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Mycobacterium A large genus of acid-fast, aerobic, thin, irregular rods that have large amounts of a large lipid called mycolic acid in their cell wall. There are about 75 species. 2. Mycolic acid constitutes about 50% of the cell wall weight of mycobacteria and conveys a number of unique characteristics to them, Slow growth. rough, tightly matted colonies on agar media and surface pellicles in broth media. C. Protection from killing inside phagocytic cells. D. Capacity for intracellular growth inside phagocytes. E. Resistance to Gram-staining, detergents, many antimicrobial drugs, dessication and acid-fastness |
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Virulence Factors of M. tuberculosis 1. M. tuberculosis produces no toxins or destructive hydrolytic enzymes. Its virulence stems from: A. Its ability to survive & replicate inside macrophages. B. Its activation of destructive host immune responses *These virulence properties are conveyed by various mycolic acid containing compounds called mycosides that are present in the cell wall of M. tuberculosis.* |
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All virulent strains of M.tuberculosis produce a mycoside called cord factor that causes M.tuberculosis cells to stick to each other and grow as large serpentine cords. causes severe inflammation, wasting and death in mice that are injected with it. 1) Cord factor does this occurs by activating macrophages to secrete excessive quantities of the inflammatory cytokine tumor necrosis factor α, which enters the circulation and causes inflammation, shock and death. |
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Mycosides called sulfitides inhibit phagosome- lysosome fusion in macrophages and enhance survival of ingested M. tuberculosis cells in macrophages |
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A complex mycoside called wax D is a potent immunological adjuvant that induces cellular immunity and delayed hypersensitivity to proteins. A. Delayed hypersensitivity to proteins produced by M. tuberculosis causes most of the tissue destruction that occurs in active tuberculosis infection. |
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TB has 4 clinical forms depending upon route of infection & the state of the host immune response. |
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A. Primary TB is the initial M. tuberculosis infection in the lungs. It results in an arrested infection in 95% of hosts; the other 5% develop progressive primary TB. B. Secondary (reactivation) TB is the reestablishment of active TB in the lungs after a period of dormancy which can be short or long in duration depending on the state of the host’s cellular immunity. About 10% of infected hosts develop reactivation TB, usually within 2 years. C. Disseminated (Miliary) TB is the spread of active TB throughout the body to many internal organs and tissues via the bloodstream. D. Ingestion TB is TB of tonsils, intestinal lymph nodes, cervical lymph nodes (scrofula) and bones. It is caused by ingestion of M. bovis or M. tuberculosis. |
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Primary Tuberculosis granulomas are called tubercles. contain live TB bacilli and necrotic, semi-solid tissue that resembles Swiss cheese.(caseous necrosis) |
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In TB Large calcified primary complex lesions are visible by X-ray & are called the Ghon complex. About 25% of infected host develop |
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dissemination of TB bacilli to multiple organs via macrophages and the bloodstream. A. It is called miliary tuberculosis because it results in the formation of thousands of small tubercles that look like millet seeds in internal organs, Miliary TB causes wasting (weigh loss, loss of vigor) and is fatal in 1-2 years. host is tuberculin positive
Disease is contained; bacteria live but are unable to replicate; 25% develop Ghon complex host is tuberculin negative
Progressive systemic disease and death 3. About 30% of hosts with active untreated TB develop miliary tuberculosis |
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TB of tonsils, intestinal lymph nodes, cervical lymph nodes (scrofula) and bones. It is caused by ingestion of M. bovis or M. tuberculosis |
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the initial M. tuberculosis infection in the lungs. It results in an arrested infection in 95% of hosts; the other 5% develop progressive primary TB |
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Secondary (reactivation) TB |
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is the reestablishment of active TB in the lungs after a period of dormancy which can be short or long in duration depending on the state of the host’s cellular immunity. About 10% of infected hosts develop reactivation TB, usually within 2 years. |
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Diagnosis of Tuberculosis |
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Active TB is diagnosed by demonstrating the presence of M. tuberculosis or M. bovis in a host’s sputum or other clinical specimen by microbial culture or other M. tuberculosis/bovis specific test. A. Microbial culture of M. tuberculosis from sputum or other lesion can take 3-6 weeks before visible growth is observed because tubercle bacilli grow very slowly The U.S. uses tuberculin skin testing as a screening tool to identify potential cases of active TB.does not distinguish active TB from inactive or previous infection, or from BCG immunization.
Two TB skin tests are in widespread use, the Old Tuberculin Tine Test and the Mantoux test. A. The tine test employs a manufactured device that has steel tines coated with tuberculin proteins. B. The Mantoux test employs intradermal injection of a purified tuberculin protein derivative called PPD. C. A positive TB skin test produces induration (a hard swelling) one cm or more in diameter at the test site. It also causes redness but the *test is read by the induration* Tuberculin-positive hosts are given a chest X-ray to determine if lesions are present in their lungs. A. Ghon complexes are usually localized to the base and central areas of the lungs. Secondary TB lesions usually occur in apical areas and are more extensive. B. Miliary TB of the lungs appears as small white lesions throughout both lungs |
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Treatment of Active Tuberculosis |
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long regimens with multiple anti-TB drug cocktails (6 months in uncomplicated cases; 12-18 months or longer with advanced TB or drug resistant tubercle bacilli). Drug-resistant tubercle bacilli quickly emerge if a single anti-tubercular drug is given, so multi-drug cocktails are given to prevent the emergence of antibiotic resistant strains. The recommended regimen for uncomplicated TB cases is isoniazid, rifampin and pyrazinamide for 2 months, then isoniazid and rifampin for 4 months. |
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Mycobacterium avium-intracellulare |
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act as opportunistic pathogen in the most common cause of opportunistic Mycobacterium infection in AIDS patients in the United States acquired by ingesting the causative organisms in contaminated food or water. B. Ingested mycobacteria initially infect Peyer’s patches in the intestinal tract. They cause diarrhea and disseminate from Peyer’s patches via lymphohematogenous spread to many organs and tissues in the body. C. These infections are difficult to treat because AIDS patients are immunodeficient, few antibiotics are effective against mycobacteria and the infections become widely |
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