Tuberculosis

Basics

Description

  • Active tuberculosis (TB) infection caused by Mycobacterium tuberculosis
    • Primary infection or reactivation of latent infection; risk increases with immunosuppression: highest risk first 2 years after infection; reactivation risk increases with comorbid disease (e.g., HIV, diabetes).
    • Well-described forms: pulmonary (85%), miliary (disseminated), meningeal, abdominal, lymphadenitis (scrofula)
  • Usually acquired by inhalation of airborne bacilli from an individual with active TB; bacilli multiply in alveoli and spread via macrophages, lymphatics, and blood. Outcomes include eradication (tissue hypersensitivity stops infection), primary TB, and latent TB infection (LTBI).

Epidemiology

Incidence

  • Worldwide (2021): an estimated 10.6 million people equivalent to 134/100,000
  • 7% of cases involve people living with HIV. Most cases are in Southeast Asia and Africa.
  • United States (2020): 7,163 (2.2/100,000); 71% of U.S. cases were in persons born outside of the United States. TB incidence has decreased by an average of 2–3% annually during the previous 10 years.

Prevalence

  • Worldwide (2020): World Health Organization estimates 9.9 million new cases of TB.
  • Mortality
    • Worldwide (2021): 1.6 million deaths due to TB; 13th leading cause of death worldwide

Etiology and Pathophysiology

  • M. tuberculosis, Mycobacterium bovis, or Mycobacterium africanum are causative organisms.
  • Spread by aerosol droplets and reach alveolar space. Alveolar macrophages ingest and migrate.
  • Cell-mediated response by activated T lymphocytes and macrophages forms a granuloma (“tubercle”) that limits bacterial replication. If bacterial replication continues, the tubercle grows with spread to regional lymph nodes. An expanding tubercle within the lung parenchyma combined with regional lymph node enlargement is called a Ranke complex.
  • As the infection is contained, destruction of the macrophages produces early “solid necrosis.” In 2 to 3 weeks, “caseous necrosis” develops and LTBI ensues. In the immunocompetent, granuloma undergoes “fibrosis” and calcification. In the immunocompromised, primary progressive TB develops. Cavitary lesions may form.

Risk Factors

  • For latent infection: homeless, correctional facilities, close contact with infected person, living in areas with high incidence of active TB, health care workers; medically underserved, low income, substance abuse
  • For development of disease once infected: renal failure; lymphoma; silicosis; diabetes; cancer of head, neck, or lung; children <5 years old; malnutrition; systemic corticosteroids; HIV; immunosuppressive drugs; IV drug abuse, alcohol abuse, cigarette smokers; <2 years since infection with M. tuberculosis; <90% of ideal body weight

General Prevention

  • Screen for and treat LTBI. Report active TB to health department; test and treat all close contacts. Without treatment, LTBI will progress to active TB disease in 5–10% of affected people.
  • Bacillus Calmette-Guérin (BCG) vaccine: used primarily in endemic countries; BCG is not recommended in the United States for high-risk children with negative PPD and ongoing exposure.

Commonly Associated Conditions

Immunosuppression; HIV coinfection; malignancy

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