1710 Symptomatic Concomitant Sarcina Associated Erosive Esophagitis and Refractory Helicobacter pylori Gastritis

Abstract

INTRODUCTION: Sarcina is a gram-positive, non-motile, anaerobic cocci that was first identified in the gastric contents of humans by John Goodsir in 1842. Since then, its precise pathogenetic role in humans still remains unclear, as clinical observations have ranged from asymptomatic to life-threatening complications such as gastric perforation and emphysematous gastritis. Our review of literature yielded a total of 7 case reports which reported 8 patients with Sarcina on esophageal biopsies. Two of these had concomitant H. pylori gastritis. We report the third case of Sarcina of the esophagus associated with H. pylori gastritis. CASE DESCRIPTION/METHODS: A 70-year-old woman presented to the Gastroenterology clinic with an increase in abdominal discomfort, nausea, and vomiting over the past several months. She had previously been taking Omeprazole for reflux symptoms without relief and Naproxen for joint pain. She underwent an EGD, which showed erythematous mucosa in the distal esophagus, gastropathy, and a hiatal hernia. Targeted esophageal and gastric mucosal biopsies showed erosive esophagitis with many colonies of Sarcina species and chronic gastritis with H. pylori infection, respectively. Patient was prescribed tetracycline, metronidazole, and bismuth subsalicylate for two weeks and her omeprazole increased to twice daily for treatment of both infections. After completing the treatment regimen, the patient reported having little improvement in symptoms. Repeat EGD showed normal appearing mucosa of the esophagus, stomach, and duodenum. Esophageal biopsies showed normal squamous mucosa. Gastric biopsies showed persistent H. pylori gastritis. She was started on a salvage treatment regimen of levofloxacin, amoxicillin, and omeprazole for two weeks. Repeat testing was noted for persistent H. pylori infection. DISCUSSION: In our case, we treated our patient with antibiotics and a proton pump inhibitor, which covered for both Sarcina and H. pylori infections. However, minimal improvement in our patient's symptoms despite successful Sarcina eradication and persistent H. pylori infection suggests that although there was endoscopic and histologic evidence of esophagitis, the majority of patient symptoms were likely due to H. pylori or non-infective etiology. This finding supports those who favor Sarcina to being a benign pathogen in the GI tract. It is unclear if H. pylori gastritis in any way can be associated with Sarcina esophagitis, but this case definitely raises a question.