A case report reveals Clostridium difficile empyema in a patient without GI infection, indicating a unique infection pathway.
Introduction Clostridium difficile is a gram-positive bacterium commonly found in the gastrointestinal (GI) tract of the human body. To date, there are only a few case reports of pulmonary C. difficile infection (CDI), which is an uncommon complication of hematogenous dissemination from primary GI infection. We describe a rare case of empyema caused by C. difficile in a patient without GI infection or bacteremia. Case Presentation A 68-year-old male with chronic obstructive pulmonary disease and gastroesophageal reflux disease presented with one month history of dyspnea on exertion. On arrival, his vitals were notable for a blood pressure of 126/77 mmHg, a heart rate of 152 beats per minute, and a pulse oximetry reading of 80% on room air. His workup revealed acute distal pulmonary embolism of intermediate risk, deep vein thrombosis of the left femoral vein, and a loculated moderate left-sided pleural effusion. The patient was started on a heparin infusion, vancomycin, and piperacillin-tazobactam, and underwent a left small-bore chest tube insertion. The pleural fluid analysis showed a leukocyte count of 48 x 103/mm3 with 100% polymorphonuclear leukocytes, 5 mg/dL glucose, 3.1 g/dL of protein with pH of 7.1. His pleural culture returned positive for C. difficile. Interestingly, the patient denied a history of GI infection, diarrhea, recent antibiotic use, healthcare exposure, or recent GI surgery, and there was no evidence of bacteremia with sterile blood cultures. Initially, the patient did not receive intrapleural enzyme due to full anticoagulation in the setting of PE, but ended up getting 2 doses of dornase later. After his antibiotic regimen was switched to metronidazole, he was discharged after chest tube removal with resolution of his symptoms. Discussion The CDI involving the pleural space is extremely rare with only a dozen case reports existing in the literature globally. The common route of acquisition of infection is through hematogenous spread from the GI tract in the setting of fulminant infection or penetrating trauma or diaphragmatic injury, where the peritoneal fluid encounters the pleural fluid by fistula formation. Interestingly, the patient reported an aspiration event at home a month before presenting to the hospital; it is possible that he developed the infection in the setting of this aspiration, with risk further heightened by his pre-existing lung injury with COPD and chronic use of a proton pump inhibitor. However, the precise mechanism by which he developed C. difficile empyema remains unclear. This abstract is funded by: none
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