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Flashcards in M tuberculosis Deck (18):

TB has been a

major human disease for 5000 years, consummately adapted to infect HUMANS (we are their natural host and reservoir, and they can be IC or EC)!!



seemed possible until AIDS


MDR (multidrug resistant) and XDR (extensively drug resistant) strains

are public health nightmares



gram stain poorly, are acid fast, and very slow-growing (has mycolic acid for its acid fastness)


Acid fast staining procedure uses

1. carbofuchsin stain (boil in water)
2. acid/alcohol decolorization
3. methylene blue counterstain;
acid-fast positives hold carbolfuchsin during the decolorization (E coli cannot!!)


Transmission almost always

to lung by inhalation, to lymph nodes, kidney, bones, CNS by hematogenous spread, to GI by swallowing infected sputum (more likely by M bovis); (alveolar macrophages try to phagocytose the inhaled bacilli, but can't kill IC mycobacteria)


Immunocompetent host

raises strong CMI response, and can hold infection latent for decades (can use CD4 helper T cells to activate some infected macrophages to kill IC bacteria); immunosenescence or -supression reactivates!!! (latency in immunocomp, active infection if also peds or HIV)


Hematogenous spread by

intracellular infection of naive macrophages; activated ones clear it (CD4 helper T cells help), CD8 cells can kill infected macrophages and establish CASEATING granulomas (mycobacteria uses phosphatides) in which infection is contained (so patient NOT CONTAGIOUS); TNF-alpha also important for containment (lose them with something like Remicade)


Classic pulmonary TB:

75% of cases: cough, weight loss ("consumpton"), fever, night sweats, hemoptysis, and chest pain (think alveolar macrophages in subpleural regions of the lung);
check sputum and chest Xray (cavity formation and maybe noncalcified round infiltrates; maybe tuberculomas that represent old infection)
(Ghon complex: bacilli spread through lymphatics to hilar node and form Ghon complex and then go hematogenously)


Extrapulmonary TB:

1. scrofula, or swollen lymph node, like cervical; more likely adults (fine needle aspirate but avoid bloodstream; surgery maybe but only after antibiotics)
2. GU with possible infertility; most common site of extrapulm infection (IV urography, urine culture); CT possible
3. CNS (MRI, spinal tap with low glucose, high protein, slight pleocytosis)
4. skeletal with bone degeneration e.g. Pott disease (MRI, joint fluid culture)
5. GI (Xray, CT of abdo; exploratory surgery maybe)
6. Miliary with hematogenous spread of TB throughout body (CXR with bright spotlight, lateral Xray, chest CT that show tiny nodules); highest risk in very young and old
7. TB meningitis: Brudzinsky sign in kids!!!



must have been recently acquired (trace source), watch for miliary TB and meningitis;
culture from gastric lavage


Determine exposure by

TST (tuberculin skin test) and/or IGRA (IFN gamma release assay with TB peptides), perform antibiotic resistance testing as soon as cultures grow (2 weeks for cultures, another 3 weeks for resistance tests)



Directly Observed Therapy (DOT) with 4-plus-drug courses featuring isoniazid; isolate patient for first two weeks


BCG vaccine

a live attenuated M bovis is used abroad, NOT cost-effective here; can create weak-moderate false positive TST


Most helpful factors for reducing

incidence of TB in a pop are good diet and housing; latent cases are NOT CONTAGIOUS!!


Pathogenic in

guinea pigs


Proliferative lesions; exudative lesions

1. develop where bacillary load is small and host cellular-immune response dominates
2. exudative lesions predominate when large numbers of bacilli are present and host defenses are weak


Risk factor for poor outcome:

1. uncontrolled HIV
2. Steroids
3. IFN-gamma deficient
4. TNF-alpha antagonists
5. Age < 5yrs