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27 Cards in this Set
- Front
- Back
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Rod shaped, non-motile, non-spore forming, acid fast aerobe
Cell envelope- waxes, mycolic acids, polysaccharides, peptidoglycan, lipids, lipoarabinomannan Slow growth. Generation time 15-20 hrs; 4-6 weeks for colonies |
Characteristics of Mycobacterium tuberculosis
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What does a Mycobacterium tuberculosis infection require for control
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CMI. There are no toxins involved
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What are the routes of transmission of Mycobacterium tuberculosis
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Respiratory- droplet nuclei containing bacteria
Ingestions- Mycobacterium bovis is causative agent via ingestion of contaminated milk and milk products |
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What is stage 1 of primary tuberculosis
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Inhalation drop reaches alveoli in mid to lower lung
Bacteria multiply in alveolar spaces Bacteria are either destroyed or grow within cells leading to death of macrophages |
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What is stage 1 of primary tuberculosis
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Inhalation drop reaches alveoli in mid to lower lung
Bacteria multiply in alveolar spaces Bacteria are either destroyed or grow within cells leading to death of macrophages |
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What is stage 2 of primary tuberculosis
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Logarithmic growth of bacteria within macrophages
Dissemination via infected macrophages into lymphatics and bloodstream and other organ systems No host defenses during first few weeks after infection |
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What is stage 3 of primary tuberculosis
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Tissue hypersensitivity 6-14 weeks post infection
Activated macrophages ingest and destroy bacteria Cytotoxic T cells recognize infected macrophages and destroy them Macrophages coalesce and fuse to form granulomas and Ghon complexes. Tissue necrosis, tubercule formation. Tissue necrosis plus calcification produces primary tubercle lesion |
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What is stage 4 of primary tuberculosis
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Bacteria multiply within granulomas and are protected from the immune response
Granulomas become necrotic Lesions heal but organisms within are not destroyed |
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What is the course of TB in healthy adults
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90% of infections in otherwise healthy adults do not progress to disease, due to containment by CMI, where activated macrophages kill bacteria
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What is extrapulmonary tuberculosis
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Bacteria can colonize and cause disease in practically any organ of the body
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What factors contribute to rise of TB incidence in the US
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Increased incidence of AIDS; Increase in homeless population; Deteriorating public health infrastructure; Refugees
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What are the current challenges to TB control in the US
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Foreign-born persons with TB; multiple drug-resistant strains of Mycobacterium tuberculosis
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How is illicit drug use and TB linked
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Illicit drug use puts a person at higher risk for exposure or infection, and at a higher risk for developing TB once infected
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How is TB diagnosed
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Sputum smear- need 10^4
Culture- 95% are niacin positive Tuberculin skin test X-ray - not sufficient by itself QuantiFERON-TB- detects IFN-gamma released from sensitized lymphocytes in patient's blood |
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What is the treatment for Mycobacterium tuberculosis
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Bacteria are intracellular and metabolically inactive in chronic lesions
Use antibiotics such as Isoniazid, Rifampin, Streptomycin, Pyrazinamide, Ethambutol, or combination therapy Patients on chemo become non-infectious within 2 weeks Duration is 6-12 months, patient compliance is essential |
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What are some prevention and control measures for TB
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Early id and treatment
ID of contacts Test high risk groups Proper use of ventilation and UV light Vaccine, though not recommended for general US use |
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What is the mycobacterium avium complex
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Mycobacterium avium and Mycobacterium intracellulare.
Opportunistic pulmonary pathogens of immunocompromised patients. Cause disseminated disease in up to 40% of patients with HIV infection in the US |
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What is the pathogen in Leprosy (Hansen disease)
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Mycobacterium leprae
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What are the characteristics of Mycobacterium leprae
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Acid fast; may stain irregularly
Obligate intracellular pathogen |
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What are the clinical manifestations of Mycobacterium Leprae
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Lesions that can be anywhere. Classically found on skin and at extremities, hands, feet nose. Clinical features are the result of bacterial proliferation, immune response of host, and peripheral neuritis
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What is TT
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Tuberculoid disease caused by Mycobacterium leprae. This is a highly specific CMI response
Skin lesions are granulomas Few or no acid-fast bacteria. Bacteria grow in macrophages and Schwann cells. Immunologic damage to nerves; demyelination by macrophages |
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What is LL (lepromatous)
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Suppression of CMI against Mycobacterium leprae.
Host responds to Mycobacterium tuberculosis yet both share cross-reacting or identical antigens. |
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What is BB-borderline
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An intermediate state of Mycobacterium leprae infections. Unstable, moves to one pole or the other
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What is the epidemiology of Mycobacterium leprae
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WHO wants to eliminate it. Transmission is man-to-man by direct contact. Low infectivity. Incubation period 3-10 years
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How is Leprosy (Hansen disease) diagnosed
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Nerve destruction- anesthetic lesions in TT
Skin scrappings- LL and BL stages yield acid fast bacteria Skin biopsy- TT yields few bacteria but grossly swollen nerve bundles infiltrated with mononuclear cells are evident Lepromin test- confirms TT, not useful for LL |
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What is the spectrum of Leprosy disease
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TT-tuberculoid
BT BB-borderline BL LL-lepromatous |
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How is leprosy treated
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Dapsone (blocks bacterial folate biosynthesis). Minimum of two years. Add Rifampin in the case of resistance
There is no vaccine |
