Pulmonary nocardiosis is an opportunistic bacterial infection caused by aerobic gram-positive filamentous, beaded, branching, partially acid-fast bacteria of the genus Nocardia. The most clinically important species in human disease are Nocardia farcinica (often more virulent and resistant), N. nova, N. cyriacigeorgica, N. asteroides complex, N. brasiliensis (more cutaneous), and N. otitidiscaviarum. Nocardia is ubiquitous in soil, decaying organic matter, water, and dust.
Infection is acquired by inhalation of aerosolized organisms or, less commonly, direct cutaneous inoculation. The lung is the primary site of infection in over 70% of cases. Risk factors include severe immunosuppression: solid organ transplantation (especially lung, kidney, heart), high-dose corticosteroids (>20 mg prednisone for prolonged periods), biologic agents (TNF-alpha inhibitors, rituximab), HIV/AIDS (CD4 less than 200), hematologic malignancies, chronic granulomatous disease, alcoholism, diabetes mellitus, and chronic lung disease (COPD, bronchiectasis, prior pulmonary tuberculosis with structural lung damage). Approximately 10-30% occur in immunocompetent individuals.
Clinical presentation is subacute (weeks to months) with productive or dry cough, fever, night sweats, weight loss, dyspnea, and pleuritic chest pain. Radiographic findings include solitary or multiple nodules with cavitation (over 50%), consolidation, abscesses, pleural effusion, and lymphadenopathy. Disseminated disease occurs in 20-50% of patients, especially in immunocompromised; CNS involvement (single or multiple brain abscesses) occurs in 20-40% (must perform brain MRI in all pulmonary cases). Skin involvement (10%) presents as nodules, abscesses, or sporotrichoid lymphocutaneous spread. Diagnosis requires direct microscopy of sputum or bronchoalveolar lavage with modified Kinyoun (modified acid-fast) staining showing branching beaded filaments, plus culture (Lowenstein-Jensen or Sabouraud media; growth slow, 5-21 days). Identification to species level (MALDI-TOF, 16S rRNA sequencing) and susceptibility testing guide therapy. Treatment of choice is high-dose trimethoprim-sulfamethoxazole (TMP-SMX, 15 mg/kg/day TMP component IV in divided doses) for severe disease, with combination therapy (imipenem + amikacin, or linezolid) for severe pulmonary or disseminated disease. Treatment duration is 6-12 months for pulmonary disease, 12 months for CNS involvement, and indefinite secondary prophylaxis in severely immunosuppressed patients.