Etiology

Mycobacterium avium complex (MAC) is commonly found in the environment, including in soil, water, and dust. It is known to colonize natural water as well as indoor water sources, pools, and hot tubs.[12][16]​​ Water transport systems act as a transmission route from water reservoirs to household water.[16]​ However, no environmental exposure or behavior has been consistently determined as a risk factor for subsequent development of MAC. Specific routes of acquisition are also rarely identified. While there may be regional differences in the prevalence of MAC in the environment, the implication of these differences in the prevalence of MAC disease is unclear.[13][17]

Mycobacteria are aerobic, nonspore-forming, nonmotile bacilli.[1] Their cell wall contains long-chained glycolipids that protect these facultative intracellular bacteria from lysosomal attack. They grow slowly over 10 to 21 days on solid media. Growth is detected earlier on liquid media (7-10 days).

There are two main species that comprise MAC: M avium and M intracellulare. The organisms are further classified into serovars based on the glycopeptidolipid content of the cell wall.[2]M avium is responsible for more than 90% to 95% of diseases in people with AIDS.[18] Serovars 1, 4, and 8 have been identified as major etiologic agents in people with AIDS.[19]

Pathophysiology

The respiratory and gastrointestinal tracts are thought to be the primary portals of entry for MAC organisms. For pulmonary disease, acquisition of the organisms is thought to be by inhalation. In contrast, the gastrointestinal tract is believed to be the primary route of infection in patients with AIDS and in patients with lymphadenitis.[20] In patients with AIDS, colonization of the intestinal tract with MAC precedes the appearance of bacteremia and disseminated disease by several months.[21] There is no known human-to-human transmission.

After entry into the body, MAC organisms colonize the respiratory and gastrointestinal tracts and invade and multiply within macrophages. This phagocytosis and processing of antigens by macrophages triggers a complex immune response that includes further activation of macrophages as well as the release of cytokines such as interleukin (IL)-12, interferon gamma and tumor necrosis factor alpha.[22][23][24] In patients with intact cellular immunity and pulmonary clearance mechanisms, this response will result in granuloma formation and intracellular killing of MAC organisms. Immune deficiency, primarily cellular immunity but also humoral immunity and cytokine genetic defects, can lead to unimpaired multiplication of the organisms within macrophages and subsequent dissemination.[25][26]

Elevated proinflammatory cytokine levels are believed to be responsible for the symptoms of fevers, night sweats, and cachexia seen in patients with MAC disease.[27]

Classification

Disease syndromes associated with Mycobacterium avium complex (MAC)

  • Pulmonary disease

  • Cervical lymphadenitis

  • Disseminated disease

  • Hypersensitivity pneumonitis

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