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  • Most cases of human tuberculosis (TB) caused by Mycobacterium tuberculosis (MTB); Mycobacterium spp. are thin, rod-shaped bacteria with hydrophobic cells walls → resistant to decolorization during Gram staining (acid-fast bacilli [AFB])
  • Risks for developing TB infection after exposure include proximity to & infectiousness of TB patient, duration of exposure, immunocompetence of exposed individual; risk of developing active TB infection highest w/in 2y of exposure; 10% of patients who acquire TB develop active infection without chemoprophylaxis
  • Cutaneous TB occurs via direct inoculation through skin
  • TB exists as rapidly growing extracellular organisms (in cavities, where resistance may exist), slow-growing organisms (in acidic/necrotic tissue, often cause for treatment failure/relapse), or dormant organisms (alternating periods of dormancy & growth → treatment failure/relapse with inadequate therapy)

Figure 34-1.

Pathophysiology of TB. (Data from Diagnostic Standards and Classification of Tuberculosis in Adults and Children. This official statement of the American Thoracic Society and the Centers for Disease Control and Prevention was adopted by the ATS Board of Directors, July 1999. This statement was endorsed by the Council of the Infectious Disease Society of America, September 1999, Am J Respir Crit Care Med 2000; Apr:161(4 Pt 1):1376.)

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Clinical Pearl 34-1

Patients with impaired cell mediated immunity (DM, HIV) & patients receiving immunosuppressive drugs are at ↑ risk of developing active TB

  • Clinical manifestations: pulmonary infection most common; systemic symptoms → fever, night sweats, malaise, ↓ appetite, weight loss (Am J Respir Crit Care Med 2000;161:1376)
  • Diagnosis: + tuberculin skin test (TST; purified protein derivative [PPD]) or + serum interferon gamma release assay (IGRA; e.g., Quantiferon®-TB Gold) identifies exposure to TB; does NOT differentiate between active/latent TB infection; further testing (e.g., CXR, cultures) required to diagnose active infection (MMWR 2010;59[RR-5]:1)
    • False-negative TST → HIV infection, immunosuppression; false + TST → prior BCG vaccination (MMWR 2000;49[RR-6]:1)
    • IGRA → only require single visit; preferred if patient cannot comply with return visit for TST reading or if prior BCG use (MMWR 2010;59[RR-5]:1)
    • CXR: upper lobe infiltrates, cavitation, mediastinal/hilar lymphadenopathy, & classic TB symptoms → active pulmonary TB; HIV/immunosuppressed patients may lack typical radiographic findings
    • AFB smear: rapid, nonspecific → presumptive evidence of TB pending culture; patients with AFB + sputum → respiratory isolation; if available, PCR may confirm presence of MTB w/in 24–48h (MMWR 2009;58:7)
    • Gold standard microbiological test for diagnosis of active TB: MTB growth from sputum, CSF, bone, urine, skin scraping, lymph node; MTB slow growing → 2–8wk for visible colony growth on solid media (Am J Respir Crit Care Med 2000;161:1376)
    • Susceptibility testing routinely performed on INH, RIF, PZA, ETH; in 2008, 6.8% of TB isolates resistant to INH & 1.2% resistant to INH & RIF (MMWR 2009:58:249)

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Clinical Pearl 34-2

Extrapulmonary TB is more common in HIV-infected patients due to failure ...

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