Sarcina Ventricularis Complicating a Patient Status Post Vertical Banded Gastroplasty: A Case Report

Shaun AC Medlicott, Fatin Adams

Shaun AC Medlicott, Department of Pathology and Laboratory Medicine, Rockyview General Hospital, University of Calgary, Calgary, Alberta, Canada
Fatin Adams, Department of Internal Medicine, Gastroenterology, Rockyview General Hospital, University of Calgary, Calgary, Alberta, Canada

Correspondence to: Shaun Medlicott MD, Rockyview General Hospital, Calgary Laboratory Services, Room 4N12, 7007, 14th Street SW, Calgary, Alberta, T2V 1P9, Canada.
Email: shaun.medlicott@cls.ab.ca
Telephone: +1-403-943-3584
Fax: +1-403-943-3333
Received: December 6, 2014
Revised: January 15, 2015
Accepted: January 21, 2015
Published online: February 21, 2015


Herein we describe the first case of Sarcina species identified on gastric biopsy material from a patient status post bariatric surgery. As Sarcina species is known to rarely behave as a pathogen, its presence is noteworthy. Our patient was treated with antibiotics with resolution of bacterial overgrowth on repeat biopsies.

Key words: Sarcina ventricularis; Bariatric surgery; Bacterial overgrowth

© 2015 The Authors. Published by ACT Publishing Group Ltd.

Medlicott SA, Adams F. Sarcina Ventricularis Complicating a Patient Status Post Vertical Banded Gastroplasty: A Case Report. Journal of Gastroenterology and Hepatology Research 2015; 4(2): 1481-1484 Available from: URL: http://www.ghrnet.org/index.php/joghr/article/view/950


Sarcina ventricularis is a known acid tolerant organism that rarely behaves as a pathogen, causing emphysematous gastritis and/or perforation[1-4]. A well documented predisposition to Sarcina species infection is overgrowth in the setting of gastroparesis or gastric outlet obstruction[2-5]. Approximately half of all reported Sarcina ventricularis cases diagnosed on gastric biopsy have complicated those individuals with histories of upper gastrointestinal surgery[2-4]. However, Sarcina ventricularis has yet to be documented in the bariatric surgery population. Herein we report the first case of Sarcina ventricularis overgrowth complicating a 53 year old female with probable diabetic gastroparesis, who is five years removed from a vertical banded gastroplasty procedure.


A 53 year old female presented with epigastric pain, post-prandial regurgitation and vomiting. In 2009 she had a vertical banded gastroplasty with a subsequent pouch ulcer diagnosed in 2011. She also has a history of a sliding hiatus hernia, irritable bowel, gastroesophageal reflux disease, diabetes, hypothyroidism and she is status post a remote cholecystectomy procedure. Present medications include: modulon, sulcrate, humalog victoza, synthroid and fenofibrate. She denies ethanol and illicit drug use.

She had an esophagogastroduodenoscopy which revealed abundant retained food in the distal stomach and polypoid mucosal lesions along the proximal- to mid-stomach staple line (Figure 1). A healed ulcer was evident in the pouch but no gastritis was noted. Endoscopic biopsies were procured from the antrum, body and polypoid lesions. Assessment of routine 4 µm hematoxylin and eosin stained slides revealed a mild chronic gastritis with rare organisms noted along the luminal surface of gastric body and polypoid mucosa (Figure 2). A gram stain proved the organisms to be gram positive cocci. There was negligible vital response to the organisms. No Helicobacter pylori, intestinal metaplasia or atrophy was identified.


The patient was empirically treated with motilium 10 mg twice daily. When Sarcina was delineated in the laboratory, metronidazole 500 mg three times daily was initiated. A repeat esophagogastroduodenoscopy was performed four months later. The proximal stomach anastomotic polyps persisted but had diminished in size. There was antral erythema of a linear antritis. Histology revealed reactive antral mucosa of a chemical gastropathy. All other mucosa was unremarkable including an absence of Sarcina and Helicobacter species.


Sarcina species was isolated as a human pathogen in 1842 by Goodsir[5]. The organism manifested as a profuse frothy and yeasty vomiting illness in the setting of pyloric obstruction[5]. Further study delineated positive Sarcina cultures almost exclusively in stool samples of healthy vegetarians compared to those who ate a mixed diet[6]. This finding collaborates with the natural history of Sarcina disease in livestock (goats, cows) and horses whose herbivorous diet presdisposes to abomasal bloat[7,8].

Sarcina ventricularis is a gram positive coccus, an obligate anaerobe with a carbohydrate fermentative metabolism and consequent vigorous gas (carbon dioxide) production[9]. The organism is exceptionally acid tolerant, growing in environments with a pH as low as 2[10]. It has distinct morphology on routine histologic stains allowing for a definitive diagnosis via microscopy[3,4]. Individual cells are 1.8-to-3 µm but replicate along at least two planes of growth resulting in tetrad or octet units, the former 8-to-10 µm[9].

There have been nine relatively recent publications in English literature of Sarcina ventricularis in the human upper gastrointestinal tract[1-4]. All patients were deemed to have gastric outlet obstruction or gastroparesis[1-4]. In particular, four patients had compromised gastric emptying due to previous surgical interventions including a Billroth II procedure and truncal vagotomy for recalcitrant ulcers, small bowel resection for malrotation, gastric pull through for esophageal atresia and a pancreaticoduodenectomy for pancreatic adenocarcinoma[2-4]. Our case is the fifth where Sarcina overgrowth complicates a patient with surgically altered gastroenteric anatomy (Table 1). Our patient is also predisposed to bacterial overgrowth in the stomach due to presumed diabetic gastroparesis.

Previous studies have delineated a management paradigm for Sarcina sp. The majority of cases represent an overgrowth of a commensal organism that potentially signifies an underlying anatomic and/or physiologic delay in gastric emptying[3,4]. Such cases may not require pharmacologic intervention. However, if Sarcina organisms are identified in a patient with prominent dysphagia or substernal burning, combined proton pump inhibitor and prokinetic therapy is indicated[3,4]. Finally, Sarcina organisms proliferating in an ulcerated or eroded stomach may cause sequela such as emphysematous gastritis or perforation[1,2]. In this setting, eradication of the organism by antibiotics is recommended[2,4]. Previous cases have been treated with either gentamycin and metronidazole or ciprofloxacin 250 mg twice daily and metrondiazole 250 mg three times daily[2,4]. As a healed ulcer was evident in our case, we decided to treat with metronidazole. Confirmation of Sarcina eradication warrants repeat endoscopy in three to six months[4].

Individuals with obesity, gastroparesis and/or metabolic syndrome have an increased prevalence of stomach and intestinal bacterial overgrowth[11,12,13]. This bacterial overgrowth can have deleterious consequences in the post-bariatric surgery population manifesting as liver toxicity and liver failure[14]. The bariatric procedure Roux-en-Y is associated with a transition to a lean weight microbiota profile in the stomach six months post-operation and may facilitate weight loss[15]. Proton pump inhibitor exposure may reverse this flora shift and propagate an obese microbiota profile, negating the benefits of surgical intervention[15].

Certainly the microbiota landscape in the surgically resected stomach has implications for patient outcome. Sarcina ventricularis is one known gastric commensal that rarely behaves as a pathogen in the setting of gastroparesis and/or outlet obstruction. In our patient, there was no deleterious outcome and the organism was eradicated by antibiotics. However, our case delineates that the bariatric surgery population is at risk for Sarcina overgrowth. Additional examples of overgrowth need to be analyzed to discern if Sarcina sp. modifies the trajectory of weight loss in this patient cohort. As this agent is known to cause emphysematous gastritis and perforation in the eroded or ulcerated stomach, clinicians should be mindful of this bacterium when surveilling their bariatric surgery patient population.


There are no conflicts of interest with regard to the present study.


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Peer reviewers: Timothy R. Koch, M.D., FACG, Professor of Medicine (Gastroenterology), Center for Advanced Laparoscopic & Bariatric Surgery, Washington Hospital Center, POB North, Suite 3400, 106 Irving Street NW, Washington, DC 20010, USA; Abdulzahra Hussain, General surgery department, Princess royal university hospital,Farnborough common, BR6 8ND, Orpington, Kent, UK.


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