Mycobacterium aviumComplex Disease

Abstract

Soil characteristics in certain regions may favor the growth of Mycobacterium avium complex (MAC), leading to regional differences in epidemiology. Laboratory abnormalities classically have reflected the disseminated nature of the disease with profound anemia out of proportion to neutropenia or thrombocytopenia, and elevated transaminases and alkaline phosphatase. Either because of improved diagnosis or concurrent antiretroviral therapy, these laboratory abnormalities may be less common among patients with disseminated Mycobacterium avium complex (DMAC) diagnosed in the present day than among those diagnosed earlier in the human immunodeficiency virus (HIV)/AIDS epidemic. One study has suggested that interferon (IFN)-ү release assays, which do not cross-react with MAC, may be useful to make the distinction between nontuberculous mycobacterial lymphadenitis. If highly active antiretroviral therapy (HAART) is ineffective, due to HIV multidrug resistance, for example, or CD4 lymphocyte improvement is delayed in a particular individual, MAC prophylaxis is still an important adjunct to care and is cost-effective. Dyspnea on initial presentation and presence of coexisting lung disease have been associated with increased mortality among patients with MAC pulmonary disease. In studies conducted for a course of clarithromycin monotherapy and a course of azithromycin monotherapy, gastrointestinal side effects were common, and changes in hearing were not infrequent. These two studies strongly suggested that clarithromycin and azithromycin have clinical utility for treatment of pulmonary MAC. DMAC is almost exclusively seen in patients with latestage AIDS and can be treated with the combination of either clarithromycin or azithromycin in combination with ethambutol, with or without rifabutin or a fluoroquinolone.