Mycobacterium xenopi: innocent bystander or emerging pathogen?

Mycobacterium xenopi is a recognized cause of smoldering pulmonary disease in patients with chronic lung disease. This organism is frequently isolated from respiratory specimens from individuals infected with human immunodeficiency virus (HIV) and is often considered nonpathogenic. Cases of pulmonary and disseminated M. xenopi disease have been described in patients with HIV infection and other immunodeficiencies. Many physicians are unaware of the clinical significance of M. xenopi isolation. Whether this organism represents a commensal or a pathogen capable of causing considerable morbidity and mortality is not fully understood. In this study, we investigated the clinical significance of M. xenopi isolation and explored the clinical spectrum of M. xenopi disease. Clinical illness occurred both in elderly people with chronic lung disease and in young individuals with HIV infection. The repeated isolation of M. xenopi in association with pulmonary lesions suggests significant infection and mandates further workup and therapy.

Mycobacterium xenopi infection masquerading as pulmonary tuberculosis in two patients infected with the human immunodeficiency virus.

Mycobacterium xenopi infections have rarely been reported among patients infected with the human immunodeficiency virus (HIV). We recently treated two HIV-infected men, neither of whom had a history of pulmonary disease or AIDS-defining conditions, and who had M. xenopi lung infections. Both patients presented with night sweats, cough, and pleuritic chest pain. Chest radiographs showed an upper-lobe nodule in the first patient and a perihilar cavitary infiltrate in the second patient. Both patients were initially believed to have pulmonary tuberculosis and were treated accordingly; however, only M. xenopi grew on cultures of multiple respiratory specimens. This diagnosis was confirmed by cultures of biopsied lung tissue from the first patient and of fluid from a peritracheal abscess in the second patient. Both patients' clinical conditions improved after multidrug therapy (isoniazid, rifampin, pyrazinamide, ethambutol, and ciprofloxacin in the first case; isoniazid, rifampin, and pyrazinamide in the second case). The second patient's condition improved despite in vitro resistance of his isolate to isoniazid and rifampin.

Intravenous and oral zidovudine pharmacokinetics and coagulation effects in asymptomatic human immunodeficiency virus-infected hemophilia patients.

Pharmacokinetic and coagulation studies were carried out over a 12-week period with 11 asymptomatic hemophilia patients with human immunodeficiency virus infection receiving zidovudine (ZDV). The patients received 300 mg every 4 h while awake (the accepted dose at the time of this study); consecutive 24-h intravenous (i.v.) and 12-h oral pharmacokinetic studies were conducted at weeks 1, 6, and 12. Coagulation studies were conducted at weeks 0, 4, 8, and 12. The numbers of units of factors VIII and IX and cryoprecipitate transfused during the 12-week periods before, during, and after ZDV treatment were recorded. Following i.v. and oral ZDV administration, the concentration in plasma declined rapidly over the first 4 h, and in some patients, ZDV was still detectable at 4 to 10 h. The i.v. total clearances (means +/- standard deviations) were 14.9 +/- 7.3, 11.2 +/- 3.7, and 15.1 +/- 4.7 ml/min/kg of body weight. The i.v. distribution volumes were 1.08 +/- 0.5, 1.0 +/- 0.4, and 1.65 +/- 1.4 liters/kg. The bioavailabilities were 0.54 +/- 0.22, 0.46 +/- 0.19, and 0.59 +/- 0.13 at weeks 1, 6, and 12, respectively. The pattern of ZDV-glucuronide (GZDV) disposition was similar to that of ZDV, and the peak plasma GZDV-to-ZDV ratio was higher after oral dosing, consistent with first-pass metabolism. In some individuals, up to 33% of an i.v. dose was excreted unchanged. At weeks 6 and 12, greater than 300 mg of total ZDV (GZDV plus ZDV) was recovered in the urine of some patients, suggesting tissue redistribution. Concentration in plasma after oral ZDV administration were variable, both within and between patients. The von Willebrand antigen level consistently decreased throughout the study but was not accompanied by a parallel change in ristocetin cofactor A activity, and no clinical adverse effects on coagulation were noted. This study demonstrates that ZDV can be used in hemophilia patients without worsening of their bleeding tendencies. The clinical significance of decreased ZDV clearance and the prolonged terminal elimination phase of ZDV will require further study with patients receiving chronic ZDV.