GS28 - Sarcina Ventriculi: An Unusual Cause of Emphysematous Gastritis

Introduction/Purpose:
Sarcina Ventriculi, also known as Clostridium Ventriculi, is a non-motile, anaerobic, Gram-positive coccus (1) with distinct morphological features including a cuboid shape, tetrad arrangement, and basophilic staining (2) which is able to survive in low pH environments (3). This bacterium has been implicated in fatal epizootic neurologic and gastroenteric syndrome (ENGS) in chimpanzees (4), acute gastric dilatation (AGD) in canines (5), and gastric dilatation in felines (6).

There have been around 65 reported cases of Sarcina Ventriculi in humans (1), where it has been associated with emphysematous gastritis (7, 8, 9, 10), delayed gastric emptying (11), and fatal gastric perforation (12, 13). The exact pathogenesis is still unclear, however it has been suggested that concomitant conditions such as gastric outlet obstruction or delayed gastric emptying may promote the overgrowth of this bacteria, and the presence of concurrent gastric ulcers may lead to emphysematous gastritis or perforation (14). We report a case of Sarcina Ventriculi in the stomach of a Jehovah’s Witness patient with anemia and a recent laparoscopic cholecystectomy for gangrenous cholecystitis who presented with concerns for ischemic gastritis and emphysematous gastritis.

Methods or Case Description:
A 64-year-old male status-post laparoscopic cholecystectomy for acute gangrenous cholecystitis presented to the emergency department on post-operative day eight with epigastric pain, frequent bowel movements, nausea, and non-bilious emesis. The patient had a past medical history of hypertension, type 2 diabetes mellitus, and anemia in the setting of being a Jehovah’s Witness.

During the initial evaluation in the emergency room he admitted to having epigastric pain for at least one year prior to this admission. He denied any fevers, chills, hematemesis, hematochezia, chest pain, or any other symptoms. Physical exam findings included diffuse abdominal tenderness and well healing incisions from the laparoscopic surgery. There were no additional abnormal findings. His initial complete blood count showed a leukocytosis of 14.34 k/uL, decreased hemoglobin of 6.7 g/dL, a decreased hematocrit of 24.1%, a normal platelet count of 400 k/uL, and a normal PT INR of 1.1. CT of the abdomen and pelvis with IV contrast showed evidence of severe gastritis with pneumatosis suggesting ischemia or necrosis. General surgery was consulted which recommended admission for further evaluation of severe gastritis and pneumatosis possibly secondary to recent laparoscopic cholecystectomy.

Due to the patient’s religious beliefs as a Jehovah’s Witness and chronic anemia, general surgery recommended initial non-operative management of the patient’s condition. Erythropoietin 20,000 unit subcutaneous injections, twice daily oral ferric gluconate 325mg, and IV ferric gluconate 125mg were given and the patient’s hemoglobin remained stable, albeit low, between 5.8 g/dL to 7.6 g/dL throughout his hospital course. Gastroenterology was consulted and an esophagogastroduodenoscopy (EGD) was ordered which revealed patchy ulceration with bleeding on contact in the antrum of the stomach, lesser curvature of the body, and angular incisura but showed no overt evidence of gastric perforation. Tissue biopsies were taken and later revealed no evidence of intestinal metaplasia, dysplasia, or immunohistochemical staining for Helicobacter pylori; however Sarcina ventriculi was identified within the acute inflammatory exudate and determined to be the culprit for the patient's emphysematous gastritis.


Figure1. Coronal and Axial images from CT-abdomen/pelvis on February 11, 2022 demonstrating emphysematous gastritis, gastric wall thickening


Figure 2a, 2b. Upper endoscopy showing ischemic changes and friability of stomach


Figure 3. Pathology results from EGD biopsy demonstrating distinct morphological features of Sarcina Ventriculi


Figure 4. Coronal and Axial images from CT-abdomen/pelvis on February 16, 2022 demonstrating resolution of emphysematous gastritis following medical management of Sarcina Ventriculi infection



Outcomes:
The patient was treated initially with IV Zosyn 3.375g, IV clindamycin 600mg, IV vancomycin 1.25g and IV fluconazole 400mg for his leukocytosis, however clindamycin and vancomycin were discontinued. The patient remained on fluconazole and zosyn for the duration of his hospital course. He also received daily Sucrulfate 1 g tablets and pantoprazole 40 mg injections for ulcer prophylaxis. His white blood cell count trended down to 7.63 k/uL from 15.09 k/uL while on antibiotic therapy. On day four of his hospital course the patient had increasing abdominal pain, nausea, and emesis with oral intake, so a peripherally inserted central catheter (PICC) line was placed to start the patient on total parenteral nutrition (TPN). On day five of his hospital course repeat CT scan of the abdomen and pelvis with oral contrast showed interval improvement of wall thickening and mural edema involving the stomach, with interval resolution of foci of gas suggesting resolved pneumonitis.

After several days on TPN the patient began to clinically improve with no additional abdominal pain, nausea, or vomiting. The patient was weaned off TPN, advanced to a GI soft diet, and continued to receive IV antibiotics along with sucrulfate and pantoprazole. The patient tolerated the GI soft diet with good oral intake for two days and was cleared for discharge from a surgical perspective. The patient was discharged with oral amoxicillin-clavulanic acid 875-125mg twice a day for seven days per infectious disease recommendations.

Conclusion:
The pathogenic role of Sarcina Ventriculi in humans is not entirely understood, although reported cases have been increasing. It has been found in blood (15), esophageal, pyloric and duodenal brushings (16, 17), fine-needle aspirations of the stomach (18), and tissue biopsies of the stomach (19). It has been implicated in bacteremia (20), esophageal stricturing (21) along with emphysematous gastritis and fatal perforations as described previously, however there have also been cases of asymptomatic patients with Sarcina found on biopsy specimens (19, 22). How Sarcina is introduced into the body or why it causes fatal complications in some populations and not others needs to be further elucidated. Many of the cases cited in this report have also indicated delayed gastric emptying and concomitant candida infections in their patients with Sarcina which may play a role in its growth.

A systematic review of literature for Sarcina infections showed that out of 66 reported cases more than 53% received antimicrobial therapy, 20% of the cases received PPIs, and surgical treatment was warranted in 23% of cases (1). The surgical interventions included partial gastrectomy, fundoplication and hiatal hernia repair, perforation suture repair with Graham patch, jejunostomy, duodenal resection, ileocecal resection associated with ileostomy, and fistula excision (1). Further research is needed to understand the indications and contraindications for surgical and non-surgical intervention of Sarcina infections. A surgical role may be required for source control in cases of emphysematous gastritis with perforation. However in clinically stable patients non-operative management with nutritional support, optimization of intestinal motility, ulcer prophylaxis and antimicrobials may prove sufficient. Further research into ideal antimicrobials is needed, as different case reviews offer varying options. In our case surgical intervention was not pursued as the patient was clinically stable and the risks of surgery outweighed the benefits. Our patient showed improvement of symptoms and improvement on imaging with antimicrobials and PPI’s, which coincides with a majority of the cases reported in the literature.