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Flashcards in Tuberculosis Deck (32)
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general characteristics of Mycobacterium tuberculosis

aerobic, non-spore forming, non-motile bacillus

high cell wall content of high-molecular-weight lipids

4.4 Mb circular genome - a very large proportion of genes encode enzymes involved in lipogenesis and lipolysis

slow growing - 22-24 hour generation time and visible growth takes 3-8 weeks on solid media


TB pathogenesis

airborne droplet nuclei

initial focus on subpleural in the midlung zone - ventillation greatest in the middle and lower lobes

ingested by alveolar macrophages

infected macrophages carried to regional lymph nodes

may spread hematogenously to lymph nodes, kidneys, epiphyses of long bones, vertebral bodies, meninges and the apical posterior areas of the lung


tuberculin reactivity

hypersensitivity to tuberculin appears 3-8 weeks after infection and makrs the development of cellular imunity an dtissue hypersensitivity

before this reaction, bacterial growth is uninhibited, both in the intial focus and in metastatic foci


Ghon complex

antigen concentration int he primarily complex after the acute TB infection

consists of the Ghon focus (pulmonary focus) and draining regional nodes

visible calcification on CXR



Ziehl-Neelsen stain

fixed smear covered with carbol-fuschin is heated, rinsed, decolorized with acid-alcohol, and counterstained with methylene blue


Kinyoun stain

modified Ziehl-Neelsen stain to make the heating step unnecessary


Fluorochrome stain (auramine-rhodamine)

slightly modified acid-alcohol decolorization step and potassium permanganate counterstaining - fluorescent mycobacteria can be easily seen with a x20 or x40 low-magnification objective


characteristic structure of granulomas

necrotic center (if caseating)

surrounded by macrophages

surrounded by T cells


caseating granuloma

cells within the ring of macrophages are lysed contributing to centralized necrosis

extracellular bacteria reside within necrosis

prevents bacteria from spreading

also prevents immune cells from reaching and eliminating those trapped bacteria


Langhans giant cell

consissts of fused macrophages oriented around tuberculosis antigen with the multiple nuclei in a peripheral position

represents the most successful type of host tissue response


What are the most important determinants of transmission of infection?

close contact and infectiousness of the source

source infectivity is a function of the number of TB in bacilli in respiratory secretions and frequency and magnitude of the cough


What does reactivation tuberculosis typically look like in chest x-rays in young people?

apical posterior infiltrates, often with cavitation

apical localization attributed to high oxygen content in the apices and the the aerobic nature of the tubercle bacillus

an alternate theory attributes it to deficient lymphatic flow at the lung apices, especially the posterior apices, wher ethe pumping effect of respiratory motion is minimal


latent TB

all bacteria are harbored within a few infected macrophages within the granuloma

diagnosis is traditionally by tuberculin skin testing - may cross reaction with BCG, have operator error, or be mistaken for other mycobaccteria

interferon-gamma release assays (IGRAs) are used today


reactivation TB

extracellular bacterial levels increase when the immune system is unable to control infection


limitations of PPD skin testing

requires follow-up visit for interpretation

"operator error" - application and interpretation

corss reactions with BCG and MAI

negative in ~25% with active disease


interferon-gamma release assays (IGRAs)

quantify release of the interferon-gamma from lymphocytes in the whole blood incubated overnight with specific M. tuberculosis antigens - early secretory antigen target-6 (ESAT-6) and culture filtrate protein-10 (CFP-10)

as sensitive and more specific than tuberculin skin testing in identifying the latent TB infection

downside is that they are expensive


clinical presentation of TB

fever, night sweats, weight loss, shortness of breath, hemoptysis

cough > 2 weeks

history of exposure to infectious TB or positive TST


common CXR findings in TB

upper lobe infiltrate

cavitary infiltrate

hilar/paratracheal adenopathy


primary vs. reactivation active pulmonary tuberculosis

primary - more common in young children, elderly, and immunosuppressed hosts; presents as lower or middle lobe infiltrates, often with hilar or mediastinal adenopathy

reactivation - typical in adolescents and adults, presents with several weeks of malaise, fever, sweats, weight loss, cough; CXR shows apical posterior infiltrates - often cavitary


milliary tuberculosis

presents as diffuse reticulonodular infiltrates

reflects widespread dissemination of TB

can occur in almost any organ, especially the lymph nodes, vertebrae, and meninges

CXR findings may not suggest TB in 50% of individuals


tuberculous meningitis

untreated death ensues within 5-8 weeks of illness onset

early diagnosis often based on CSF formula - lymphocytic or mixed pleocytosis, high protein, low glucose, negative cultures


types of media used for culture of mycobacteria

egg-based (Lowenstein Jensen) and agar-based  (Middlebrook 7H11) - 3-8 weeks of incubation

liquid broth (Middlebrook 7H12) - 1-3 weeks of incubation


Xpert MTB/RIF test

automatic nucleic acid amplification test for TB and rifampin resistant TB

very sensitive and specific

takes about an hour to get results


first-line drugs for TB treatment








second-line drugs for TB







p-aminosalicylic acid




treatment for latent TB

isoniazid x9 months


rifampin x 4 months


isoniazid plus rifapentine weekly x2 months (directly observed therapy)


treatment for active TB

standard regimen - 2 months of isoniazid, rifampin, thambutol, and pyrazinamide followed by 4 months of isoniazid plus rifampin

extended treatment is recommended for cavitary disease on initial CXR and positive sputum cultures at 2 months of treatment


What is multi-drug resistant TB? What are the categories of MDRTB?

TB that is resistant to at least INH and rifampin

primary - patient initially infected with MDR-TB

acquired - poor adherence to Rx, selection of resistant bacteria


Why does drug resistance emerg during therapy? What is the likelihood of this happening?

selection - resistant variants pre-exist in the bacterial population

about 108 bacteria in a cavity

1in 108 are rifampin resistant

1 in 106 are isoniazid resistant

1 in 105 are ethambutol resistant

overall resistance probability to isoniazid and rifampin is 10-14


extensively drug resistant TB (XDR-TB)

resistance to INH and rifampin plus any fluoroquinolone and any one of the second-line anti-TB injectable drugs