A 60-year-old African American male with a history of recently diagnosed focal segmental glomerulosclerosis on prednisone 60 mg daily, HTN, and diabetes mellitus type II, complicated by steroid-induced hyperglycemia, presented with one week of progressive dyspnea on exertion, nonproductive cough, and subjective fevers. Physical exam was notable for bibasilar rales and left lower lobe bronchial breath sounds. Labs showed leukocytosis to 21, 000 with 80% neutrophils and creatinine of 2.8, which was his baseline. Chest radiograph demonstrated perihilar infiltrates and left lower lobe consolidation. Despite 3 days of treatment for community acquired pneumonia and 2 days subsequent empiric therapy with atovaquone for PJP pneumonia, he was persistently febrile and short of breath.
Induced sputum grew PJP and gram positive, weakly acid-fast filamentous rods, consistent with Nocardia species. He received trial of trimethoprim-sulfamethoxazole, before eventual transition to linezolid and atovaquone because of worsening hyperkalemia and rising creatinine. On this regimen, fevers resolved after 2 days and complete resolution of respiratory symptoms was reported after 3 weeks.
Discussion:
Pulmonary nocardiosis is rare, but more prevalent in the immunosuppressed and poorly controlled diabetic populations. Delay in diagnosis is common, as it can be easily masked by co-infection with other pathogens. The diagnosis of nocardiosis is challenging and often requires bronchoscopy, as the organism is difficult to isolate and culture. Once the diagnosis is established, neuroimaging to rule out CNS involvement is recommended, as Nocardia has affinity for neural tissue. Treatment for Nocardia is equally difficult as there are no established recommendations for empiric therapy prior to speciation. A process that can take at least 2 weeks for this fastidious organism. Two agent therapy is recommended initially, such as trimethroprim-sulfamethoxazole plus amikacin. However, the patient’s kidney disease prompted our team to explore alternative therapies.
Conclusions:
Identifying the causative agent of pulmonary infections in the immunosuppressed can be difficult. Immunosuppressed patients may require early bronchoscopy to obtain an adequate specimen for culture, as the differential for pneumonia in these patients is broad. A delay in diagnosis and appropriate therapy is common. Respiratory symptoms can be masked by co-infection with other equally culpable infections, as in our patient’s case.