Mycobacterium avium complex
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Mycobacterium avium complex (MAC), also called Mycobacterium avium-intracellulare complex, is a microbial complex of 2 Mycobacterium species, Mycobacterium avium and Mycobacterium intracellulare.[1] It causes Mycobacterium avium-intracellulare infection.[2][3]
Some sources also include Mycobacterium avium subspecies paratuberculosis (MAP).[4]
Mycobacterium avium complex (MAC) include ubiquitous atypical bacterium found in the environment which can infect patients with HIV and low CD4 cell count (below 100/microliter); mode of infection is usually inhalation or ingestion.
MAC causes disseminated disease in up to 40% of patients with human immunodeficiency virus (HIV) in the United States, producing fever, sweats, weight loss, and anemia.[5][6][7] Disseminated MAC characteristically affects patients with advanced HIV disease and peripheral CD4+ T-lymphocyte counts less than 100 cells/uL. Effective prevention and therapy of MAC has the potential to contribute substantially to improved quality of life and duration of survival for HIV-infected persons.[8]
Diagnosis
Disseminated MAC is most readily diagnosed by one positive blood culture. Blood cultures should be performed in patients with symptoms, signs, or laboratory abnormalities compatible with mycobacterium infection. Blood cultures are not routinely recommended for asymptomatic persons, even for those who have CD4+ T-lymphocyte counts less than 100 cells/uL.[8]
Prevention
Patients with HIV infection and less than 50 CD4+ T-lymphocytes/uL should be administered prophylaxis against MAC. Prophylaxis should be continued for the patient's lifetime unless multiple drug therapy for MAC becomes necessary because of the development of MAC disease.[8]
Clinicians must weigh the potential benefits of MAC prophylaxis against the potential for toxicities and drug interactions, the cost, the potential to produce resistance in a community with a high rate of tuberculosis, and the possibility that the addition of another drug to the medical regimen may adversely affect patients' compliance with treatment. Because of these concerns, therefore, in some situations rifabutin prophylaxis should not be administered.[8]
Before prophylaxis is administered, patients should be assessed to ensure that they do not have active disease due to MAC, M. tuberculosis, or any other mycobacterial species. This assessment may include a chest radiograph and tuberculin skin test.[8]
Rifabutin, 300 mg by mouth daily, is recommended for the patient's lifetime unless disseminated MAC develops, which would then require multiple drug therapy. Although other drugs, such as azithromycin and clarithromycin, have laboratory and clinical activity against MAC, none has been shown in a prospective, controlled trial to be effective and safe for prophylaxis. Thus, in the absence of data, no other regimen can be recommended at this time.The 300-mg dose of rifabutin has been well tolerated. Adverse effects included neutropenia, thrombocytopenia, rash, and gastrointestinal disturbances.[8]
Treatment
Although studies have not yet identified an optimal regimen or confirmed that any therapeutic regimen produces sustained clinical benefit for patients with disseminated MAC, the Task Force concluded that the available information indicated the need for treatment of disseminated MAC. The Public Health Service therefore recommends that regimens be based on the following principles:[8]
- Treatment regimens outside a clinical trial should include at least two agents.
- Every regimen should contain either azithromycin or clarithromycin; many experts prefer ethambutol as a second drug. Many clinicians have added one or more of the following as second, third, or fourth agents: clofazimine, rifabutin, rifampin, ciprofloxacin, and in some situations amikacin. Isoniazid and pyrazinamide are not effective for the therapy of MAC.
- Therapy should continue for the lifetime of the patient if clinical and microbiologic improvement is observed.
Clinical manifestations of disseminated MAC—such as fever, weight loss, and night sweats—should be monitored several times during the initial weeks of therapy. Microbiologic response, as assessed by blood culture every 4 weeks during initial therapy, can also be helpful in interpreting the efficacy of a therapeutic regimen.Most patients who ultimately respond show substantial clinical improvement in the first 4–6 weeks of therapy. Elimination of the organisms from blood cultures may take somewhat longer, often requiring 4–12 weeks.[8]
HIV-infected children
HIV-infected children less than 12 years of age also develop disseminated MAC. Some age adjustment is necessary when clinicians interpret CD4+ T-lymphocyte counts in children less than 2 years of age. Diagnosis, therapy, and prophylaxis should follow recommendations similar to those for adolescents and adults.[8]
References
This article incorporates public domain material from the Centers for Disease Control and Prevention document "Recommendations on Prophylaxis and Therapy for Disseminated Mycobacterium avium Complex for Adults and Adolescents Infected with Human Immunodeficiency Virus".
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