A 26-year-old homosexual man with human immunodeficiency virus type 1 infection presented with fever, productive cough, and progressive respiratory distress for 2 weeks. He had not taken antimicrobial prophylaxis for Pneumocystis jirovecii pneumonia or antiretroviral therapy. The CD4 lymphocyte count was 45 cells/μl on admission. High-resolution computed tomography of the chest revealed diffuse ground-glass opacities and numerous cystic lesions in both lungs (Figure 1A). This patient developed respiratory failure soon after admission to the hospital and two episodes of pneumothorax during the stay in the ICU, which required mechanical ventilator support. The consulting chest physician and intensivist decided that bronchoscopy might be hazardous on his admission to the ICU. Examination of the lung biopsy specimen obtained by video-assisted thoracoscopy revealed P. jirovecii in the alveolar exudates. He received highly active antiretroviral therapy (HAART) consisting of lamivudine, abacavir, and atazanavir with good viral suppression and increases of CD4 lymphocyte count. Follow-up high-resolution computed tomography of the chest revealed significant regression of cystic and ground-glass lesions 8 months later when his CD4 count had increased to 120 cells/μl (Figure 1B) and he had returned to his usual activities as a bicyclist.
Figure 1.
The incidence of P. jirovecii pneumonia among HIV-infected patients has significantly decreased since the introduction of HAART and use of chemoprophylaxis with trimethoprim-sulfamethoxazole (1, 2). However, P. jirovecii pneumonia remains the most common cause of respiratory failure in the HAART era (3), for which the mortality rate remains around 10% (4). Predictors of mortality include age of 40 years or more, intravenous drug use in the previous 6 months, total bilirubin greater than 0.6 mg/dl, serum albumin less than 3 g/dl, and alveolar–arterial oxygen gradient greater than 50 mm Hg (5). HAART use is not only associated with a lower mortality rate in patients admitted to ICU with confirmed P. jirovecii pneumonia (6), but also contributes to earlier discontinuation of primary or secondary prophylaxis in patients who achieve viral suppression (7, 8).
Previous studies have shown that the prevalence of cysts on chest roentgenograms or computed tomography ranges from 10% to 34% in HIV-infected patients with P. jirovecii pneumonia (9, 10). These cystic lesions are associated with an increased incidence of spontaneous pneumothorax (10), as is demonstrated by the two episodes of pneumothorax in our patient. The pathogenesis of cyst formation is not well known and several theories have been proposed, such as check-valve bronchiolar obstruction with distal cyst formation, elastase release from the macrophages with destruction of alveolar tissue, cytotoxic effect of HIV, or direct tissue destruction by P. jirovecii (11–13). Similar to our observation in this case, several studies have reported that both the radiologic changes and impaired pulmonary function are reversible after treatment (14–17). The time to resolution may range from 5 days to 1 year (18).
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