B Levine1, R E Chaisson. 1. Johns Hopkins University School of Medicine, Baltimore, Maryland.
Abstract
OBJECTIVE: To assess the clinical features and response to therapy of Mycobacterium kansasii infection in patients with human immunodeficiency virus (HIV) infection. DESIGN: We reviewed the records of all patients with M. kansasii and HIV infection treated between January 1985 and June 1990. SETTING: The Johns Hopkins Hospital, Baltimore, Maryland. RESULTS: Nineteen patients with M. kansasii and HIV infection were identified; 14 patients had exclusive pulmonary infection, 3 patients had pulmonary and extrapulmonary infection, and 2 patients had exclusive extrapulmonary infection. At the time of diagnosis of M. kansasii infection, the median CD4+ lymphocyte count was 49 cells/microL (range, 0 to 198 cells/microL), and 16 of 19 patients had a previous diagnosis of the acquired immunodeficiency syndrome (AIDS). All 17 patients with pulmonary infection presented with fever and cough of at least 2 weeks duration. Chest radiographs showed either focal upper lobe infiltrates (n = 8) or diffuse interstitial infiltrates (n = 9); 9 patients also had thin-walled cavitary lesions. Nine patients with pulmonary M. kansasii infection were treated with antituberculosis chemotherapy, with resolution of fever and respiratory symptoms, improvement of radiographic infiltrates, and sputum conversion; 1 patient with M. kansasii osteomyelitis also responded to antituberculosis therapy. Autopsies done on 3 treated patients did not reveal any evidence of M. kansasii infection. Nine patients did not receive any antituberculosis chemotherapy; 2 untreated patients developed progressive cavitary pulmonary disease and died from M. kansasii pneumonia. CONCLUSIONS: Mycobacterium kansasii causes serious and potentially life-threatening pulmonary disease in patients with advanced HIV-related immunosuppression. In contrast to previous reports, our findings indicate that disease produced by M. kansasii in patients with HIV infection is responsive to antituberculosis chemotherapy.
OBJECTIVE: To assess the clinical features and response to therapy of Mycobacterium kansasiiinfection in patients with human immunodeficiency virus (HIV) infection. DESIGN: We reviewed the records of all patients with M. kansasii and HIV infection treated between January 1985 and June 1990. SETTING: The Johns Hopkins Hospital, Baltimore, Maryland. RESULTS: Nineteen patients with M. kansasii and HIV infection were identified; 14 patients had exclusive pulmonary infection, 3 patients had pulmonary and extrapulmonary infection, and 2 patients had exclusive extrapulmonary infection. At the time of diagnosis of M. kansasiiinfection, the median CD4+ lymphocyte count was 49 cells/microL (range, 0 to 198 cells/microL), and 16 of 19 patients had a previous diagnosis of the acquired immunodeficiency syndrome (AIDS). All 17 patients with pulmonary infection presented with fever and cough of at least 2 weeks duration. Chest radiographs showed either focal upper lobe infiltrates (n = 8) or diffuse interstitial infiltrates (n = 9); 9 patients also had thin-walled cavitary lesions. Nine patients with pulmonary M. kansasiiinfection were treated with antituberculosis chemotherapy, with resolution of fever and respiratory symptoms, improvement of radiographic infiltrates, and sputum conversion; 1 patient with M. kansasiiosteomyelitis also responded to antituberculosis therapy. Autopsies done on 3 treated patients did not reveal any evidence of M. kansasiiinfection. Nine patients did not receive any antituberculosis chemotherapy; 2 untreated patients developed progressive cavitary pulmonary disease and died from M. kansasiipneumonia. CONCLUSIONS:Mycobacterium kansasii causes serious and potentially life-threatening pulmonary disease in patients with advanced HIV-related immunosuppression. In contrast to previous reports, our findings indicate that disease produced by M. kansasii in patients with HIV infection is responsive to antituberculosis chemotherapy.
Authors: I Nachamkin; R R MacGregor; J L Staneck; A Y Tsang; J C Denner; M Willner; S Barbagallo Journal: J Clin Microbiol Date: 1992-05 Impact factor: 5.948
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