Atypical Mycobacterial Infection Follow-up

Updated: Feb 07, 2018
  • Author: Arry Dieudonne, MD; Chief Editor: Russell W Steele, MD  more...
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Follow-up

Further Outpatient Care

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  • Decrease in fever and a decline in quantity of mycobacteria in blood or tissue can be expected within 2-4 weeks after initiation of appropriate therapy; however, for those with more extensive disease or advanced immunosuppression, clinical response may be delayed. [44, 60] A repeat blood culture for MAC should be obtained in 4-8 weeks after initiation of antimycobacterial therapy for patients who do not have a clinical response to their initial treatment regimen (ie, demonstrate little or no reduction in fever or systemic symptoms). Treatment failure is defined by the absence of clinical response and the persistence of mycobacteremia after 4-8 weeks of treatment.

  • Testing of MAC isolates for susceptibility to azithromycin and clarithromycin is recommended for patients who do not respond microbiologically to initial therapy, who have relapse after initial response, or who develop MAC disease while receiving clarithromycin or azithromycin for prophylaxis. Results of susceptibility should be used to construct a new multidrug regimen consisting of at least 2 new drugs not previously used and to which the isolate is susceptible, including the following: ethambutol, rifabutin, ciprofloxacin or levofloxacin, or amikacin. [33] Resistance to clarithromycin in patients with pulmonary disease caused by MAC has been reported. [83] Data are insufficient to support the use of adjunctive treatment with immunomodulators, such as IFN-gamma, TNF-alpha, granulocyte-macrophage colony stimulating factor, and IL-12 alone or in combination with other cytokines, which appear to inhibit intracellular replication or invitrointracellular killing of M avium.

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Further Inpatient Care

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  • Inpatient care is not mandatory for immunocompromised patients with M avium complex (MAC) disease unless their treatment is complicated by the presence of severe diarrhea with moderate-to-severe dehydration requiring intravenous fluid replacement and hyperalimentation, severe anemia requiring transfusion of blood products, or for further medical investigation.

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Inpatient & Outpatient Medications

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  • See Medication.

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Deterrence/Prevention

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  • Because optimal therapy does not guarantee a better outcome, disseminated MAC disease still carries significant morbidity. Therefore, preventing its occurrence may be the best approach. Data from multicenter studies have shown the presence of resistant strains in patients receiving prophylaxis. With a high frequency rate and a high rate of antimicrobial resistance, primary chemoprophylaxis for MAC infection, in conjunction with effective antiretroviral therapy, should be considered. Prophylaxis for prevention should be offered to children younger than 13 years with the following CD4+ T-lymphocyte counts: [66]

    • Children aged 6 years or older with fewer than 50 cells/µL

    • Children aged 2-6 years with fewer than 75 cells/µL

    • Children aged 1-2 years with fewer than 500 cells/µL

    • Children younger than 12 months with fewer than 750 cells/µL

  • Azithromycin or clarithromycin is recommended. Rifabutin is another alternative prophylactic agent. However, it should not be used until active tuberculosis has been excluded to avoid the development of rifampin-resistant tuberculosis. Disseminated MAC disease should also be excluded based on a negative blood culture result before prophylaxis is initiated. [66, 84] Discontinuation of prophylaxis for MAC disease in adult patients infected with HIV who have a response to antiretroviral therapy is supported by some published data. [85] Children with a history of disseminated MAC disease should be administered lifelong prophylaxis to prevent recurrence. The safety of discontinuing MAC prophylaxis has not been studied in children whose CD4+ lymphocyte counts have increased in response to HAART. [33]

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Complications

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  • Gastrointestinal obstruction and gastrointestinal bleeding caused by bulky intra-abdominal adenopathy or extensive ileal disease have been reported. [58] Pulmonary complications from disseminated MAC disease are uncommon in children. Culture and histologic evidence of infection have been reported in the heart, eye (keratitis), brain, skin, thyroid, tongue, adrenals, stomach, pancreas, skeletal system, and peripheral nerves. [86, 87, 88]

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Prognosis

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  • In the early years of the HIV epidemic, descriptive and retrospective studies were mostly aimed at defining the population of children infected with HIV at risk for MAC infection and at analyzing the predictors of survival in patients with AIDS and disseminated MAC disease. [38, 89, 90] MAC was a contributor to mortality in HIV infection, and its presence was considered an indication that death is imminent. [59, 91]

  • The development of HAART has resulted in marked changes in the outcome of HIV disease, with reductions in hospitalizations and death as well as opportunistic infections, including MAC. [64] Established treatment, previously discussed, has reduced the morbidity and mortality caused by disseminated MAC disease. MAC infection is still a problem in developing countries where access to antiretroviral therapy is still limited and in severely immunocompromised patients whose adherence and tolerance to treatment raise a lot of questions. The prognosis for children without HIV with disseminated mycobacterial infection secondary to IFN-gamma receptor ligand-binding deficiency is poor.

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Patient Education

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