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53 Cards in this Set
- Front
- Back
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Microbiology Chapter 23
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Mycobacteria: Tuberculosis and Leprosy
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percent of individuals infected with Tb who become ill
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10%
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oxygen status of mycobacterium
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obligate aerobes
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staining characteristics of mycobacteria
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acid fast, resistant to drying, slow growing
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most abundant wax in mycobacteria
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mycolic acid
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acid fast stain procedure
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heat in presense of basic red fuschsin dye. Treat with acid which removes red dye in most cases. Counterstain with blue dye. Mycobacteria will appear as slender red rods
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flurochrome dyes
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now being used instead of fushin because they can be detected with fluorescense microscopy
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waxy coat makes mycobacteria
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resistant to drying and allows them to evade killing by phagocytes
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waxy coat does not protect mycobacteria against
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withstanding heat (pasteurization)
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why does it take so long to culture mycobacteria
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mycobacteria grow slowly due to reduced ability to transfer nutrients across their waxy coats
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TB is a major cause of death in these patients
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immuno comprimised/ AIDS
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source of TB infection
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inhalation of droplet nuclei
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pulmonary cavities
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can be formed by host inflammatory response to initial TB infection. These cavities allow TB particles to be coughed into the air
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clinical manifestations of TB are a result of
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host immune response
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toxins produced by tubercle bacilli
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none
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where does primary infection usually occur
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in the middle lung zone where airflow is greatest
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facultative intracelllular pathogen
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TB is able to multiply both inside and outside of cell
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describe the formation of the Ghon complex
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TB infected macrophages/monocyres travel to regional lymphocytes resulting in inflammation of the lung region and hilar lymph nodes
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where do TB organisms preferably settle during lymphohematogenous dissemination
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lymph nodes, vertebral bodies, meninges, and apices of lungs
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what occurs when primary infection is not fully contained by the initial immune response
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progresses to progressive primary TB
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most important consequence of lymphohematogenous dissemination
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seeding of lung apices where progressive primary/secondary disease occurs
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endogenous reactivation can be triggered by
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malnutrition, steroid therapy, immunosupresive drugs, renal failure, malignancy, HIV
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most common site of reactivation
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apex of lung
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what becomes of reactivated lesion
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undergo caseous necrosis resulting in larger lesions with a well aerated cavity
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tuberculosis pneumonia
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discharge of caseous material distributes TB organism throughout the lungs
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what type of immune response is required for TB control
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cellular
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how do CD4+ T cells recognice mycobacterial antigens
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presented to them by MHC-II proteins on APCs (macrophages)
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when/how does sensitivity to tubercillin occur
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activated lymphocytes (CD4) proliferate and release lymphokines which further activate macrophages. When tubercillin is injected these cells will flock to it, as tubercillin mimics the mycobacterial antigens
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pattern that symbolizes sucessful immune control of TB infection
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granulomas
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miliary TB
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seen in IC patients who cannot control the primary infection. The organisms seed the bloodstream and disseminate
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cytokines that contribute to symptoms of TB
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IL-1 and TNF-a
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tuberculin conversion
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positive PPD test after negative one. May indicate recent infection, indication for chemoprophylaxis
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IFN gamma and TB
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IFN gamma assays can identify latent infections. IFN gamma is released in response to TB antigens. As such we can use these assays similarly to PPD testing
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Pott disease
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chronic back pain associated with TB reactivation in vertebrae
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2 main defensive strategies against TB
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1. cellular immunity (macrophages and T cells) 2. fibrosis and walling off of lesion
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diagnosis for active and asymptomatic TB
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acid fast stain/culture and tuberculin skin test respectively
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gold standard for TB diagnosis
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culture
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mycobacterium avium complex and M kansassi
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mycobacterial infections resembling TB that are pretty much only seen in advanced AIDS and immunosupression
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4 drug TB cocktail
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INH, Rifampin, PZA, ethambutol
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drug used in chemoprophylaxis of TB
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INH, there are so few organisms present in latent tb that only 1 drug is needed
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primary drug resistant TB
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person is infected with drug resistant strain
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secondary drug resistant TB
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person who has received TB therapy becomes resistant (noncompliance causes this)
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MDR TB
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resistant to INH and rifampin
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how we grow M leprae
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we cannot culture it in vitro but have been able to grow it in the foot pads of mice
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critter that is associated with high amounts of M leprae
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nine banded armadillo
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phenolic glycolipid
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surface lipid of M leprae that provides a defense against oxidative killing
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why do leprosy bacilli grow best in skin and superficial tissues
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lower temperatures
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drugs used in treatment of leprosy
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dapsone, rifampin, clofazimine
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tuberculoid leprosy
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associated with red blotchy lesions and locan anesthesia, lepromin sensitivity
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lepromin + test indicitates
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tuberculoid leprosy
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type of leprosy with better prognoisis
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tuberculoid because it is self limited
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bacterial load is higher in what type of leprosy, why
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lepromatous. There is no immune response so the bacteria grow unchecked, tuberculoid leprosy requires only a small amount of organism present for a robust immune response
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lepromatous leprosy
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no reaction to lepromin, minimal immunity, highest bacterial load of any human disease, analgous to miliary TB. Involvment of skin and nerves with secondary infection common
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