Introduction: Gastric perforation is most commonly caused by peptic ulcer disease, malignancy, or trauma. Isolated gastric candidiasis leading to perforation is an exceptionally rare event, almost exclusively reported in severely immunocompromised hosts. We present a case of peritonitis secondary to Candida -mediated gastric perforation in a patient with no identifiable immunodeficiency. Case presentation: A 25-year-old previously healthy man presented with a 2-day history of acute-onset, severe epigastric pain, and signs of peritonitis. He reported no history of antibiotic exposure, smoking, alcohol, nonsteroidal anti-inflammatory drug (NSAID) use, peptic ulcer disease/proton pump inhibitor use, or any immunocompromising conditions. Laboratory findings revealed leukocytosis. An upright abdominal X-ray demonstrated free subdiaphragmatic air, consistent with a hollow viscus perforation. An urgent exploratory laparotomy revealed a 1.5 cm perforated ulcer on the pre-pyloric region. A modified Graham patch repair was performed. Intraoperatively, a full-thickness biopsy of the ulcer margin was taken for histopathological examination. The pathology report revealed necrotic tissue with invasive fungal hyphae morphologically consistent with Candida species invading the gastric wall. There was no evidence of malignancy, Helicobacter pylori -like organisms, or features of chronic peptic ulcer disease. Postoperatively, an infectious disease workup was initiated, which found no evidence of underlying human immunodeficiency virus, diabetes mellitus, or neutropenia. The patient was successfully treated with appropriate antifungal therapy and made a full recovery. Discussion: Primary invasive gastric candidiasis resulting in perforation is exceptionally rare in immunocompetent hosts, with only sporadic cases reported in the literature. Although Candida colonizes 20–40% of benign gastric ulcers, true tissue invasion is uncommon and requires disruption of mucosal integrity allowing yeast-to-hypha transition – the critical step enabling deep tissue penetration. This case is notable because the patient lacked classic risk factors including immunosuppression, NSAID use, or chronic illness, yet presented with acute peritonitis from a 1.5 cm perforated ulcer demonstrating invasive hyphae on histopathology. The diagnostic ambiguity of fungal perforation, which is radiologically and intraoperatively indistinguishable from peptic ulcer disease, underscores the critical importance of routine biopsy and special staining (periodic acid–Schiff/Gomori’s methenamine silver) of perforation margins. Early surgical source control combined with targeted antifungal therapy resulted in complete recovery. Conclusion: This case highlights that invasive gastric candidiasis can be a primary cause of life-threatening complications like perforation and peritonitis in immunocompetent individuals. It should be considered in the differential diagnosis of spontaneous gastric perforation, even in the absence of classic risk factors. Histopathological evaluation of perforation margins is crucial for diagnosis and guiding appropriate antifungal therapy.
Memon et al. (Tue,) studied this question.