Abstract
A 66-year-old Chinese man with chronic hepatitis B treated with tenofovir disoproxil fumarate, a history of liver transplantation approximately 17 months earlier, hypertension, and atrial fibrillation treated with apixaban presented with progressive weakness, weight loss, and inability to ambulate. His only anti-rejection agent was tacrolimus. One month earlier, he had been hospitalized for multifocal pneumonia and treated with intravenous piperacillin-tazobactam for seven days after outpatient cefdinir failed. He was discharged without antibiotics. Bronchoscopy showed no endobronchial lesions or mucosal abnormalities. The initial routine microbiologic results were negative, but mycobacterial cultures remained in prolonged incubation. After discharge but before his subsequent readmission, a sputum culture from the prior hospitalization identified Mycobacterium fortuitum. On readmission, he had profound hyponatremia with a serum sodium concentration of 105 mmol/L, requiring intensive care and hypertonic saline. Imaging showed progressive right upper lobe consolidation concerning for infection or malignancy. Several days into the readmission, a biopsy of a technically accessible right lower lobe nodule showed inflammation without malignancy or caseating granulomas. Shortly thereafter, a bronchoalveolar lavage culture obtained during the prior hospitalization identified Mycobacterium tuberculosis after prolonged incubation. Tissue culture from the lung biopsy later identified Nocardia beijingensis. Given the patient’s immunosuppression and progressive pulmonary abnormalities, all three isolates were treated as potentially pathogenic with imipenem, trimethoprim-sulfamethoxazole, moxifloxacin, isoniazid, pyrazinamide, and a rifamycin, with tacrolimus adjustment for drug interactions. The relative contribution of each organism could not be established with certainty. This case highlights the diagnostic and therapeutic complexity of concurrent pulmonary organism detection in a transplant recipient.