Pulmonary Nocardiosis in a Patient With Human Immunodeficiency Virus

Abstract

A man was admitted to the hospital with a 3-week history of dry cough, anorexia, weakness, and weight loss. The patient was positive for human immunodeficiency virus and was noncompliant with prescribed antiretroviral medications. His CD4 count and viral load were unknown at the time of admission. A chest radiograph revealed diffuse cystic and bullous changes and coarse reticular markings throughout both lung fields, consistent with chronic, most likely postinfectious, fibrotic changes, possibly with a superimposed active infectious process (Figure 1). The patient underwent bronchoscopy and bronchoalveolar lavage. Transbronchial biopsies of the right lower lobe were obtained. Material was submitted for bacterial, fungal, and viral cultures, and for histopathologic examination. Acid-fast bacilli were seen on the smear from bronchial secretions by the auramine-rhodamine method. A presumptive diagnosis of mycobacterial infection was made. Mycobacterium xenopi was subsequently isolated from mycobacterial culture. Routine bacterial, fungal, and viral cultures were negative. Microscopic examination of transbronchial biopsies demonstrated extensive inflammatory infiltrate involving bronchial tissue and expanding adjacent alveolar interstitium. The infiltrate consisted of plasma cells, lymphocytes, histiocytes, neutrophils, and rare multinucleated giant cells (Figure 2, original magnification 3400). Well-formed granulomas were not seen. Ziehl-Neelsen stains for acid-fast bacilli were negative. Gomori methenamine silver stain, Gram stain, and modified acid-fast Fite stain (Figure 3, oil immersion, original magnification 31000) revealed the presence of gram-positive, branching, filamentous, beaded bacteria morphologically diagnostic of Nocardia species. Nocardia species belong to the group of aerobic bacteria generically designated as actinomycetes. They are ubiquitous environmental saprophytes living in soil, organic matter, and water.1 Nocardiae have long been known to cause disease in animals and are being recognized increasingly as opportunistic human pathogens. The organism does not elicit a humoral response and is eliminated from the body via cell-mediated mechanisms. Thus, individuals with impaired T-cell function are at increased risk for nocardial infection. Groups at the highest risk in-