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27 Cards in this Set

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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
What does a Mycobacterium tuberculosis infection require for control
CMI. There are no toxins involved
What are the routes of transmission of Mycobacterium tuberculosis
Respiratory- droplet nuclei containing bacteria
Ingestions- Mycobacterium bovis is causative agent via ingestion of contaminated milk and milk products
What is stage 1 of primary tuberculosis
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
What is stage 1 of primary tuberculosis
Inhalation drop reaches alveoli in mid to lower lung
Bacteria multiply in alveolar spaces
What is stage 2 of primary tuberculosis
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
What is stage 3 of primary tuberculosis
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
What is stage 4 of primary tuberculosis
Bacteria multiply within granulomas and are protected from the immune response
Granulomas become necrotic
Lesions heal but organisms within are not destroyed
What is the course of TB in healthy adults
90% of infections in otherwise healthy adults do not progress to disease, due to containment by CMI, where activated macrophages kill bacteria
What is extrapulmonary tuberculosis
Bacteria can colonize and cause disease in practically any organ of the body
What factors contribute to rise of TB incidence in the US
Increased incidence of AIDS; Increase in homeless population; Deteriorating public health infrastructure; Refugees
What are the current challenges to TB control in the US
Foreign-born persons with TB; multiple drug-resistant strains of Mycobacterium tuberculosis
How is illicit drug use and TB linked
Illicit drug use puts a person at higher risk for exposure or infection, and at a higher risk for developing TB once infected
How is TB diagnosed
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
What is the treatment for Mycobacterium tuberculosis
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
What are some prevention and control measures for TB
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
What is the mycobacterium avium complex
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
What is the pathogen in Leprosy (Hansen disease)
Mycobacterium leprae
What are the characteristics of Mycobacterium leprae
Acid fast; may stain irregularly
Obligate intracellular pathogen
What are the clinical manifestations of Mycobacterium Leprae
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
What is TT
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
What is LL (lepromatous)
Suppression of CMI against Mycobacterium leprae.
Host responds to Mycobacterium tuberculosis yet both share cross-reacting or identical antigens.
What is BB-borderline
An intermediate state of Mycobacterium leprae infections. Unstable, moves to one pole or the other
What is the epidemiology of Mycobacterium leprae
WHO wants to eliminate it. Transmission is man-to-man by direct contact. Low infectivity. Incubation period 3-10 years
How is Leprosy (Hansen disease) diagnosed
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
What is the spectrum of Leprosy disease
How is leprosy treated
Dapsone (blocks bacterial folate biosynthesis). Minimum of two years. Add Rifampin in the case of resistance
There is no vaccine