S5099 Rare Sarcina and H. pylori Co-Infection in Gastric Outlet Obstruction Complicated by Perforation

Introduction: Sarcina ventriculi is an anaerobic Gram-positive bacterium associated with delayed gastric emptying and gastric outlet obstruction (GOO). While often considered a benign colonizer, it has been linked to complications such as emphysematous gastritis and perforation. Co-infection with H. pylori is exceedingly rare, and its clinical significance remains unclear. We present, to our knowledge, the first reported adult case of Sarcina and H. pylori co-infection in the setting of GOO complicated by perforation. Case Description/Methods: A 48-year-old woman with history of GERD and Barrett’s esophagus presented with nausea, vomiting, and 30-pound weight loss. Computed tomography (CT) showed a massively distended stomach with abrupt tapering at the pylorus. Esophagogastroduodenoscopy revealed complete circumferential pyloric obstruction with ulcerated, fibrotic, mass-like mucosa. Biopsies showed chronic active inflammation with ulceration, reactive changes, and no evidence of malignancy. H. pylori and Sarcina were identified on HandE stain. She was treated with intravenous proton pump inhibitors (PPI) and broad-spectrum antibiotics. She left against medical advice amidst surgical planning and returned days later with severe abdominal pain and pneumoperitoneum on x-ray. Emergent laparotomy revealed a small pyloric perforation for which she underwent distal gastrectomy and gastrojejunostomy. Surgical pathology revealed active serositis, chronic gastritis, and no evidence of malignancy. Sarcina was not detected, and H. pylori immunostain was negative. Discussion: While both H. pylori and Sarcina have been implicated in gastric ulceration and perforation, there are no prior reports of co-infection with both organisms leading to perforation in adults. Although the pathogenicity of Sarcina remains uncertain, its gas-forming nature, known to cause fatal bloating in animals, has been proposed as a mechanism for mucosal damage in humans. Sarcina in the setting of H. pylori infection may compound mucosal injury or impair healing. This case suggests Sarcina may serve as a marker of high-risk gastric stasis rather than a benign finding. Identification on biopsy should prompt consideration for antibiotics and PPI, though optimal regimens have not been established. Thorough evaluation for obstruction is essential, and early surgical consultation should be considered. Further research is needed to determine whether co-infection with Sarcina and H. pylori confers unique risk or simply reflects the need to treat H. pylori and address underlying impaired gastric motility.