TB and NTM Flashcards
how is TB spread? where does it land initially?
by carriers with ACTIVE disease via airborne droplet nuclei. Lands in mid or lower lungs. Hilar or mediastinal adenopathy
Where does TB most commonly spread? how does it spread?
Lymph nodes, vertebrae, meninges. hematogenously or via macrophages in lymph
What does the immune response to TB involve?
Activated lymphocytes but no antibodies. Caseating or noncaseating granulomas.
When does tissue hypersensitivity develop?
3-9 wks after infection
What are epithelioid and Langhans giant cells?
Epithelioid-highly stimulated macrophages
Langhans-fused macrophages (multiple peripheral nuclei)
What is the rate of reactivation infection?
5% w/in first two years, additional 5% after that. Higher in AIDS pts
How are primary TB infections characterized?
Majority-PPD +. Minority-primary (Ghon) comple. Necrosis and calcification of initial focus. Rarely-progressive Tb (in children,AIDS)
Where are bacteria harbored during latent TB infection?
w/in macrophages in the granuloma
What are the three main TB test?
PPD (TST), Interferon Gamma. Second has higher sens and spec but is more expensive
Where does TB usually reactivate?
Apical posterior lung (usually no hilar adenopathy). Extrapulmonary. Miliary.
Miliary TB
represents widespread dissemination of disease. Presents on CXR as reticulonodular infiltrates
What is the formula for tuberculous meningitis?
Pleocytosis (esp lymphocytic), high protein, low glucose, negative cultures
What is the fastest way to culture TB? Other ways?
Broth (1-3 wks). Solid media takes 3-8 wks. Fastest is Xpert MTB/RIF use nucleic acid amplification (same day) also test RIF resistance
What is the probability of resistance to a regimen?
the product of the probabilities of a resistant strain being present
What defines MDR-TB? XDR-TB?
Resistance to RIf/INH. Rif/INH plus fluoroquinolones and other second lines
What is BCG good for?
children, TB meningitis, lasts 10-20 yrs
How does NTM usually present?
chronic granulomatous pneumonia or bronchiectasis. 75% pulmonary although can be bacteremic, cutaneous, or lymph nodes
How does NTM differ from TB?
no latent infection, no person2person transmission.
How are NTM classified? Which are the main ones? Why are they the ones that infect lungs?
Rapid vs slow growing. MAC/MAI and M. kansasii are slow growers. Cause they grow at 36*C
what are the criteria for diagnosis of NTM lung disease?
MULTIPLE (+) sputum samples. (+) bronchial lavage. (+) biopsy
What are the three major disease complexes of M. avium and M. intracellulare?
Pulmonary disease, disseminated disease (AIDS), cervical lymphadenitis.
Lady Windemere Syndrome
MAC pulm infection in tall, thin women with chest wall abnormalities. Old white ladies w/ CF
M. kansasii
infection mimics pulmonary TB
M. gordonae
noninfectious mycobacterium
What NTM can cause cutaneous infection
marinum, abcessus, chelonae, fortuitum
