some fimbriae can contain lectins. The lectins are necessary to adhere to target cells, because they can recognize oligosaccharide units on the surface of these target cells. Other fimbriae bind to components of the extracellular matrix. Fimbriae are found in both Gram-negative and Gram-positive bacteria. In Gram-positive bacteria, the pilin subunits are covalently linked.
Key Points
• The process of bacterial conjugation allow for the exchange of genes via the formation of “sex pili”.
• All pili are primarily composed of oligomeric pilin proteins.
• Conjugative pili allow the transfer of DNA between bacteria in the process of bacterial conjugation.
Key Terms
• pilus: A hair-like appendage found on the cell surface of many bacteria. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.03%3A_Penetrating_Host_Defenses/14.3B%3A_Pili_and_Pilus_Assembly.txt |
Biofilms will form on virtually every non-shedding surface in a non-sterile aqueous (or very humid) environment.
Learning Objectives
• Discuss the importance of biofilms in the biomedical community
Key Points
• Biofilms have been found to be involved in a wide variety of microbial infections in the body.
• Microbes form a biofilm in response to many factors, which may include cellular recognition of specific or non-specific attachment sites on a surface and nutritional cues.
• Bacterial biofilms may impair cutaneous wound healing and reduce topical antibacterial efficiency in healing or treating infected skin wounds.
Key Terms
• biofilm: A thin film of mucus created by and containing a colony of bacteria and other microorganisms.
• sterile: unable to reproduce (or procreate)
A biofilm is an aggregate of microorganisms in which cells adhere to each other on a surface. These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS).
Microbes form a biofilm in response to many factors, which may include cellular recognition of specific or non-specific attachment sites on a surface, nutritional cues, or in some cases, by exposure of planktonic cells to sub-inhibitory concentrations of antibiotics. When a cell switches to the biofilm mode of growth, it undergoes a phenotypic shift in behavior in which large suites of genes are differentially regulated.
Biofilms are ubiquitous. Nearly every species of microorganism, not only bacteria and archaea, have mechanisms by which they can adhere to surfaces and to each other. Biofilms will form on virtually every non-shedding surface in a non-sterile aqueous (or very humid) environment.
Biofilms have been found to be involved in a wide variety of microbial infections in the body, by one estimate in 80% of all infections. Infectious processes in which biofilms have been implicated include common problems such as urinary tract infections, catheter infections, middle-ear infections, formation of dental plaque, gingivitis, and coating contact lenses. Biofilms have also been implicated in less common but more lethal processes such as endocarditis, infections in cystic fibrosis, and infections of permanent indwelling devices such as joint prostheses and heart valves.
More recently it has been noted that bacterial biofilms may impair cutaneous wound healing and reduce topical antibacterial efficiency in healing or treating infected skin wounds. It has recently been shown that biofilms are present on the removed tissue of 80% of patients undergoing surgery for chronic sinusitis. The patients with biofilms were shown to have been denuded of cilia and goblet cells, unlike the controls without biofilms who had normal cilia and goblet cell morphology. Biofilms were also found on samples from two of 10 healthy controls mentioned. The species of bacteria from interoperative cultures did not correspond to the bacteria species in the biofilm on the respective patient’s tissue. In other words, the cultures were negative though the bacteria were present.
Biofilms can also be formed on the inert surfaces of implanted devices such as catheters, prosthetic cardiac valves, and intrauterine devices. New staining techniques are being developed to differentiate bacterial cells growing in living animals, e.g. from tissues with allergy-inflammations.
Pseudomonas aeruginosa biofilms
The achievements of medical care in industrialized societies are markedly impaired due to chronic opportunistic infections that have become increasingly apparent in immunocompromised patients and the aging population. Chronic infections remain a major challenge for the medical profession and are of great economic relevance because traditional antibiotic therapy is usually not sufficient to eradicate these infections.
Pseudomonas aeruginosa is not only an important opportunistic pathogen and causative agent of emerging nosocomial infections but can also be considered a model organism for the study of diverse bacterial mechanisms that contribute to bacterial persistence. In this context the elucidation of the molecular mechanisms responsible for the switch from planktonic growth to a biofilm phenotype and the role of inter-bacterial communication in persistent disease should provide new insights. It should help researchers learn about the pathogenicity of P. aeruginosa, contribute to a better clinical management of chronically infected patients, and lead to the identification of new drug targets for the development of alternative anti-infective treatment strategies.
Dental plaque
Dental plaque is a biofilm that adheres to teeth surfaces and consists of bacterial cells, salivary polymers, and bacterial extracellular products. This accumulation of microorganisms subject the teeth and gingival tissues to high concentrations of bacterial metabolites which results in dental disease. The biofilms attached to the surfaces of some dental alloys, impression materials, dental implants, restorative and cement materials play an essential role concerning the biofilms establishment dynamics toward the physical-chemical properties of the materials which biofilms are attached to.
Legionellosis
Legionella bacteria are known to grow under certain conditions in biofilms, in which they are protected against disinfectants. Workers in cooling towers, persons working in air conditioned rooms, and people taking a shower are exposed to Legionella by inhalation when the systems are not well designed, constructed, or maintained. Neisseria gonorrhoeae is an exclusive human pathogen. Recent studies have demonstrated that it utilizes two distinct mechanisms for entry into human urethral and cervical epithelial cells involving different bacterial surface ligands and host receptors. In addition, it has been demonstrated that the gonococcus can form biofilms on glass surfaces and over human cells. There is evidence for the formation of gonococcal biofilms on human cervical epithelial cells during natural disease. Evidence also suggests that the outer membrane blebbing by the gonococcus is crucial in biofilm formation over human cervical epithelial cells.
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Learning Objectives
• Describe the major toxin types (bacterial toxins and mycotoxins) and their mechanisms of action
Toxins are poisonous substances produced within living cells or organisms and can include various classes of small molecules or proteins that cause disease on contact. The severity and type of diseases caused by toxins can range from minor effects to deadly effects. The organisms which are capable of producing toxins include bacteria, fungi, algae, and plants. Some of the major types of toxins include, but are not limited to, environmental, marine, and microbial toxins. Microbial toxins may include those produced by the microorganisms bacteria (i.e. bacterial toxins) and fungi (i.e. mycotoxins).
Bacterial Toxins
Bacterial toxins are typically classified under two major categories: exotoxins or endotoxins. Exotoxins are immediately released into the surrounding environment whereas endotoxins are not released until the bacteria is killed by the immune system. The release of toxins into the surrounding environment, regardless of when released, results in the disruption of metabolic pathways in the host eukaryote. These metabolic pathways include damaging cell membranes, disrupting protein synthesis, inhibiting neurotransmitter release, or activating the host immune system. The mechanisms of action by which toxins disrupt eukaryotic cell processes are dependent on the target. For example, the bacteria Listeria monocytogenes, associated with food-borne illnesses, specifically targets cholesterol by producing a pore-forming toxin protein, listeriolysin O. This exotoxin affects intracellular processes and creates unregulated pores within the cell membranes of the host. Another example of an exotoxin includes an enterotoxin produced by the bacteria Staphlycoccal aureus. S. aureus can producestaphylococcal enterotoxin B (SEB), associated with intestinal illness, which promotes activation of the immune system. Upon activation of the immune system, the release of large amounts of cytokines, inflammatory related molecules, causes significant inflammation. Lastly, an example of an endotoxin, includes the protein lipopolysaccharide (LPS) produced by gram-negative bacteria. The LPS is a component of the bacteria’s outer membrane and promotes structural integrity. Upon destruction of the membrane by an immune response, the LPS is released and functions as a toxin.
However, bacterial toxins are also currently serving as new sources for potential drug development. Toxins have been shown to exhibit anticancer characteristics and fight again microbial virulence. The investigation of toxins as potential medicinal compounds is currently underway.
Mycotoxins
Mycotoxins are the classes of toxins produced by fungi. Mycotoxins are numerous and production of a specific mycotoxin is not restricted to one specific species. Mycotoxins are secondary metabolites that are toxic to humans and produced by fungi. There are various types of mycotoxins including, but not limited to, aflatoxins, ochratoxins, citrinin, and ergot alkaloids.
Aflatoxins
Aflatoxins are a type of mycotoxin that are produced by certain strains of Aspergillus fungi. The aflatoxins are further broken down into types: AFB1, AFB2, AFG1, and AFG2. These strains are present in a wide range of agricultural commodities associated with tropic and subtropic zones. These commodities include species of peanuts and corn. The most potent toxin is AFB1 and it is associated with carcinogenic effects.
Ochratoxin
Ochratoxin is a type of toxin produced by both Penicillium and Aspergillus species. Ochratoxins are further classified in types A, B and C and differ in structure. Ochratoxins have demonstrated carcinogenic properties and are often found in beverages such as beer and wine, as the fungal species which produce ochratoxins are often found on the plants used to produce these products.
Citrinin
Citrinin is a mycotoxin that has been isolated in numerous species of both Penicillium and Aspergillus. Many of these fungal species are utilized in food processing and are often found in foods including cheese, wheat, rice, corn, and soy sauce. Citrinin is known to function as a nephrotoxin, indicating it has toxic effects on kidney function.
Ergot Alkaloids
Ergot Alkaloids are specific compounds that are produced as toxic alkaloids in Claviceps, a group of fungi associated with grasses, rye, and related plants. The disease caused by ingestion of this fungi is called ergotism. Ergotism is characterized by detrimental effects on the vascular system in particular, including vasoconstriction of blood vessels resulting in gangrene, and eventually, limb loss if left untreated. Additionally, ergotism can present as hallucinations and convulsions as ergot alkaloids target the central nervous system. Due to the vascular system effects of ergot alkaloids, they have been used for medicinal purposes.
Key Points
• Microbial toxins may include those produced by the microorganisms bacteria (i.e. bacterial toxins) and fungi (i.e. mycotoxins ).
• Bacterial toxins can include both endotoxins and exotoxins, which vary in mechanism of action and are species -specific.
• Exotoxins are immediately released into the surrounding environment whereas endotoxins are not released until the bacteria is killed by the immune system.
• Mycotoxins can be classified into numerous categories and are not species-specific because the same mycotoxin can be produced by different fungal species.
Key Terms
• endotoxin: Any toxin secreted by a microorganism and released into the surrounding environment only when it dies.
• exotoxin: Any toxin secreted by a microorganism into the surrounding environment.
• cytokines: Regulatory proteins that function in the regulation of the cells involved in immune system function | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.04%3A_Damaging_Host_Cells/14.4A%3A_Toxins.txt |
Direct damage to the host is a general mechanism utilized by pathogenic organisms to ensure infection and destruction of the host cell.
Learning Objectives
• Describe the different processes used by pathogens to damage the host and ensure infection
Key Points
• Pathogenic organisms must have mechanisms in place to evade attack by the immune system.
• Pathogens can produce enzymes that disrupt normal tissue and allow for further invasion into the tissues.
• Pathogens can produce toxins that interfere with protein function deemed necessary by the host cell for proper maintenance.
Key Terms
• diphtheria: A disease of the upper respiratory tract caused by a toxin secreted by Corynebacterium diphtheriae.
• phagocytosis: the process by which a cell incorporates foreign particles intracellularly.
Direct damage to the host is a general mechanism utilized by pathogenic organisms to ensure infection and destruction of the host cell. The pathogenic organism typically causes damage due to its own growth process. The promotion of disease is characterized by the ability of a pathogenic organism to enter a host and inflict damage and destruction onto the host cell. The pathogenic organism must exhibit specific characteristics that promote its growth into a host cell including, but not limited to, the ability to invade, colonize, and attach to host cells.
The ability of a pathogen to gain entrance to a host cell is fundamental in the ability of the pathogen to promote and cause disease. The ability to manipulate the process of phagocytosis is a mechanism often utilized by bacteria to ensure they effectively invade a host. Phagocytosis is a process utilized by phagocytes (white blood cells) as a defense mechanism to protect from foreign bodies. The phagocytes engulf invaders and present them to additional factors within the immune system that result in their destruction. However, a successful and destructive pathogen often exhibits the ability to evade phagocytosis.
The mechanism(s) utilized by pathogens to avoid phagocytosis include avoiding both contact and engulfment. Pathogens that exhibit the ability to avoid contact utilize various processes to accomplish this, including: the ability to grow in regions of the body where phagocytes are incapable of reaching; the ability to inhibit the activation of an immune response; inhibiting and interfering with chemotaxis which drives the phagocytes to site of infection; and ‘tricking’ the immune system to identify the bacteria as ‘self. ‘ Additional mechanism(s) by which bacteria can avoid destruction is by avoiding engulfment. This is accomplished by the ability of the bacteria to exhibit produce molecules that interfere with the phagocytes ability to internalize the bacteria. Molecules that interfere with this process include certain types of proteins and sugars that block engulfment.
Once the pathogen has successfully evaded engulfment and destruction by the immune system, it is detrimental because the bacteria then multiply. Often times, bacteria will directly attach themselves to host cells and utilize nutrients from the host cell for their own cellular processes. Upon the use of host nutrients for its own cellular processes, the bacteria may also produce toxins or enzymes that will infiltrate and destroy the host cell. The production of these destructive products results in the direct damage of the host cell. The waste products of the microbes will also damage to the cell. Examples of bacteria that will damage tissue by producing toxins, include, Corynebacterium diphtheriae and Streptococcus pyogenes. Specifically, Corynebacterium diphtheriae causes diphtheria, which isa disease of the upper respiratory tract. It produces a toxin, diphtheria toxin, which alters host protein function. The toxin can then result in damage to additional tissues including the heart, liver, and nerves. Streptococcus pyogenes is associated with strep throat and “flesh-eating disease. ” The bacteria produce enzymes which function in disrupting fibrin clots. Fibrin clots will form at sites of injury, in this case, at the site of foreign invasion. The enzymes, capable of digesting fibrin, will open an area within the epithelial cells and promote invasion of the bacteria into the tissues. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.04%3A_Damaging_Host_Cells/14.4B%3A_Direct_Damage.txt |
Type III and IV secretion systems are utilized by pathogenic bacteria to transfer molecules from the bacterial cell to the host cell.
Learning Objectives
• Distinguish between Type III and IV secretion systems
Key Points
• Type III secretion system use a process which injects the secretory molecule into the host cell.
• Type IV secretion systems use a process which is similar to the bacterial conjugation machinery.
• Type IV secretion systems require attachment to the host cell by direct cell-to-cell contact or via a bridge-like apparatus.
• Type IV secretion systems can be used to both transport and receive molecules.
• Type III secretion systems requires a large protein complex to ensure proper transfer of secretory molecules.
Key Terms
• peptidoglycan: A polymer of glycan and peptides found in bacterial cell walls.
• effector: a small molecule that effects additional molecules
• bacterial conjugation: transfer of genetic material between bacterial cells by direct contact
In regards to pathogenecity, secretion in microorganisms such as bacterial species involves the movement of effector molecules from the interior of a pathogenic organism to the exterior. The secretion of specific molecules allows for adaptation to occur, thereby promoting survival. Effector molecules secreted include proteins, enzymes or toxins. The mechanisms by which pathogenic bacteria secrete proteins involve complex and specialized secretion systems. Specifically, Type III and Type IV secretion systems are utilized by gram-negative pathogenic bacteria to transport proteins that function as pathogenic components.
Type III Secretion Systems
Type III secretion systems are characterized by the ability to inject a protein directly from the bacterial cell to the eukaryotic cell. It is often compared to the bacterial flagellar basal body which functions as a motor unit and extracellular appendage that is comprised of numerous proteins. The pathogenic bacteria which exhibit this capability contain a critical structural component, considered a protein appendage, that allows the injection of the protein into the host cell. The type III secretion system involves the formation of a complex, roughly ~20 proteins, that reside within the cytoplasmic membrane of the bacterial cell. The process of injecting or transferring the secretory protein from the bacterial cell to the host eukaryotic cell requires a membrane-associated ATPase. Certain species of pathogenic bacteria, including: Salmonella, Shigella, Yersinia and Vibrio exhibit type III secretion systems. The system is regulated by Ca2+ concentrations which regulate the opening and closing of gates present in the membrane by which the type III secretion system complexes can utilize for translocation. For example, in Salmonella, most commonly associated with Enteritis salmonellosis, or food poisoning, the bacteria injects a toxin, AvrA, that inhibits activation of the innate immune system of the host. The mechanism by which AvrA is injected involves exact and proper assembly of proteins which promote invasion of the host cell. Misalignment or improper organization of proteins involved in the type III secretion system prevent injection of secretory substances from the pathogen into the host cell. Another pathogen, Shigella, which utilizes type III secretion systems is able to successfully carry out its infection by evading the immune system. The movement between neighboring cells and evading the immune system, enhances its ability to inject its secretory protein into the host cell.
Type IV Secretion Systems
Type IV secretion systems are characterized by the ability to transfer secretory molecules via a mechanism similar to the bacterial conjugation machinery. The type IV secretion systems can either secrete or receive molecules. The bacterial conjugation machinery allows transfer of genetic material to occur via direct cell-to-cell contact or by a bridge-like apparatus between the two cells. The type IV secretion system utilizes a process similar to this. However, the exact mechanism(s) this process utilizes is unknown but there is a general understanding.
This specific secretion system can transport both DNA and proteins. An example of a pathogenic bacteria that utilizes the type IV secretion system is Helicobacter pylori. H. pylori, most commonly associated with stomach ulcers, attaches itself to epithelial cells within the stomach, then via a type IV secretion system, injects a secretory molecule. The secretory molecule injected into the epithelial cells is an inflammation-inducing agent derived from their own cellular wall. The secretory molecule, peptidoglycan, is recognized by the host system as a foreign substance and activates expression of cytokines which promotes an inflammatory response. This inflammatory response of the stomach is a key characteristic of individuals with ulcers. Peptidoglycan is not the only secretory molecule transferred to the stomach epithelial cells but additional proteins, such as CagA, which function in disruption of host cell cellular activities can be transferred as well. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.04%3A_Damaging_Host_Cells/14.4C%3A_Type_III_and_Type_IV_Secretion.txt |
Learning Objectives
• Distinguish between plasmids and lysogeny in regards to pathogenecity
Plasmids
Plasmids are DNA molecules that are capable of replicating independently from the chromosomal DNA. Plasmids are often characterized by their circular appearance and double-strands; they also vary in size and number. Plasmids are present in the three major domains (Archaea, Bacteria and Eukarya) and are considered to be ‘naked DNA’. ‘Naked DNA’ refers to a specific type of DNA which does not encode for genes promoting the transfer of genetic material to a new host. The plasmids are present within the cells as extra chromosomal genomes and are a common tool used in molecular biology to integrate new DNA into a host. In the field of molecular biology, plasmid DNA is often referred to as ‘ vectors ‘ due to their ability to transfer DNA between organisms. The use of plasmid DNA in molecular biology is considered to be recombinant DNA technology. In addition, plasmid DNA provides a mechanism by which horizontal gene transfer can occur, contributing to antibiotic resistance.
Horizontal gene transfer is a major mechanism promoting bacterial antibiotic resistance, as the plasmid DNA can transfer genes from one species of bacteria to another. The plasmid DNA which is transferred often has developed genes that encode for resistance against antibiotics. The ability to transfer this resistance from one species to another is increasingly becoming an issue in clinics for treatment of bacterial infections. The process of horizontal gene transfer can occur via three mechanisms: transformation, transduction and conjugation. Plasmid DNA transfer is associated with conjugation as the host-to-host transfer requires direct mechanical transfer. The advantages of plasmid DNA transfer allow for survival advantages.
Lysogeny
Lysogeny is the process by which a bacteriophageintegrates its nucleic acids into a host bacterium’s genome. Lysogeny is utilized by viruses to ensure the maintenance of viral nucleic acids within the genome of the bacterium host. The virus displays the ability to infect the bacterium host and integrate its own genetic materials into the host bacterium genome. The bacteriophages newly integrated genetic material, called a prophage, is transferred to new bacterial daughter cells upon cell division. The prophage is integrated into the bacterium genome at this point. The lysogenic cycle is key to ensure the transmittance of bacteriophage nucleic acids to host bacterium’s genome. Lysogeny is one of two major methods of viral reproduction utilized by viruses.
Lysogenic cycles are utilized by specific types of viruses to ensure viral reproduction, but they also need the second major method of viral reproduction, the lytic cycle, as well. The lytic cycle, considered the primary method of viral replication, results in the actual destruction of the infected cell. Upon destruction of the infected cell, the new viruses, which have developed after undergoing biosynthesis and maturation, are free to infect other cells. The lytic cycle is characterized by the breakdown of the bacteria cell wall intracellularly. The viruses cause disruption of the bacterial cell by producing enzymes which facilitate this process. An example of a virus which can promote the transformation of bacterium from a nontoxic to toxic strain via lysogeny is the CTXφ virus. Specifically, the bacterium, Vibrio cholerae, is transformed into a toxic strain upon infection with the bacteriophage. This bacterium is then able to produce a cholera toxin, the cause of the disease cholera.
Key Points
• Plasmids are double-stranded circular forms of ‘naked DNA ‘.
• Plasmids are responsible for horizontal gene transfer which promotes the development of antibiotic resistance in bacterium.
• Lysogeny is a major method of viral reproduction characterized by the integration of viral nucleic acids in the bacterium genome.
Key Terms
• bacteriophage: A virus that specifically infects bacteria.
• lysogeny: the process by which a bacteriophage incorporates its nucleic acids into a host bacterium | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.04%3A_Damaging_Host_Cells/14.4D%3A_Plasmids_and_Lysogeny.txt |
Learning Objectives
• Compare and contrast the role of various siderophores in pathogenecity, including: yersiniabactin, enterobactin and ferrichromes
Siderophores are specific types of molecules utilized by microorganisms to obtain iron from the environment. Specifically, in regards to pathogenicity, organisms that exhibit the ability to produce siderophores release these iron-specific molecules and scavenge iron from their hosts organisms. The siderophores are then utilized by the pathogen to obtain iron. Therefore, siderophores are chelating agents that bind the iron ions. The ability of pathogens to obtain iron from the host is essential for survival because the iron is limited in the host environment, in particular, the host tissues and fluids. The iron is used to allow for formation of soluble ferric ion (Fe3+) complexes that are necessary for maintenance of homeostatic mechanisms within the pathogen.
The ability to form water soluble Fe3+ complexes is a key component to the active transport of the Fe-siderophore complex across the cellular membrane. In iron deficient environments, the siderophores are released and allow for the formation of water soluble-Fe3+ complexes to increase iron acquisition. The complexes then generally bind to the cellular membrane using cell specific receptors. They are transported across the membrane utilized for the necessary processes. However, there are differences in the mechanisms employed by various sideorophobes to obtain iron and the specific type of siderophore utilized varies.
Yersiniabactin
The pathogenic bacteria, Yersinia pestis, Yersinia pseduotuberculosis, and Yersinia enterocolitica have the ability to produce a siderophore called yersiniabactin. Pathogenic yersinia is responsible for numerous diseases including the bubonic plague. The ability of pathogenic Yersinia to establish and spread disease is based on its ability to obtain iron for fundamental cellular processes. In areas of low iron, the organism will release yersiniabactin to form Fe3+ complexes. The yersiniabactin-Fe3+ complex will then bind to the outer membrane of the bacteria based on specific receptor recognition. The complex is then translocated through the membrane via membrane-embedded proteins and iron is released from the yersiniabactin. The iron will then be utilized in numerous cellular processes.
Enterobactin
Pathogenic bacteria such as Escherichia coli and Salmonella typhimurium have the ability to produce a siderophore called enterobactin. This specific type of siderophore is the strongest identified siderophore, to date, with an extremely high binding affinity to Fe3+. Upon a decrease in iron, the bacterial cells release enterobactin which forms a complex with Fe3+. The complex is then transported intracellularly via an ATP-binding cassette transporter. Once the enterobactin-Fe3+ complex arrives intracellularly, it is necessary to remove the Fe3+ from the complex. Due to the high-binding affinity of enterobactin, the bacteria require a highly specific enzyme, ferrienterobactin esterase, to cleave the iron from the complex. The iron released from the complex will then be utilized in metabolic processes.
Ferrichrome
Another type of siderophore produced by pathogenic fungi includes a ferrichrome. Fungi that have been shown to produce ferrichromes include those in the genera Aspergillus, Ustilago, and Penicillum. The ferrichrome allows for formation of a ferrichrome-iron complex which can then interact with a protein receptor on the cell surface. The ferrichrome promotes iron transport within the organism to allow metabolic processes to occur.
The discovery and identification of siderophores have allowed for the development of treatments targeting these siderophore-iron complexes. By targeting these complexes, the pathogenic microorganisms can be targeted by inhibiting necessary cellular processes. The production and importance of these siderophores to pathogenic organisms is key to their survival.
Key Points
• Siderophore – iron complexes are necessary for iron acquisition to various pathogenic organisms for metabolic processes.
• The types of siderophores produced are species specific and exhibit different properties.
• The siderophores are necessary to obtain iron by binding to cell surfaces and transporting the siderophore-iron complexes intracellularly.
• Siderophores are produced in environments that have low iron concentration, such as host tissues and fluids. They are considered advantageous to pathogenic organisms.
Key Terms
• siderophore: Any medium-sized molecule that has a high specificity for binding or chelating iron; they are employed by microorganisms to obtain iron from the environment
• chelating agent: A compound that reacts with a metal ion to produce a chelate.
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• Bacterial Toxins: Friends or Foes?. Provided by: Centers for Disease Control and Prevention. Located at: http://wwwnc.cdc.gov/eid/article/5/2...06_article.htm. License: Public Domain: No Known Copyright
• Claviceps. Provided by: Wikipedia. Located at: en.Wikipedia.org/wiki/Claviceps. License: CC BY-SA: Attribution-ShareAlike
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• Figure 1 - Bacterial Toxins: Friends or Foes?n- Volume 5, Number 2u2014April 1999 - Emerging Infectious Disease journal - CDC. Provided by: Centers for Disease Control and Prevention. Located at: http://wwwnc.cdc.gov/eid/article/5/2/99-0206-f1.htm. License: Public Domain: No Known Copyright
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• Figure 1 - Bacterial Toxins: Friends or Foes?n- Volume 5, Number 2u2014April 1999 - Emerging Infectious Disease journal - CDC. Provided by: Centers for Disease Control and Prevention. Located at: http://wwwnc.cdc.gov/eid/article/5/2/99-0206-f1.htm. License: Public Domain: No Known Copyright
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• Figure 1 - Bacterial Toxins: Friends or Foes?n- Volume 5, Number 2u2014April 1999 - Emerging Infectious Disease journal - CDC. Provided by: Centers for Disease Control and Prevention. Located at: http://wwwnc.cdc.gov/eid/article/5/2/99-0206-f1.htm. License: Public Domain: No Known Copyright
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• Figure 1 - Bacterial Toxins: Friends or Foes?n- Volume 5, Number 2u2014April 1999 - Emerging Infectious Disease journal - CDC. Provided by: Centers for Disease Control and Prevention. Located at: http://wwwnc.cdc.gov/eid/article/5/2/99-0206-f1.htm. License: Public Domain: No Known Copyright
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Learning Objectives
• Recognize examples of intracellular pathogens
A pathogen or infectious agent is a microorganism such as a virus, bacterium, prion, or fungus that causes disease in its host. The host may be an animal, a plant, or even another microorganism. Not all pathogens are undesirable to humans. In entomology, pathogens are one of the “Three P’s” (predators, pathogens, and parasitoids) that serve as natural or introduced biological controls to suppress arthropod pest populations.
There are several types of intracellular pathogens. Pathogenic viruses are mainly those of the families of Adenoviridae, bacteria Picornaviridae, Herpesviridae, Hepadnaviridae, Flaviviridae, Retroviridae, Orthomyxoviridae, Paramyxoviridae, Papovaviridae, Polyomavirus, Rhabdoviridae, and Togaviridae. Viruses typically range between 20 to 300 nanometers in length. Although the vast majority of bacteria are harmless or beneficial, a few pathogenic bacteria can cause infectious diseases. Bacteria can often be killed by antibiotics because the cell wall in the outside is destroyed, expelling the DNA out of the body of the pathogen, therefore making the pathogen incapable of producing proteins, so it dies. They typically range between 1 and 5 micrometers in length.
Pathogenic fungi comprise a eukaryotic kingdom of microbes that are usually saprophytes but can cause diseases in humans, animals, and plants. Fungi are the most common cause of diseases in crops and other plants. The typical fungal spore size is 1 to 40 micrometers in length.
Some eukaryotic organisms, such as protists and helminths, cause disease. According to the prion theory, prions are infectious pathogens that do not contain nucleic acids. These abnormally-folded proteins are found characteristically in some diseases such as scrapie, bovine spongiform encephalopathy (mad cow disease), and Creutzfeldt–Jakob disease. Although prions fail to meet the requirements laid out by Koch’s postulates, the hypothesis of prions as a new class of pathogen led Stanley B. Prusiner to receive the Nobel Prize in Physiology or Medicine in 1997.
Key Points
• The host may be an animal, a plant, or even another microorganism.
• Pathogenic viruses are mainly those of the families of Adenoviridae, bacteria Picornaviridae, Herpesviridae, Hepadnaviridae, Flaviviridae, Retroviridae, Orthomyxoviridae, Paramyxoviridae, Papovaviridae, Polyomavirus, Rhabdoviridae, and Togaviridae.
• Although the vast majority of bacteria are harmless or beneficial, a few pathogenic bacteria can cause infectious diseases.
Key Terms
• prion: A self-propagating misfolded conformer of a protein that is responsible for a number of diseases that affect the brain and other neural tissue.
• pathogen: Any organism or substance, especially a microorganism, capable of causing disease, such as bacteria, viruses, protozoa, or fungi. Microorganisms are not considered to be pathogenic until they have reached a population size that is large enough to cause disease.
14.5B: Extracellular Immune Avoidance
A pathogen’s success depends on its ability to evade the host’s immune responses.
Learning Objectives
• List the mechanisms that bacteria use for intracellular pathogenesis
Key Points
• Bacteria usually overcome physical barriers by secreting enzymes to digest the barrier in the manner of a type II secretion system.
• Some pathogens avoid the immune system by hiding within the cells of the host, a process referred to as intracellular pathogenesis.
• Other pathogens invade the body by changing the non-essential epitopes on their surface rapidly, while keeping the essential epitopes hidden.
Key Terms
• pathogen: Any organism or substance, especially a microorganism, capable of causing disease, such as bacteria, viruses, protozoa, or fungi. Microorganisms are not considered to be pathogenic until they have reached a population size that is large enough to cause disease.
• biofilm: A thin film of mucus created by and containing a colony of bacteria and other microorganisms.
• antigenic variation: The mechanism by which an infectious organism changes its surface proteins in favor of circumventing a host immune response.
Extracellular Immune Avoidance
A pathogen’s success depends on its ability to evade the host’s immune responses. Thus, pathogens have evolved several methods that allow them to successfully infect a host by evading the immune system’s detection and destruction. Bacteria usually overcome physical barriers by secreting enzymes that digest the barrier in the manner of a type II secretion system. They also use a type III secretion system that allows bacteria to insert a hallow tube, which provides proteins a direct route to enter the host cell. These proteins often shutdown the defenses of the host.
Some pathogens avoid the immune system by hiding within the cells of the host, a process referred to as intracellular pathogenesis. The pathogen hides inside the host cell where it is protected from direct contact with the complement, antibodies, and immune cells. A lot of pathogens release compounds that misdirect or diminish the host’s immune response. Some bacteria even form biofilms which protect them from the proteins and cells of the immune system. Many successful infections often involve biofilms. Some bacteria create surface proteins, such as Streptococcus, that will bind to antibodies making them ineffective.
Other pathogens invade the body by changing the non-essential epitopes on their surface rapidly while keeping the essential epitopes hidden. This is referred to as antigenic variation. HIV rapidly mutates so the proteins that are on its viral envelope, which are essential for its entry into the host’s target cell, are consistently changing. The constant change of these antigens is why vaccines have not been created. Another common strategy that is used is to mask antigens with host molecules in order to evade detection by the immune system. With HIV, the envelope covering the viron is created from the host cell’s outermost membrane making it difficult for the immune system to identify as a non-self structure. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.05%3A_Surviving_Within_the_Host_and_Exiting_the_Host/14.5A%3A_Intracellular_Pathogens.txt |
Virulence regulation is a combination of the specific traits of the pathogen and the evolutionary pressures that lead to virulent traits.
Learning Objectives
• Compare and contrast the hypotheses that explain why a pathogen evolves as it does: Trade-Off, Short-Sighted Evolution and Coincidental Evolution Hypotheses
Key Points
• Virulence is the degree of pathogenicity within a group or species of parasites as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host.
• The ability of a microorganism to cause disease is described in terms of the number of infecting bacteria, the route of entry into the body, the effects of host defense mechanisms, and intrinsic characteristics of the microorganism called virulence factors.
• Optimal virulence increases with horizontal transmission (between non-relatives) and decreases with vertical transmission (from parent to child).
• The pathogen population can evolve once it is in the host.
• The three main hypotheses about why a pathogen evolves as it does are the Trade-Off Hypothesis, the Short-Sighted Evolution Hypothesis, and the Coincidental Evolution Hypothesis.
Key Terms
• virulence: The degree of pathogenicity within a group or species of parasites as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host and it is determined by virulence factors.
Virulence is the degree of pathogenicity within a group or species of parasites as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. The pathogenicity of an organism – its ability to cause disease – is determined by its virulence factors. In an ecological context, virulence can be defined as the host’s parasite-induced loss of fitness. Virulence can be understood in terms of proximate causes—those specific traits of the pathogen that help make the host ill—and ultimate causes—the evolutionary pressures that lead to virulent traits occurring in a pathogen strain.
The ability of a microorganism to cause disease is described in terms of the number of infecting bacteria, the route of entry into the body, the effects of host defense mechanisms, and intrinsic characteristics of the microorganism called virulence factors. Host-mediated pathogenesis is often important because the host can respond aggressively to infection with the result that host defense mechanisms do damage to host tissues while the infection is being countered.
According to evolutionary medicine, optimal virulence increases with horizontal transmission (between non-relatives) and decreases with vertical transmission (from parent to child). This is because the fitness of the host is bound to the fitness in vertical transmission but is not so bound in horizontal transmission.The pathogen population can evolve once it is in the host. There are three main hypotheses about why a pathogen evolves as it does. These three models help to explain the life history strategies of parasites, including reproduction, migration within the host, virulence, etc.
1. Trade-off hypothesis argues that pathogens tend to evolve toward ever decreasing virulence because the death of the host (or even serious disability) is ultimately harmful to the pathogen living inside. For example, if the host dies, the pathogen population inside may die out entirely. Therefore, it was believed that less virulent pathogens that allowed the host to move around and interact with other hosts should have greater success reproducing and dispersing. But this is not necessarily the case. Pathogen strains that kill the host can increase in frequency as long as the pathogen can transmit itself to a new host, whether before or after the host dies. The evolution of virulence in pathogens is a balance between the costs and benefits of virulence to the pathogen.
2. Short-sighted evolution hypothesis suggests that the traits that increase reproduction rate and transmission to a new host will rise to high frequency within the pathogen population. These traits include the ability to reproduce sooner, reproduce faster, reproduce in higher numbers, live longer, survive against antibodies, or survive in parts of the body the pathogen does not normally infiltrate. These traits typically arise due to mutations, which occur more frequently in pathogen populations than in host populations, due to the pathogens’ rapid generation time and immense numbers. After only a few generations, the mutations that enhance rapid reproduction or dispersal will increase in frequency. The same mutations that enhance the reproduction and dispersal of the pathogen also enhance its virulence in the host, causing much harm (disease and death). If the pathogen’s virulence kills the host and interferes with its own transmission to a new host, virulence will be selected against. But as long as transmission continues despite the virulence, virulent pathogens will have the advantage.
3. Coincidental evolution hypothesis argues that some forms of pathogenic virulence did not co-evolve with the host. For example, tetanus is caused by the soil bacterium Clostridium tetani. After C. tetani bacteria enter a human wound, the bacteria may grow and divide rapidly, even though the human body is not their normal habitat. While dividing, C. tetani produce a neurotoxin that is lethal to humans. But it is selection in the bacterium’s normal life cycle in the soil that leads it to produce this toxin, not any evolution with a human host. The bacterium finds itself inside a human instead of in the soil by mere happenstance. We can say that the neurotoxin is not directed at the human host. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.05%3A_Surviving_Within_the_Host_and_Exiting_the_Host/14.5C%3A_Regulating_Virulence.txt |
Pathogens must have a way to be transmitted from one host to another to ensure their species’ survival.
Learning Objectives
• Distinguish between horizontal and vertical disease transmission
Key Points
• Transmission of microorganisms can happen directly from one person to another by: droplet contact, direct physical contact, indirect physical contact, airborne transmission, or fecal-oral transmission.
• Transmission can also be indirect, via another organism, either a vector or an intermediate host.
• Disease can also be transmitted in two ways: horizontally from one individual to another in the same generation and vertically from parent to offspring, such as through perinatal transmission.
Key Terms
• transmission: Transmission is the passing of a communicable disease from an infected host individual or group to a conspecific individual or group, regardless of whether the other individual was previously infected.
Transmission is the passing of a communicable disease from an infected host individual or group to a conspecific individual or group by one or more of the following means: droplet contact, direct physical contact, indirect physical contact, airborne transmission, and fecal-oral transmission.
Transmission can also be indirect, via another organism. Indirect transmission could involve zoonoses or, more typically, larger pathogens like macroparasites with more complex life cycles. Disease can be directly transmitted in two ways. The first is horizontal disease transmission – from one individual to another in the same generation by either direct contact, or indirect contact air, such as via a cough or sneeze. The second is vertical disease transmission – passing a disease causing agent vertically from parent to offspring, such as through perinatal transmission.
Pathogens must have a way to be transmitted from one host to another to ensure their species ‘ survival. Infectious agents are generally specialized for a particular method of transmission. For example, a virus or bacteria that causes its host to develop coughing and sneezing symptoms has a great survival advantage – it is much more likely to be ejected from one host and carried to another. This is also the reason that many microorganisms cause diarrhea.
The respiratory route is a typical mode of transmission among many infectious agents. If an infected person coughs or sneezes on another person, the microorganisms, suspended in warm, moist droplets, may enter the body through the nose, mouth, or eye surfaces. Diseases that are commonly spread by coughing or sneezing include: bacterial meningitis and chickenpox.
When viruses are shed by an infected person through coughing or sneezing into the air, the mucus coating on the virus starts to evaporate. Once this mucus shell evaporates the remaining viron is called a droplet nucleus or quanta. The mucus evaporation rate is determined by the temperature and humidity inside the room. The lower the humidity, the quicker the mucus shell evaporates thus allowing the droplet nuclei to stay airborne and not drop to the ground. The low indoor humidity levels in wintertime buildings ensure that higher levels of droplet nuclei will survive: droplet nuclei are so microscopic that they are able to stay airborne indefinitely on the air currents present within indoor spaces. When an infected person coughs or sneezes, a percentage of their viruses will become droplet nuclei. If these droplet nuclei gain access to the eyes, nose, or mouth of an uninfected person (known as a susceptible) – either directly, or indirectly by touching a contaminated surface – then the droplet nuclei may penetrate into the deep recesses of their lungs. Viral diseases that are commonly spread by coughing or sneezing droplet nuclei include the common cold and influenza.
Direct fecal-oral transmission is rare for humans at least. More common are the indirect routes: foodstuffs or water become contaminated and the people who eat and drink them become infected. This is the typical mode of transmission for infectious agents such as cholera, hepatitis A, and polio.
Sexual transmission refers to any disease that can be caught during sexual activity with another person, including vaginal or anal sex or (less commonly) through oral sex. Transmission is either directly between surfaces in contact during intercourse or from secretions which carry infectious agents that get into the partner’s blood stream through tiny tears in the penis, vagina, or rectum. Some diseases transmissible by the sexual route include: HIV/AIDS and chlamydia.
Sexually transmitted diseases such as HIV and Hepatitis B are thought to not normally be transmitted through mouth-to-mouth contact, although it is possible to transmit some STDs between the genitals and the mouth during oral sex. In the case of HIV this possibility has been established. It is also responsible for the increased incidence of herpes simplex virus 1 (which is usually responsible for oral infections ) in genital infections and the increased incidence of the type 2 virus (more common genitally) in oral infections.
Diseases that can be transmitted by direct contact are called contagious. These diseases can also be transmitted by sharing a towel (where the towel is rubbed vigorously on both bodies) or items of clothing in close contact with the body (socks, for example) if they are not washed thoroughly between uses.
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A fungus is a member of a large group of eukaryotic organisms that includes microorganisms that exhibit pathogenicity.
Learning Objectives
• Give examples of pathogenic fungi
Key Points
• There are various examples of pathogenic fungi including but not limited too: Candida species, Aspergillosis, Cryptococcus, Histoplasma, Pneumocystis and Stachybotrys.
• Many fungal species produce bioactive compounds called mycotoxins, such as alkaloids and polyketides that are toxic to animals including humans, contributing to pathogenecity and disease.
• The study of pathogenic fungi is referred to as a medical mycology.
Key Terms
• symbiont: An organism that lives in a symbiotic relationship; a symbiote.
• mycotoxin: Any substance produced by a mold or fungus that is injurious to vertebrates upon ingestion, inhalation, or skin contact.
• opportunist: when an organism takes advantage of any opportunity to advance its own situation.
A fungus is a member of a large group of eukaryotic organisms that includes microorganisms such as yeasts and molds. These organisms are classified as kingdom Fungi, separate from plants, animals, and bacteria. Fungi have a worldwide distribution and cangrow in a wide range of habitats, including extreme environments such as deserts or areas with high salt concentrations or ionizing radiation, as well as in deep sea sediments. Most fungi are inconspicuous because of the small size of their structures and their cryptic lifestyles in soil, on dead matter, and as symbionts of plants, animals, or other fungi. Fungi perform an essential role in the decomposition of organic matter and have fundamental roles in nutrient cycling and exchange. Many fungal species produce bioactive compounds called mycotoxins, such as alkaloids and polyketides that are toxic to animals including humans, contributing to pathogenecity and disease.
The study of pathogenic fungi is referred to as a medical mycology. There are various examples of pathogenic fungi including but not limited too: Candida species, Aspergillosis, Cryptococcus, Histoplasma, Pneumocystis and Stachybotrys.
Candida species are commonly known to cause opportunist infections in immunocompromised hosts. The immunocompromised hosts that commonly become infected with Candida include transplant patients, cancer patients and AIDS sufferers. Candida infections are difficult to treat and can result in systemic infections leading to death.
One of the most commons fungal pathogenic species includes Aspergillus strains, specifically Aspergillus fumigatus and Aspergillus flavus. Aspergillus can cause disease via production of mycotoxins, induction of allergic responses and through localized or systemic infections. Aspergillus flavus specifically produces aflatoxin which is both a toxin and carcinogen whereas Aspergillus fumigatus causes allergic disease. Symptoms of diseases caused by Aspergillus can include fever, cough, chest pain or breathlessness.
Cryptococcus neoformans causes severe forms of meningitis and meningo-encephalitis in patients with HIV infection and AIDS. Cryptococcus species live in the soil and do not cause disease in humans thus, Cryptococcus neoformans is the major pathogen in both human and animals.
Histoplasma capsulatum results in the formation of histoplasmosis in humans, dogs and cats. This specific fungus is endemic in certain areas of the United States and infection is due to inhaling contaminated air.
Pneumocystis jirovecii results in the formation of pneumonia in individuals with weakened immune systems including premature children, the elderly and AIDS patients.
Stachybotrys chartarum, also referred to as black mold, causes respiratory damage and severe headaches. This type of black mold frequently occurs in households that are chronically damp. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.06%3A_Pathogenicity_and_Other_Microbes/14.6A%3A_Fungi.txt |
Protozoa are a diverse group of unicellular eukaryotic organisms, many of which can cause disease.
Learning Objectives
• Compare and contrast the proliferative and dormant stages in pathogenic protozoa and the diseases protazoa cause
Key Points
• Examples of human diseases caused by protozoa are: malaria, amoebiasis, giardiasis, toxoplasmosis, cryptosporidiosis, trichomoniasis, Chagas disease, leishmaniasis, and dysentery.
• The life stages of these protozoa play a major role in their ability to function as pathogens and infect various hosts.
• Protozoa were regarded as the partner-group of protists to protophyta, which have plant-like behavior (e.g., photosynthesis). In general, protozoa are referred to as animal-like protists because they are capable of movement, or motile.
• Some protozoa are human parasites, causing diseases.
Key Terms
• trophozoite: A protozoan in the feeding stage of its life cycle.
• protozoa: Protozoa are a diverse group of unicellular eukaryotic organisms, many of which are motile. Originally, protozoa had been defined as unicellular protists with animal-like behavior, e.g., movement. Protozoa were regarded as the partner group of protists to protophyta, which have plant-like behavior, e.g., photosynthesis.
• dormant cyst: A resting or dormant stage of a microorganism
• cyst: a pouch or sac without opening, usually membranous and containing morbid matter, which develops in one of the natural cavities or in the substance of an organ
Protozoa (or protozoans) are a diverse group of unicellular eukaryotic organisms, many of which are motile. Originally, protozoa had been defined as unicellular protists with animal-like behavior (e.g., movement). Protozoa were regarded as the partner-group of protists to protophyta, which have plant-like behavior (e.g., photosynthesis). In general, protozoa are referred to as animal-like protists because they are capable of movement, or motile. While there is no exact definition for the term protozoa, it often refers to a unicellular heterotrophic protist, such as the amoebas and ciliates.
Protozoa can display pathogenicity and are the cause of various diseases. The life stages of these protozoa play a major role in their ability to function as pathogens and infect various hosts. Some protozoa have life stages alternating between proliferative stages (e.g., trophozoites ) and dormant cysts. As cysts, protozoa can survive harsh conditions, such as exposure to extreme temperatures or harmful chemicals, or long periods without access to nutrients, water, or oxygen for a period of time. The ability of protozoa to thrive under extreme environments contributes to their ability to evade immune system responses, drug therapies and survive for prolonged periods of time before infection. Being a cyst enables parasitic species to survive outside of a host, and allows their transmission from one host to another. When protozoa are in the form of trophozoites they actively feed. The conversion of a trophozoite to cyst form is known as encystation, while the process of transforming back into a trophozoite is known as excystation.
Protozoa such as the malaria parasites (Plasmodium spp. ), trypanosomes, and leishmania are also important as parasites and symbionts of multicellular animals. Examples of human diseases caused by protozoa are: malaria, amoebiasis, giardiasis, toxoplasmosis, cryptosporidiosis, trichomoniasis, Chagas disease, leishmaniasis, and dysentery. The life cycle of protozoan are successful based on successful transmission between hosts and host and environment. Infection and disease by protozoan parasites are often times associated with developing countries with poor hygiene and sanitation conditions that may promote transmission of these protozoa. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.06%3A_Pathogenicity_and_Other_Microbes/14.6B%3A_Protozoa.txt |
Parasitic worms, often referred to as helminths, are a division of eukaryotic parasites.
Learning Objectives
• List the four groups of parasitic worms (helminths), routes of transmission and risk factors
Key Points
• Helminths are worm-like organisms that live and feed off of living hosts, receiving nourishment and protection while disrupting the nutrient absorption of their hosts, which causes weakness and disease.
• Helminths that live inside the digestive tract are called intestinal parasites.
• Helminths often find their way into a host through contaminated food or water, soil, mosquito bites, and sexual acts.
• Response to worm infection in humans is a Th2 response in the majority of cases.
Key Terms
• helminth: A parasitic roundworm or flatworm.
• lymphatic system: In mammals, including humans, a network of lymph vessels and lymph nodes that transport fluid, fats, proteins, and lymphocytes to the bloodstream as lymph, and remove microorganisms and other debris from tissues.
Parasitic worms, often referred to as helminths, are a division of eukaryotic parasites. They are worm-like organisms that live and feed off of living hosts, receiving nourishment and protection while disrupting the nutrient absorption of their hosts, which causes weakness and disease. Those that live inside the digestive tract are called intestinal parasites. They can live inside humans as well as other animals.
Parasitic worms belong to four groups:
• Monogeneans
• Cestodes (tapeworms)
• Nematodes (roundworms)
• Trematodes (flukes)
Helminths often find their way into a host through contaminated food or water, soil, mosquito bites, and even sexual acts. Poorly washed vegetables eaten raw may contain eggs of nematodes such as Ascaris, Enterobius, Thichuris, and or cestodes such as Taenia, Hymenolepis, and Echinococcus. Plants may also be contaminated with fluke metacercaria, such as Fasciola. Schistosomes and nematodes such as hookworms (Ancylostoma an Necator) and Strongyloides can penetrate the skin. Finally, Wuchereria, Onchocerca, and Dracunculus are transmitted by mosquitoes and flies.
Populations in the developing world are at particular risk for infestation with parasitic worms. Risk factors include the following:
• Inadequate water treatment
• Use of contaminated water for drinking, cooking, washing food, and irrigation
• Undercooked food of animal origin
• Walking barefoot
Simple measures—such as use of shoes, soaking vegetables with 1.5% bleach, adequate cooking of foods (not microwaving), and sleeping under mosquito-proof nets—can have a strong impact on prevention.
Response to worm infection in humans is a Th2 response in the majority of cases. Inflammation of the gut may also occur, resulting in cyst-like structures forming around the egg deposits throughout the body. The host’s lymphatic system is also increasingly taxed the longer helminths propagate, as they excrete toxins after feeding. These toxins are released into the intestines and absorbed by the host’s bloodstream, making the host susceptible to more common diseases such as seasonal viruses and bacterial infections.
Parasitic worms have been used as a medical treatment for various diseases, particularly those involving an overactive immune response. As humans have evolved with parasitic worms, proponents argue that they are needed for a healthy immune system. Scientists are looking to see if there is a connection between the prevention and control of parasitic worms and the increase in allergies such as hay-fever in developed countries. Parasitic worms may be able to damp down the immune system of their host, making it easier for them to live in the intestine without coming under attack. This may be one mechanism for their proposed medicinal effect. | textbooks/bio/Microbiology/Microbiology_(Boundless)/14%3A_Pathogenicity/14.06%3A_Pathogenicity_and_Other_Microbes/14.6C%3A_Helminths.txt |
Algae can act as pathogens like any other microbe.
Learning Objectives
• Discuss the various types of pathogenic algae
Key Points
• While algal blooms can lead to negative consequences, the effect of an algal bloom are often indirect, the alga is not directly infecting a host.
• Cephaleuros are a genus of parasitic alga which infect plants, causing red rust, which affects many commercial crops that humans consume.
• Prototheca are a type of green alga that lack chlorophyll, that can infect mammals including humans causing the disease protothecosis.
• To some degree the distribution of algae is subject to floristic discontinuities caused by geographical features, such as Antarctica, long distances of ocean, or general land masses.
Key Terms
• thalloid: Of a plant, alga, or fungus lacking complex organization, especially lacking distinct stems, roots, or leaves.
• alga: any of many aquatic photosynthetic organisms, whose size ranges from a single cell to giant kelps and whose form is very diverse
• basionym: An earlier valid scientific name of a species that has since been renamed and from which the new name is partially derived.
Algae, are not normally considered common pathogens. Algal blooms are often associated with negative impacts on humans and the surrounding environment in which they occur. A harmful algal bloom (HAB) is an algal bloom that causes negative impacts to other organisms via production of natural toxins, mechanical damage to other organisms, or by other means. HABs are often associated with large-scale marine mortality events and have been associated with various types of shellfish poisonings. However, the damage to other organisms is not due to the algae infecting a host but rather indirectly excreting a toxin, or in some cases blocking out light or competing for resources.
However notable examples of algae acting as pathogens are known. For example Cephaleuros which is a genus of parasitic thalloid alga comprising approximately 14 species. Its common name is red rust. Chrooderma is its basionym. Specimens can reach around 10 mm in size. Dichotomous branches are formed. The alga is parasitic on some important economic plants of the tropics and subtropics such as tea, coffee, mango and guava causing damage limited to the area of algal growth on leaves (algal leaf spot), or killing new shoots, or disfiguring fruit. Members of the genera may also grow with a fungus to form a lichen that does not damage the plants.
Examples of algae acting as a mammalian pathogen are known as well, notably the disease Protothecosis. Protothecosis is a disease found in dogs, cats, cattle, and humans caused by a type of green alga known as Prototheca that lacks chlorophyll. It and its close relative Helicosporidium are unusual in that they are actually green algae that have become parasites.The two most common species are Prototheca wickerhamii and Prototheca zopfii. Both are known to cause disease in dogs, while most human cases are caused by P. wickerhami. Prototheca is found worldwide in sewage and soil. Infection is rare despite high exposure, and can be related to a defective immune system. In dogs, females and Collies are most commonly affected. The first human case was identified in 1964 in Sierra Leone.
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Thumbnail: Sir Charles Bell’s portrait of a soldier dying of tetanus.
15: Diseases
• 15.1A: Chagas Disease (American Trypanosomiasis)
Chagas disease is caused by the protozoan parasite Trypanosoma cruzi and transmitted via the reduviid bug.
• 15.1B: Toxoplasmosis
Toxoplasmosis is a parasitic disease caused by the protozoan Toxoplasma gondii and its life cycle mandates a definitive host which are cats.
• 15.1C: Malaria
Malaria is a mosquito-borne infectious disease that affects humans and other animals caused by various species of the protist Plasmodium.
• 15.1D: Leishmaniasis
Leishmaniasis is caused by the protozoan parasite Leishmania and presents itself in two forms: cutaneous or visceral leishmaniasis.
• 15.1E: Babesiosis
Babesiosis is a malaria-like parasitic disease caused by infection with Babesia, a parasite transmitted to human hosts by ticks.
• 15.1F: Schistosomiasis
Schistosomiasis is a parasitic disease caused by various species of trematodes or “flukes,” which are of the genus Schistosoma.
• 15.1G: Swimmer’s Itch
15.01: Protozoan and Helminthic Diseases of the Cardiovascular and Lymphatic Systems
Learning Objectives
• Describe the life cycle of Trypanosoma cruzi
Chagas disease, also known as American trypanosomiasis, is caused by the parasite Trypanosoma cruzi. It is transmitted to humans via the reduviid bug (the “kissing bugs”), and is therefore characterized as a zoonotic disease.
Chagas disease is similar to African sleeping sickness which is caused by the African trypanosome. The risk factors for Chagas disease include living where reduviid bugs live, including areas of Central and South America. In addition, it is possible to obtain Chagas via blood transfusion from an individual with the active disease.
The reduviid bug itself becomes infected by feeding on the blood of an already-infected person or animal. The bugs are nocturnal, emerge at night and typically feed on an individual’s face. The bug then proceeds to defecate on the person, passing Trypanosoma cruzi parasites in its feces in posterior station infection. These parasites surround the bite wound and, when the bite is scratched, the parasites are able to pass into the host. The reduviid bud often bites the tender skin around the eyes, leaving a swollen bump called a chagoma or Ramona’s sign.
At this specific stage, the parasites are referred to as trypomastigotes, and these invade the host cells and differentiate into intracellular amastigotes where they continue to multiply by binary fission. These amastigotes then differentiate into trypomastigotes which circulate into the bloodstream. At this time, if the infected individual is re-bitten by a reduviid bug, the cycle will start again.
Chagas disease can be characterized by two phases: acute and chronic. The acute phase is presents with mild symptoms which include: fever, swelling of an eye and/or the area surrounding the insect bite.
The acute phase will then enter remission and, over time, additional symptoms will develop that include: constipation, gastrointestinal issues, heart failure, abdominal pain and difficulties swallowing. It can sometime take upwards of 20 years from the time of infection for these later heart and digestive issues to present. American trypanosomiasis causes megacolon and megaesophagus and an enlarged heart in pediatric patients and is very serious.
Key Points
• Chagas disease is prevalent in areas with reduviid bugs such as Central and South America.
• Chagas disease is transmitted via a vector, the reduviid bug, which becomes infected when it bites an already-infected individual.
• The life cycle of Trypanosoma cruzi requires two hosts, the reduviid bug and the human or animal host.
Key Terms
• zoonotic: of or relating to zoonosis, the transmission of an infectious disease between species. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.01%3A_Protozoan_and_Helminthic_Diseases_of_the_Cardiovascular_and_Lymphatic_Systems/15.1A%3A_Chagas_Disease_%28American_Trypanosomiasis%29.txt |
Learning Objectives
• Compare and contrast: acute and latent toxoplasmosis and outline the life cycle of the protazoan that causes it
Toxoplasmosis is an infection caused by the parasite Toxoplasma gondii. Toxoplasmosis is found in humans worldwide, but the definitive hosts are cats. Humans may become infected as a result of infected blood transfusions, organ transplants, ingesting contaminated soil, raw or undercooked meat, and most commonly from the careless handling of cat litter, which can lead to accidental ingestion of the parasite. Toxoplasmosis can also be passed from an infected mother to her baby via the placenta (transplacentally). Symptoms that may occur from toxplasmosis include: enlarged lymph nodes, headache, fever, muscle pain, and sore throat. Individuals with immunocompromised or weakened systems display more severe symptoms, such as: confusion, fever, headache, blurred vision and seizures. The three categories of toxoplasmosis include acute, latent, and cutaneous toxoplasmosis.
Symptoms
Acute toxoplasmosis is characterized by swollen lymph nodes found in the neck or under the chin, followed by the axillae, and the groin area. Enlarged lymph nodes will occur at different times after the initial infection. Latent toxoplasmosis is characterized by the formation of cysts in both the nervous and muscle tissue due to the bradyzoite form of the parasite. Often times, individuals infected with latent toxoplasmosis do not present with symptoms, as the infection enters a latent phase. In individuals with cutaneous toxoplasmosis, skin lesions will occur due to the tachyzoite form of the parasite and its presence in the epidermis.
Hosts, Life Cycle
The known definitive hosts for Toxoplasma gondii are members of family Felidae (domestic cats and their relatives). In the life cycle of this parasite, unsporulated oocysts are shed in the cat’s feces. The cat will shed large numbers of these cysts over a short period of time. The oocysts will then take 1-5 days to sporulate in the environment and become infective. The intermediate hosts in nature (including birds and rodents) become infected after ingesting contaminated soil, water, or plant material. The oocysts, upon ingestion, will transform into tachyzoites, which will localize in the neural and muscle tissue. After localizing to these sites, they will develop into tissue cyst bradyzoites. Cats, can become infected after consuming intermediate hosts that are infected with tissue cysts or by ingesting sporulated oocysts.
Key Points
• Cats are the definitive hosts for Toxoplasma gondii and are the primary source of infection to humans.
• Toxoplasmosis can occur in either acute, latent or cutaneous forms.
• Toxoplasmosis is found worldwide and can be transmitted by eating undercooked meat of animals which may contain cysts, ingesting contaminated food or water, transplacentally or from coming in contact with infected cat feces.
Key Terms
• definitive host: a host in which the parasite reaches maturity and, if possible, reproduces sexually
• axillae: The armpit
• transplacental: Through or across the placenta
15.1C: Malaria
Learning Objectives
• Reconstruct the route of transmission and life cycle for Plasmodium species that cause malaria and describe its symptoms
Malaria is a parasitic disease that is caused by the bite of an infected Anopheles mosquito. Malaria can be transmitted from mother to baby and by blood transfusions. The Anopheles mosquito transmits the parasites, called sporozoites, upon biting the hosts, into the bloodstream to the liver, where the parasites continue their life cycle. In the liver, the parasites mature and release another form called merozoites, which enter the bloodstream and infect the red blood cells. In the red blood cells, they develop into ring forms called trophozoites and schizonts that in turn, produce further merozoites. Upon infection of the red blood cells, the parasite is able to multiply within the cell, break open and continue infecting additional red blood cells. The symptoms occur in a cyclical manner every 48-72 hours. Malaria is characterized by the development of symptoms that include high fevers, shaking chills, flu-like symptoms, and anemia. The symptoms that persist due to parasitic infection are a result of the release of merozoites into the bloodstream, destruction of the red blood cells and the free circulation of large amounts of hemoglobin in the red blood cells due to disruption.
The five types of malaria parasites include species of Plasmodium. The fives species include: Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, Plasmodium malariae, and Plasmodium knowlesi. Plasmodium falciparum is responsible for the majority of deaths caused by infection and Plasmodium vivax, ovale and malariaecause a milder form of malaria. The species, Plasmodium knowlesi, commonly causes malaria in macaques but can also cause severe infections in humans.
Malaria is common in temperate climates and the Centers for Disease Control and Prevention (CDC) estimates 300-500 million cases each year. In addition, it is estimated that 1 million people die from it each year as well. Malaria is typically diagnosed by microscopic examination of blood or with antigen-based rapid diagnostic tests. Disease transmission can be reduced by preventing mosquito bites through the use of mosquito nets and insect repellents. However, the mosquitoes which transmit malaria have begun to develop resistance to insecticides and the parasite itself has developed resistance to commonly used antibiotics. As a result of increased resistance, it is extremely difficult to contain the spread of this disease.
Key Points
• The five common species of Plasmodium that cause malaria include: Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, Plasmodium malariae and Plasmodium knowlesi.
• Mosquitoes transmit the protists by injecting sporozoites into the bloodstream of humans.
• The sporozoites injected into the bloodstream, travel to the liver where they multiply into merozoites, rupture the liver cells, and then return to the bloodstream.
• A mosquito, upon feeding off an already infected individual, will carry the protists and become infectious.
• The symptoms of malaria can present in a cyclic manner.
Key Terms
• merozoites: the organisms formed by multiple fission of a sporozoite within the body of the host.
• antigen: A substance that induces an immune response, usually foreign.
• sporozoites: Any of the minute active bodies into which a sporozoan divides just before it infects a new host cell. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.01%3A_Protozoan_and_Helminthic_Diseases_of_the_Cardiovascular_and_Lymphatic_Systems/15.1B%3A_Toxoplasmosis.txt |
Learning Objectives
• Outline the life cycle of Leishmania and distinguish between cutaneous or viseral leishmaniasiss within the Ideal Gas Law
Leishmaniasis is a disease transmitted by the bite of a female sandfly. There various types of leishmaniasis that exist including cutaneous leishmaniasis, systemic, or visceral leishmaniasis. Cutaneous leishmaniasis is characterized by infection of the skin and mucous membranes. The symptoms include skin sores which present at the site of the sandfly bite. In addition, cutaneous leishmaniasis includes breathing difficulty, stuffy nose, runny nose, nose bleeds, swallowing difficulty and ulcers in the mouth, tongue, gums, lips, nose, and inner nose. Systemic or visceral leishmaniasis present as an infection of the entire body. There is a delay of symptoms, ranging from 2-8 months post bite, and the effects on the immune system can result in deadly complications. The parasites damage the immune system by targeting the disease-fighting cells. Symptoms present much more quickly in children and include a cough, diarrhea, fever, and vomiting. In adults, there is fatigue, weakness, loss of appetite, abdominal pain, night sweats, fever, weight loss, and changes in the color and texture of the skin. In combination, cutaneous and visceral leishmaniasis are caused by more than 20 different leishmanial species.
Leishmaniasis is vector-borne because it is transmitted via a bite from a sandfly. The sandflies that cause leishmaniasis are infected by an obligate intracellular protozoa of the genus Leishmania. The species of Leishmania that can cause leishmaniasis include: L. donovani complex with 2 species (L. donovani, L. infantum, also known as L. chagasi); the L. mexicana complex with 3 main species (L. mexicana, L. amazonensis, and L. venezuelensis); L. tropica; L. major; L. aethiopica; and the subgenus Viannia with 4 main species (L. (V.) braziliensis, L. (V.) guyanensis, L. (V.) panamensis, and L. (V.) peruviana). These various species are indistinguishable via morphology but can be identified using advanced techniques such as isoenzyme analysis.
Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies which can transmit the infection Leishmania. The sandflies inject the infective stage, metacyclic promastigotes, during blood meals. Metacyclic promastigotes that reach the puncture wound are phagocytized by macrophages and transform into amastigotes. Amastigotes multiply in infected cells and affect different tissues, depending in part on which Leishmania species is involved. These differing tissue specificities cause the differing clinical manifestations of the various forms of leishmaniasis. Sandflies become infected during blood meals on infected hosts when they ingest macrophages infected with amastigotes. In the sandfly’s midgut, the parasites differentiate into promastigotes, which multiply, differentiate into metacyclic promastigotes, and migrate to the proboscis.
Key Points
• Leishmaniasis is a vector-borne disease and is transmitted by the sand fly.
• Cutaneous leishmaniasis is the most common form of leishmaniasis and symptoms include skin sores.
• Visceral leishmaniasis is more severe and is characterized by the migration of parasites to the vital organs and tissues.
Key Terms
• visceral: of or relating to the viscera – the internal organs of the body
• cutaneous: of, relating to, existing on, or affecting the exterior skin; especially the cutis
• phagocytosis: the process by which a cell incorporates foreign particles intracellularly. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.01%3A_Protozoan_and_Helminthic_Diseases_of_the_Cardiovascular_and_Lymphatic_Systems/15.1D%3A_Leishmaniasis.txt |
Learning Objectives
• Outline the life cycle of the Babesia microti parasite that causes babesiosis
Babesiosis is a malaria-like parasitic disease caused by Babesia. Babesia is a genus of protozoal piroplasms which are characterized by their ability to divide by binary fission. Also, protozoal piroplasms are sporozoan parasites, and so they possess both sexual and asexual phases. The piroplasm is categorized under Phylum Apicomplexa and specifically, Babesia, is a parasite transmitted via a tick vector. Many of the cases of Babesia infection are asymptomatic but can include mild fevers and diarrhea. The more severe cases are plagued with high fevers, shaking chills, and severe anemia, similar to symptoms seen in individuals infected with malaria. If the disease progresses without treatment and it is severe, the infected individual can suffer from organ failure and adult respiratory distress syndrome. Recently, there has been an increase in babesiosis diagnosis due to an increase in the number of individuals with immunodeficiencies coming into contact with ticks.
The life cycle of Babesia parasites is characterized by their ability to undergo reproduction in the erythrocytes. These parasites, within the red blood cells, form a distinctive structure called a “Maltese Cross” that is composed of four attached merozoites undergoing asexual budding. This asexual process results in hemolytic anemia. The Babesia microti life cycle includes two hosts, a rodent, primarily the white-footed mouse, and a tick.
During a blood meal, the tick introduces sporozoites into the mouse host. The sporozoites enter the erythrocytes and undergo asexual reproduction as previously mentioned. In the blood, the parasites will then differentiate into male and female gametes. The definitive host, the tick, will then ingest both types of gametes (upon another blood meal). The gametes will unite and undergo a sporogonic cycle resulting in sporozoite. The humans play a role in this cycle if they are bitten by an infected tick. The tick will introduce the sporozoites and the cycle will proceed. Diagnosis of babesiosis is performed using a Giemsa-test for parasitic identification. The “Maltese Cross” is observed on blood films and both serological testing for antibodies and PCR testing for Babesia from the peripheral blood is performed.
Key Points
• Babesia, the parasite, is capable of undergoing both sexual and asexual reproduction in its life cycle.
• A majority of individuals infected with babesiosis are asymptomatic but severe cases display malaria-like symptoms which include high fevers, chills, shakes, and hemolytic anemia.
• A definitive characteristic of Babesia infection is the formation of a “Maltese Cross” structure within the erythrocytes that represents the asexual budding of four attached merozoites.
Key Terms
• piroplasms: a protozoan parasite of the phylum Apicomplexa.
• sporozoite: any of the minute active bodies into which a sporozoan divides just before it infects a new host cell
• hemolytic: producing hemolysis; destroying red blood cells
15.1F: Schistosomiasis
Learning Objectives
• Outline the life cycle of the trematodes of the genus Schistosoma that cause schistosoomiasis
Schistosomiasis is a parasitic disease caused by various species of trematodes or “flukes,” which are of the genus Schistosoma. For parasites categorized as schistosomes, the snail is the intermediary agent between the mammalian hosts. Schistosomiasis is common in countries that lack the facilities to maintain proper water supplies and sanitation facilities. These supplies and facilities are often exposed to contaminated water that contains infected snails. Individuals infected with schistosomiasis display chronic illness that can result in the damage of internal organs and in children, targets growth and cognitive development. Children will often acquire the disease by swimming or playing in contaminated water. Upon contact with contaminated water, the parasitic larvae can penetrate the skin and mature within the organ tissues.
The life cycle of the various human schistosomes is similar. The parasitic eggs are released into the environment from already-infected individuals and hatch on contact with water, releasing free-swimming miracidia. These infect freshwater snails by penetrating their skin. The site of penetration will promote the transformation of the miracidium into a primary sporocyst. This contains germ cells which will divide to produce secondary sporocysts. In turn, these migrate to the snails’ hepatopancreas and the germ cells, now present within the secondary sporocysts, will divide to form thousands of new parasites called cercariae. These are the larvae capable of infecting mammals.
Interestingly, the cercariae are released from the snail host in a circadian rhythm and depend on ambient temperature and light. Penetration of the human skin occurs after the cercariae have attached to and explored the skin. The parasite secretes enzymes that break down the skin’s protein to enable penetration of the cercarial head through the skin. As the cercaria penetrates the skin, it transforms into a migrating schistosomulum stage.
The various species which can infect humans include:
• Schistosoma mansoni, Schistosoma intercalatum: cause intestinal schistosomiasis
• Schistosoma haematobium: causes urinary schistosomiasis
• Schistosoma japonicum, Schistosoma mekongi: cause Asian intestinal schistosomiasis
• Avian schistosomiasis species: cause swimmer’s itch and clam digger itch
Key Points
• For parasites categorized as schistosomes, the snail is the intermediary agent between the mammalian hosts.
• Schistosomiasis is common in countries that lack the facilities to maintain proper water supplies and sanitation facilities. These supplies and facilities are often exposed to contaminated water that contains infected snails.
• Individuals infected with schistosomiasis display chronic illness that can result in the damage of internal organs and in children, affects target growth and cognitive development.
Key Terms
• hepatopancreas: An organ of the digestive tract of arthropods and fish which provides the function which in mammals is provided separately by the liver and pancreas. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.01%3A_Protozoan_and_Helminthic_Diseases_of_the_Cardiovascular_and_Lymphatic_Systems/15.1E%3A_Babesiosis.txt |
Swimmer’s itch is a result of an immune reaction in response to the penetration of the skin by a schistosome.
Learning Objectives
• Outline the general life cycle of the Schistosomatidae parasite that causes schistosome cercarial dermatitis
Key Points
• Swimmer’s itch is commonly referred to as lake itch, duck itch, cercarial dermatitis and Schistosome cercarial dermatitis.
• The cercaria, the larvae stage of the parasite, will accidentally penetrate the skin of a human host and die within the skin. The cercaria cannot continue the life cycle in a human and requires its normal host, a waterfowl.
• The penetration of the skin by the cercaria result in an inflammatory immune reaction that causes itchy spots and raised papules in humans.
Key Terms
• swimmer’s itch: Swimmer’s itch, also known as lake itch, duck itch, cercarial dermatitis, and Schistosome cercarial dermatitis, is a short-term, immune reaction occurring in the skin of humans that have been infected by water-borne schistosomatidae.
• papules: A small, inflammatory, irritated spot on skin; similar in appearance to a pimple, without containing pus.
• cercaria: The parasitic larva of trematodes; its tail disappears when adult.
Swimmer’s itch is a condition often referred to as lake itch, duck itch, cercarial dermatitis and Schistosome cercarial dermatitis. It is caused by an immune response that is activated upon the entry of a water-borne flatworm parasite named schistosomatidae into the skin. The schistosomatidae results in an immune reaction in the skin that results in itchy, raised papules that occur within hours of infection.
There are numerous types of flatworm parasites within the family Schistosomatidae that can cause swimmer’s itch. The schistosomatidae which are responsible for swimmer’s itch include the genera Trichobilharzia and Gigantobilharzia. A species that is often implicated in cases of cercarial dermatitis is Austrobilharzia variglandis. The hosts of this species are ducks and the snail is the intermediate host for this species.
The life cycle of these parasites is characterized by their use of both freshwater snails and vertebrates as hosts. More specifically, waterfowl are used as the vertebrate host. During the life stage of these parasites, the larvae of the parasite, cercaria, exit the water snails and can accidentally come into contact with the skin of a swimmer. Upon contact with the skin of the swimmer, the cercaria will penetrate the skin and immediately die in the skin. Interestingly, the cercaria are unable to survive within a human host and cause infection. The symptoms and reactions exhibited in individuals diagnosed with swimmer’s itch are a result of the dead cercaria larvae.
If indeed the cercaria encounter a water bird, their normal host, the cercaria will penetrate the skin of the birds and migrate to the blood vessels to complete the cycle. For completion of the cycle, adult worms will form in the blood vessels and produce eggs which are passed in the feces. The eggs, upon exposure to water, will hatch into a miracidium that is ciliated. This form in the life cycle infects the snail intermediate host. In turn, the cercaria which are responsible for swimmer’s itch are produced.
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The respiratory system include lungs, airways and respiratory muscles. Ventilation is the rate at which gas enters or leaves the lung.
Learning Objectives
• Summarize the the functional anatomy of the respiratory system
Key Points
• Ventilation occurs under the control of the autonomic nervous system from parts of the brain stem—the medulla oblongata and the pons —that together form the respiration regulatory center.
• The three types of ventilation are minute ventilation, alevolar ventilation, and dead space ventilation.
• Inhalation is initiated by the diaphragm and supported by the external intercostal muscles. Additional accessory muscles include sternocleidomastoid, platysma, the scalene muscles of the neck, pectoral muscles, and the latissimus dorsi.
• When the diaphragm contracts, the ribcage expands and the contents of the abdomen are moved downward, resulting in a larger thoracic volume and negative pressure (with respect to atmospheric pressure) inside the chest.
• Exhalation is generally a passive process since the lungs have a natural elasticity; they recoil from the stretch of inhalation and air flows back out until the pressures in the chest and the atmosphere reach equilibrium.
• Gas exchange occurs at the alveoli, the tiny sacs that are the basic functional component of the lungs. The alveoli are interwoven with capillaries that connect to the larger bloodstream.
Key Terms
• elastic recoil: The lungs’ rebound from the stretch of inhalation that passively removes air from the lungs during exhalation.
• Dead space: Any space in the airways that is not involved in alveolar gas exhange, such as the conducting zones.
• ventilation: The bodily process of breathing, the inhalation of air to provide oxygen, and the exhalation of spent air to remove carbon dioxide.
The Respiratory System
The primary function of the respiratory system is gas exchange between the external environment and an organism ‘s circulatory system. In humans and other mammals, this exchange balances oxygenation of the blood with the removal of carbon dioxide and other metabolic wastes from the circulation.
As gas exchange occurs, the acid-base balance of the body is maintained as part of homeostasis. If proper ventilation is not maintained, two opposing conditions could occur: respiratory acidosis (a life threatening condition) and respiratory alkalosis.
At the molecular level, gas exchange occurs in the alveoli—tiny sacs which are the basic functional component of the lungs. The alveolar epithelial tissue is extremely thin and permeable, allowing for gas exchange between the air inside the lungs and the capillaries of the blood stream. Air moves according to pressure differences, in which air flows from areas of high pressure to areas of low pressure.
The Ventilation Rate
In respiratory physiology, ventilation rate is the rate at which gas enters or leaves the lung. There are several different terms used to describe the nuances of the ventilation rate.
• Minute Ventilation (VE): The amount of air entering the lungs per minute. It can be defined as tidal volume (the volume of air inhaled in a single breath) times the amount of breaths in a minute.
• Alveolar Ventilation (VA): The amount of gas per unit of time that reaches the alveoli (the functional part of the lungs where gas exchange occurs). It is defined as tidal volume minus dead space (the space in the lungs where gas exchange does not occur) times the respiratory rate.
• Dead Space Ventilation (VD): The amount of air per unit of time that doesn’t reach the alveoli. It is defined as volume of dead space times the respiratory rate.
Dead space is any space that isn’t involved in alveolar gas exchange itself, and it typically refers to parts of the lungs that are conducting zones for air, such as the trachea and bronchioles.
If someone breathes through a snorkeling mask, the length of their conducting zones increases, which increases dead space and reduces on alveolar ventilation. Feedback mechanisms increase the ventilation rate in such a case, but if dead space becomes too great, they won’t be able to counteract the effect.
The ventilation rate is controlled by several centers of the autonomic nervous system in the brain, primarily the medulla and the pons.
Mechanisms of Inhalation
Inhalation is initiated by the activity of the diaphragm and supported by the external intercostal muscles. A normal human respiratory rate is 10 to 18 breaths per minute.
During vigorous inhalation (at rates exceeding 35 breaths per minute), or in approaching respiratory failure, accessory muscles—such as the sternocleidomastoid, platysma, and the scalene muscles of the neck—are recruited to help sustain the increased respiratory rate. Pectoral muscles and latissimus dorsi are also accessory muscles for the activity of the lungs.
Under normal conditions, the diaphragm is the primary driver of inhalation. When the diaphragm contracts, the rib cage expands and the contents of the abdomen are moved downward, resulting in a larger thoracic volume and negative pressure (with respect to atmospheric pressure) inside the thorax.
As air moves from zones of high pressure to zones of low pressure, the contraction of the diaphragm allows the air to enter the conducting zone (such as the trachea, bronchioles, etc.), where it is filtered, warmed, and humidified as it flows to the lungs.
Mechanisms of Exhalation
Exhalation is generally a passive process. The lungs have high degree of elastic recoil, so they rebound from the stretch of inhalation and air flows out until the pressures in the lungs and the atmosphere reach equilibrium.
The reason for the elastic recoil of the lung is the surface tension from water molecules on the epithelium of the lungs. A molecule called surfactant (secreted by the alveoli) prevents the surface tension from becoming too great and collapsing the lungs.
Active or forced exhalation is achieved by the abdominal and the internal intercostal muscles. During this process, air is forced or exhaled out. During forced exhalation, as when blowing out a candle, the expiratory muscles, including the abdominal muscles and internal intercostal muscles, generate abdominal and thoracic pressure that force air out of the lungs.
Forced exhalation is often used as an indicator to measure airway health, as people with obstructive lung diseases (such as emphysema, asthma, and bronchitis) will not be able to actively exhale as much as a healthy person because of obstruction in the conducting zones from inhlation, or from a loss of elastic recoil of the lungs. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.02%3A_Microbial_Diseases_of_the_Respiratory_System/15.2A%3A_Functional_Anatomy_of_the_Respiratory_System.txt |
Airborne diseases are characterized by diseases that are transmitted through the air via the presence of a pathogen.
Learning Objectives
• Give examples of airborne pathogens and various routes of transmission
Key Points
• Airborne transmission results in the inhalation of pathogens that can affect an individual’s respiratory system or the rest of the body.
• Airborne diseases are caused by pathogens which can ride on either dust particles or small respiratory droplets that can stay suspended in the air and travel distances on air currents.
• Airborne diseases are commonly seen in unsanitary household conditions and overcrowded areas, and thrive in areas of poverty and poor hygienic conditions.
Key Terms
• droplet nuclei: Droplet nuclei are an important mode of transmission among many infectious viruses such as Influenza A. When viruses are shed by an infected person through coughing or sneezing into the air, the mucus coating on the virus starts to evaporate. Once this mucus shell evaporates the remaining viron is called a droplet nucleus or quanta.
Airborne Transmission of Disease
Airborne diseases are characterized by diseases that are transmitted through the air via the presence of a pathogen. These pathogens can include both viruses and bacteria that are spread by coughing, sneezing, laughing, or through personal contact. The pathogens are capable of traveling distances on air currents when they are present on either dust particles or small respiratory droplets. The airborne transmission that occurs utilizes small particles or droplet nucleithat contains these infectious agents or pathogens. These particles and droplets are capable of remaining suspended in air for extended periods of time. Inhalation of these particles results in respiratory tract infection. The ability of these droplets to remain suspended for long periods of time result in the lack of face-to-face contact for infection. The ability of these pathogens to survive and retain their ability to infect for relatively long periods of time add to the difficulty encountered in their prevention and targeting.
Often times, these airborne pathogens can result in inflammation in the nose, throat, sinuses, and the lungs. The symptoms such as sinus congestion, coughing, and sore throats are examples of inflammation of the upper respiratory airway. Many types of infections that can be a result of airborne transmission include: Anthrax, Chickenpox, Influenza, Measles, Smallpox, and Tuberculosis. Airborne diseases are caused by exposure to a source such as an infected individual or animal.
Airborne transmission of disease is common in unsanitary household conditions and overcrowded areas, and pathogens that are transmitted in this manner thrive in areas of poverty and poor hygienic conditions. For example, tuberculosis is common in individuals from developing areas in the world, adding to 95% of cases worldwide.
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Pharyngitis is an inflammation of the throat that has many causes, some of which are bacterial infections.
Learning Objectives
• List the symptoms and bacterial causes associated with pharyngitis
Key Points
• In most cases, pharyngitis is caused by a systemic viral infection and is typified by a painful swelling inflammation of the throat. This can cause difficulty swallowing or breathing.
• The most common bacterial cause of pharyngitis is streptococcus.
• Several types of bacteria can cause pharyngitis. The most common and effective treatment for these infections are antibiotics.
Key Terms
• hemolytic: producing hemolysis; destroying red blood cells
• peritonsillar abscess: Peritonsillar abscess (PTA), also called a quinsy, or abbreviated as a PTA, is a recognized complication of tonsillitis. It consists of a collection of pus beside the tonsil in what is referred to as Peritonsilar space (Peri – meaning surrounding).
Pharyngitis
Pharyngitis is an inflammation of the throat. In most cases, it is quite painful and is the most common cause of a sore throat. Like many types of inflammation, pharyngitis can be acute or chronic. Acute cases are characterized by a rapid onset and, typically, a relatively short course of inflammation. Pharyngitis can result in very large tonsils. This can make swallowing and breathing difficult. It can be accompanied by a cough or fever, for example, if it is caused by a systemic infection. Most acute cases are caused by viral infections (40–80%). The remainder are caused by bacterial infections, fungal infections, or irritants such as pollutants or chemical substances. The treatment of viral causes is mainly symptomatic. Bacterial or fungal causes are often amenable to antibiotics and anti-fungal treatments, respectively.
Bacterial Causes of Pharyngitis
A number of different bacteria can infect the human throat. The most common is Group A streptococcus, but others include Corynebacterium diphtheriae, Neisseria gonorrhoeae, Chlamydophila pneumoniae, and Mycoplasma pneumoniae.
Streptococcal pharyngitis, more commonly known as strep throat, is caused by group A beta-hemolytic streptococcus (GAS). This is the most common bacterial cause of pharyngitis (15–30%). Common symptoms of strep throat include fever, sore throat, and large lymph nodes. It is a contagious infection, spread by close contact with an infected individual. A throat culture is the gold standard for the diagnosis of streptococcal pharyngitis, with a sensitivity of 90–95%. A rapid strep test (also called rapid antigen detection testing, or RADT) is also occasionally used as a diagnostic. While the rapid strep test is quicker, it has a lower sensitivity (70%) and a statistically equal specificity (98%) as a throat culture. For step throat, antibiotics are useful in preventing complications and expediting recovery.
Fusobacterium necrophorum are normal inhabitants of the oropharyngeal flora. Occasionally, however, these bacteria can create a peritonsillar abscess. In 1 out of 400 untreated cases, Lemierre’s syndrome can occur as a result of these abscesses.
Diphtheria is a potentially life threatening upper respiratory infection caused by Corynebacterium diphtheriae. As a result of childhood vaccination programs, diphtheria has has been largely eradicated in developed nations, but it is still reported in the Third World, and, increasingly, in some areas in Eastern Europe. Antibiotics are effective in the early stages, but recovery is generally slow.
15.3A: Pharyngitis
Learning Objectives
• Describe the bacterium Streptococcus pyogenes that causes scarlet fever
A Bacteriophage Hitchhiker
Scarlet fever is an infectious disease which most commonly affects 4-8 year-old children. Symptoms include sore throat, fever, and a characteristic red rash. It is usually spread by inhalation. There is no vaccine, but the disease is effectively treated with antibiotics. Scarlet fever is caused by an erythrogenic toxin, a substance produced by the bacterium Streptococcus pyogenes (group A strep. ) when it is infected by a certain bacteriophage.
Scarlet fever is caused by secretion of pyrogenic (fever inducing) exotoxins by the infected Streptococcus. Exotoxin A (speA) is probably the best studied of these toxins. It is carried by the bacteriophage T12, which integrates into the Streptococcal genome, from where the toxin is transcribed.
The phage itself integrates into a serine tRNA gene on the chromosome. The T12 virus itself has not been placed into a taxon by the International Committee on Taxonomy of Viruses. It has a double stranded DNA genome; on morphological grounds it appears to be a member of the Siphoviridae. The speA gene was cloned and sequenced in 1986. It is 753 base pairs in length and encodes a 29.244 kiloDalton (kDa) protein. The protein contains a putative 30 amino acid signal peptide. Removal of the signal sequence gives a predicted molecular weight of 25.787 (kDa) for the secreted protein. Both a promoter and a ribosome-binding site (Shine-Dalgarno sequence) are present upstream of the gene. A transcriptional terminator is located 69 bases downstream from the translational termination codon. The carboxy terminal portion of the protein exhibits extensive homology with the carboxy terminus of Staphylococcus aureus enterotoxins B and C1. Streptococcal phages other than T12 may also carry the speA gene.
Key Points
• Scarlet fever usually affects children. Historically, it had devastating effects.
• While antibiotics are effective against scarlet fever, the illness is actually caused by a bacteriophage infecting Streptococcus that has infected a person.
• The bacteriophage T12 inserts into the genome of Streptococcus. This leads to the expression of an exotoxin, which causes scarlet fever.
Key Terms
• scarlet fever: a streptococcal infection, mainly occurring among children, and characterized by a red skin rash, sore throat and fever
• Shine-Dalgarno sequence: A ribosomal binding site in the mRNA of prokaryotes.
• exotoxin: Any toxin secreted by a microorganism into the surrounding environment.
• enterotoxin: Any of several toxins produced by intestinal bacteria | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.03%3A_Bacterial_Diseases_of_the_Respiratory_System/15.3A%3A_Pharyngitis/1.01%3A_Scarlet_Fever.txt |
Diphtheria is an upper respiratory infection that is largely benign unless left untreated, at which point very harmful toxins are produced.
Learning Objectives
• Discuss the role of diphtheria toxin in diphtheria
Key Points
• Diptheria is caused bu the bacteria Corynebacterium diphtheriae, and is easily treated with antibiotics. It is now a fairly rare disease in developed countries.
• If left untreated and if infected by a bacteriophage, then Corynebacterium diphtheriae produces toxins that can lead to mortality.
• Diphtheria toxinis comprised of two fragments, fragment A and fragment B;. Fragment B binds to the target cell surface and allows entry into cells through endosomes; fragment A inhibits protein translation.
• Fragment A inhibits protein synthesis by catalyzing EF-2 a protein essential for tRNA movement during protein translation.
Key Terms
• ribosylation: The attachment of a ribose or ribosyl group to a molecule, especially to a polypeptide or protein
• translation: A process occurring in the ribosome, in which a strand of messenger RNA (mRNA) guides assembly of a sequence of amino acids to make a protein.
Overview of Diphtheria
Diphtheria is an upper respiratory tract illness caused by Corynebacterium diphtheriae, a facultative, anaerobic, Gram-positive bacterium. It is characterized by sore throat, low fever, and an adherent membrane (a pseudomembrane) on the tonsils, pharynx, and/or nasal cavity. A milder form of diphtheria can be restricted to the skin. Less common consequences include myocarditis (about 20% of cases) and peripheral neuropathy (about 10% of cases).
Diphtheria is a contagious disease spread by direct physical contact or breathing the aerosolized secretions of infected individuals. Historically quite common, diphtheria has largely been eradicated in industrialized nations through widespread vaccination. In the United States, for example, there were 52 reported cases of diphtheria between 1980 and 2000; between 2000 and 2007, there were only three cases as the diphtheria–pertussis–tetanus (DPT) vaccine is recommended for all school-age children. Boosters of the vaccine are recommended for adults, since the benefits of the vaccine decrease with age without constant re-exposure; they are particularly recommended for those traveling to areas where the disease has not been eradicated.
Advanced Cases of Diphtheria
In cases that progress beyond a throat infection, diphtheria toxin spreads through the blood and can lead to potentially life-threatening complications that affect other organs, such as the heart and kidneys. The toxin can cause damage to the heart that affects its ability to pump blood or the kidneys’ ability to clear wastes. It can also cause nerve damage, eventually leading to paralysis. About 40% to 50% of those left untreated can die.
Diphtheria toxin is produced by C. diphtheriae only when it is infected with a bacteriophage that integrates the toxin-encoding genetic elements into the bacteria. Diphtheria toxin is a single, 60,000 dalton molecular weight protein composed of two peptide chains, fragment A and fragment B, held together by a disulfide bond. Fragment B is a recognition subunit that gains the toxin entry into the host cell by binding to the EGF-like domain of heparin-binding EGF-like growth factor (HB-EGF) on the cell surface. This signals the cell to internalize the toxin within an endosome via receptor-mediated endocytosis. Inside the endosome, the toxin is split by a trypsin-like protease into its individual A and B fragments. The acidity of the endosome causes fragment B to create pores in the endosome membrane, thereby catalyzing the release of fragment A into the cell’s cytoplasm.
Fragment A inhibits the synthesis of new proteins in the affected cell. It does this by catalyzing ADP-ribosylation of elongation factor EF-2—a protein that is essential to the translation step of protein synthesis. This ADP-ribosylation involves the transfer of an ADP-ribose from NAD+ to a diphthamide (a modified histidine) residue within the EF-2 protein. Since EF-2 is needed for the moving of tRNA from the A-site to the P-site of the ribosome during protein translation, ADP-ribosylation of EF-2 prevents protein synthesis. ADP-ribosylation of EF-2 is reversed by giving high doses of nicotinamide (a form of vitamin B3), since this is one of the reaction ‘s end-products, thus high amounts will drive the reaction in the opposite direction counteracting the toxin. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.03%3A_Bacterial_Diseases_of_the_Respiratory_System/15.3C%3A_Diphtheria.txt |
Otitis media, or earache, is the inflammation of the middle ear and is often due to bacterial infections.
Learning Objectives
• Discuss the causes and symptoms associated with otitis media
Key Points
• Bacterial-caused earaches are often due to Streptococcus pneumoniae, a common bacterial infection.
• Trimeric Autotransporter Adhesins on the surface of bacteria are the proteins responsible for earaches.
• TAA proteins bind to host cells, allowing the invading bacteria to transfer virulence factors which then cause inflammation of the middle ear.
Key Terms
• Eustachian tube: In humans and other land vertebrates, a tube that links the pharynx to the cavity of the middle ear to allow the equalization of the pressure on both sides of the eardrum.
• tympanic: relating to the eardrum or middle ear; tympanal
Otitis media is inflammation of the middle ear. It occurs in the area between the tympanic membrane and the inner ear, also effecting a duct known as the eustachian tube. It is one of the two most common causes of earache – the other being otitis externa. Diseases other than ear infections can also cause ear pain, including various cancers of any structure that share nerve supply with the ear. Though painful, otitis media is not threatening and usually heals on its own within 2–6 weeks. Typically, acute otitis media follows a cold. After a few days of a stuffy nose, the ear becomes involved and can cause severe pain. The pain will usually settle within a day or two, but can last over a week. Sometimes the ear drum ruptures, discharging pus from the ear, but the ruptured drum will usually heal rapidly.
Otitis media is most commonly caused by infection with viral, bacterial, or fungal pathogens. The most common bacterial pathogen is Streptococcus pneumoniae. Others include Pseudomonas aeruginosa, nontypeable Haemophilus influenzae and Moraxella catarrhalis. Among older adolescents and young adults, the most common cause of ear infections is Haemophilus influenzae. Viruses like respiratory syncytial virus (RSV) and those that cause the common cold may also result in otitis media by damaging the normal defenses of the epithelial cells in the upper respiratory tract. A major risk factor for developing otitis media is Eustachian tube dysfunction, which leads to the ineffective clearing of bacteria from the middle ear.
Otitis media caused by bacterial infections are due to Trimeric Autotransporter Adhesins (TAA; proteins found on the outer membrane of Gram-negative bacteria. Bacteria use TAAs in order to infect their host cells via a process called cell adhesion. TAAs are virulence factors; an infective agent that infects the host cell by attaching to them and secreting the virulence factor by a secretion pathway. The UspA1 protein domain is a TAA found in the bacteria Moraxella catarrhalis, which causes middle ear infections in humans.
15.3E: Whooping Cough
Pertussis, more commonly known as whooping cough, is a bacterial infection of the upper respiratory system.
Learning Objectives
• Describe the mechanism of action and causes of pertussis causing bacteria
Key Points
• Whooping cough is caused by the bacteria Bordetella pertussis, which infects the respiratory system.
• There is no zoonotic reservoir of Bordetella pertussis, meaning that humans appear to be the only host of this bacteria.
• Bordetella pertussis produces a number of virulence factors, notably Ptx, which inhibits the ability of phagocytes to respond to infections. This helps Bordetella pertussis spread throughout a host.
Key Terms
• zoonotic: of or relating to zoonosis, the transmission of an infectious disease between species.
• glottis: an organ of speech, located in the larynx, and consisting of the true vocal cords and the opening between them
• lymphocytes: type of white blood cells in the vertebrate immune system
Pertussis
Pertussis, also known as whooping cough, is an infection of the respiratory system characterized by a “whooping” sound that an afflicted person makes when breathing inwards. Only 50% of patients actually display the classic sound as they attempt to draw breath over a partially closed glottis. In the U.S., the infection was responsible for 5,000 to 10,000 deaths per year before a vaccine was developed and made available. Vaccination has transformed this. Between 1985 and 1988, fewer than 100 children died from pertussis. In 2000, according to the WHO, around 39 million people worldwide were being infected annually. Of these, about 297,000 died.
Causes of Pertussis
Pertussis is caused by the bacteria, Bordetella pertussis, a gram-negative, aerobic coccobacillus capsulate of the genus Bordetella. Bordetella pertussis infects its host by colonizing lung epithelial cells. The bacterium contains a surface protein, filamentous haemagglutinin adhesin, which binds to the sulfatides found on the cilia of epithelial cells. Once anchored, the bacterium produces tracheal cytotoxin, which stops the cilia from beating. This prevents the cilia from clearing debris from an organism ‘s lungs, and the body responds by sending the host into a coughing fit. These coughs expel some bacteria into the air, which are free to infect other hosts. There does not appear to be a zoonotic reservoir for B. pertussis. Humans are its only host. The bacterium is spread by airborne droplets, and its incubation period is one to two weeks.
B. pertussis has the ability to inhibit the function of a host’s immune system, through virulence factors. Its virulence factors include pertussis toxin, filamentous hæmagglutinin, pertactin, fimbria, and tracheal cytotoxin. The pertussis toxin, or PTx, inhibits G protein coupling that regulates an adenylate cyclase-mediated conversion of ATP to cyclic AMP. The end result is that phagocytes convert too much ATP to cyclic AMP, which can cause disturbances in cellular signaling mechanisms. This prevents phagocytes from correctly responding to an infection. PTx, formerly known as lymphocytosis -promoting factor, causes a decrease in the entry of lymphocytes into lymph nodes. This can lead to a condition known as lymphocytosis, which is a large increase in the number of lymphocytes in an organism’s blood. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.03%3A_Bacterial_Diseases_of_the_Respiratory_System/15.3D%3A_Otitis_Media.txt |
Tuberculosis is a common, and in many cases lethal, infectious bacterial disease that mainly affects the lungs.
Learning Objectives
• Summarize the risk factors associated with tuberculosis (TB)
Key Points
• Tuberculosis is spread through the air when people who have an active TB infection cough, sneeze, or otherwise transmit their saliva through the air.
• The classic symptoms of active TB infection are a chronic cough with blood -tinged sputum, fever, night sweats, and weight loss.
• Diagnosis of active TB relies on radiology (commonly chest x-rays) as well as microscopic examination and microbiological culture of body fluids. Diagnosis of latent TB relies on the Mantoux tuberculin skin test.
• Antibiotic resistance is a growing problem in the treatment of tuberculosis.
Key Terms
• latent: Existing or present but concealed or inactive.
• tuberculosis: An infectious disease of humans and animals caused by a species of mycobacterium mainly infecting the lungs where it causes tubercles characterized by the expectoration of mucus and sputum, fever, weight loss, and chest pain. It is transmitted through inhalation or ingestion of bacteria.
• pleurisy: inflammation of lung pleura
• sputum: Matter coughed up and expectorated from the mouth, composed of saliva and discharges from the respiratory passages such as mucus, phlegm, or pus.
Tuberculosis (TB; short for tubercle bacillus) is a common, and in many cases lethal, infectious disease caused by various strains of mycobacteria, usually Mycobacterium tuberculosis . Tuberculosis typically attacks the lungs, but can also affect other parts of the body. It is spread through the air when people who have an active TB infection cough, sneeze, or otherwise transmit their saliva through the air. Most infections are asymptomatic and latent, but about one in 10 latent infections eventually progresses to active disease which, if left untreated, kills more than 50% of those infected. One third of the world’s population is thought to have been infected with M. tuberculosis with new infections occurring at a rate of about one per second.
Symptoms
The classic symptoms of active TB infection are a chronic cough with blood-tinged sputum, fever, chills night sweats, and weight loss. Tuberculosis may infect any part of the body, but most commonly occurs in the lungs, known as pulmonary tuberculosis. Extrapulmonary TB occurs when tuberculosis develops outside of the lungs, but may co-exist with pulmonary TB as well. Extrapulmonary TB occurs more commonly in immunosuppressed persons and young children. In those with HIV this occurs in more than 50% of cases. Notable extrapulmonary infection sites include the pleura (in tuberculous pleurisy), the central nervous system (in tuberculous meningitis), the lymphatic system (in scrofula of the neck), the genitourinary system (in urogenital tuberculosis), and the bones and joints (osseous tuberculosis). Tuberculosis may become a chronic illness and cause extensive scarring in the upper lobes of the lungs.
Diagnostics
Diagnosing active tuberculosis based merely on signs and symptoms is difficult, as is diagnosing the disease in those who are immunosuppressed. A diagnosis of TB should, however, be considered in those with signs of lung disease or constitutional symptoms lasting longer than two weeks. A chest x-ray and multiple sputum cultures for acid-fast bacilli are typically part of the initial evaluation. A definitive diagnosis of TB is made by identifying M. tuberculosis in a clinical sample such as sputum, pus, or a tissue biopsy. However, the difficult culture process for this slow-growing organism can take two to six weeks for blood or sputum culture.
The Mantoux tuberculin skin test is often used to screen people at high risk for TB. It involves injecting an protein extraction of the tuberculosis bacteria under the skin, and then examining the site 36-48 hours later. A person who has been exposed to the bacteria and has previously formed antibodies is expected to mount an immune response, displaying a raised, red area of skin at the site of injection. The test does have limited accuracy, especially in immunosuppressed people, and is typically used in combination with clinical findings and x-rays to reach a diagnosis.
Risk Factors
A number of factors make people more susceptible to TB infections. The most important risk factor globally is HIV; 13% of all TB cases are infected by the virus. This is a particular problem in sub-Saharan Africa, where rates of HIV are high. Tuberculosis is closely linked to both overcrowding and malnutrition, making it one of the principal diseases of poverty. Those at high risk thus include: people who inject illicit drugs, inhabitants and employees of locales where vulnerable people gather, such as prisons and homeless shelters; medically underprivileged and resource-poor communities; high-risk ethnic minorities, children in close contact with high-risk category patients, and health care providers serving these clients. Chronic lung disease is another significant risk factor. Those who smoke cigarettes have nearly twice the risk of TB than non-smokers. Other disease states can also increase the risk of developing tuberculosis, including alcoholism and diabetes mellitus. Certain medications that cause immunosuppression such as corticosteroids and infliximab, are becoming increasingly important risk factors, especially in the developed world.
Treatment
Treatment of TB uses antibiotics to kill the bacteria. Effective TB treatment is difficult, due to the unusual structure and chemical composition of the mycobacterial cell wall, which hinders the entry of drugs and makes many antibiotics ineffective. The two antibiotics commonly used are isoniazid and rifampicin. Treatments can be prolonged, from months to even years. A barrier to effective treatment is patient noncompliance. Due to the long duration of treatment, patients will often forget to take their antibiotics periodically or stop taking them altogether. This contributes to the development of drug-resistant tuberculosis. Many strains of tuberculosis have already become resistant to previous treatments, including a strain that is resistant to all antibiotics.
Latent TB treatment usually employs a single antibiotic, while active TB disease is best treated with combinations of several antibiotics to reduce the risk of the bacteria developing antibiotic resistance. People with latent infections are also treated to prevent them from progressing to active TB disease later in life. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.03%3A_Bacterial_Diseases_of_the_Respiratory_System/15.3F%3A_Tuberculosis.txt |
Pneumonia is an inflammatory lung disease that can lead to problems with breathing, often caused by bacterial infections.
Learning Objectives
• List the various causes of bacterial pneumonia
Key Points
• Most cases of pneumonia are caused by bacterial infections, and most of the bacterial infections are caused by the bacteria Streptococcus pneumoniae.
• The bacteria that cause pneumonia are split into three groups, gram-negative, gram-positive and atypical.
• Alcoholism is asociated with Streptococcus pneumoniae induced pneumonia and smoking exacerbates the situation.
Key Terms
• pneumonia: Pneumonia is an inflammatory condition of the lung, affecting primarily the microscopic air sacs known as alveoli.
• infection: An uncontrolled growth of harmful microorganisms in a host.
• Alveoli: alveolus (plural alveoli) a small air sac in the lungs, where oxygen and carbon dioxide are exchanged with the blood.
Pneumonia is an inflammatory condition of the lung, affecting primarily the microscopic air sacs known as alveoli. It is usually caused by infection with viruses or bacteria and less commonly other microorganisms, certain drugs and other conditions such as autoimmune diseases. Typical symptoms include a cough, chest pain, fever, and difficulty breathing. Diagnostic tools include x-rays and culture of the sputum. Vaccines to prevent certain types of pneumonia are available. Treatment depends on the underlying cause. Presumed bacterial pneumonia is treated with antibiotics. If the pneumonia is severe, the affected person is generally admitted to hospital.
Bacteria are the most common cause of community-acquired pneumonia (CAP), with Streptococcus pneumoniae isolated in nearly 50% of cases. Other commonly isolated bacteria include: Haemophilus influenzae in 20%, Chlamydophila pneumoniae in 13%, and Mycoplasma pneumoniae in 3% of cases; Staphylococcus aureus; Moraxella catarrhalis; Legionella pneumophila and Gram-negative bacilli. A number of drug-resistant versions of the above infections are becoming more common, including drug-resistant Streptococcus pneumoniae (DRSP) and methicillin-resistant Staphylococcus aureus (MRSA). The spreading of organisms is facilitated when risk factors are present. Alcoholism is associated with Streptococcus pneumoniae, anaerobic organisms and Mycobacterium tuberculosis; smoking facilitates the effects of Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Legionella pneumophila. Exposure to birds is associated with Chlamydia psittaci; farm animals with Coxiella burnetti; aspiration of stomach contents with anaerobic organisms; and cystic fibrosis with Pseudomonas aeruginosa and Staphylococcus aureus. Streptococcus pneumoniae is more common in the winter, and should be suspected in persons who aspirate a large amount anaerobic organisms.
Bacteria caused pneumonia fall into 3 groups:
1. Gram Positive. Streptococcus pneumoniae is the most common bacterial cause of pneumonia in all age groups except newborn infants. Streptococcus pneumoniae is a Gram-positive bacterium that often lives in the throat of people who do not have pneumonia. Other important Gram-positive causes of pneumonia are Staphylococcus aureus and Bacillus anthracis.
2. Gram Negative. Gram-negative bacteria are seen less frequently: Haemophilus influenzae, Klebsiella pneumoniae, Escherichia coli, Pseudomonas aeruginosa, and Moraxella catarrhalis are the most common. These bacteria often live in the gut and enter the lungs when contents of the gut (such as vomit or faeces) are inhaled.
3. Atypical bacteria. “Atypical” bacteria are Coxiella burnetii, Chlamydophila pneumoniae, Mycoplasma pneumoniae, and Legionella pneumophila. Many people falsely believe they are called “atypical” because they are uncommon and/or do not respond to common antibiotics and/or cause atypical symptoms. In reality, they are “atypical” because they do not gram stain as well as gram-negative and gram-positive organisms. Pneumonia caused by Yersinia pestis is usually called pneumonic plague.
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The common cold is caused by several different viruses and is the most common human viral infection.
Learning Objectives
• Recognize the major viruses known to cause the common cold: rhinovirus, human parainfluenza virus and the human respiratory syncytial virus (RSV)
Key Points
• Over 200 virus types have been found that cause the common cold, with rhinoviruses being the most common.
• Rhinoviruses are a sub-type of picornavirus, a non-enveloped RNA virus, which is very small in size.
• The symptoms of the common cold are not due to the viral infection directly but rather the bodies response to the virus.
• There is no cure for the common cold, and in fact antibiotics which often prescribed are detrimental to patients.
Key Terms
• serotypes: A group of microorganisms characterized by a specific set of antigens; serovar.
• capsid: The outer protein shell of a virus.
The common cold (also known as nasopharyngitis, rhinopharyngitis, acute coryza, or a cold) is a viral infectious disease of the upper respiratory tract which affects primarily the nose. Symptoms include coughing, sore throat, runny nose, and fever which usually resolve in seven to ten days, with some symptoms lasting up to three weeks. Well over 200 viruses are implicated in the cause of the common cold. The most commonly implicated virus is a rhinovirus (30–80%), a type of picornavirus with 99 known serotypes. A picornavirus is a virus belonging to the family Picornaviridae. Picornaviruses are non-enveloped RNA viruses with an icosahedral capsid. The name is derived from pico, meaning small, and RNA, referring to the ribonucleic acid genome, so “picornavirus” literally means small RNA virus. Others include: coronavirus (10–15%), human parainfluenza viruses, human respiratory syncytial virus, adenoviruses, enteroviruses, and metapneumovirus. Frequently more than one virus is present.
The symptoms of the common cold are believed to be primarily related to the immune response to the virus. The mechanism of this immune response is virus specific. For example, the rhinovirus is typically acquired by direct contact; it binds to human ICAM-1 receptors through unknown mechanisms to trigger the release of inflammatory mediators. These inflammatory mediators then produce the symptoms. It does not generally cause damage to the nasal epithelium. The respiratory syncytial virus (RSV) on the other hand is contracted by both direct contact and air born droplets. It then replicates in the nose and throat before frequently spreading to the lower respiratory tract. RSV does cause epithelium damage. Human parainfluenza virus typically results in inflammation of the nose, throat, and bronchi. In young children when it affects the trachea it may produce the symptoms of croup due to the small size of their airway.
No cure for the common cold exists, but the symptoms can be treated. Antibiotics have no effect against viral infections and thus have no effect against the viruses that cause the common cold. Due to their side effects they cause overall harm; however, they are still frequently prescribed.It is the most frequent infectious disease in humans with the average adult contracting two to three colds a year and the average child contracting between six and twelve. These infections have been with humanity since antiquity. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.04%3A_Viral_Diseases_of_the_Respiratory_System/15.4A%3A_Colds.txt |
Viral pneumonia, one of the two leading causes of pneumonia, more commonly affects children.
Learning Objectives
• Outline the route of infection for a virus that causes pneumonia
Key Points
• Viral pneumonia is caused by both viral infection which leads to cell death. The body’s response to clear the cellular debris leads to further inflammation and the blockage of respiration.
• Many different viruses can cause viral pneumonia, but they all enter the lungs and damage the alveoli.
• The best prevention for viral pneumonia is to vaccinate against the viruses that can cause pneumonia.
Key Terms
• Alveoli: alveolus (plural alveoli) a small air sac in the lungs, where oxygen and carbon dioxide are exchanged with the blood.
• cytokines: Regulatory proteins that function in the regulation of the cells involved in immune system function
• apoptosis: The process of programmed cell death by which cells undergo an ordered sequence of events which lead to death of the cell. This occurs during growth and development of the organism, as a part of normal cell aging, or as a response to cellular injury.
Pneumonia is an inflammatory condition of the lung that particularly affects microscopic air sacs (alveoli). It is associated with fever and chest symptoms, and it appears as a lack of space on a chest x-ray. The inflammation may be caused by infection from viruses, bacteria, or other microorganisms. Less commonly, it is caused by certain drugs and other conditions. Viruses and bacteria are the two leading causes of pneumonia, while fungi and parasites are less common. Viruses are the most common cause of pneumonia in children, while bacteria are the most common cause in adults.
How Viruses Cause Pneumonia
Many types of viral infections can cause pneumonia, but in order to do this, these viruses must first invade cells in order to reproduce. Typically, a virus will reach the lungs by traveling in droplets through the mouth and nose during inhalation. Once there, the virus will invade the cells that line the airways and the alveoli. This invasion often leads to cell death, in which either the virus directly kills the cell, or the cell self-destructs through apoptosis. Further damage to the lungs occurs when the immune system responds to the infection. White blood cells, in particular lymphocytes, are responsible for activating a variety of chemicals (cytokines) which cause fluid to leak into the alveoli. The combination of cellular destruction and fluid-filled alveoli interrupts the transportation of oxygen into the bloodstream. Thus, in large part, as with other viral infections, it is the body’s response to the virus that causes the symptoms of pneumonia, and not necessarily the viral infection itself. In addition to their effects on the lungs, many viruses affect other organs and can lead to illnesses that affect other bodily functions. Viruses also make the body more susceptible to bacterial infection. For this reason, bacterial pneumonia often complicates viral pneumonia.
Which Viruses Cause Pneumonia
Common viruses that cause pneumonia include influenza viruses A and B, respiratory syncytial viruses (RSV), and human parainfluenza viruses (hPIV), the last of which particularly affects children. Rarer viruses that commonly cause pneumonia include adenoviruses (in military recruits), metapneumoviruses, and severe acute respiratory syndrome virus (SARS coronavirus). Viruses that primarily cause other diseases, but sometimes cause pneumonia, include herpes simplex virus (HSV, mainly in newborns), varicella- zoster virus (VZV), measles virus, rubella virus, and cytomegalovirus (CMV, mainly in people with immune system problems). In children with pneumonia, the most commonly identified agents are respiratory syncytial virus, rhinovirus, human metapneumovirus, human bocavirus, and parainfluenza viruses. Because of this, the best prevention against viral pneumonia is vaccination against influenza, adenovirus, chickenpox, herpes zoster, measles, and rubella. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.04%3A_Viral_Diseases_of_the_Respiratory_System/15.4B%3A_Viral_Pneumonia.txt |
Human respiratory syncytial virus (RSV) causes respiratory tract infections in humans.
Learning Objectives
• Recognize the traits associated with the human respiratory syncytial virus (RSV) and its mode of infection
Key Points
• RSV is a single stranded virus, the genome of which encodes 11 proteins which play different roles in RSV infection.
• RSV can induce syncytia (aggregates of host cells), providing further fertile ground for RSV to propagate.
• There is no direct treatment of RSV except to mitigate the symptoms, giving the patient’s body time to fight off the infection.
Key Terms
• cannula: A hose or tube that connects directly to an oxygen (O2) bottle/source from the user’s nose, commonly used by aircraft pilots or others needing a direct oxygen breathing apparatus.
• prophylactic: A medicine that preserves or defends against disease; a preventive.
• hypertonic: Having a greater osmotic pressure than another.
Respiratory Syncytial Virus Infection
Human respiratory syncytial virus (RSV) is a virus that causes respiratory tract infections. It is a major cause of lower respiratory tract infections and hospital visits during infancy and childhood. A prophylactic medication (not a vaccine) exists for preterm-birth (under 35 weeks gestation) infants, and for infants with a congenital heart defect or bronchopulmonary dysplasia. Of those infected with RSV, 2–3% will develop bronchiolitis, necessitating hospitalization.
RSV is a negative-sense, single-stranded RNA virus of the family Paramyxoviridae, which includes common respiratory viruses such as those causing measles and mumps. RSV is a member of the paramyxovirus subfamily Pneumovirinae. RSV has ten genes encoding 11 proteins. There are two open reading frames of M2. NS1 and NS2 inhibit type I interferon activity. N encodes the nucleocapsid protein that associates with the genomic RNA forming the nucleocapsid. M encodes the matrix protein required for viral assembly. SH, G and F form the viral coat. The G protein is a surface protein; it functions as the attachment protein, the protein which attaches the virus to target cells. The F protein is another important surface protein. RSV’s name comes from the fact that F proteins on the surface of the virus cause the cell membranes on nearby cells to merge, forming syncytia.
Syncytia are aggregates of cells that can form when cells are infected with certain types of viruses, notably HIV and paramyxoviruses such as RSV. During infection, viral fusion proteins used by the virus to enter the cell are transported to the cell surface where they can cause the host cell membrane to fuse with neighboring cells. This presumably works to the virus’s advantage, as aggregates of target cells provide more hosts for the virus to infect and multiply. F proteins also mediate viral fusion, allowing entry of the virus into the cell cytoplasm and also allowing the formation of syncytia. Antibodies directed at the F protein are neutralizing. M2 is the second matrix protein required for viral transcription; it encodes M2-1 (elongation factor) and M2-2 (transcription regulation), while L encodes the RNA polymerase. The phosphoprotein P is a cofactor for L. The genome is transcribed sequentially from NS1 to L with reduction in expression levels along its length.
Treatment of RSV is limited to supportive care, including oxygen therapy. Studies of nebulized hypertonic saline (HS) have shown that the “use of nebulized 3% HS is a safe, inexpensive, and effective treatment for infants hospitalized with moderately severe viral bronchiolitis” where “RSV accounts for the majority of viral bronchiolitis cases. ” Supportive care includes fluids and oxygen until the illness runs its course. Increased airflow, humidified and delivered via nasal cannula, may be supplied in order to reduce the effort required for respiration. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.04%3A_Viral_Diseases_of_the_Respiratory_System/15.4C%3A_Respiratory_Syncytial_Virus_Infection.txt |
Influenza is an infectious disease caused by RNA viruses of the family Orthomyxoviridae that affects birds and mammals.
Learning Objectives
• Differentiate between the respiratory system disorders of influenza and coryza
Key Points
• The most common symptoms of the disease are chills, fever, sore throat, muscle pains, severe headache, coughing, weakness/fatigue, and general discomfort.
• Influenza is transmitted through the air by coughs or sneezes, by direct contact with bird droppings or nasal secretions, or through contact with contaminated surfaces.
• Coryza is a word describing the symptoms of a cold and refers to the inflammation of the mucous membranes lining the nasal cavity which usually gives rise to the symptoms of congestion.
Key Terms
• coryza: Inflammation of the mucous membranes lining the nasal cavity, usually causing a running nose, nasal congestion, and loss of smell.
• RNA virus: Any of many viruses that possess ribonucleic acid as their genetic material and do not replicate using DNA.
• influenza: An acute contagious disease of the upper airways and lungs, caused by a virus, which rapidly spreads around the world in seasonal epidemics.
Influenza, commonly referred to as the flu, is an infectious disease caused by RNA viruses of the family Orthomyxoviridae that affects birds and mammals. The most common symptoms of the disease are chills, fever, sore throat, muscle pains, severe headache, coughing, weakness/fatigue, and general discomfort. Although it is often confused with other influenza-like illnesses, especially the common cold, influenza is a more severe disease than the common cold. The general symptoms of influenza are summarized in.
Typically, influenza is transmitted through the air by coughs or sneezes, creating aerosols containing the virus. Influenza can also be transmitted by direct contact with bird droppings or nasal secretions, or through contact with contaminated surfaces. Reasonably effective ways to reduce the transmission of influenza include good personal health and hygiene habits such as: not touching your eyes, nose or mouth; frequent hand washing, covering coughs and sneezes, avoiding close contact with sick people and staying home yourself if you are sick.
Vaccinations against influenza are usually made available to people in developed countries. The most common human vaccine is the trivalent influenza vaccine (TIV) that contains purified and inactivated antigens against three viral strains. Typically, this vaccine includes material from two influenza A virus subtypes and one influenza B virus strain. The TIV carries no risk of transmitting the disease, and it has very low reactivity. A vaccine formulated for one year may be ineffective in the following year, since the influenza virus evolves rapidly, and new strains quickly replace the older ones.
Influenza viruses A, B, and C are very similar in overall structure and a diagram of the structure of the virus can be seen in Figure 2. The viral particles of all influenza viruses are similar in composition. They are made of a viral envelope containing two main types of glycoproteins, wrapped around a central core. The central core contains the viral RNA genome and other viral proteins that package and protect this RNA. RNA tends to be single stranded, but in special cases it is double. Unusually for a virus, its genome is not a single piece of nucleic acid but seven or eight pieces of segmented negative-sense RNA. Each piece of RNA contain either one or two genes, which code for a gene product (protein). Hemagglutinin (HA) and neuraminidase (NA) are the two large glycoproteins on the outside of the viral particles. HA is a lectin that mediates binding of the virus to target cells and entry of the viral genome into the target cell, while NA is involved in the release of progeny virus from infected cells, by cleaving sugars that bind the mature viral particles. Furthermore, they are antigens to which antibodies can be raised. Influenza A viruses are classified into subtypes based on antibody responses to HA and NA. These different types of HA and NA form the basis of the H and N distinctions in, for example, H5N1. There are 16 H and 9 N subtypes known, but only H 1, 2, and 3, and N 1 and 2 are commonly found in humans.
Antiviral medication can be effective, but some strains of influenza can show resistance to the standard antiviral drugs. The two classes of antiviral drugs used against influenza are neuraminidase inhibitors and M2 protein inhibitors (adamantane derivatives). Neuraminidase inhibitors are currently preferred for flu virus infections since they are less toxic and more effective.
Coryza is a word describing the symptoms of a “cold. ” It describes the inflammation of the mucous membranes lining the nasal cavity which usually gives rise to the symptoms of nasal congestion and loss of smell, among other symptoms. Coryza may not always have an infectious or allergenic etiology and can be due to something as innocuous as a cold wind, spicy food, or tender points in the muscles of the neck such as the sternocleidomastoid. It is also a symptom of narcotic withdrawal. Coryza is classically used in association with the “four Cs” of measles infection: cough, conjunctivitis, Koplik’s spots, and coryza.
Treatment of coryza depends on etiology. Coryza from any allergic causes usually gets relieved if contact with the allergen (dust, pollen, cold wind, etc.) is avoided. Nasal sprays, antihistamines, and decongestants are beneficial. However, if it is due to any virus it usually takes three to seven days to improve.
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Histoplasmosis is a disease caused by the fungus Histoplasma capsulatum.
Learning Objectives
• Describe the traits associated with and mode of transmission for Histoplasma capsulatum
Key Points
• Histoplasmosis is s a disease caused by the fungus Histoplasma capsulatum, which is usually found in soil, and often associated with decaying bat guano or bird droppings.
• Cases of histoplasmosis have declined acutely since the Industrial Revolution as quality of life improved dramatically and humans were no longer living in their own squalor.
• Symptoms of this infection vary greatly, but the disease affects primarily the lungs. Occasionally, other organs are affected, and it can be fatal if left untreated.
Key Terms
• Histoplasmosis: Histoplasmosis is a disease caused by the fungus Histoplasma capsulatum. Symptoms of this infection vary greatly, but the disease primarily affects the lungs. Other organs are occassionally affected; this is called disseminated histoplasmosis and can be fatal if left untreated.
• fungus: Any member of the kingdom Fungi; a eukaryotic organism typically having chitin cell walls but no chlorophyll or plastids. Fungi may be unicellular or multicellular.
Histoplasmosis (also known as “Cave disease,” “Darling’s disease,” “Ohio valley disease,” “Reticuloendotheliosis,” “Spelunker’s Lung,” and “Caver’s disease”) is a disease caused by the fungus Histoplasma capsulatum. Symptoms of this infection vary greatly, but the disease primarily affects the lungs. Other organs are occasionally affected; this is called disseminated histoplasmosis and can be fatal if left untreated. Histoplasmosis is common among AIDS patients due to their suppressed immune system.
If symptoms of histoplasmosis infection occur, they will start within 3 to 17 days after exposure, with the average being 12 to 14 days. Most affected individuals have clinically silent manifestations and show no apparent ill effects. The acute phase of histoplasmosis is characterized by non-specific respiratory symptoms, often cough or flu-like. Chest X-ray findings are normal in 40 to 70% of cases. Chronic histoplasmosis cases can resemble tuberculosis, and disseminated histoplasmosis affects multiple organ systems and is fatal unless treated.
Histoplasmosis may be divided into the following types: primary pulmonary histoplasmosis, progressive disseminated histoplasmosis, primary cutaneous histoplasmosis, and African histoplasmosis.
Histoplasma capsulatum is found throughout the world. It is endemic in certain areas of the United States, particularly in states bordering the Ohio River valley and the lower Mississippi River. It is also common in caves in southern and East Africa. Positive histoplasmin skin tests occur in as many as 90% of the people living in areas where Histoplasma capsulatum is common, such as the eastern and central United States.
Histoplasma capsulatum grows in soil and material contaminated with bird or bat droppings (guano). The fungus has been found in poultry house litter, caves, areas harboring bats, and in bird roosts (particularly those of starlings). The fungus is thermally dimorphic: in the environment it grows as a brownish mycelium, and at body temperature (37 °C in humans) it morphs into a yeast. The inoculum is represented principally by microconidia that, once inhaled into the alveolar spaces, germinate and then transform into budding yeast cells. Histoplasmosis is not contagious, but is contracted by inhalation of the spores from disturbed soil or guano.
Histoplasmosis can be diagnosed by samples containing the fungusken from sputum, blood, or infected organs. It can also be diagnosed by detection of antigens in blood or urine samples by ELISA or PCR. It can also be diagnosed by a test for antibodies against Histoplasma in the blood. Histoplasma skin tests indicate whether a person has been exposed, but do not indicate whether they have the disease. Formal histoplasmosis diagnoses are often confirmed only by culturing the fungus directly. Cutaneous manifestations of disseminated disease are diverse and often present as a nondescript rash with systemic complaints. Diagnosis is best established by urine antigen testing. Blood cultures may take up to 6 weeks for diagnostic growth to occur and serum antigen testing often comes back with a false negative before 4 weeks of disseminated infection.
It is not practical to test or decontaminate most sites that may be contaminated with Histoplasma capsulatum, so precautions to reduce a person’s risk of exposure are important. Precautions common to all geographical locations would be to avoid accumulations of bird or bat droppings.
Antifungal medications are used to treat severe cases of acute histoplasmosis and all cases of chronic and disseminated disease. Typical treatment of severe disease first involves treatment with amphotericin B, followed by oral itraconazole. Treatment with itraconazole will need to continue for at least a year in severe cases.
In many milder cases, oral itraconazole or ketoconazole is sufficient. Asymptomatic disease is typically not treated. Past infection results in partial protection against ill effects if reinfected. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.05%3A_Fungal_Diseases_of_the_Respiratory_System/15.5A%3A_Histoplasmosis.txt |
Coccidioidomycosis is a fungal disease caused by Coccidioides immitis or C. posadasii.
Learning Objectives
• Describe the mode of transmission, symptoms and diagnostic test associated with Coccidioidomycosis immitis
Key Points
• C. immitis resides in the soil in certain parts of the southwestern United States, northern Mexico, and parts of Central and South America.
• Infection is caused by inhalation of the particles.
• The disease is usually mild, with flu-like symptoms and rashes.
Key Terms
• Coccidioidomycosis: Coccidioidomycosis is a fungal disease caused by Coccidioides immitis or C. posadasii. It is endemic in certain parts of Arizona, California, Nevada, New Mexico, Texas, Utah and northwestern Mexico.
• fungal: Of or pertaining to a fungus or fungi
• inhalation: The substance (medicament) which is inhaled.
Coccidioidomycosis (commonly known as “Valley fever”, as well as “California fever”, “Desert rheumatism”, and “San Joaquin Valley fever”) is a fungal disease caused by Coccidioides immitis or C. posadasii. It is endemic in certain parts of Arizona, California, Nevada, New Mexico, Texas, Utah and northwestern Mexico.
C. immitis resides in the soil in certain parts of the southwestern United States, northern Mexico, and parts of Central and South America. It is dormant during long dry spells, then develops as a mold with long filaments that break off into airborne spores when the rains come. The spores, known as arthroconidia, are swept into the air by disruption of the soil, such as occurs during construction, farming, or an earthquake.
Infection is caused by inhalation of the particles. The disease is not transmitted from person to person. The infection ordinarily resolves leaving the patient with a specific immunity to re-infection. C. immitis is a dimorphic saprophytic organism that grows as a mycelium in the soil and produces a spherule form in the host organism.
The disease is usually mild, with flu-like symptoms and rashes. The Mayo Clinic estimates that half the population in some affected areas have suffered from the disease. On occasion, those particularly susceptible may develop a serious or even fatal illness. Serious complications include severe pneumonia, lung nodules, and disseminated disease, where the fungus spreads throughout the body. The disseminated form of Valley Fever can devastate the body, causing skin ulcers, abscesses, bone lesions, severe joint pain, heart inflammation, urinary tract problems, meningitis, and often death. In order of decreasing risk, people of Filipino, African, Native American, Hispanic, and Asian descent are susceptible to the disseminated form of the disease. Men and pregnant women, and people with weakened immune systems (such as from AIDS), are more susceptible than non-pregnant women.
It has been known to infect humans, cattle, deer, dogs, elk, fish, mules, livestock, apes, kangaroos, wallabies, tigers, bears, badgers, otters and marine mammals.
Symptomatic infection (40% of cases) usually presents as an influenza-like illness with fever, cough, headaches, rash, and myalgia (muscle pain). Some patients fail to recover and develop chronic pulmonary infection or widespread disseminated infection (affecting meninges, soft tissues, joints, and bone). Severe pulmonary disease may develop in HIV-infected persons.
An additional risk is that health care providers who are unfamiliar with it or are unaware that the patient has been exposed to it may misdiagnose it as cancer and subject the patient to unnecessary surgery.
Coccidioidomycosis may be divided into the following types: Primary pulmonary coccidioidomycosis; Disseminated coccidioidomycosis; and Primary cutaneous coccidioidomycosis.
The fungal infection can be demonstrated by microscopic detection of diagnostic cells in body fluids, exudates, sputum and biopsy-tissue. With specific nucleotide primers, C.immitis DNA can be amplified by PCR. It can also be detected in cultures by morphological identification, or by using molecular probes that hybridize with C.immitis RNA. An indirect demonstration of fungal infection can be achieved also by serologic analysis detecting fungal antigen or host antibody produced against the fungus.
There are no published prospective studies that examine optimal antifungal therapy for coccidioidomycosis. Mild cases often do not require treatment. Oral Fluconazole and intravenous Amphotericin B are used in progressive or disseminated disease, or in which patients are immunocompromised. Alternatively, itraconazole or ketoconazole may be used. Posaconazole and voriconazole have also been used. There is currently no practical preventative measures available for people who live or travel through Valley Fever endemic areas. It is recommended to avoid airborne dust or dirt, though this is not a guaranteed manner of prevention. People in certain occupations may be advised to wear face masks. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.05%3A_Fungal_Diseases_of_the_Respiratory_System/15.5B%3A_Coccidiomycosis.txt |
Pneumocystis pneumonia (PCP) or pneumocystosis is a form of pneumonia, caused by the yeast-like fungus Pneumocystis jirovecii.
Learning Objectives
• Review the symptoms associated with pneumocystis pneumonia and the methods of diagnosis
Key Points
• Pneumocystis jirovecii is a pathogen that is specific to humans.
• Pneumocystis is commonly found in the lungs of healthy people, but, being a source of opportunistic infection, it can cause a lung infection in people with a weak immune system.
• Symptoms of PCP include fever, non-productive cough, shortness of breath, weight loss, and night sweats.
Key Terms
• Pneumocystis pneumonia: Pneumocystis pneumonia (PCP) or pneumocystosis is a form of pneumonia, caused by the yeast-like fungus Pneumocystis jirovecii. This pathogen is specific to humans; it has not been shown to infect other animals.
• Opportunistic: An opportunistic infection is an infection caused by pathogens, particularly opportunistic pathogens—those that take advantage of certain situations—such as bacterial, viral, fungal or protozoan infections that usually do not cause disease in a healthy host, one with a healthy immune system. A compromised immune system, however, presents an “opportunity” for the pathogen to infect.
• Symptoms: A symptom is a departure from normal function or feeling which is noticed by a patient, indicating the presence of disease or abnormality. A symptom is subjective, observed by the patient, and cannot be measured directly.
Pneumocystis pneumonia (PCP) or pneumocystosis is a form of pneumonia, caused by the yeast-like fungus (which had previously been erroneously classified as a protozoan) Pneumocystis jirovecii. This pathogen is specific to humans; it has not been shown to infect other animals. Other species of Pneumocystis that parasitize other animals have not been shown to infect humans.
Pneumocystis is commonly found in the lungs of healthy people, but being a source of opportunistic infection, it can cause a lung infection in people with a weak immune system. Pneumocystis pneumonia is especially seen in people with cancer, HIV/AIDS and the use of medications that affect the immune system.
Nomenclature of Pneumocystis Pneumonia
The older name Pneumocystis carinii (which now only applies to the Pneumocystis species that is found in rats), is still in common usage. As a result, Pneumocystis pneumonia (PCP) is also known as Pneumocystis jiroveci[i] pneumonia and (incorrectly) as Pneumocystis carinii pneumonia.
Regarding nomenclature, when the name of Pneumocystis pneumonia changed from P. carinii pneumonia to P. jirovecii pneumonia, it was at first felt that it could no longer be referred to as “PCP”. However, because the term PCP was already in common usage, it was rationalized that the term PCP could continue to be used, as it stood for PneumoCystis (jirovecii) Pneumonia.
Symptoms of Pneumocystis Pneumonia
Symptoms of PCP include fever, non-productive cough (because sputum is too viscous to become productive), shortness of breath (especially on exertion), weight loss, and night sweats. There is usually not a large amount of sputum with PCP unless the patient has an additional bacterial infection. The fungus can invade other visceral organs (such as the liver, spleen, and kidney), but only in a minority of cases.
Pneumothorax is a well-known complication of PCP. An acute history of chest pain with breathlessness and diminished breath sounds is typical of pneumothorax.
The risk of pneumonia due to Pneumocystis jirovecii increases when CD4 positive cell levels are less than 200 cells/μl. In these immunosuppressed individuals the manifestations of the infection are highly variable. The disease attacks the interstitial, fibrous tissue of the lungs, with marked thickening of the alveolar septa and alveoli, leading to significant hypoxia which can be fatal if not treated aggressively. In this situation LDH levels increase and gas exchange is compromised. Oxygen is less able to diffuse into the blood, leading to hypoxia. Hypoxia, along with high arterial carbon dioxide (CO2) levels, stimulates hyper-ventilatory effort, thereby causing dyspnea (breathlessness).
Diagnosis and Treatment of Pneumocystis Pneumonia
The diagnosis can be confirmed by the characteristic appearance of the chest x-ray, which shows widespread pulmonary infiltrates, and an arterial oxygen level (PaO2) that is strikingly lower than would be expected from symptoms. Gallium 67 scans are also use in the diagnosis. They are abnormal in approximately 90% of cases and are often positive before the chest x-ray becomes abnormal. The diagnosis can be definitively confirmed by histological identification of the causative organism in sputum or bronchio-alveolar lavage (lung rinse). Staining with toluidine blue, silver stain, periodic-acid schiff stain, or an immunofluorescence assay will show the characteristic cysts. The cysts resemble crushed ping-pong balls and are present in aggregates of 2 to 8 (and not to be confused with Histoplasma or Cryptococcus, which typically do not form aggregates of spores or cells). A lung biopsy would show thickened alveolar septa with fluffy eosinophilic exudate in the alveoli. Both the thickened septa and the fluffy exudate contribute to dysfunctional diffusion capacity which is characteristic of this pneumonia.
Pneumocystis infection can also be diagnosed by immunofluorescent or histochemical staining of the specimen, and more recently by molecular analysis of polymerase chain reaction products comparing DNA samples. Notably, simple molecular detection of Pneumocystis jirovecii in lung fluids does not mean that a person has Pneumocystis pneumonia or infection by HIV. The fungus appears to be present in healthy individuals in the general population.
Antipneumocystic medication is used with concomitant steroids in order to avoid inflammation, which causes an exacerbation of symptoms about four days after treatment begins if steroids are not used. By far the most commonly used medication is trimethoprim-sulfamethoxazole, but some patients are unable to tolerate this treatment due to allergies. Other medications that are used, alone or in combination, include pentamidine, trimetrexate, dapsone, atovaquone, primaquine, pafuramidine maleate (under investigation), and clindamycin. Treatment is usually for a period of about 21 days. However, pneumocystis pneumonia can be prevented by the drug TMP-SMX.
Pentamidine is less often used as its major limitation is the high frequency of side effects. These include acute pancreatitis, renal failure, hepatotoxicity, leukopenia, rash, fever, and hypoglycemia. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.05%3A_Fungal_Diseases_of_the_Respiratory_System/15.5C%3A_Pneumocystis_Pneumonia.txt |
Blastomycosis is a fungal infection caused by the organism Blastomyces dermatitidis.
Learning Objectives
• Describe the causes and symptoms of blastomycosis
Key Points
• Infection occurs by inhalation of the fungus from its natural soil habitat.
• Once suspected, the diagnosis of blastomycosis can usually be confirmed by demonstration of the characteristic, broad-based budding organisms in sputum or tissues by KOH prep, cytology, or histology.
• Once inhaled in the lungs, Blastomycosis multiply and may disseminate through the blood and lymphatics to other organs, including the skin, bone, genitourinary tract, and brain.
Key Terms
• fungal: Of or pertaining to a fungus or fungi
• Blastomycosis: Blastomycosis is a fungal infection caused by the organism Blastomyces dermatitidis. Endemic to portions of North America, blastomycosis causes clinical symptoms similar to histoplasmosis.
• inhalation: The substance (medicament) which is inhaled.
Blastomycosis (also known as “North American blastomycosis,” “Blastomycetic dermatitis,” and “Gilchrist’s disease”) is a fungal infection caused by the organism Blastomyces dermatitidis. Endemic to portions of North America, blastomycosis causes clinical symptoms similar to histoplasmosis.
Symptoms
Blastomycosis can present in one of the following ways:
• A flu-like illness with fever, chills, myalgia, headache, and a nonproductive cough which resolves within days
• An acute illness resembling bacterial pneumonia, with symptoms of high fever, chills, a productive cough, and pleuritic chest pain
• A chronic illness that mimics tuberculosis or lung cancer, with symptoms of low-grade fever, a productive cough, night sweats, and weight loss
• A fast, progressive, and severe disease that manifests as ARDS, with fever, shortness of breath, tachypnea, hypoxemia, and diffuse pulmonary infiltrates
• Skin lesions, usually asymptomatic, that appear as ulcerated lesions with small pustules at the margins
• Bone lytic lesions that can cause bone or joint pain.
• Prostatitis may be asymptomatic or may cause pain on urinating. Laryngeal involvement causes hoarseness.
Infection occurs by inhalation of the fungus from its natural soil habitat. Once inhaled in the lungs, Blastomycosis multiply and may disseminate through the blood and lymphatics to other organs, including the skin, bone, genitourinary tract, and brain. The incubation period is 30 to 100 days, although infection can be asymptomatic.
Diagnosis
Once suspected, the diagnosis of blastomycosis can usually be confirmed by demonstration of the characteristic, broad-based budding organisms in sputum or tissues by KOH prep, cytology, or histology. Tissue biopsy of skin or other organs may be required in order to diagnose extra-pulmonary disease. Blastomycosis is histologically associated with granulomatous nodules. Commercially available urine antigen testing appears to be quite sensitive in suggesting the diagnosis in cases where the organism is not readily detected. While culture of the organism remains the definitive diagnostic standard, its slow growing nature can lead to delays in treatment of up to several weeks.
Treatment
Itraconazole given orally is the treatment of choice for most forms of the disease. Ketoconazole may also be used. Cure rates are high, and the treatment over a period of months is usually well tolerated. Amphotericin B is considerably more toxic, and is usually reserved for immunocompromised patients who are critically ill and those with central nervous system disease. Fluconazole has also been tested on patients in Canada. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.05%3A_Fungal_Diseases_of_the_Respiratory_System/15.5D%3A_Blastomycosis.txt |
Sporotrichosis is a disease caused by the fungus Sporothrix schenckii.
Learning Objectives
• Compare and contrast the various forms of sporotrichosis: cutaneous/skin, pulmonary and disseminated sporotrichosis
Key Points
• In cases of sporotrichosis affecting the lungs, the fungal spores enter through the respiratory pathways.
• Sporotrichosis progresses slowly – the first symptoms may appear from one to 12 weeks (average three weeks) after the initial exposure to the fungus.
• Forms and symptoms of sporotrichosis include: cutaneous or skin sporotrichosis; pulmonary sporotrichosis; and disseminated sporotrichosis.
Key Terms
• fungus: Any member of the kingdom Fungi; a eukaryotic organism typically having chitin cell walls but no chlorophyll or plastids. Fungi may be unicellular or multicellular.
• Sporotrichosis: A disease caused by the infection of the fungus Sporothrix schenckii, usually affecting the skin, although other rare forms can affect the lungs, joints, bones, and even the brain. Because roses can spread the disease, it is often referred to as rose-thorn or rose-gardeners’ disease.
Sporotrichosis (also known as “Rose gardener’s disease”) is caused by the infection of the fungus Sporothrix schenckii . This fungal disease usually affects the skin, although other rare forms can affect the lungs, joints, bones, and even the brain. Because roses can spread the disease, it is one of a few diseases referred to as rose-thorn or rose-gardeners’ disease.
Because S. schenckii is naturally found in soil, hay, sphagnum moss, and plants, it usually affects farmers, gardeners, and agricultural workers. It enters through small cuts and abrasions in the skin to cause the infection. In cases of sporotrichosis affecting the lungs, the fungal spores enter through the respiratory pathways. Sporotrichosis can also be acquired from handling cats with the disease; it is an occupational hazard for veterinarians.
Sporotrichosis progresses slowly – the first symptoms may appear from one to 12 weeks (average three weeks) after the initial exposure to the fungus. Serious complications can also develop in patients who have a compromised immune system.
Forms and symptoms of sporotrichosis include: cutaneous or skin sporotrichosis; pulmonary sporotrichosis; and disseminated sporotrichosis.
Cutaneous or skin sporotrichosis: This is the most common form of the disease. Symptoms include nodular lesions or bumps in the skin at the point of entry and also along lymph nodes and vessels. The lesion starts off small and painless, and ranges in color from pink to purple. Left untreated, the lesion becomes larger and looks similar to a boil. More lesions will appear, until a chronic ulcer develops. Usually, cutaneous sporotrichosis lesions occur in the finger, hand, and arm.
Pulmonary sporotrichosis: This rare form of the disease occurs when S. schenckii spores are inhaled. Symptoms include productive coughing, nodules and cavitations of the lungs, fibrosis, and swollen hilar lymph nodes. Patients with this form of sporotrichosis are susceptible to developing tuberculosis and pneumonia.
Disseminated sporotrichosis: this occurs when the infection spreads from the primary site to secondary sites in the body and develops into a rare and critical form. The infection can spread to joints and bones (called osteoarticular sporotrichosis) as well as the central nervous system and the brain (called sporotrichosis meningitis). The symptoms include weight loss, anorexia, and the appearance of bony lesions.
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The human gastrointestinal tract refers to the stomach and intestine, and sometimes to all the structures from the mouth to the anus.
Learning Objectives
• Outline the anatomical organization of the digestive system
Key Points
• The major organs of the digestive system are the stomach and intestine.
• The upper gastrointestinal tract consists of the esophagus, stomach, and duodenum.
• The lower gastrointestinal tract includes the small intestine and the large intestine.
• Digestive juices are produced by the pancreas and the gallbladder.
• The small intestine includes the duodenum, jejunum, and ileum.
• The large intestine includes the cecum, colon, rectum, and anus.
Key Terms
• upper gastrointestinal tract: This tract consists of the esophagus, stomach, and duodenum.
• lower gastrointestinal tract: This tract includes most of the small intestine and all of the large intestine.
The human gastrointestinal tract refers to the stomach and intestine, and sometimes to all the structures from the mouth to the anus.
Upper Gastrointestinal Tract
The upper gastrointestinal tract consists of the esophagus, stomach, and duodenum. The exact demarcation between upper and lower can vary. Upon gross dissection, the duodenum may appear to be a unified organ, but it is often divided into two parts based upon function, arterial supply, or embryology.
The upper gastrointestinal tract includes the:
• Esophagus, the fibromuscular tube that food passes through—aided by peristaltic contractions—the pharynx to the stomach.
• Stomach, which secretes protein -digesting enzymes called proteases and strong acids to aid in food digestion, before sending the partially digested food to the small intestines.
• Duodenum, the first section of the small intestine that may be the principal site for iron absorption.
Lower Gastrointestinal Tract
The lower gastrointestinal tract includes most of the small intestine and all of the large intestine. According to some sources, it also includes the anus.
The small intestine has three parts:
• Duodenum: Here the digestive juices from the pancreas ( digestive enzymes ) and the gallbladder ( bile ) mix together. The digestive enzymes break down proteins and bile and emulsify fats into micelles. The duodenum contains Brunner’s glands that produce bicarbonate, and pancreatic juice that contains bicarbonate to neutralize hydrochloric acid in the stomach.
• Jejunum: This is the midsection of the intestine, connecting the duodenum to the ileum. It contains the plicae circulares and villi to increase the surface area of that part of the GI tract.
• Ileum: This has villi, where all soluble molecules are absorbed into the blood ( through the capillaries and lacteals).
The large intestine has four parts:
1. Cecum, the vermiform appendix that is attached to the cecum.
2. Colon, which includes the ascending colon, transverse colon, descending colon, and sigmoid flexure. The main function of the colon is to absorb water, but it also contains bacteria that produce beneficial vitamins like vitamin K.
3. Rectum.
4. Anus.
The ligament of Treitz is sometimes used to divide the upper and lower GI tracts.
15.6B: Normal Gastrointestinal Microbiota
Gut flora consist of microorganisms that live in the digestive tracts of animals and are the largest reservoir of human flora.
Learning Objectives
• Summarize the relationship between the nonpathogenic gastrointestinal microbiota and the human hosts
Key Points
• The relationship between gut flora and humans is not merely commensal (a non-harmful coexistence), but rather a mutualistic relationship.
• Gut flora perform functions, such as fermenting unused energy substrates, training the immune system, preventing growth of harmful bacteria, regulating the development of the gut, producing vitamins for the host, and producing hormones to direct the host to store fats.
• In certain conditions, some gutflora are thought to be capable of causing disease by producing infection or increasing cancer risk for the host.
Key Terms
• commensal: A term for a form of symbiosis in which one organism derives a benefit while the other is unaffected
• microflora: Microscopic plant life, especially the bacterial colonies found in the gut of normal, healthy animals and humans.
Gut flora consists of microorganisms that live in the digestive tracts of animals and is the largest reservoir of human flora. In this context, gut is synonymous with intestinal, and flora with microbiota and microflora; the word microbiome is also in use.
The human body, consisting of about 10 trillion cells, carries about ten times as many microorganisms in the intestines. The metabolic activities performed by these bacteria resemble those of an organ, leading some to liken gut bacteria to a “forgotten” organ. It is estimated that these gut flora have around 100 times as many genes in aggregate as there are in the human genome.
Bacteria make up most of the flora in the colon and up to 60% of the dry mass of feces. Somewhere between 300 and 1000 different species live in the gut, with most estimates at about 500. However, it is probable that 99% of the bacteria come from about 30 or 40 species. Fungi and protozoa also make up a part of the gut flora, but little is known about their activities.
Research suggests that the relationship between gut flora and humans is not merely commensal (a non-harmful coexistence), but rather a mutualistic relationship. Though people can survive without gut flora, the microorganisms perform a host of useful functions, such as: fermenting unused energy substrates, training the immune system, preventing growth of harmful, pathogenic bacteria, regulating the development of the gut, producing vitamins for the host (such as biotin and vitamin K), and producing hormones to direct the host to store fats. However, in certain conditions, some species are thought to be capable of causing disease by producing infection or increasing cancer risk for the host.
Over 99% of the bacteria in the gut are anaerobes, but in the cecum, aerobic bacteria reach high densities. Not all the species in the gut have been identified because most cannot be cultured, and identification is difficult. Populations of species vary widely among different individuals but stay fairly constant within an individual over time, even though some alterations may occur with changes in lifestyle, diet and age. An effort to better describe the microflora of the gut and other body locations has been initiated (such as the Human Microbiome Project). In 2009, scientists from INRA (France) highlighted the existence of a small number of species shared by all individuals constituting the human intestinal microbiota phylogenetic core. Most bacteria belong to the genera Bacteroides, Clostridium, Fusobacterium, Eubacterium, Ruminococcus, Peptococcus, Peptostreptococcus, and Bifidobacterium. Other genera, such as Escherichia and Lactobacillus, are present to a lesser extent. Species from the genus Bacteroides alone constitute about 30% of all bacteria in the gut, suggesting that this genus is especially important in the functioning of the host. The currently known genera of fungi of the gut flora include Candida, Saccharomyces, Aspergillus, and Penicillium. An enterotype is a classification of living organisms based on its bacteriological ecosystem in the human gut microbiome. Three human enterotypes have been discovered.
Bacteria in the gut fulfill a host of useful functions for humans, including digestion of unutilized energy substrates, stimulating cell growth, repressing the growth of harmful microorganisms, training the immune system to respond only to pathogens, and defending against some diseases.
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The mouth contains a wide variety of oral bacteria, but only a few specific species of bacteria are believed to cause tooth and gum infections.
Learning Objectives
• List the types of bacteria and issues associated with oral bacteria: Streptococci spp and Lactobaccilus acidophilus
Key Points
• Dental caries, also known as tooth decay or cavity, is a bacterial infection that causes demineralization and destruction of the hard tissues (enamel, dentin, and cementum).
• Tooth decay results from the production of acid by bacterial fermentation of the food debris accumulated on the tooth surface.
• Bacteria occupy the ecological niche provided by both the tooth surface and gingival epithelium. However, a highly efficient innate host defense system constantly monitors the bacterial colonization and prevents bacterial invasion of local tissues.
• Porphyromonas gingivalis is a Gram-negative oral anaerobe strongly associated with chronic adult periodontitis.
• Dental plaque is the material that adheres to the teeth and consists of bacterial cells (mainly S. mutans and S. sanguis), salivary polymers, and bacterial extracellular products.
Key Terms
• cavity: A soft area in a decayed tooth.
• plaque: a clearing in a bacterial lawn caused by a virus
• dental plaque: Dental plaque is the material that adheres to the teeth and consists of bacterial cells (mainly S. mutans and S. sanguis), salivary polymers, and bacterial extracellular products.
• biofilm: A thin film of mucus created by and containing a colony of bacteria and other microorganisms.
Tooth and Gum Infections
Dental caries, also known as tooth decay or cavity, is a bacterial infection that causes demineralization and destruction of the hard tissues (enamel, dentin, and cementum). This usually happens from the production of acid by bacterial fermentation of the food debris accumulated on the tooth surface. If demineralization exceeds saliva and other remineralization factors, such as from calcium and fluoridated toothpastes, these hard tissues progressively break down, producing dental caries (cavities, holes in the teeth). The bacteria most responsible for dental cavities are the mutans streptococci, most prominently Streptococcus mutans and Streptococcus sobrinus, and lactobacilli. If left untreated, the disease can lead to pain, tooth loss, and infection. Today, caries remain one of the most common diseases throughout the world.
The mouth contains a wide variety of oral bacteria, but only a few specific species of bacteria are believed to cause dental caries: Streptococcus mutans and Lactobacilli among them. Lactobacillus acidophilus, Actinomyces viscosus, Nocardia spp., and Streptococcus mutans are most closely associated with caries, in particular root caries. Bacteria collect around the teeth and gums in a sticky, creamy-colored mass called plaque, which serves as a biofilm. Some sites collect plaque more commonly than others. Grooves on the occlusal surfaces of molar and premolar teeth provide microscopic retention sites for plaque bacteria, as do the approximal sites. Plaque may also collect above or below the gingiva where it is referred to as supra- or sub-gingival plaque respectively.
Oral bacteria have evolved mechanisms to sense their environment and evade or modify the host. Bacteria occupy the ecological niche provided by both the tooth surface and gingival epithelium. However, a highly efficient innate host defense system constantly monitors the bacterial colonization and prevents bacterial invasion of local tissues. A dynamic equilibrium exists between dental plaque bacteria and the innate host defense system. The oral cavity of the newborn baby does not contain bacteria but rapidly becomes colonized with bacteria such as Streptococcus salivarius. With the appearance of the teeth during the first year, colonization by Streptococcus mutans and Streptococcus sanguinis occurs as these organisms colonize the dental surface and gingiva. Other strains of streptococci adhere strongly to the gums and cheeks but not to the teeth. The gingival crevice area (supporting structures of the teeth) provides a habitat for a variety of anaerobic species. Bacteroides and spirochetes colonize the mouth around puberty.
The levels of oral spirochetes are elevated in patients with periodontal diseases. Among this group, Treponema denticola is the most studied and is considered one of the main etiological bacteria of periodontitis. Treponema denticola is a motile and highly proteolytic bacterium.
Spirochetes and fusi-form bacilli live as normal flora in the mouth, but the bacteria can cause infection and diseases to the oral cavity.
Porphyromonas gingivalis is a Gram-negative oral anaerobe strongly associated with chronic adult periodontitis. The bacterium produces a number of well-characterized virulence factors and can be manipulated genetically. The availability of the genome sequence is aiding our understanding of the biology of P. gingivalis and how it interacts with the environment, other bacteria, and the human host.
Aggregatibacter actinomycetemcomitans is considered an oral pathogen due to its virulence factors, its association with localized aggressive periodontitis in young adolescents, and studies indicating that it can cause bone loss.
Dental plaque is the material that adheres to the teeth and consists of bacterial cells (mainly S. mutans and S. sanguis), salivary polymers, and bacterial extracellular products. Plaque is a biofilm on the surfaces of the teeth. This accumulation of microorganisms subject the teeth and gingival tissues to high concentrations of bacterial metabolites which results in dental disease. If not taken care of, via brushing or flossing, the plaque can turn into tartar (its hardened form) and lead to gingivitis or periodontal disease. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.07%3A_Bacterial_Diseases_of_the_Mouth/15.7A%3A_Tooth_and_Gum_Infections.txt |
Dental caries cause demineralization of the hard tissues and destruction of the organic matter of the tooth.
Learning Objectives
• Explain how dental caries can be prevented
Key Points
• Dentin is produced continuously throughout life by odontoblasts.
• Caries can be classified by location, etiology, rate of progression, and affected hard tissues.
• Enamel is a highly mineralized acellular tissue. Enamel rods, which are the basic unit of the enamel structure, run perpendicularly from the surface of the tooth to the dentin.
• There are four main criteria required for caries formation: a tooth surface (enamel or dentin), caries-causing bacteria, fermentable carbohydrates (such as sucrose), and time.
• Dental caries can occur on any surface of a tooth that is exposed to the oral cavity, but not the structures that are retained within the bone.
• The two bacteria most commonly responsible for dental cavities are Streptococcus mutans and Lactobacillus.
• The use of dental sealants is a means of prevention.
• Professional hygiene care consists of regular dental examinations and cleanings.
• An extraction can also serve as treatment for dental caries.
• In general, early treatment is less painful and less expensive than treatment of extensive decay.
• Recurrent caries, also described as secondary, are caries that appears at a location with a previous history of caries.
• Dentin is produced continuously throughout life by odontoblasts.
• Personal hygiene care consists of proper brushing and flossing daily. The purpose of oral hygiene is to minimize any etiologic agents of disease in the mouth.
• Primary diagnosis involves inspection of all visible tooth surfaces using a good light source, dental mirror and explorer. Dental radiographs (X-rays) may show dental caries before it is otherwise visible, in particular caries between the teeth.
• Caries can be classified by location, etiology, rate of progression, and affected hard tissues.
• In dentin from the deepest layer to the enamel, the distinct areas affected by caries are the advancing front, the zone of bacterial penetration, and the zone of destruction.
• Intrauterine and neonatal lead exposure promote tooth decay. Other divalent cations, such as cadmium, mimic the calcium ion and therefore exposure may promote tooth decay.
• From the deepest layer of the enamel to the enamel surface, the identified areas are the: translucent zone, dark zones, body of the lesion, and surface zone.
• Enamel is a highly mineralized acellular tissue. Enamel rods, which are the basic unit of the enamel structure, run perpendicularly from the surface of the tooth to the dentin.
• Some brands of smokeless tobacco contain high sugar content, increasing susceptibility to caries. Tobacco use is a significant risk factor for periodontal disease, which can cause the gingiva to recede.
• Reduced saliva is associated with increased caries.
• There are four main criteria required for caries formation: a tooth surface (enamel or dentin); caries-causing bacteria; fermentable carbohydrates (such as sucrose); and time.
• If demineralization exceeds saliva and other remineralization factors such as from calcium and fluoridated toothpastes, these tissues progressively break down, producing dental caries (cavities, holes in the teeth).
• The presentation of caries is highly variable.
• Bacteria collect around the teeth and gums in a sticky, creamy-coloured mass called plaque, which serves as a biofilm.
• Dental caries can occur on any surface of a tooth that is exposed to the oral cavity, but not the structures that are retained within the bone.
• The mineral content of teeth is sensitive to increases in acidity from the production of lactic acid.
• Radiographs are used for less visible areas of teeth and to judge the extent of destruction.
• Depending on the extent of tooth destruction, various treatments can be used to restore teeth to proper form, function, and aesthetics, but there is no known method to regenerate large amounts of tooth structure. Instead, dental health organizations advocate preventive and prophylactic measures, such as regular oral hygiene and dietary modifications, to avoid dental caries.
• Tooth decay disease is caused by specific types of bacteria that produce acid in the presence of fermentable carbohydrates such as sucrose, fructose, and glucose.
• Before the cavity forms, the process is reversible, but once a cavity forms, the lost tooth structure cannot be regenerated.
• The two bacteria most commonly responsible for dental cavities are Streptococcus mutans and Lactobacillus.
Key Terms
• cementum: A bony substance that covers the root of a tooth; cement.
• enamel: The hard covering on the exposed part of a tooth.
• dentin: The hard, dense calcareous material that makes up the bulk of a tooth
Dental caries, also known as tooth decay or a cavity, is an infection, usually bacterial in origin, that causes demineralization of the hard tissues (enamel, dentin, and cementum ) and destruction of the organic matter of the tooth, usually by production of acid by hydrolysis of the food debris accumulated on the tooth surface. If demineralization exceeds saliva and other remineralization factors such as from calcium and fluoridated toothpastes, these tissues progressively break down, producing dental caries (cavities, holes in the teeth). The two bacteria most commonly responsible for dental cavities are Streptococcus mutans and Lactobacillus. If left untreated, the disease can lead to pain, tooth loss, and infection. Today, caries remain one of the most common diseases throughout the world.
Caries can be classified by location, etiology, rate of progression, and affected hard tissues. These forms of classification can be used to characterize a particular case of tooth decay in order to more accurately represent the condition to others and also indicate the severity of tooth destruction.
Tooth decay disease is caused by specific types of bacteria that produce acid in the presence of fermentable carbohydrates such as sucrose, fructose, and glucose. The mineral content of teeth is sensitive to increases in acidity from the production of lactic acid. To be specific, a tooth (which is primarily mineral in content) is in a constant state of back-and-forth demineralization and remineralization between the tooth and surrounding saliva. For people with little saliva, especially due to radiation therapies that may destroy the salivary glands, there also exists remineralization gel. These patients are particularly susceptible to dental caries. When the pH at the surface of the tooth drops below 5.5, demineralization proceeds faster than remineralization (meaning that there is a net loss of mineral structure on the tooth’s surface). Most foods are in this acidic range and without remineralization result in the ensuing decay.
As the enamel and dentin are destroyed, the cavity becomes more noticeable. The affected areas of the tooth change color and become soft to the touch. Once the decay passes through enamel, the dentinal tubules, which have passages to the nerve of the tooth, become exposed, causing a toothache. The pain may worsen with exposure to heat, cold, or sweet foods and drinks. Dental caries can also cause bad breath and foul tastes. In highly progressed cases, infection can spread from the tooth to the surrounding soft tissues. Complications such as cavernous sinus thrombosis and Ludwig’s angina can be life-threatening.
There are four main criteria required for caries formation: a tooth surface (enamel or dentin) caries-causing bacteria, fermentable carbohydrates (such as sucrose), and time. The caries process does not have an inevitable outcome, and different individuals will be susceptible to different degrees depending on the shape of their teeth, oral hygiene habits, and the buffering capacity of their saliva. Dental caries can occur on any surface of a tooth that is exposed to the oral cavity, but not the structures that are retained within the bone. All caries occur from acid demineralization that exceeds saliva and fluoride remineralization, and almost all acid demineralization occurs where food (containing carbohydrate like sugar) is left on teeth. Though most trapped food is left between teeth, over 80% of cavities occur inside pits and fissures on chewing surfaces where brushing, fluoride, and saliva cannot reach to remineralize the tooth as they do on easy-to-reach surfaces that develop few cavities.
In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Ninety-six percent of tooth enamel is composed of minerals. These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5. Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content. Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, however, the tooth is susceptible to dental caries.
Bacteria in a person’s mouth convert glucose, fructose, and most commonly sucrose (table sugar) into acids such as lactic acid through a glycolytic process called fermentation. If left in contact with the tooth, these acids may cause demineralization, which is the dissolution of its mineral content. The process is dynamic, however, as remineralization can also occur if the acid is neutralized by saliva or mouthwash.
At times, pit and fissure caries may be difficult to detect. Bacteria can penetrate the enamel to reach dentin, but then the outer surface may remineralize, especially if fluoride is present. These caries, sometimes referred to as “hidden caries”, will still be visible on x-ray radiographs, but visual examination of the tooth would show the enamel intact or minimally perforated. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.07%3A_Bacterial_Diseases_of_the_Mouth/15.7B%3A_Dental_Caries.txt |
Plaque-induced inflammatory lesions make up the vast majority of periodontal diseases, which are divided into peridontitis or gingivitis.
Learning Objectives
• Differentiate between peridontitis and gingivitis
Key Points
• Peridontal tissues are the cementum, or the outer layer of the roots of teeth; the gingiva, or gums; the alveolar bone, or the bony sockets into which the teeth are anchored; and the periodontal ligament, which are the connective tissue fibers that run between the cementum and the alveolar bone.
• Periodontitis is an inflammatory disease affecting the periodontium, or the tissues that surround and support the teeth. Periodontitis involves progressive loss of the alveolar bone around the teeth, and if left untreated, can lead to the loosening and subsequent loss of teeth.
• Periodontitis is caused by microorganisms that adhere to and grow on the tooth ‘s surfaces, along with an overly aggressive immune response against these microorganisms.
• In the early stages, periodontitis has very few symptoms and in many individuals the disease has progressed significantly before they seek treatment. The gingival inflammation and bone destruction of peridontitis are largely painless.
• Gingivitis, or inflammation of the gums, is a non-destructive peridontal disease. The primary cause of gingivitis is poor oral hygiene which leads to the accumulation dental plaque at the gum line. Gingivitis can progress to periodontitis.
• Daily oral hygiene measures to prevent periodontal disease include brushing and flossing daily and using an antiseptic mouthwash.
• There are many surgical approaches used in treatment of advanced periodontitis, including open flap debridement, osseous surgery, as well as guided tissue regeneration and bone grafting.
• Several conditions and diseases, including Down syndrome, diabetes, and other diseases that affect one’s resistance to infection also increase susceptibility to periodontitis.
• The primary etiology (cause) of gingivitis is poor oral hygiene which leads to the accumulation of a mycotic and bacterial matrix at the gum line, called dental plaque. Other contributors are poor nutrition and underlying medical issues such as diabetes.
• Once successful periodontal treatment has been completed, with or without surgery, an ongoing regimen of “periodontal maintenance” is required.
• In the early stages, periodontitis has very few symptoms and in many individuals the disease has progressed significantly before they seek treatment. Symptoms may include the following: redness or bleeding of gums, gum swelling that recurs, spitting out blood after brushing teeth, halitosis, or bad breath, and a persistent metallic taste in the mouth, gingival recession, resulting in apparent lengthening of teeth, deep pockets between the teeth and the gums, and loose teeth
• Periodontitis is caused by microorganisms that adhere to and grow on the tooth’s surfaces.
• The extent of disease refers to the proportion of the dentition affected by the disease in terms of percentage of sites. Generally, six probing sites around each tooth are recorded, as follows: mesiobuccal, mid-buccal, distobuccal, mesiolingual, mid-lingual, and distolingual.
• The severity of disease refers to the amount of periodontal ligament fibers that have been lost, termed clinical attachment loss.
• Smoking is a factor that increases the occurrence of periodontitis
• The 1999 classification system for periodontal diseases and conditions listed seven major categories of periodontal diseases, of which the last six are termed destructive periodontal disease because the damage is essentially irreversible. The seven categories are as follows:
• Gingivitis
• Chronic periodontitis
• Aggressive periodontitis
• Periodontitis as a manifestation of systemic disease
• Necrotizing ulcerative gingivitis/periodontitis
• Abscesses of the periodontium
• Combined periodontic-endodontic lesions
Key Terms
• periodontitis: An inflammatory disease that affects the periodontium—the tissues that surround and support the teeth–and can lead to tooth loss.
• periodontium: The specialized tissues that both surround and support the teeth, maintaining them in the maxillary and mandibular bones; the tissues including alveolar bone, cementum, gums, and periodontal ligament.
• gingivitis: Inflammation of the gums or gingivae.
Periodontal disease is a type of disease that affects one or more of the periodontal tissues, which include:
• the cementum, or the outer layer of the roots of teeth
• the gingiva, or gum tissue
• the alveolar bone, or the bony sockets into which the teeth are anchored
• the periodontal ligament, which are the connective tissue fibers that run between the cementum and the alveolar bone.
While many different diseases affect the tooth-supporting structures, plaque-induced inflammatory lesions make up the vast majority of periodontal diseases and have traditionally been divided into two categories: peridontitis or gingivitis.
Peridontitis
Periodontitis is an inflammatory disease affecting the periodontium, or the tissues that surround and support the teeth. Periodontitis involves progressive loss of the alveolar bone around the teeth, and if left untreated, can lead to the loosening and subsequent loss of teeth. Periodontitis is caused by microorganisms that adhere to and grow on the tooth’s surfaces, along with an overly aggressive immune response against these microorganisms.
In the early stages, periodontitis has very few symptoms and in many individuals the disease has progressed significantly before they seek treatment. Symptoms may include the following:
• Redness or bleeding of gums while brushing teeth, using dental floss, or biting into hard food
• Gum swelling that recurs
• Spitting out blood after brushing teeth
• Halitosis, or bad breath, and a persistent metallic taste in the mouth
• Gingival recession, resulting in apparent lengthening of teeth
• Deep pockets between the teeth and the gums, that are sites where the attachment has been gradually destroyed by collagen-destroying enzymes, known as collagenases
• Loose teeth, in the later stages
The gingival inflammation and bone destruction of peridontitis are largely painless. Hence, people may wrongly assume that painless bleeding after teeth cleaning is insignificant, although this may be a symptom of progressing periodontitis in that patient.
A diagnosis of periodontitis is established by inspecting the soft gum tissues around the teeth with a probe and by evaluating the patient’s x-ray films to determine the amount of bone loss around the teeth.
Gingivitis
Gingivitis, or inflammation of the gums, is a non-destructive peridontal disease. The primary cause of gingivitis is poor oral hygiene which leads to the accumulation of bacterial matrix at the gum line, called dental plaque. Other contributors are poor nutrition and underlying medical issues such as diabetes.
In some people, gingivitis progresses to periodontitis –- with the destruction of the gingival fibers, the gum tissues separate from the tooth, forming pockets between the tooth and gum. Subgingival microorganism (those that exist under the gum line) colonize the periodontal pockets and cause further inflammation in the gum tissues and progressive bone loss.
If left undisturbed, microbic plaque calcifies to form calculus, which is commonly called tartar. Calculus above and below the gum line must be removed completely by the dental hygienist or dentist to treat gingivitis and periodontitis. Although the primary cause of both gingivitis and periodontitis is the microbic plaque that adheres to the tooth surface, there are many other modifying factors. A very strong risk factor is one’s genetic susceptibility. Several conditions and diseases, including Down syndrome, diabetes, and other diseases that affect one’s resistance to infection also increase susceptibility to periodontitis.
Prevention
Daily oral hygiene measures to prevent periodontal disease include:
• Brushing teeth properly at least twice daily, with the patient attempting to direct the toothbrush bristles underneath the gum-line, to help disrupt the bacterial-mycotic growth and formation of subgingival plaque.
• Flossing daily and using interdental brushes as well as cleaning behind the last tooth, the third molar, in each quarter.
• Using an antiseptic mouthwash. Chlorhexidine gluconate-based mouthwash in combination with careful oral hygiene may cure gingivitis, although they cannot reverse any attachment loss due to periodontitis.
• Using periodontal trays to maintain dentist-prescribed medications at the source of the disease. The use of trays allows the medication to stay in place long enough to penetrate the biofilms where the microorganism are found.
Regular dental check-ups and professional teeth cleaning as required. Dental check-ups serve to monitor the person’s oral hygiene methods and levels of attachment around teeth, identify any early signs of periodontitis, and monitor response to treatment.
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Gastroenteritis is characterized by inflammation of the gastrointestinal tract that involves both the stomach and the small intestine.
Learning Objectives
• Describe the cause and effect of bacterial gastroenteritis
Key Points
• Gastroenteritis typically involves both diarrhea and vomiting, or less commonly, presents with only one or the other.
• Transmission rates are also related to poor hygiene, especially among children, in crowded households, and in those with pre-existing poor nutritional status.
• A supply of easily accessible uncontaminated water and good sanitation practices are important for reducing rates of infection and clinically significant gastroenteritis.
Key Terms
• inflammation: A condition of any part of the body, consisting in congestion of the blood vessels, with obstruction of the blood current, and growth of morbid tissue. It is manifested outwardly by redness and swelling, attended with heat and pain.
• gastroenteritis: Inflammation of the mucous membranes of the stomach and intestine; often caused by an infection.
Gastroenteritis is a medical condition characterized by inflammation (“-itis”) of the gastrointestinal tract that involves both the stomach (“gastro”-) and the small intestine (“entero”-), resulting in some combination of diarrhea, vomiting, and abdominal pain and cramping. Although unrelated to influenza, it has also been called ‘stomach flu’ and ‘gastric flu’.
Globally, most cases in children are caused by rotavirus. Less common causes include other bacteria (or their toxins) and parasites. Transmission may occur due to consumption of improperly prepared foods, contaminated water, or via close contact with individuals who are infectious. The foundation of management for this illness is adequate hydration. For mild or moderate cases, this can typically be achieved via oral rehydration solution. For more severe cases, intravenous fluids may be needed. Gastroenteritis primarily affects children and those in the developing world. Gastroenteritis typically involves both diarrhea and vomiting, or less commonly, presents with only one or the other. Abdominal cramping may also be present.
Signs and symptoms usually begin 12–72 hours after contracting the infectious agent. Some bacterial infections may be associated with severe abdominal pain and may persist for several weeks. In the developed world, Campylobacter jejuni is the primary cause of bacterial gastroenteritis, with half of these cases associated with exposure to poultry. In children, bacteria are the cause in about 15% of cases, with the most common types being Escherichia coli, Salmonella, Shigella, and Campylobacter species. If food becomes contaminated with bacteria and remains at room temperature for a period of several hours, the bacteria multiply and increase the risk of infection in those who consume the food. Toxigenic Clostridium difficile is an important cause of diarrhea that occurs more often in the elderly. Infants can carry these bacteria without developing symptoms. It is a common cause of diarrhea in those who are hospitalized and is frequently associated with antibiotic use. Staphylococcus aureus infectious diarrhea may also occur in those who have used antibiotics. “Traveler’s diarrhea” is usually a type of bacterial gastroenteritis. Acid-suppressing medication appears to increase the risk of significant infection after exposure to a number of organisms, including Clostridium difficile, Salmonella, and Campylobacter species.
Transmission rates are also related to poor hygiene, especially among children, in crowded households, and in those with pre-existing poor nutritional status. After developing tolerance, adults may carry certain organisms without exhibiting signs or symptoms, and thus act as natural reservoirs of contagion. While some agents (such as Shigella) only occur in primates, others may occur in a wide variety of animals (such as Giardia).
Gastroenteritis is typically diagnosed clinically, based on a person’s signs and symptoms. Determining the exact cause is usually not needed as it does not alter management of the condition. However, stool cultures should be performed in those with blood in the stool, those who might have been exposed to food poisoning, and those who have recently traveled to the developing world. Electrolytes and kidney function should also be checked when there is a concern about severe dehydration.
A supply of easily accessible uncontaminated water and good sanitation practices are important for reducing rates of infection and clinically significant gastroenteritis. Personal measures (such as hand washing) have been found to decrease incidence and prevalence rates of gastroenteritis in both the developing and developed world by as much as 30%.
15.8B: Staphylococcal Food Poisoning
Staphylococcal toxins are a common cause of food poisoning, as they can be produced in improperly-stored food.
Learning Objectives
• Recognize the causes of staphylococcal food poisoning
Key Points
• Staphylococcus is a Gram-positive bacteria which includes several species that can cause a wide variety of infections in humans and other animals through infection or the production of toxins.
• Foodborne illness usually arises from improper handling, preparation, or storage of food.
• Good hygiene practices before, during, and after food preparation can reduce the chances of contracting an illness.
Key Terms
• toxin: A toxic or poisonous substance produced by the biological processes of biological organisms.
• norovirus: The genus of a number of species of virus, family Caliciviridae, causing human gastroenteritis, of which Norwalk virus is the prototype.
Staphylococcus is a Gram-positive bacteria which includes several species that can cause a wide variety of infections in humans and other animals through infection or the production of toxins. Staphylococcal toxins are a common cause of food poisoning, as they can be produced in improperly-stored food. The main coagulase-positive staphylococcus is Staphylococcus aureus. These bacteria can survive on dry surfaces, increasing the chance of transmission.
Any S. aureus infection can cause the staphylococcal scalded skin syndrome, a cutaneous reaction to exotoxin absorbed into the bloodstream. It can also cause a type of septicaemia called pyaemia. The infection can be life-threatening. Problematically, Methicillin-resistant Staphylococcus aureus (MRSA) has become a major cause of hospital-acquired infections and is being recognized with increasing frequency in community-acquired infections.
Foodborne illness usually arises from improper handling, preparation, or food storage. Good hygiene practices before, during, and after food preparation can reduce the chances of contracting an illness. There is a consensus in the public health community that regular hand-washing is one of the most effective defenses against the spread of foodborne illness. The action of monitoring food to ensure that it will not cause foodborne illness is known as food safety.
Foodborne disease can also be caused by a large variety of toxins that affect the environment, such as pesticides or medicines in food, and naturally toxic substances such as poisonous mushrooms or reef fish. In the past, bacterial infections were thought to be more prevalent because few places had the capability to test for norovirus and no active surveillance was being done for this particular agent. Toxins for bacterial infections are delayed because the bacteria need time to multiply. Their symptoms are usually not seen until 12–72 hours or more after eating contaminated food. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.08%3A_Bacterial_Diseases_of_the_Digestive_System/15.8A%3A_Bacterial_Gastroenteritis.txt |
Salmonellosis is an infection by the Salmonella bacteria that results in diarrhea, fever, vomiting, and abdominal cramps.
Learning Objectives
• Distinguish between nontyphoidal and typhoidal Salmonella
Key Points
• In severe cases, the Salmonella infection may spread from the intestines to the bloodstream, and then to other body sites, and can cause death unless the person is treated with antibiotics.
• The type of Salmonella usually associated with infections in humans, nontyphoidal Salmonella, is often contracted from contaminated food or reptiles.
• The Salmonella bacterium induces responses in the animal it is infecting, and this is what typically causes the symptoms, rather than any direct toxin that is produced.
Key Terms
• typhoid fever: An illness caused by the bacterium Salmonella typhi. Not to be confused with typhus.
• endotoxin: Any toxin secreted by a microorganism and released into the surrounding environment only when it dies.
• arthritis: Inflammation of a joint or joints causing pain and/or disability, swelling, and stiffness; and due to various causes such as infection, trauma, degenerative changes, or metabolic disorders.
Salmonellosis is an infection with the Salmonella bacteria. Most people infected with Salmonella develop diarrhea, fever, vomiting, and abdominal cramps 12 to 72 hours after infection. In most cases, the illness lasts four to seven days, and most people recover without treatment. However, in some cases the diarrhea may be so severe that the patient becomes dangerously dehydrated and must be taken to a hospital. At the hospital, the patient may receive intravenous fluids to treat the dehydration, and may be given medications to relieve symptoms, such as fever reducers. In severe cases, the Salmonella infection may spread from the intestines to the bloodstream, and then to other body sites, and can cause death unless the person is promptly treated with antibiotics. The elderly, infants, and those with impaired immune systems are more likely to develop severe illness. Some people afflicted with Salmonellosis later experience reactive arthritis, which can have long-lasting, disabling effects.
Different Kinds of Salmonella
The different kinds of Salmonella include S. bongori and S. enterica. The type of Salmonella usually associated with infections in humans, nontyphoidal Salmonella, is usually contracted from: poultry, pork, and beef when the meat is prepared incorrectly or is infected with the bacteria after preparation; infected eggs, egg products, and milk when not prepared, handled, or refrigerated properly; reptiles (such as turtles, lizards, and snakes) which can carry the bacteria in their intestines; and tainted fruits and vegetables.
The typhoidal form of Salmonella can lead to typhoid fever. Typhoid fever is a life-threatening illness, and about four hundred cases are reported in the United States each year, with 75% of those acquired while traveling out of the country. It is carried only by humans and is usually contracted through direct contact with the fecal matter of an infected person. Typhoidal Salmonella is more commonly found in poorer countries, where unsanitary conditions are more likely to occur, and can affect as many as 21.5 million people a year.
Salmonella Infection
The Salmonella bacterium induces responses in the animal it is infecting, and this is what typically causes the symptoms rather than any direct toxin that is produced. Symptoms are usually gastrointestinal, including nausea, vomiting, abdominal cramps, and bloody diarrhea with mucus. Headache, fatigue, and rose spots are also possible. These symptoms can be severe, especially in young children and the elderly. Symptoms last generally up to a week, and can appear 12 to 72 hours after ingesting the bacterium. After bacterial infections, reactive arthritis (Reiter’s syndrome) can develop.
An infectious process can only begin after living salmonellae (not only their toxins) reach the gastrointestinal tract. Some of the microorganisms are killed in the stomach, while the surviving salmonellae enter the small intestine and multiply in tissues (this is the localized form). By the end of the incubation period, the macro-organisms are poisoned by endotoxins that are released from the dead salmonellae. The local response to the endotoxins is enteritis and gastrointestinal disorder. In the generalized form of the disease, salmonellae pass through the lymphatic system of the intestine into the blood of the patients (typhoid form) and are carried to various organs (liver, spleen, kidneys) to form secondary foci (septic form).
Endotoxins first act on affected organs’ vascular and nervous systems, manifested by: increased permeability and decreased tone of the vessels, upset thermal regulation, vomiting, and diarrhea. In severe forms of the disease, enough liquid and electrolytes are lost to upset the body’s metabolism of water and salt, decreasing the circulating blood volume and arterial pressure to enough of a degree to cause hypovolemic shock. Septic shock may also develop. Shock of mixed character (with signs of both hypovolemic and septic shock) is more common in severe salmonellosis. Oliguria and azotemia develop in severe cases as a result of kidney involvement due to hypoxia and bacteremia. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.08%3A_Bacterial_Diseases_of_the_Digestive_System/15.8C%3A_Salmonellosis.txt |
Learning Objectives
• Summarize the four stages of untreated typhoid fever and methods of preventing it
Typhoid fever, also known as typhoid, is a common, worldwide bacterial disease. It is transmitted by the ingestion of food or water that has been contaminated with the feces of a person infected by the bacterium Salmonella typhi, serotype Typhi. The disease has been known by many names, such as gastric fever, abdominal typhus, infantile remittant fever, slow fever, nervous fever or pythogenic (originating from filth or putrefaction) fever. The name “typhoid” means “resembling typhus” and comes from the neuropsychiatric symptoms common to typhoid and typhus. The term “enteric fever” is a collective term that refers to typhoid and paratyphoid. The impact of this disease fell sharply with the improved sanitation techniques of the 20th century.
STAGES
Classically, the course of untreated typhoid fever is divided into four individual stages, each lasting approximately one week.
First stage: the temperature rises slowly and fever fluctuations are seen with relative bradycardia (slow pulse), malaise, headache and cough. Nose bleeds (epistaxis) are seen in 25% of cases and abdominal pain can occur. There is leukopenia (a decrease in the number of circulating white blood cells), with eosinopenia and relative lymphocytosis. The classic Widal test is negative in the first week.
Second stage: the patient lies prostrate with high fever in plateau around 40 °C (104 °F) and bradycardia, classically with a dicrotic pulse wave. Delirium is frequent; patients may be calm, but sometimes agitated. This delirium gives typhoid its nickname of “nervous fever”. Rose spots appear on the lower chest and abdomen in around a third of patients. The Widal test is strongly positive with antiO and antiH antibodies. Blood cultures may be still positive at this stage. (The major symptom of typhoid is that the fever usually rises in the afternoon in the first and second stages. )
Third stage: a number of complications can occur: intestinal hemorrhage due to bleeding in congested Peyer’s patches and intestinal perforation in the distal ileum.
Fourth stage: by the end of the third week the fever starts subsiding (defervescence). This carries on into the fourth and final week.
PREVENTION
The bacteria which cause typhoid fever may be spread through poor hygiene habits and public sanitation conditions and, sometimes, also by flying insects feeding on infected feces. Public education campaigns encouraging people to wash their hands after defecating and before handling food are an important component in controlling the spread of the disease. A person may become an asymptomatic carrier of typhoid fever, suffering no symptoms, but capable of infecting others.
DIAGNOSIS
Diagnosis is made by any blood, bone marrow or stool cultures and with the Widal test (demonstration of salmonella antibodies against antigens O-somatic and H-flagellar). In epidemics and less wealthy countries, after excluding malaria, dysentery or pneumonia, a therapeutic trial time with chloramphenicol is generally undertaken while awaiting the results of the Widal test, and cultures of the blood and stool. The Widal test is time-consuming and often, when a diagnosis is reached, it is too late to start an antibiotic regimen.
VACCINATION
There are two vaccines licensed for use for the prevention of typhoid: the live, oral Ty21a vaccine (sold as Vivotif Berna) and the injectable Typhoid polysaccharide vaccine (sold as Typhim Vi by Sanofi Pasteur and Typherix by GlaxoSmithKline).
TREATMENT
The rediscovery of oral rehydration therapy in the 1960s provided a simple way to prevent many of the deaths of diarrheal diseases in general. Where resistance is uncommon, the treatment of choice is a fluoroquinolone such as ciprofloxacin otherwise, a third-generation cephalosporin such as ceftriaxone or cefotaxime. Cefixime is a suitable oral alternative. Typhoid fever in most cases is not fatal. Antibiotics, such as ampicillin, chloramphenicol, trimethoprim-sulfamethoxazole, amoxicillin and ciprofloxacin have been commonly used to treat typhoid fever.
Key Points
• The impact of Typhoid fever fell sharply with the improved sanitation techniques of the 20th century.
• Classically, the course of untreated typhoid fever is divided into four individual stages, each lasting approximately one week.
• Diagnosis is made by any blood, bone marrow or stool cultures and with the Widal test (demonstration of salmonella antibodies against antigens O-somatic and H-flagellar).
Key Terms
• dicrotic: A type of pulse associated with low systemic vascular resistance and a compliant aorta, e.g sepsis
• Peyer’s patch: Peyer’s patches (or aggregated lymphoid nodules) are usually found in the lowest portion of the small intestine, the ileum, in humans.
• Widal test: The agglutination test for typhoid fever.
• eosinopenia: Eosinopenia is a form of agranulocytosis where the number of eosinophil granulocyte is lower than expected; usually a predictor of bacterial infection.
• lymphocytosis: An increase in the number or proportion of lymphocytes in the blood. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.08%3A_Bacterial_Diseases_of_the_Digestive_System/15.8D%3A_Typhoid_Fever.txt |
Cholera is an infection in the small intestine caused by the bacterium Vibrio cholerae.
Learning Objectives
• Describe the mode of transmission for Vibrio cholerae and the steps that can be taken to prevent this
Key Points
• The primary symptoms of cholera are profuse, painless diarrhea and vomiting of clear fluid.
• V. cholerae bacteria that survive the gastric juices produce the hollow cylindrical protein flagellin to make flagella, the cork-screw helical fibers they rotate to propel themselves through the mucus of the small intestine.
• A number of safe and effective oral vaccines for cholera are available.
Key Terms
• flagella: A flagellum is a lash-like appendage that protrudes from the cell body of certain prokaryotic and eukaryotic cells.
• electrolyte: any of the various ions (such as sodium or chloride) that regulate the electric charge on cells and the flow of water across their membranes
Vibrio Cholerae
Cholera is an infection in the small intestine caused by the bacterium Vibrio cholerae. The primary symptoms of cholera are profuse, painless diarrhea and vomiting of clear fluid. These symptoms usually start suddenly, one to five days after ingestion of the bacteria. The diarrhea is frequently described as “rice water” in nature and may have a fishy odor. If the severe diarrhea is not treated with intravenous rehydration, it can result in life-threatening dehydration and electrolyte imbalances.
Transmission
Cholera is typically transmitted by either contaminated food or water. In the developed world, seafood is the usual cause, while in the developing world it is more often water. Cholera is rarely spread directly from person to person. Both toxic and nontoxic strains exist.
Most V. cholerae bacteria, when consumed, do not survive the acidic conditions of the human stomach. The few surviving bacteria conserve their energy and stored nutrients during the passage through the stomach by shutting down much protein production. When the surviving bacteria exit the stomach and reach the small intestine, they need to propel themselves through the thick mucus that lines the small intestine to get to the intestinal walls, where they can thrive. V. cholerae bacteria begin production of the hollow cylindrical protein flagellin to make flagella. These flagella are cork-screw helical fibers that rotate to propel the bacteria through the mucus of the small intestine.
Once the cholera bacteria reach the intestinal wall, they no longer need the flagella to move. The bacteria stop producing the protein flagellin, again conserving energy and nutrients by changing the mix of proteins they manufacture in response to the changed chemical surroundings. The V. cholerae start producing the toxic proteins that give the infected person a watery diarrhea.
The diarrhea carries new generations of V. cholerae bacteria out into the drinking water of the next host if proper sanitation measures are not in place. A rapid dip-stick test is available to determine the presence of V. cholerae in a water supply. Samples that test positive should be further tested to determine antibiotic resistance. In epidemic situations, a clinical diagnosis may be made by taking a patient history and doing a brief examination. Treatment is usually started without or before confirmation by laboratory analysis. Although cholera may be life-threatening, prevention of the disease is normally straightforward if proper sanitation practices are followed. In developed countries, due to nearly universal advanced water treatment and sanitation practices, cholera is no longer a major health threat.
Breaking the Transmission Path
Effective sanitation practices, if instituted and adhered to in time, are usually sufficient to stop an epidemic. There are several points along the cholera transmission path at which its spread may be halted.
• Sterilization or proper disposal and treatment of infected fecal waste water produced by cholera victims and all contaminated materials (e.g. clothing, bedding, etc.) is essential. All materials that come in contact with cholera patients should be sanitized by washing in hot water, using chlorine bleach if possible. Hands that touch cholera patients or their clothing, bedding, etc., should be thoroughly cleaned and disinfected with chlorinated water or other effective antimicrobial agents.
• Antibacterial treatment of general sewage by chlorine, ozone, ultraviolet light or other effective treatment before it enters the waterways or underground water supplies helps prevent undiagnosed patients from inadvertently spreading the disease.
• Warnings about possible cholera contamination should be posted around contaminated water sources with directions on how to decontaminate the water (boiling, chlorination etc.) for possible use.
• All water used for drinking, washing, or cooking should be sterilized by either boiling, chlorination, ozone water treatment, ultraviolet light sterilization (e.g. by solar water disinfection), or antimicrobial filtration in any area where cholera may be present.
• Public health education and adherence to appropriate sanitation practices are of primary importance to help prevent and control transmission of cholera and other diseases.
Prevention and Treatment
A number of safe and effective oral vaccines for cholera are available. In most cases, cholera can be successfully treated with oral rehydration therapy (ORT), which is effective, safe, and simple to administer. Rice-based solutions are more efficient than glucose-based ones. In cases of severe dehydration, intravenous rehydration may be necessary. Antibiotic treatments for one to three days shorten the course of the disease and reduce the symptoms. People will recover without them, however, if sufficient hydration is maintained. Doxycycline is typically used first line, although some strains of V. cholerae have shown resistance. Testing for resistance during an outbreak can help determine appropriate future choices. Other antibiotics proven to be effective include cotrimoxazole, erythromycin, tetracycline, chloramphenicol, and furazolidone. Fluoroquinolones, such as norfloxacin, also may be used, but resistance has been reported.
15.8F: Noncholera Vibrios
Vibrio is a Gram-negative bacteria possessing a curved rod shape (comma shape), several species of which can cause foodborne infection.
Learning Objectives
• Discuss the difference between cholera and noncholera causing Vibrios
Key Points
• Vibrio species are prevalent in estuarine and marine environments. Seven species can cause food borne infections associated with seafood.
• Patients with noncholera Vibrio wound infection or septicemia are much more ill and frequently have other medical conditions.
• Early medical intervention is paramount and consists of antimicrobial therapy, intensive medical therapy for disease symptoms, and surgical removal of infected tissues if necessary.
Key Terms
• necrotizing fasciitis: Necrotizing fasciitis, commonly known as flesh-eating disease or flesh-eating bacteria syndrome, is a rare infection of the deeper layers of skin and subcutaneous tissues, that easily spreads across the fascial plane within the subcutaneous tissue.
• hemolysin: any substance that damages the membranes of red blood cells and thus releases hemoglobin
• septicemia: A disease caused by the presence of pathogenic organisms, especially bacteria or their toxins in the bloodstream, characterized by chills and fever.
• vibrio: Any of several bacteria, of the genus Vibrio, shaped like a curved rod.
Vibrio is a genus of Gram-negative bacteria possessing a curved rod shape (comma shape). Several species of Vibro can cause food borne infection, usually associated with eating undercooked seafood. Vibrio species are prevalent in estuarine and marine environments. Seven species can cause food borne infections associated with seafood. Vibrio cholerae O1 and O139 serovtypes produce cholera toxin and are agents of cholera. Vibrio species are facultative anaerobes that test positive for oxidase and do not form spores. All members of the genus are motile and have polar flagella with sheaths.
Patients with noncholera Vibrio wound infection or septicemia are much more ill and frequently have other medical conditions. Medical therapy consists of the following: prompt initiation of effective antibiotic therapy (doxycycline or a quinolone), intensive medical therapy with aggressive fluid replacement, vasopressors for hypotension and septic shock, early fasciotomy within 24 hours after development of clinical symptoms in patients with necrotizing fasciitis, early debridement of the infected wound, expeditious and serial surgical evaluation and intervention to prevent rapid deterioration, especially in patients with necrotizing fasciitis or compartment syndrome. Reconstructive surgery, such as skin graft, is indicated in the recovery phase.
Fecal-oral route infections in the terrestrial environment are responsible for epidemic cholera. Most strains cause gastroenteritis such as V. cholerae non-O1/O139 strains and Vibrio parahaemolytitcus strains capable of producing thermostable direct hemolysin (TDH) and/or TDH-related hemolysin. Vibrio vulnificus is responsible for seafood borne primary septicemia. Its infectivity depends primarily on the risk factors of the host. V. vulnificus infection has the highest fatality rate (50%) of any food borne pathogen. Four other species (V. mimicus, V. hollisae, V. fluvialis, and V. furnissii) can cause gastroenteritis. Some strains of these species produce known toxins, but the pathogenic mechanism is largely not understood. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.08%3A_Bacterial_Diseases_of_the_Digestive_System/15.8E%3A_Cholera.txt |
Most E. coli strains are harmless, but some serotypes are pathogenic and can cause serious food poisoning in humans and other species.
Learning Objectives
• Distinguish between the different types of pathogenic E. coli in regards to classification and mode of transmission
Key Points
• Pathogenic E. coli strains can be categorized based on elements that can elicit an immune response in animals. The different categories are: O antigen, K antigen, H antigen, and F antigen in the lipopolysaccharide.
• In humans and in domestic animals, virulent strains of E. coli can cause gastroenteritis, urinary tract infections, and neonatal meningitis.
• Bacterial infections are usually treated with antibiotics.
Key Terms
• bacteraemia: The medical condition of having bacteria in the bloodstream.
• lipopolysaccharide: any of a large class of lipids conjugated with polysaccharides
• flora: the microorganisms that inhabit some part of the body, such as intestinal flora
• enterohemorrhagic E. coli: strains of the bacterium Escherichia coli that, when infecting humans, have been linked with the severe complication hemolytic-uremic syndrome
Escherichia coli (E. coli) is a Gram-negative, rod-shaped bacterium that is commonly found in the lower intestine of warm-blooded organisms (endotherms). Most E. coli strains are harmless, but some serotypes are pathogenic and can cause serious food poisoning in humans and other species. The harmless strains are part of the normal flora of the gut, and can benefit their hosts by producing vitamin K2, and by preventing the establishment of pathogenic bacteria within the intestine.
Pathogenic E. coli
Pathogenic E. coli strains can be categorized based on elements that can elicit an immune response in animals, namely: O antigen, K antigen, H antigen, and F antigen in the lipopolysaccharide (LPS) molecules found in the outer membrane of the E. coli cell. The O antigen is a polymer of immunogenic repeating oligosaccharides which is used for serotyping E.coli. It should be noted though that antibodies towards several O antigens cross-react with other O antigens and partially to K antigens not only from E. coli, but also from other Escherichia species and Enterobacteriaceae species. There are two separate groups of K-antigen groups, named group I and group II (while a small in-between subset (K3, K10, and K54/K96) has been classified as group III). Group I consists of 100 kDa (large) capsular polysaccharides, while those in Group II, associated with extraintestinal diseases, are under 50 kDa in size.
In humans and in domestic animals, virulent strains of E. coli can cause various diseases. In humans, gastroenteritis, urinary tract infections, and neonatal meningitis can occur. In rarer cases, virulent strains are also responsible for haemolytic-uremic syndrome, peritonitis, mastitis, septicemia, and Gram-negative pneumonia. Certain strains of E. coli produce potentially lethal toxins. Food poisoning caused by E. coli can result from eating unwashed vegetables or undercooked meat. If E. coli bacteria escape the intestinal tract through a perforation (for example from an ulcer, a ruptured appendix, or due to a surgical error) and enter the abdomen, they usually cause peritonitis that can be fatal without prompt treatment.
Transmission of pathogenic E. coli often occurs via fecal–oral transmission. Common routes of transmission include unhygienic food preparation, farm contamination due to manure fertilization, irrigation of crops with contaminated greywater or raw sewage, feral pigs on cropland, or direct consumption of sewage-contaminated water. According to the U.S. Food and Drug Administration, the fecal-oral cycle of transmission can be disrupted by cooking food properly, preventing cross-contamination, instituting barriers such as gloves for food workers, instituting health care policies so food industry employees seek treatment when they are ill, pasteurization of juice or dairy products and proper hand washing requirements.
Uropathogenic E. coli
Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy. In ascending infections, fecal bacteria colonize the urethra and spread up the urinary tract to the bladder, as well as to the kidneys (causing pyelonephritis), or the prostate in males. Because women have a shorter urethra than men, they are 14 times more likely to suffer from an ascending UTI. Uropathogenic E. coli use P fimbriae (pyelonephritis-associated pili) to bind urinary tract endothelial cells and colonize the bladder. UPEC can evade the body’s innate immune defences (e.g. the complement system) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs). They also have the ability to form K antigen, capsular polysaccharides that contribute to biofilm formation. Descending infections in turn, though relatively rare, occur when E. coli cells enter the upper urinary tract organs (kidneys, bladder or ureters) from the blood stream.
E. coli and Meningitis
Neonatal meningitis is produced by a serotype of E. coli that contains a capsular antigen called K1. The colonization of the newborn’s intestines with these stems, that are present in the mother’s vagina, lead to bacteraemia, which leads to meningitis. Severe meningitis in the neonates are caused because of the absence of the IgM antibodies from the mother (these do not cross the placenta because FcRn only mediates the transfer of IgG), plus the fact that the body recognizes as self the K1 antigen, as it resembles the cerebral glicopeptides. In stool samples, microscopy will show Gram-negative rods, with no particular cell arrangement.
Treating E. coli
Bacterial infections are usually treated with antibiotics. However, the antibiotic sensitivities of different strains of E. coli vary widely. As Gram-negative organisms, E. coli are resistant to many antibiotics that are effective against Gram-positive organisms. Antibiotics which may be used to treat E. coli infection include amoxicillin, as well as other semisynthetic penicillins, many cephalosporins, carbapenems, aztreonam, trimethoprim-sulfamethoxazole, ciprofloxacin, nitrofurantoin, and the aminoglycosides. Researchers have actively been working to develop safe, effective vaccines to lower the worldwide incidence of E. coli infection. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.08%3A_Bacterial_Diseases_of_the_Digestive_System/15.8G%3A_Pathogenic_Escherichia_coli.txt |
Campylobacter (meaning ‘twisted bacteria’) is a genus of bacteria that are Gram-negative, spiral, and microaerophilic.
Learning Objectives
• Discuss the method of transmission for Campylobacter
Key Points
• Campylobacter jejuni is now recognized as one of the main causes of bacterial foodborne disease in many developed countries.
• The common routes of transmission are fecal-oral, ingestion of contaminated food or water, and the eating of raw meat.
• It produces an inflammatory, sometimes bloody, diarrhea, periodontitis or dysentery syndrome, mostly including cramps, fever and pain.
Key Terms
• microaerophilic: living and thriving in an environment low in oxygen
• enteritis: Inflammation of the intestines, generally the small intestine, that may lead to diarrhea.
• flagella: A flagellum is a lash-like appendage that protrudes from the cell body of certain prokaryotic and eukaryotic cells.
Description of Campylobacter Bacteria
Campylobacter is a genus of bacteria that are Gram-negative, spiral, and microaerophilic. The name means “twisted bacteria” because of the spiral formation; motile, with either unipolar or bipolar flagella, the organisms have a characteristic spiral/corkscrew appearance and are oxidase-positive.
Campylobacter jejuni is now recognized as one of the main causes of bacterial foodborne disease in many developed countries. At least a dozen species of Campylobacter have been implicated in human disease, with C. jejuni and C. coli the most common. C. fetus is a cause of spontaneous abortions in cattle and sheep, as well as an opportunistic pathogen in humans.
Campylobacter species contain two flagellin genes in tandem for motility: flaA and flaB. These genes undergo intergenic recombination, further contributing to their virulence. Nonmotile mutants do not colonize.
Methods of Transmission and Treatment
The common routes of transmission are fecal-oral; the bacteria are introducted through ingestion of contaminated food or water and by the eating of raw meat. Infection produces an inflammatory, sometimes bloody diarrhea, periodontitis, or dysentery syndrome, mostly including cramps, fever and pain. The infection is usually self-limiting. In most cases symptomatic treatment by liquid and electrolyte replacement is enough in human infections. The use of antibiotics, on the other hand, is controversial.
Diagnosis
Symptoms typically last for five to seven days. The sites of tissue injury include the jejunum, the ileum, and the colon. Most strains of C. jejuni produce a toxin (cytolethal distending toxin) that hinders the cells from dividing and activating the immune system. This symptom helps the bacteria evade the immune system and survive for a limited time in the cells. A cholera-like enterotoxin was also once thought to be made, but this appears not to be the case. The organism produces diffuse, bloody, edematous, and exudative enteritis. Although rarely has the infection been considered a cause of hemolytic uremic syndrome and thrombotic thrombocytopenic purpura, no unequivocal case reports exist. In some cases, a Campylobacter infection can be the underlying cause of Guillain-Barré syndrome. Gastrointestinal perforation is a rare complication of ileal infection.
Diagnosis of the illness is made by testing a specimen of faeces (bowel motion). Standard treatment is now azithromycin and, on occassion, terbinafine. Quinolone antibiotics such as ciprofloxacin or levofloxacin are no longer as effective due to resistance. Dehydrated children may require intravenous (by vein) fluid treatment in a hospital. The illness is contagious, and children must be kept at home until they have been clear of symptoms for at least two days. Good hygiene is important to avoid contracting the illness or spreading it to others. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.08%3A_Bacterial_Diseases_of_the_Digestive_System/15.8H%3A_Campylobacter.txt |
A peptic ulcer, also known as peptic ulcer disease, is an erosion in the wall of the stomach, duodenum, or esophagus.
Learning Objectives
• List the causes of and treatments for peptic ulcer disease
Key Points
• 70–90% of peptic ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach.
• Diagnosis is mainly established based on the characteristic symptoms. Stomach pain is usually the first signal of a peptic ulcer.
• Treatment of H. pylori usually leads to clearing of infection, relief of symptoms, and eventual healing of ulcers.
• Gas in the peritoneal cavity, shown on an erect chest x-ray or supine lateral abdominal x-ray, is an omen of perforated peptic ulcer disease, which requires emergency surgery.
• Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery.
• Most bleeding ulcers require endoscopy urgently to stop bleeding with cautery, injection, or clipping.
• During the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue.
• A gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and muscularis propria, produced by acid-pepsin aggression.
• Ulcers are not purely an infectious disease and that psychological factors do play a significant role.
• Diagnosis is mainly established based on the characteristic symptoms. Stomach pain is usually the first signal of a peptic ulcer.
• Gastric ulcers are most often localized on the lesser curvature of the stomach.
• Gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.
• Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery.
• Burning or gnawing feeling in the stomach area lasting between 30 minutes and 3 hours commonly accompanies ulcers.
• Typical ulcers tend to heal and recur and as a result the pain may occur for few days and weeks and then wane or disappear.
Key Terms
• prostaglandin: Any of a group of naturally occurring lipids derived from the C20 acid prostanoic acid; they have a number of physiological functions and may be considered to be hormones.
• NSAID: Any drug of the non-steroidal anti-inflammatory class used as a pain reliever.
• gastrin: A hormone that stimulates the production of gastric acid in the stomach.
• gastritis: Inflammation of the lining of the stomach, characterized by nausea, loss of appetite, and upper abdominal discomfort or pain.
A peptic ulcer, also known as peptic ulcer disease, is an erosion in the wall of the stomach, duodenum, or esophagus. As many as 70–90% of such ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach. Ulcers can also be caused or worsened by drugs such as aspirin, ibuprofen, and other NSAIDs.
Symptoms
Symptoms of a peptic ulcer include abdominal pain, classically near the stomach with severity relating to mealtimes, about three hours after eating a meal; bloating and abdominal fullness; nausea; copious vomiting; loss of appetite and weight loss; vomiting of blood; and melena, which are tarry, foul-smelling feces due to oxidized iron from hemoglobin. Rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis. This is extremely serious and requires immediate surgery.
Causes
A major causative factor of ulcers is chronic inflammation due to Helicobacter pylori that colonizes the mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis, resulting in a defect in the regulation of gastrin production by that part of the stomach. Gastrin secretion can either be increased, or as in most cases, decreased, resulting in a too basic or too acidic stomach environment, respectively. A decrease in acid can promote H. pylori growth and an increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation.
Another major cause is the use of NSAIDs. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins.
Researchers also continue to look at stress as a possible cause, or at least complication, in the development of ulcers. There is debate as to whether psychological stress can influence the development of peptic ulcers. Burns and head trauma, however, can lead to physiologic stress ulcers, which are reported in many patients who are on mechanical ventilation.
Diagnosis
The diagnosis is mainly established based on the characteristic symptoms. Stomach pain is usually the first signal of a peptic ulcer. In some cases, doctors may treat ulcers without diagnosing them with specific tests and observe whether the symptoms resolve, this indicating that their primary diagnosis was accurate.
Confirmation of the diagnosis is made with the help of tests such as endoscopies or barium contrast x-rays. The tests are typically ordered if the symptoms do not resolve after a few weeks of treatment. Tests are also given when first appear in a person who is over age 45 or who has other symptoms such as weight loss, because stomach cancer can cause similar symptoms. Also, when severe ulcers resist treatment, particularly if a person has several ulcers or the ulcers are in unusual places, a doctor may suspect an underlying condition that causes the stomach to overproduce acid.
An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.
If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to “free gas” within the peritoneal cavity. If the patient stands erect, as when having a chest x-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest x-ray or supine lateral abdominal x-ray, is an omen of perforated peptic ulcer disease.
Treatment
Younger patients with ulcer-like symptoms are often treated with antacids. The ability of antacids to neutralize acidity by increasing the pH or blocking the secretion of acid by gastric cells is critical in reducing acidity in the stomach. Patients who are taking NSAIDs may also be prescribed a prostaglandin analogue in order to help prevent peptic ulcers by replacing the prostaglandins whose formation is blocked by NSAID use.
When H. pylori infection is present, the most effective treatments are combinations of two antibiotics, such as Clarithromycin, Amoxicillin, Tetracycline, and Metronidazole; and one proton pump inhibitor, sometimes in combination with antacids. In complicated, treatment-resistant cases, three antibiotics may be used together with a proton pump inhibitor. Treatment of H. pylori usually leads to clearing of infection, relief of symptoms and eventual healing of ulcers. Recurrence of infection can occur and retreatment may be required, if necessary with other antibiotics.
Perforated peptic ulcer is a surgical emergency and requires surgical repair of the perforation. Most bleeding ulcers require endoscopy urgently to stop bleeding with cautery, injection, or clipping. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.08%3A_Bacterial_Diseases_of_the_Digestive_System/15.8I%3A_Peptic_Ulcer_Disease.txt |
Listeriosis is a bacterial infection caused by a Gram-positive, motile bacterium called Listeria monocytogenes.
Learning Objectives
• Discuss the mechanism of action for listeriosis
Key Points
• Listeriosis has a low incidence in humans and occurs in pregnant women, newborn infants, elderly patients, and patients who are immunocompromised.
• Listeria can invade through unusually tough barriers in humans: the blood-brain barrier and the feto-placental barrier, which contain high levels of cadherin protein on their membrane.
• The main route of acquisition of Listeria is through the ingestion of contaminated food products.
Key Terms
• incidence: a measure of the risk that a person develops a new condition within a specified period of time, usually a year
• listeriosis: An infectious disease of humans and animals caused by the bacteria Listeria monocytogenes and Listeria ivanovii, often through contaminated food.
• meningitis: Inflammation of the meninges, characterized by headache, neck stiffness and photophobia and also fever, chills, vomiting, and myalgia.
• cadherin: Any of a class of transmembrane proteins important in maintaining tissue structure.
• blood-brain barrier: a structure in the central nervous system (CNS) that keeps various substances found in the bloodstream out of the brain while allowing in the substances essential to metabolic function
Listeriosis is a bacterial infection caused by a Gram-positive, motile bacterium, Listeria monocytogenes. Listeriosis has a low incidence in humans and occurs in pregnant women, newborn infants, elderly patients, and patients who are immunocompromised. Pregnant women are the most susceptible and infection can lead to early delivery, infection of the newborn, and death of the baby.
The symptoms of listeriosis usually last 7–10 days, with the most common symptoms being fever, muscle aches, and vomiting. Diarrhea is another symptom, but less common. If the infection spreads to the nervous system it can cause meningitis, an infection of the covering of the brain and spinal cord.
Listeria originally evolved to invade membranes of the intestines, as an intracellular infection, and developed a chemical mechanism to do so. This involves a bacterial protein “internalin” which attaches to a protein on the intestinal cell membrane “cadherin. ” These adhesion molecules are also to be found in two other unusually tough barriers in humans – the blood-brain barrier and the feto-placental barrier, and this may explain the apparent affinity that Listeria has for causing meningitis and affecting babies in-utero. Particular strains of a food-borne bacteria are able to invade the heart, leading to serious and difficult-to-treat heart infections.
Listeria monocytogenes is ubiquitous in the environment. The main route of acquisition is by the ingestion of contaminated food products. Listeria has been isolated from raw meat, dairy products, vegetables, fruit and seafood. Soft cheeses, unpasteurized milk and unpasteurised pâté are potential dangers too. The main prevention is through the promotion of safe handling, cooking and consumption of food. This includes washing raw vegetables and cooking raw food thoroughly, as well as reheating leftover or ready-to-eat foods, like hot dogs, until steaming hot. Another preventative measure is to advise high-risk groups such as pregnant women and immunocompromised patients to avoid unpasteurized pâtés and foods such as soft cheeses.
In the advent of listeriosis, bacteremia should be treated for two weeks, meningitis for three weeks, and brain abscess for at least six weeks. Ampicillin generally is considered the antibiotic of choice and gentamicin is added frequently for its synergistic effects. About 10 percent of serious listeria infections involve cardiac infections that are difficult to treat, with more than one-third proving fatal.
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• Listeria monocytogenes - Columbia Horse Blood Agar -Detail | Flickr - Photo Sharing!. Provided by: Flickr. Located at: http://www.flickr.com/photos/nathanreading/6268795918/. License: CC BY: Attribution | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.08%3A_Bacterial_Diseases_of_the_Digestive_System/15.8J%3A_Listeriosis.txt |
Mumps was a common childhood viral disease, but widespread vaccination has now made it rare in developed countries.
Learning Objectives
• Analyze the cause, symptoms, and prevention of mumps
Key Points
• Mumps is a contagious disease that is spread from person to person through contact with respiratory secretions, such as saliva from an infected person. The common symptoms of mumps include inflammation of the salivary glands, pancreas, and testicles; fever; and headache.
• A physical examination confirms the presence of the swollen glands. Usually, the disease is diagnosed on clinical grounds and no confirmatory laboratory testing is needed.
• The most common preventative measure against mumps is a vaccination with a mumps vaccine. The vaccine may be given separately or as part of the routine MMR immunization vaccine which also protects against measles and rubella.
• Like many other viral illnesses, there is no specific treatment for mumps, other than supportive treatment. Death from mumps is very unusual. The disease is self-limiting, and general outcome is good. Known rare complications of mumps include infertility in men and profound hearing loss.
Key Terms
• orchitis: A painful inflammation of one or both testes.
• salivary gland: Any of several exocrine glands that produce saliva to break down carbohydrates in food enzymatically.
• prodromal symptoms: A prodrome is an early symptom (or set of symptoms) that might indicate the start of a disease before specific symptoms occur.
• parotid gland: Either of a pair of salivary glands located in front of, and below each ear in humans.
Mumps, also known as epidemic parotitis, was a common childhood viral disease caused by the mumps virus. Before the development of vaccination and the introduction of a vaccine in 1949, it was common worldwide, but now, outbreaks are largely confined to developed countries.
Symptoms
The common symptoms of mumps include inflammation of the salivary glands, pancreas, and testicles; fever, and headache. Swelling of the salivary glands, specifically the parotid gland, is known as parotitis, and it occurs in 60–70% of infections and 95% of patients with symptoms. Parotitis causes swelling and local pain, particularly when chewing. It can occur on one side but is more common on both sides in about 90% of cases. Painful inflammation of the testicles in mumps in known as orchitis. Other symptoms of mumps can include dry mouth, sore face and/or ears and occasionally, in more serious cases, loss of voice. In addition, up to 20% of persons infected with the mumps virus do not show symptoms, so it is possible to be infected and spread the virus without knowing it. Fever and headache are prodromal symptoms of mumps, together with malaise and loss of appetite.
Causes
Mumps is a contagious disease that is spread from person to person through contact with respiratory secretions, such as saliva from an infected person. When an infected person coughs or sneezes, the droplets aerosolize and can enter the eyes, nose, or mouth of another person. Mumps can also be spread by sharing food and drinks. The virus can survive on surfaces and then be spread after contact in a similar manner. A person infected with mumps is contagious from approximately six days before the onset of symptoms until about nine days after symptoms start. The incubation period can be anywhere from 14–25 days, but is more typically 16–18 days.
Diagnostics
A physical examination confirms the presence of the swollen glands. Usually, the disease is diagnosed on clinical grounds, and no confirmatory laboratory testing is needed. If there is uncertainty about the diagnosis, a test of saliva or blood may be carried out. An estimated 20–30% of cases are asymptomatic. As with any inflammation of the salivary glands, the level of amylase in the blood is often elevated.
Prevention
The most common preventative measure against mumps is a vaccination with a mumps vaccine. The vaccine may be given separately or as part of the routine MMR immunization vaccine which also protects against measles and rubella. The MMR vaccine is given at ages 12–15 months and then again at four to six years.
Treatment and Complications
Like many other viral illnesses, there is no specific treatment for mumps. Symptoms may be relieved by the application of intermittent ice or heat to the affected neck/testicular area and by the acetaminophen or ibuprofen for pain relief. Warm salt water gargles, soft foods, and extra fluids may also help relieve symptoms. Patients are advised to avoid acidic foods and beverages, since these stimulate the salivary glands, which can be painful.
Death from mumps is very unusual. The disease is self-limiting, and general outcome is good, even if other organs are involved. Known complications of mumps include:
• In teenage males and men, complications from orchitis such as infertility or sub-fertility are rare, but present.
• Spontaneous abortion in about 27% of cases during the first trimester of pregnancy.
• Mild forms of meningitis in up to 10% of cases.
• Profound hearing loss is very rare, but mumps was the leading cause of acquired deafness before the advent of the mumps vaccine.
After the illness, life-long immunity to mumps generally occurs; re-infection is possible but tends to be mild and atypical. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.09%3A_Viral_Diseases_of_the_Digestive_System/15.9A%3A_Mumps.txt |
Hepatitis is the inflammation of the liver. Causes include viruses, bacterial infections, alcohol, autoimmune disorders, drugs, and toxins.
Learning Objectives
• Differentiate between acute and chronic hepatitis
Key Points
• Hepatitis is acute when it lasts less than six months and chronic when it persists longer.
• The initial symptoms of hepatitis are nonspecific flu-like symptoms, common to almost all acute viral infections and may include malaise, muscle and joint aches, fever, nausea or vomiting, diarrhea, and headache.
• A diagnosis of hepatitis is usually made by a combination of blood work and physical examination. When the liver is inflamed, levels of certain liver enzymes that are found in the blood will be elevated. If a patient has viral hepatitis, the presence of the virus can be detected in the blood.
• There are many causes of liver inflammation or hepatitis. The most common cause of acute hepatitis is infection with the Hepatitis B, C, or D viruses. Bacterial diseases can also cause liver inflammation, such as tuberculosis and tick-borne diseases.
• Non-infectious causes of hepatitis include alcohol, autoimmune conditions, drugs, circulatory insufficiency, metabolic diseases, pregnancy, and toxins.
• For those with alcohol-induced hepatitis, cessation of drinking is recommended, as alcoholic hepatitis is often the beginning of more serious drinking-related liver disorders.
Key Terms
• ascites: An accumulation of fluid in the peritoneal cavity, frequently symptomatic of liver disease.
• jaundice: A yellowish pigmentation of the skin, the whites of the eyes (sclera), and other mucous membranes caused by increased levels of bilirubin in the blood that build up in extracellular fluid, usually due to liver disease.
• cirrhosis: A chronic disease of the liver caused by damage from toxins (including alcohol), metabolic problems, hepatitis, or nutritional deprivation. It is characterized by an increase of fibrous tissue and the destruction of liver cells.
• hepatitis: inflammation of the liver, sometimes caused by a viral infection
Hepatitis is the inflammation of the liver. The condition can be self-limiting (healing on its own) or can progress to fibrosis (scarring) and cirrhosis.
Hepatitis may occur with limited or no symptoms, but often leads to jaundice, poor appetite, and malaise. Hepatitis is acute when it lasts less than six months and chronic when it persists longer. A group of viruses, known as the hepatitis viruses, cause most cases of hepatitis worldwide, but it can also be due to toxins, notably alcohol, certain medications, some industrial organic solvents, and plants.
Symptoms
The initial symptoms of hepatitis are nonspecific flu-like symptoms, common to almost all acute viral infections and may include malaise, muscle and joint aches, fever, nausea or vomiting, diarrhea, and headache. More specific symptoms, which can be present in acute hepatitis from any cause, are profound loss of appetite, aversion to smoking among smokers, dark urine, yellowing of the eyes and skin and abdominal discomfort. Physical findings are usually minimal, apart from jaundice and liver swelling. Some patients exhibit enlarged lymph nodes or enlargement of the spleen.
Acute Hepatitis
Acute viral hepatitis is more likely to be asymptomatic in younger people. Symptomatic individuals may present after convalescent stage of 7 to 10 days, with the total illness lasting 2 to 6 weeks.
A small proportion of people with acute hepatitis progress to acute liver failure, in which the liver is unable to clear harmful substances from the circulation, leading to confusion and coma due liver insufficiency, and unable to produce blood proteins, leading to peripheral edema and bleeding. This may become life-threatening and, occasionally, requires a liver transplant.
Chronic Hepatitis
Chronic hepatitis often leads to nonspecific symptoms, such as malaise, tiredness and weakness, and often causes no symptoms at all. It is commonly identified on blood tests performed either for screening or to evaluate nonspecific symptoms. The occurrence of jaundice indicates advanced liver damage. On physical examination, there may be enlargement of the liver.
Extensive damage and scarring of liver, known as cirrhosis, leads to weight loss, easy bruising and bleeding tendencies, peripheral edema and accumulation of ascites, or fluid in the abdominal cavity. Eventually, cirrhosis may lead to various complications, including esophageal varices, which are enlarged veins in the wall of the esophagus that can cause life-threatening bleeding; hepatic encephalopathy, which causes confusion and coma; and kidney dysfunction.
Diagnoses
A diagnosis of hepatitis is usually made by a combination of blood work and physical examination. When the liver is inflamed, levels of certain liver enzymes that are found in the blood will be elevated. If a patient has viral hepatitis, the presence of the virus can be detected in the blood. Patients with progressing liver damage will often display jaundice, or yellowing of the whites of the eyes and skin, and their livers will be visibly enlarged.
Causes
There are many causes of liver inflammation, or, hepatitis. The most common cause of acute hepatitis is infection with the Hepatitis B, C, or D viruses. Bacterial diseases can also cause liver inflammation, such as tuberculosis and tick-borne diseases.
Non-infectious causes of hepatitis include alcohol, autoimmune conditions, drugs, circulatory insufficiency, metabolic diseases, pregnancy, and toxins.
Alcohol is a significant cause of hepatitis worldwide. Usually alcoholic hepatitis comes after a period of increased alcohol consumption. Alcoholic hepatitis is characterized by a variable constellation of symptoms, which may include feeling unwell, enlargement of the liver, development of fluid in the abdomen ascites, and a modest elevation of liver blood tests. Alcoholic hepatitis can vary from mild with only liver test elevation to severe liver inflammation with development of jaundice and liver failure.
Alcoholic hepatitis is distinct from cirrhosis caused by long-term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long-term alcohol consumption.
Treatment
Treatment of hepatitis typically involves treating the underlying condition that caused the inflammation.
In acute hepatitis caused by the hepatitis viruses, often, the liver inflammation will subside when the viral illness has subsided. Antiviral medications, such as interferon, can be used to treat the hepatitis viruses. There is currently a vaccination for Hepatitis B, but not for C or D. Similarly, hepatitis caused by a bacterial disease will typically resolve once the bacterial illness is treated with antibiotics.
For non-infectious causes of hepatitis, treatment of the underlying cause is necessary. For those with alcohol-induced hepatitis, cessation of drinking is recommended, as alcoholic hepatitis is often the beginning of more serious drinking-related liver disorders. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.09%3A_Viral_Diseases_of_the_Digestive_System/15.9B%3A_Hepatitis.txt |
Gastroenteritis is caused by two different virus types in adults and children.
Learning Objectives
• Recognize the viruses that cause gastroenteritis and their mode of transmission
Key Points
• Rotaviruses typically causes gastroenteritis in children. These are double-stranded viruses, which have two coats or capsids.
• Noroviruses, which cause most adult cases of gastroenteritis, are fast mutating viruses.
• The key to the treatment of gastroenteritis is rehydration, either orally or, in severe cases, intravenously.
Key Terms
• replication: Process by which an object, person, place or idea may be copied mimicked or reproduced.
• kbp: kilobase pair
• substitutions per site per year: A DNA mutation where one DNA base pair is replaced with another; often used synonymous with the term mutation rate.
Gastroenteritis is a medical condition characterized by inflammation (“-itis”) of the gastrointestinal tract that involves both the stomach (“gastro”-) and the small intestine (“entero”-), resulting in some combination of diarrhea, vomiting, abdominal pain and cramping. Gastroenteritis has also been referred to as gastro, stomach bug, and stomach virus. Although unrelated to influenza, it has also been called stomach flu and gastric flu.
Viruses that are known to cause gastroenteritis include rotavirus, norovirus, adenovirus, and astrovirus. Globally, Rotavirus is the most common cause of gastroenteritis in children, and produces similar incidence rates in both the developed and developing world. In adults, norovirus and Campylobacter are more common causes.
Viruses cause about 70% of episodes of infectious diarrhea in the pediatric age group. Rotavirus is a genus of double-stranded RNA virus in the family Reoviridae. Reoviruses are non-enveloped and have an icosahedral capsid composed of an outer and inner protein shell. The genomes of viruses in Reoviridae contains 10-12 segments which are grouped into three categories corresponding to their size: L (large), M (medium) and S (small). Segments range from ~ 3.9 kbp – 1kbp and each segment encodes 1-3 proteins. Since these viruses have dsRNA genomes, replication occurs exclusively in the cytoplasm and the virus encodes several proteins which are needed for replication.
The virus can enter the host cell via a receptor on the cell surface. The receptor is not known. After binding to the receptor the outer shell is partially digested to allow cell entry. The inner shell particle then enters the cytoplasm by a yet unknown process to start replication. Viral particles begin to assemble in the cytoplasm 6–7 hours after infection.
Rotavirus is a less common cause in adults due to their acquired immunity. Norovirus is the leading cause of gastroenteritis among adults in America, causing greater than 90% of outbreaks. Noroviruses contain an RNA genome of approximately 7.5 kbp, encoding a major structural protein (VP1) and a minor capsid protein (VP2). The virus particles demonstrate an amorphous surface structure when visualized using electron microscopy and are between 27-38 nm in size.
The most variable region between different viruses of the same type is a portion of the viral capsid. Specifically a region which contains antigen-presenting sites and carbohydrate-receptor binding regions, which is probably the region of the virus that binds to target cells. The estimated mutation rate (1.21 x 10-2 to 1.41 x 10-2 substitutions per site per year) in this virus is high, even compared with other RNA viruses. Norovirus epidemics typically occur when groups of people spend time in close physical proximity to each other, such as on cruise ships, in hospitals, or in restaurants. People may remain infectious even after their diarrhea has ended. Norovirus is the cause of about 10% of cases in children.
The foundation of management of gastroenteritis, viral-caused or otherwise, is adequate hydration. For mild or moderate cases, this can be typically achieved via oral rehydration solution. For more severe cases, intravenous fluids may be needed. Gastroenteritis primarily affects children and those in the developing world.
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Ergot poisoning is caused by ingestion of the alkaloids produced by the ergot fungi.
Learning Objectives
• List the causes and effects of ergot poisoning
Key Points
• Ergot fungi typically infect rye, wheat and forage plants.
• Ingestion of the alkaloid toxins produced by the fungi can result in ergot poisoning in humans and foraging animals.
• Ergot poisoning can have either convulsive central nervous system effects or gangrenous symptoms caused by vasoconstriction effects.
Key Terms
• alkaloids: A class of organic heterocyclic bases.
• gangrenous: To be afflicted with gangrene.
Ergot poisoning is a type of illness associated with the ingestion of alkaloids produced by the fungi Claviceps purpurea (C. purpurea). Claviceps purpurea is a fungus classified under the fungi genus Claviceps. This specific type of fungus is found on rye, and also on crops like wheat and barley. In addition, Claviceps purpurea can effect plants and crops that are typically considered forage plants. Thus, this type of fungus can also result in diseases within livestock.
The life cycle of C. purpurea begins when an ergot kernel, called a sclerotium, infects the host. The fungi continues to undergo proliferation and destroys the plant ovary. The first stage of ergot infection is a white soft tissue, called Sphacelia segetum, that drops out of the host. The white soft tissue contains asexual spores which infect additional host plants. This tissue, present within the host, is then converted into a hard Sclerotium clavus within the husk. At this specific stage, the alkaloids and lipids accumulate.
The alkaloids, responsible for the ergot poisoning, are naturally occurring compounds that are mainly comprised of basic nitrogen atoms. Alkaloids are produced within various organisms as a secondary metabolite. Secondary metabolites are most commonly produced in plants as a defense system. The alkaloids produced by fungi are often toxic. Specifically, the alkaloid produced by Claviceps purpurea is ergoline based.
In cases of ergot poisoning (also known as ergotoxicosis or traditionally, Saint Anthony’s Fire) alkaloids accumulate in the system due to the consumption of contaminated grain products. The symptoms which present in individuals with ergot poisoning can be classified as convulsive symptoms and gangrenous symptoms. The convulsive symptoms include seizures and effects on the central nervous system that range from hallucinations to psychotic episodes. The gangrenous symptoms are a result of vasoconstriction induced by the alkaloids. Peripheral systems, such as fingers and toes, are typically affected. More recently, ergot poisoning has been associated with an increased intake of ergot-based drugs. These drugs include those that promote vasoconstriction for treating migraines and Parkinson’s disease.
15.10B: Aflatoxin Poisoning
Aflatoxin poisoning is a result of ingestion of aflatoxins produced by Aspergillus that have contaminated a food source.
Learning Objectives
• Summarize the causes and effects of alfatoxin poisoning
Key Points
• Aspergillus flavus and Aspergillus parasiticus are two commonly known species of Aspergillus that can aflatoxin poisoning.
• Aflatoxin poisoning can result in either acute aflatoxicosis, which is a result of moderate to high level ingestion; or chronic aflatoxicosis, which results from ingestion of low to moderate levels of aflatoxins.
• Aspergillus species which cause aflatoxin poisoning are often found in crops in underdeveloped countries, due to lack of detection techniques and inadequate harvesting and storage.
Key Terms
• mycotoxins: a substance produced by a mold or fungus.
Aflatoxins are categorized as mycotoxins that are typically produced by species of Aspergillus. Aflatoxins, although only synthesized by a few Aspergillus species, are considered to be one of the most important mycotoxins identified to date. Both Aspergillus flavus and Aspergillus parasiticus are well known for their production of aflatoxins. Aflatoxins are most commonly transmitted to humans through the diet. Aflatoxins grow on whole grains and contaminate food supplies during processing, storage, or transport when there are favorable conditions for mold growth, specifically for the Aspergillus species.
Aflatoxin poisoning, or aflatoxicosis, occurs when there is ingestion of aflatoxin contaminated foods. Upon ingestion or exposure to aflatoxin, it is common to see injury to the liver. Aflatoxicosis is a primarily hepatic disease, as the liver is the target organ for this toxin in mammals. Although the liver demonstrates the ability to metabolize the ingested aflatoxins, the intermediate formed is a reactive epoxide or a less harmful hydroxylated form referred to as M1. There have been various studies stating that metabolic activation of aflatoxins is required for the aflatoxin to exert its carcinogenic effects. These metabolites are harmful to the liver and have been implicated in liver cancer development. The aflatoxins produced by these Aspergillus species have been show to produce adducts (altered forms of DNA). These adducts are now used as a diagnostic factor to test for aflatoxin exposure by testing blood and urine.
Aflatoxin poisoning or aflatoxicosis is rarely diagnosed in developed countries but continues to be an issue in underdeveloped countries. In developed countries, commercial crops are screened for the presence of aflatoxins. However, in underdeveloped or developing countries, screening methods are lacking, or are in the process of being introduced. Interestingly, a rise in homegrown food has been correlated with a slight increase in aflatoxin exposure via diet.
Aflatoxin poisoning can be diagnosed as either acute or chronic. In cases of acute aflatoxicosis, an individual has been exposed to moderate to high levels of aflatoxins. Acute aflatoxicosis is characterized by symptoms such as hemorrhaging; acute liver damage and issues with digestion; and absorption and metabolism of nutrients. In cases of chronic aflatoxicosis, an individual has been exposed to low to moderate levels of aflatoxins. Chronic aflatoxicosis is characterized by symptoms such as dysfunctional food conversion and slow growth rates. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.10%3A_Fungal_and_Protozoan_Diseases_of_the_Digestive_System/15.10A%3A_Ergot_Poisoning.txt |
Giardiasis, sometimes referred to as beaver fever, is caused by the protozoan Giardia lamblia and results in diarrheal illness.
Learning Objectives
• Summarize the life cycle and route of transmission for Giardia lamblia
Key Points
• Giardia lamblia is transmitted by exposure or ingestion of fecal contaminated sources such as soil, food, and water.
• Giardiasis is a common worldwide cause of gastroenteritis.
• The structure and life cycle of Giardia lamblia allow for survival in harsh environments and resistance against numerous types of disinfectants.
Key Terms
• giardiasis: an infectious diarrheal disease caused by the Giardia lamblia parasite
• zoonotic: of or relating to zoonosis, the transmission of an infectious disease between species.
• hematuria: The presence of blood in the urine.
Giardiasis is a protozoan disease caused by Giardia lamblia. Giardiasis, referred to as beaver fever, is a common cause of gastroenteritis worldwide. The protozoa, Giardia lamblia, also referred to as Giardia intestinalis or Giardia duodenalis, infects humans via the fecal-oral route and is also suspected to be zoonotic. The organism is commonly found in soil, food, or water that has been contaminated with fecal matter from infected humans or animals. Beavers typically spread the parasite in their fecal matter in rivers and streams hence, giardiasis is commonly referred to as beaver fever. Individuals susceptible to infection by Giardia lamblia are those who come in frequent contact with individuals already infected. Travelers that spend time in wilderness area are at an increased risk due to ingestion of contaminated food or water sources and a lack of medical care or supplies.
The life cycle, structure, and organization of Giardia lamblia promotes its survival for long periods of time outside the body. The organism itself is protected by an outer shell that provides protection against numerous harsh environments. In addition, the shell provides protection against disinfectants including chlorine. The cysts and trophozoites, found in the fecal matter, are extremely resistant to harsh environments. It is the cysts that are ingested and passed from exposure to contaminated food, water, or by the fecal-oral route. Once in the host, the trophozoites multiply via binary fission. They can either remain free within the lumen or attach to the mucosa by a sucking disk. Once the parasites move towards the colon, the encystation phase occurs and the cysts are infectious when passed in the stool.
Giardiasis is characterized as a disease of the gastrointestinal system. The symptoms include from fever, diarrhea, hematuria, stomach cramping, vomiting, flatulence, and loose stool. The symptoms are typically present one to two weeks post infection and can disappear and reappear cyclically. The pathogenecity of Giardia lamblia is characterized by its ability to coat the inside of the intestinal wall and inhibit nutrient absorption. The ability of the protozoan to block nutrient absorption can result in vitamin B12 deficiency. Additionally, a development of lactose intolerance is often associated with giardiasis infection.
15.10D: Cryptosporidiosis
Learning Objectives
• Outline the life cycle of Cryptosporidium
Cryptosporidiosis is a type of parasitic disease caused by the parasite Cryptosporidium. Cryptosporidiosis is typically spread through the fecal-oral route and can be spread through contaminated water as well. Cryptosporiodiosis is one of most common waterborne diseases identified worldwide. The transmission of Cryptosporidium is based on successful ingestion of oocysts which are able to implant and infect the epithelial tissue of the intestine, hence, the gastrointestinal symptoms associated with cryptosporidiosis.
Cryptosporidium is classified as a protozoan within the Phylum Apicomplexa. Other pathogens classified in this phylum include the malaria parasite and the parasite that causes toxoplasmosis. The life cycle of Cryptosporidium allows for growth in a single host. The spore phase of the life cycle, also referred to as the oocyst stage, is the stage that allows survival of the pathogen in numerous harsh environments. The oocyst allows for survival against harsh chemicals including harsh disinfectants such as chlorine. The life cycle is characterized by the presence of both an asexual and sexual stage. The oocysts, once ingested, excyst within the small intestine and release sporozoites which attach to the microvilli. The sporozoites then develop into trophozoites and undergo asexual reproduction via schizogony. The trophozoites then develop into Type 1 and Type 2 merozoites which can either cause auto infection (Type 1) or undergo releasal and attach the epithelial cells (Type 2). Once released and attached, they will either develop in macrogamonts or microgamonts which correlate with male and female forms. Sexual reproduction occurs than zyogotes are developed. The zygote further develops into the oocyst which can either reinfect the host by rupturing and releasing sporozoites or be excreted into the environment.
The major symptom associated with individuals infected with Cryptosporidium is diarrhea. However, cryptosporidiosis is prevalent in immunocompromised individuals, such as those infected with the HIV virus. The symptoms of cryptosporidiosis in these cases are much more severe and can be fatal. The oocysts can initiate infections by attaching to the brush border of the small intestine and attacking the epithelial cells. Additional symptoms associated with cryptosporidiosis include abdominal cramping, malnutrition, weight loss, and nausea.
Key Points
• Cryptosporidium is commonly transmitted through food and water that has been contaminated with the feces of an infected individual.
• Cryptosporidium is commonly found in immunocompromised individuals that exhibit symptoms associated with this disease such as acute or persistent diarrhea.
• The life cycle of Cryptosporidium involves both asexual and sexual reproduction.
Key Terms
• excyst: The break down of a cyst wall.
• schizogony: A form of asexual reproduction in protozoans characterized by multiple divisions. | textbooks/bio/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.10%3A_Fungal_and_Protozoan_Diseases_of_the_Digestive_System/15.10C%3A_Giardiasis.txt |
Cyclospora diarrheal infection is commonly referred to as traveler’s diarrhea and is caused by the parasite Cyclospora cayetanensis.
Learning Objectives
• Outline the life cycle of Cyclospora cayetanensis
Key Points
• The life cycle of Cyclospora begins as the host ingests the oocyst form.
• Cyclospora is transmitted through fecal matter and is commonly found on contaminated fruits and vegetables in countries or areas with a lack of stringent health regulations.
• Cyclospora causes gastroenteritis with symptoms ranging from diarrhea to loss of appetite, weight loss, cramping, nausea and fatigue.
Key Terms
• meronts: After infecting a host cell, a trophozoite increases in size and during this process, the organism is referred to as a meront.
• sporocysts: a cysts that develops from a sporoblasts and results in the production of sporozoites.
Cyclospora diarrheal infection, commonly referred to as travelers diarrhea or cyclosporiasis, is caused by a specific species of Cyclospora. The protozoan that are categorized as cyclospora are defined by the spherical shape of the sporocysts. Specifically, Cyclospora cayetanensis is the species associated with the disease in both humans and primates. Cyclospora can be transmitted by consuming contaminated food or water. In 2012, cyclospora caused about 500 infections in 2012 in the US from a salad mix imported from Mexico and used in restaurants in Texas and Arkansas.
Life Cycle of Cyclospora
The life cycle of Cyclospora begins when the host is exposed and ingests the pathogen either in its oocyst or spore form. The oocyst is comprised of sporocytes which contain sporozoites. Upon release of the sporozoites, the epithelial cells of the intestine are penetrated. Within the intestinal cells, the sporozoites undergo multiple fission and develop into meronts which contain merozoites. The merozoites then undergo division and produce micro- and macro-gametes representing male and female gametes, respectively.
These gametes then reproduce and result in the formation of oocysts. It is the oocysts which pass through the intestinal tract and are released into the feces. The oocysts demonstrate the ability to undergo sporulation in a crop and water host as well beginning with the oocyst stage. It is during the oocyst stage that cyclospora exhibit a high resistance to disinfectants.
Symptoms of Cyclospora
The symptoms associated with this disease are categorized as gastroenteritis based issues. The symptoms range from watery, loose stool, weight loss, cramping, fatigue, vomiting, fever and nausea. The symptoms can be extremely severe if presented in an immunocompromised patient, such as a patient living with AIDS. The transmission of cyclospora to humans most often occurs by ingesting contaminated foods. In regions of the world where there is lack of health regulations, the chances of cyclospora exposure is increased. Often times, the contaminants include fresh fruits and vegetables which have been exposed to contaminated soil. Individuals exposed to these pathogens in these of regions are at high risk for developing cyclosporiasis, hence, the origin of the commonly known name, traveler’s diarrhea.
15.10F: Amoebic Dysentery (Amoebiasis)
Amoebic dysentery is caused by the parasite Entamoeba histolytica and infected individuals suffer from severe diarrhea, cramps, and fever.
Learning Objectives
• Outline the life cycle of Entamoeba histolytica
Key Points
• Amoebiasis is transmitted via food or water contaminated with fecal matter from an infected individual.
• The pathogen, Entamoeba histolytica, is mainly found in tropical areas and is protected from degradation and destruction by its protective shell, formed during its cyst stage.
• The cyst stage is typically passed in the feces and then ingested to cause infection.
• The amoebas are able to burrow into the walls of the intestines, causing damage.
Key Terms
• trophozoites: A protozoan in the feeding stage of its life cycle.
Amoebic dysentery, also referred to as amoebiasis, is caused by the ameoba Entamoeba histolytica. Dysentery is characterized as an inflammatory disorder of the intestine that results in severe diarrhea containing both mucus and blood in the feces, often accompanied with fever and abdominal pain.
The route of transmission for ameobic dysentery is the fecal-oral route. Transmission and infection occur upon exposure or ingestion of contaminated food and water. The infective cysts are passed via infected stool. The ameoba also demonstrates the ability to spread as free amoebae or trophozoites, meaning the cysts are not absolutely necessary; however, these states do not survive long outside of the host.
Ameobic dysentery is seen in both developing and industrialized countries, although it is most common in tropical areas. Ameobic cysts are often found in areas of the world where the use of human feces for fertilizer is common, often referred to as ‘night soil’. Upon ingestion of contaminated foods or water, the cysts will move into the intestinal area. These cysts are protected from stomach acids and are able to evade destruction. Once in the intestine, the cyst breaks open and releases the amoebas which then burrow into and damage the intestinal walls.
The amoebae or trophozoites are able to divide via binary fission and and produce cysts. If they are passed in the feces as is, instead of developing into cysts, their survival rate decreases as they are unable to survive in harsh environments. Interestingly, individuals can be asymptomatic if infected with trophozoites and can function as carriers by passing cysts in their stool.
Symptoms of individuals infected with Entamoeba histolytica include ulcers, abdominal cramps, diarrhea, bloody stools, liquid stools, fever and vomiting.
15.10G: Legionellosis
Legionellosis is most commonly caused by the Gram-negative bacteria Legionella pneumophila which is an aquatic organism.
Learning Objectives
• Discuss the mode of infection for the bacteria Legionella
Key Points
• Legionella pneumophila is an aquatic organism that is transmitted via aerosols.
• Legionellosis is caused by exposure to contaminated water sources including water towers, spas, fountains, swimming pools and cooling towers.
• Legionellosis-infected individuals have pneumonia -like symptoms with moderate to high fever ranges, chills and a dry cough.
Key Terms
• macrophages: A type of white blood cell that targets foreign material, including bacteria and viruses.
• Legionnaire’s disease: The more severe form of legionellosis which produces high fever and pneumonia.
Legionellosis, commonly referred to as Legionnaire’s disease, is caused by the pathogenic, gram-negative bacteria Legionella. It is characterized by flu- and pneumonia -like symptoms, including fevers and chills. In advanced stages of the disease, there are gastrointestinal and nervous system issues which result in diarrhea and nausea.
Legionella are a type of bacterium that reside within amoebae in the natural environment. The specific species most associated with legionellosis is Legionella pneumophilia, an aquatic organism. Legionella transmission occurs via aerosols and infection occurs when upon inhalation of the bacteria. After being inhaled, the bacteria infect the macrophages of the alveolar and exploit the host machinery to create an environment that promotes bacterial replication. However, the bacteria are not spread from one person to another. In the 1970s, the CDC investigated a large outbreak of legionellosis at Baptist Hospital that was spread through its air conditioner.
Individuals infected with legionellosis have similar symptoms as those diagnosed with pneumonia. Symptoms include high fevers, chills, cough, muscle aches and headaches. For a diagnosis of legionellosis, x-rays and diagnostic tests are used to identify the bacteria. Individuals particularly at risk are older individuals, those immunocompromised or with chronic lung disease.
Legionellosis can take on two distinct forms commonly referred to as legion fever or pontiac fever. Legion fever resembles acute influenza and is the more severe form of the disease, characterized by high fever and pneumonia. Pontiac fever is a milder version and results in mild respiratory illness without the development of pneumonia.
Common sources of Legionella include swimming pools, cooling towers, hot-water systems such as spas, fountains, freshwater ponds and creeks. As seen, the major source for Legionella bacteria is infected water. The bacteria can become suspended in water droplets which are then inhaled into the lungs.
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Learning Objectives
• Compare and contrast the various methods used to diagnose microbial diseases: microbial culture, microscopy, biochemical tests and molecular diagnostics
The process of identifying infectious diseases is complex and requires identification of the agent through direct or indirect means. In regards to many microbial diseases, it is often difficult to diagnose an individual based on clinical presentation. As such, further testing is required. The methods used to diagnose microbial disease include microbial culture, microscopy, biochemical tests, and molecular diagnostics.
Microbial Culture
The first tool in diagnosing microbial disease is microbial cultures. The sample is obtained from the infected individual and tested for the presence of an infectious agent or microbe that is capable of growing in specific media. It is critical to isolate the infectious agent in a pure culture containing only the infectious bacteria. The most common method to isolate individual cells and produce a pure culture is to prepare a streak plate. The streak plate method is a way to physically separate the microbial population, and is done by spreading the inoculate back and forth with an inoculating loop over the solid agar plate. Upon incubation, colonies will arise and single cells will have been isolated from the biomass.
It is established that most pathogenic bacteria can be grown on nutrient agar, and the addition or subtraction of specific nutrients can aid in further identification. The use of microbial cultures is common to help in the clinical identification of pathogenic microbes. However, there are specific classes of microbe that require culture within live animals. The bacteria Mycobacterium leprae is such a microbe, as it can only be cultured in animals.
There are also specific types of infectious agents that require the use of xenodiagnosis to promote growth. The parasite responsible for Chagas disease, Trypanosoma cruzi, requires a vector for diagnosis. For example, an uninfected reduviid bug is used to feed from an individual suspected of having Chagas. Once the blood is taken, the bug will be analyzed for Trypanosoma cruzi growth.
Microscopy
An additional tool utilized for microbial disease diagnosis is microscopy. To ensure proper identification of a pathogen, microscopy, in combination with biochemical staining techniques, is often used to ensure definitive identification. Biochemical staining techniques that are used to aid in identification include stains such as Giemsa, crystal violet, and other stains that help distinguish between gram positive and gram negative.
Biochemical Tests
Biochemical tests are also used to help in microbial disease diagnosis. They will specifically test for metabolic and enzymatic products that an infectious agent may use. Biochemical tests will also test for fermentation products, acids, alcohol or gases that may be products of metabolic pathways.
Molecular Diagnostics
The identification of infectious agents is now often done by using molecular based techniques such as polymerase chase reactions ( PCR ). PCR allows for the identification and testing for nucleic acids which are specific to the infectious agent. The need of an infectious agent to amplify its own nucleic acids to ensure successful infection has allowed us to use PCR to detect the presence of these nucleic acids. In combination with the advances made in genome sequencing, the tools and information needed to establish PCR as the gold-standard for diagnosing microbial disease is present.
Key Points
• Microbial culture is a technique utilized to help in microbial disease diagnosis and can include nutrient plates, liquid cultures, culture within live animals, and use of a vector as well.
• Microscopy is an additional technique used to identify pathogenic microbes by utilizing specialized stains to help identification and characterization based on specific principes.
• Biochemical tests are used to help identify pathogenic microbes and focus on metabolic or enzymatic products that are specific to microbes based on their metabolic pathways.
Key Terms
• xenodiagnosis: The diagnosis of an infectious disease by exposure to a vector of that disease and performing analysis on the vector for the disease.
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