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26 Cards in this Set
- Front
- Back
How is M. tuberculae visualized? Why is this technique used?
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*Acid-fast staining
*waxy coat prevents Gram staining |
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What is the O2 preference of M. TB? Does it like to live inside or outside of cells?
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*obligate aerobe
*facultative intracellular pathogen |
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How is TB transmitted?
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Aerosol - inhalation of droplet nuclei.
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What caused the rise of TB in the early 1980's?
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*HIV/AIDS
*influx of immigrants from endemic areas *dismantling of public health infrastructure |
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After the microbe has entered the body, what does M. TB do next?
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*ingested by alveolar macrophages
*prevents phagosome-lysosome fusion in inactivated phages *IC replication followed by host cell lysis *may be transported throughout RES |
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What symptoms are seen in primary TB? What's the course of this condition?
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*flu sx
*cell-mediated immune response results in granuloma (casein) formation *viable bugs remain in granuloma |
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How does secondary TB occur? What symptoms are seen?
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*Oranisms inside granuloma are re-activated and spread
*fever, night sweats, wt loss *tissue damage may result in cavitation |
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Is infection by TB restricted to the lungs?
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No - M. TB can infect virtually any part of the body.
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What are some ways TB is detected? What are some problems with each?
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*PPD: false+ for BCG recipients, false- for HIV pts
*culture: slow-growing *sputum smear: poor sample *Bac-Tec *CXR: non-specific |
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How is TB treated? What are some difficulties? What's been done to lessen these?
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*6-8 month course of rifampin, INH, ethambutol
*poor compliance *DOTS has increased compliance |
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Is there a vaccine for TB? What are its drawbacks?
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Yes - the BCG vaccine. Efficacy is variable and all recipients will give a false+ PPD.
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What's been the biggest obstacle with the study of M. leprae?
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Unable to culture in vitro - animal models must be used.
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Describe the transmission and incubation of M. leprae.
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*not highly infectious
*transmitted by inhalation *5-yr incubation period *lepromatous nodules contain numerous bacteria |
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What 2 symptoms appear in both forms of disease caused by M. leprae?
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*disfigurement
*dennervation |
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Where in the body does M. leprae live?
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In macrophages and Schwann cells.
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What are the 2 disease forms caused by M. leprae? What are the characteristics of each?
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1.Tuberculoid: good Th-1 immune response; hypopigmented lesion; neuropathy
2.Lepromatous: poor immune response; large, bacteria-filled nodules on skin |
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How is infection with M. leprae treated?
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6-12 month triple antibiotic regimen
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What distinguishes the photochromagens?
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They are slow growing and produce a yellow pigment when grown in the light.
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What class of MOTT is M. kansasii? What type of disease does it cause?
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*photochromagens
*pulmonary disease common among HIV pts in the midwest |
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What class of MOTT is M. marinum? What kind of disease does it cause?
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*photochromogen
*"swimming pool granuloma" *chronic draining ulcer *2-6 week incubation |
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What distinguishes the scotochromogens? Describe 2 microbes that fall in this class.
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*slow growing
*produce a yellow pigment in lighth or dark *M. scrofulaceum - lymphadenitis *M. gordonae - culture contaminant |
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How might nonchromagens be recognized? Name 2.
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Their slow growth and inability to produce pigment under any conditions.
*M. avium complex, M. paratuberculosis |
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How is MAC acquired? What patient population does it affect most often? Treatibility?
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*inhalation or ingestion of contaminated water
*causes pulmonary disease in HIV, COPD, and CF pts. *high multi-rx resistance |
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With what disease has M. paratuberculosis been linked?
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Crohn's disease.
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The majority of Runyon Class IV MOTT (rapid-growers) are associated with a single disease type. What is this?
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*M. fortuitum, M. chelonei, and M. abscessus are associated with skin abscesses and wound infection
*M. smegmatis is non-pathogenic |
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What is the only MOTT that doesn't fall under Runyon classification? What does it cause?
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*M. ulcerans
*necrotizing skin ulcer associated with trauma (Buruli ulcer) |