Pulmonary infiltrates in immunocompromised patients (patients with HIV disease, absolute neutrophil counts less than 1000/mcL [less than 1.0 × 109/L], current or recent exposure to myelosuppressive or immunosuppressive medications, or those currently taking more than 5 mg/day of prednisone) may arise from infectious or noninfectious causes. Infection may be due to bacterial, mycobacterial, fungal, protozoal, helminthic, or viral pathogens. Noninfectious processes, such as pulmonary edema, alveolar hemorrhage, medication reactions, pulmonary thromboembolic disease, malignancy, and radiation pneumonitis, may mimic infection.
Although almost any pathogen can cause pneumonia in an immunocompromised host, two clinical tools help the clinician narrow the differential diagnosis. The first is knowledge of the underlying immunologic defect. Specific immunologic defects are associated with particular infections. Defects in humoral immunity predispose to bacterial infections; defects in cellular immunity lead to infections with viruses, fungi, mycobacteria, and protozoa. Neutropenia and impaired granulocyte function predispose to infections from S aureus, Aspergillus, gram-negative bacilli, and Candida. Second, the time course of infection also provides clues to the etiology of pneumonia in immunocompromised patients. A fulminant pneumonia is often caused by bacterial infection, whereas an insidious pneumonia is more apt to be caused by viral, fungal, protozoal, or mycobacterial infection. Pneumonia occurring within 2–4 weeks after organ transplantation is usually bacterial, whereas several months or more after transplantation P jirovecii, viruses (eg, cytomegalovirus) and fungi (eg, Aspergillus) are encountered more often.