Mycobacterium kansasii is a bacterium which belongs to the same family as the organisms which cause tuberculosis (M. tuberculosis) and Mycobacterium avium intracellulare (MAI; M. avium and M. intracellulare). In people with damaged immune systems, such as a CD4 cell count below 100 cells/mm³, it can cause lung problems, and can occasionally spread to other parts of the body.

M. kansasii is a common opportunistic infection in southern Africa miners with HIV infection. Its incidence is unknown in other groups in southern Africa, and has not been reported in other parts of the world. M. kansasii is not transmitted from person to person, but is believed to be acquired from contaminated water sources.

Symptoms and diagnosis

Symptoms include fever, cough, and shortness of breath. The organisms can be detected by examining a sputum smear, fluid that has been flushed within the throat and lungs (bronchoalveolar lavage) or samples of lung tissue, or by trying to grow the bacteria from these samples. Chest X-rays frequently show the presence of thin-walled hollow lesions within the lungs.

Treatment

There is no standard treatment for M. kansasii, although it seems to be sensitive to some anti-tuberculosis medications. One team of researchers has recommended early aggressive therapy consisting of rifampicin (Rifadin / Rimactane) or rifabutin (Mycobutin) and ethambutol with either ciprofloxacin (Ciproxin), clarithromycin (Klaricid / Klaricid XL) or clofazimine.

M. kansasii can be difficult to treat. A recent study of 79 HIV-positive patients with M. kansasii has shown that treatment with three antimycobacterial drugs for nine months resulted in 53% mortality. Patients with low CD4 cell counts, inadequate treatment of the bacteria, no HAART and presence of bacteria in a sputum smear (Marras 2004). However, these investigators concluded that witholding treatment in HIV-positive patients with M. kansasii should only be considered in patients with negative smear microscopy, few positive cultures and mild immunosuppression.

Research

Marras (2004) studied 127 patients with pulmonary M. kansasii. 33% fulfilled American Thoracic Society criteria for the disease. 29% received at least 1 drug for at least 3 months. 53% died. Mortality was associated with lower CD4 cell count (hazard ratio [HR] 1.6, 95% confidence interval [CI] 1.1, 2.3) and positive smear microscopy (HR 2.8, 95% CI 1.3, 6.1). Antiretroviral therapy (HR 0.3, 95% CI 0.1, 0.8) and M. kansasii treatment (HR 0.4, 95% CI 0.2, 0.9) were associated with survival.

Klein (1998) conducted a retrospective study of all cases of M. kansasii at two London hospitals. 19 cases were identified, including 10 with pulmonary disease and 9 with disseminated infection. 7 patients appeared to be colonized with M. Kansasii but had not symptoms of disease. A third had M. kansasii in their faeces. Disseminated M. kansasii infection occurred in 0.44% of all AIDS cases attending the two units. 11/13 patients with M. kansasii-related disease responded to anti-mycobacterial therapy. 4 patients received sub-optimal treatment and subsequently relapsed.

Levine (1991) conducted a retrospective chart review of 19 patients with AIDS and M. kansasii. Median CD4 count at diagnosis was 49. 14/19 had exclusively pulmonary disease, 3/19 had pulmonary and extrapulmonary disease, and 2/19 had exclusively extrapulmonary disease. 10/19 received anti-tuberculosis therapy (nine had pulmonary disease and one had M. kansasii osteomyelitis). Patients received isoniazid and rifampicin with ethambutol, streptomycin, or pyrazinamide. All treated patients improved clinically, with no evidence of relapse. All isolates were susceptible to rifampicin and ethambutol. INH resistance was found in 4/10 patients, and all isolates were resistant to pyrazinamide. 5/9 untreated patients died with respiratory failure caused by M. kansasii.

Bamberger (1994) reported the results of a retrospective chart review of 35 HIV-infected patients with M. kansasii, 28 of whom had symptomatic infection. Average CD4 cell count was 12/microL. The majority presented with pulmonary disease with symptoms such as fever, cough, and dyspnea, but only 8/22 patients had radiographic evidence of either pulmonary cavitation or predominantly upper-lobe disease. M. kansasii was detected in the blood or bone marrow of 10. The majority responded to therapy but 11 patients died either before mycobacterial infection was diagnosed or early in the course of treatment.

Rooney (1996) conducted another retrospective analysis of 10 cases of M. kansasii, 6 of which were disseminated. All but one had a CD4 count below 20 and 8 had fever and malaise. All isolates were sensitive to ethambutol and all but one were sensitive to rifampicin. All isolates were resistant to isoniazid and pyrazinamide. The majority had chest infections and the organism was isolated on induced sputum.

References

Bamberger DM et al. Mycobacterium kansasii among patients infected with human immunodeficiency virus in Kansas City. Kansas City AIDS Research Consortium. Clinical Infectious Diseases 18(3): 395-400, 1994.

Klein JL et al. Mycobacterium kansasii and human immunodeficiency virus co-infection in London. J Infect 37(3): 252-259, 1998.

Levine B et al. Mycobacterium kansasii: a cause of treatable pulmonary disease associated with advanced HIV infection. Annals of Internal Medicine 114: 861-868, 1991.

Marras TK et al. Mortality prediction in pulmonary Mycobacterium kansasii infection and human immunodeficiency virus. Am J Respir Crit Care Med 170: 793-398, 2004.

Rooney G et al. Mycobacterium kansasii: its presentation, treatment and outcome in HIV infected patients. Journal of Clinical Pathology 49(10): 821-823, 1996.