Gastrointestinal mucormycosis with no classical immunosuppression and the potential for Qat leaves chewing as an unidentified risk factor: a case report
This case describes gastric mucormycosis in a patient without profound immunosuppression but with severe physiological stress and chronic Qat exposure as well as a hypothesis-generating factor because of possible fungal contamination of leaves and repeated mucosal injury.
Abstract
Gastrointestinal mucormycosis is a rare, life-threatening invasive fungal infection that is often diagnosed late because of nonspecific clinical and endoscopic findings. Khat or Qat (Catha edulis) leaves may harbor environmental fungi, including Mucor species, and chronic chewing may contribute to gastrointestinal mucosal injury. However, a possible association between Qat use and gastrointestinal mucormycosis has not been established. We report a case of a 60-year-old man with diet-controlled type 2 diabetes mellitus and long-standing Qat chewing who was admitted after an out-of-hospital cardiac arrest secondary to acute myocardial infarction. He had no history of malignancy, transplantation, neutropenia, or immunosuppressive therapy. Return of spontaneous circulation was achieved after 34 min of cardiopulmonary resuscitation, followed by temporary venoarterial extracorporeal membrane oxygenation. On hospital day 14, coffee-ground material was observed through the nasogastric tube, accompanied by a decline in hemoglobin from 14.0 to 9.5 g/dL. Esophagogastroduodenoscopy revealed a fungating, ulcerated lesion involving the gastric fundus and body. Histopathological examination demonstrated extensive necrosis, angioinvasion, and broad, ribbon-like, pauci-septate fungal hyphae with irregular branching, consistent with gastric mucormycosis. Intravenous liposomal amphotericin B was initiated at 8 mg/kg/day. Gastrointestinal bleeding resolved without surgery. Repeat endoscopy one month later showed marked healing, and follow-up biopsy revealed no residual fungal elements. The patient completed six weeks of antifungal therapy and achieved clinical and histopathological resolution. Fungal culture and molecular identification were not performed, precluding species-level confirmation. In conclusion, this case describes gastric mucormycosis in a patient without profound immunosuppression but with severe physiological stress and chronic Qat exposure. Critical illness, gastric hypoperfusion, and mucosal disruption may have facilitated fungal invasion. Qat chewing is presented as a hypothesis-generating factor because of possible fungal contamination of leaves and repeated mucosal injury; nevertheless, causality cannot be inferred from a single case. Further microbiological and epidemiological studies are required to investigate this potential association.
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