Sarcina ventriculi: An incidental finding or a byproduct of a more concerning underlying disease?

Abstract

Sarcina ventriculi is a rare, acid-resistant, carbohydrate-fermenting, Gram-positive bacterium most often reported in the setting of delayed gastric emptying or gastric stasis and obstruction. Its clinical relevance is variable, ranging from incidental colonisation to potentially severe complications such as emphysematous gastritis and perforation. Diagnosis is typically suggested by the characteristic basophilic tetrads on routine hematoxylin–eosin staining. An 81-year-old male presented with a 3-month history of atypical epigastric pain, postprandial vomiting, and general deterioration. Initial laboratory evaluation showed severe anemia and an inflammatory response. Upper gastrointestinal endoscopy revealed a traversable ulcerated, exophytic antral lesion extending toward the greater curvature. Histopathology of multiple biopsies demonstrated a poorly differentiated gastric carcinoma with concomitant Helicobacter pylori infection and S ventriculi identified on hematoxylin–eosin slides. Contrast-enhanced CT confirmed a locally advanced antrum–pyloric tumor with nodal, hepatic, and peritoneal metastases T4N2M1 (according to the eighth edition of the AJCC TNM staging system). The patient received symptomatic management, Helicobacter pylori eradication therapy, and was referred for palliative oncologic care. He died shortly thereafter. The detection of S ventriculi on gastric biopsies should prompt clinicians to actively search for an underlying cause of gastric stasis or obstruction, including malignancy. Management should prioritise treatment of the precipitating condition. Antibiotic therapy for S ventriculi may be considered in symptomatic patients or when complications are suspected, and H pylori should be treated according to standard guideline-based regimens when present.

Case report

Patient information

An 81-year-old male patient weighing 70 kg (BMI 22.9) with a history of benign prostatic hyperplasia presented with atypical epigastric pain progressing over 3 months, associated with postprandial vomiting and deterioration in general condition, with unintentional weight loss of 5 kg. The patient reported no self-medication with proton pump inhibitors or NSAIDs, and no history of tobacco or alcohol consumption.

Clinical findings

Clinically, the patient was adequately hydrated, and his vital signs were stable: heart rate 80 bpm, respiratory rate 14 cpm, blood pressure 130/60 mmHg. Abdominal examination showed slight epigastric tenderness without palpable masses or other abnormalities.

Diagnostic assessment

An initial blood panel showed hypochromic anemia with hemoglobin 9.7 g/dL; MCV 80 fL; MCHC 29.6 g/dL and a mildly elevated CRP at 11.7 mg/L, associated with elevated tumor markers (CA 19-9: 66.0 U/mL; CEA: 9.9 µg/L). Ferritin was low at 13 ng/mL. Renal function panel showed a creatinine of 0.7 mg/dL and a BUN of 26 mg/dL. Liver function was not impacted, with no signs of cytolysis or cholestasis.

Given persistent postprandial vomiting and constitutional decline, an upper gastrointestinal endoscopy was performed after an overnight fast to optimize visualization. The examination showed a traversable, exophytic, ulcerated antral lesion extending toward the greater curvature; no signs of stasis were noted, likely due to fasting and frequent emesis. Multiple biopsies of the lesion were performed in addition to biopsies of the duodenum, antrum, and fundus.

Histopathology (Fig. 1) showed a poorly differentiated gastric adenocarcinoma, intestinal type, with concomitant Helicobacter pylori and Sarcina ventriculi colonies identified within the glandular lumen and lamina propria on hematoxylin–eosin–saffron stains (Fig. 2), grouped in packets of tetrads and octets of highly basophilic and moderately sized cuboid organisms. No special stains or immunohistochemistry were performed for the neoplasm or the infections due to their characteristic morphology. No specific signs of emphysematous gastritis were noted.

Fig. 1.

Carcinomatous tumour proliferation invading the submucosa. The neoplastic cells are mainly isolated or arranged in small aggregates. Their cytoplasm is abundant and eosinophilic, rarely clarified. The nuclei are large, ovoid and hyperchromatic, with irregular contours and prominent nucleoli (H&E ×400).

Fig. 2.

Tetrads of spherical, basophilic structures are present within the lamina propria (arrows), consistent with Sarcina ventriculi infection (H&E ×400).

Further imaging by contrast-enhanced CT scan (Fig. 3, Fig. 4) was consistent with a locally advanced antrum–pyloric tumor with 24-mm depth of invasion and a 59 mm longitudinal extent, coming into intimate contact with the left hepatic lobe, with metastases in segments III, V, and VI (Fig. 5). In addition, metastases were present in multiple lymph nodes of the gastric lymphatic system, the peri-gastric fat, and the peritoneum, with a suspicious sclerotic lesion suggesting secondary osseous involvement (Fig. 6). The tumor was staged as T4N2M1. Notably, despite the patient having fasted, the CT revealed gastric distension (Fig. 3, Fig. 4), and retained solid debris—objective signs of gastric retention that explained the permissive environment for S ventriculi (SV) overgrowth.

Fig. 3.

Axial contrast-enhanced CT demonstrating focal antropyloric gastric wall thickening (24 mm) associated with gastric distension (arrow).

Fig. 4.

Coronal contrast-enhanced CT showing antropyloric mass with marked gastric dilatation.

Fig. 5.

Axial contrast-enhanced CT showing profound gastric stasis with massive intraluminal retention associated with hepatic metastases (arrows).

Fig. 6.

Sagittal contrast-enhanced CT reconstruction demonstrating marked gastric distension with severe intragastric stasis and a focal sclerotic lesion within the L5 vertebral body suspicious for secondary osseous involvement (arrow).

Therapeutic intervention

Symptomatic management was initiated, including antiemetic therapy as needed. An intravenous omeprazole regimen of 20 mg twice daily for 14 days to reduce gastric acidity and promote mucosal protection. Antibiotic therapy was introduced with a dual purpose: amoxicillin (1 g intravenously twice daily for 7 days) was aimed at the associated bacterial findings in the setting of an obstructive gastric lesion and persistent vomiting. Subsequently, a standard Helicobacter pylori eradication regimen was added—clarithromycin 500 mg and metronidazole 500 mg twice daily for 7 additional days—based on local data showing acceptable eradication rates with this regimen. No SV-directed antibiotics were administered. Nutritional support and prokinetic therapy were not provided. The patient was referred to oncology for palliative-intent management.

Follow-up and outcomes

The case was managed with palliative intent after confirmation of metastatic disease. Clinical follow-up was limited due to advanced-stage malignancy. The clinical course was unfavorable, and the patient died 2 months after diagnosis.

Discussion

We present an 81-year-old man with metastatic gastric adenocarcinoma in whom SV was identified on gastric biopsy. This case illustrates a recurring pattern in the literature: SV as a histologic marker of impaired gastric emptying, with a potential underlying malignancy.

SV, also reported as Clostridium ventriculi, is a rare, anaerobic, Gram-positive coccus with a distinctive packet-like (tetrad/octet) morphology readily identifiable on routine hematoxylin–eosin staining. In clinical practice, SV should primarily be interpreted as a marker of impaired gastric emptying or gastric outlet dysfunction rather than an obligate pathogen, because it is most frequently encountered in settings where food retention and carbohydrate-rich substrates promote overgrowth [[1], [2], [3], [4]].

Although SV remains uncommon in humans, its clinical relevance spans a broad spectrum—from incidental colonization to severe, life-threatening presentations such as deep ulceration, emphysematous gastritis, and, rarely, perforation [1,2,5,6]. Consequently, when SV is reported on gastric biopsy, the key question is not simply “SV present or absent,” but rather “what is the underlying driver of gastric outlet dysfunction, and are there signs of mucosal or transmural injury [[2], [3], [4]]?”

From a diagnostic standpoint, histology remains the cornerstone. SV has a distinctive morphology, appearing as packets within surface mucus or luminal material, composed of tetrads or octets of cuboid-shaped, intensely basophilic organisms measuring approximately 2-3 μm, with frequent flattening of the cell walls at areas of intercellular contact. This morphology is typically easily recognizable on H&E slides and requires no special staining; molecular confirmation (e.g., 16S rRNA sequencing) may be reserved for selected scenarios (diagnostic uncertainty or research) but is not routinely necessary [[1], [2], [3], [4],7]. A key pitfall is over-attribution—assigning symptoms to SV alone—when the underlying cause of stasis (tumor, stenosis, gastroparesis) is often the dominant driver of the clinical presentation [[2], [3], [4]].

What this case adds

In our patient, the clinical picture of postprandial vomiting, epigastric pain, weight loss, and iron-deficiency anemia pointed toward a structural lesion. Endoscopy confirmed an ulcerated, budding antral process extending toward the greater curvature. Importantly, no endoscopic signs of food retention were noted. This was explained by the fasting required for the procedure and the patient’s frequent vomiting, which mechanically emptied the stomach before visualization. The absence of stasis at endoscopy does not exclude it as the underlying mechanism; rather, it illustrates how clinical context must override a single negative intraprocedural finding.

Radiologic correlation

In our case, endoscopy with biopsy was performed first, establishing the diagnosis of adenocarcinoma and identifying SV. CT subsequently confirmed metastatic dissemination (T4N2M1) and, importantly, revealed objective signs of gastric stasis, that being gastric distension and retained solid debris despite a fasting state, which explained the permissive environment for SV overgrowth. The absence of endoscopic stasis, therefore, does not contradict the CT findings; rather, it reflects the intermittent relief of stasis by fasting and vomiting, while CT captured the persistent functional defect.

Even when endoscopy does not reveal an obvious malignancy, the presence of SV should raise suspicion for occult gastric stasis and its causes. In such cases, contrast-enhanced CT should be reviewed for signs of retention: gastric distension, retained solid food or debris in a fasting patient, delayed passage of oral contrast, or layering of particulate material in the dependent stomach. When mechanical obstruction is present (as here, with an antro-pyloric tumor), CT will often show wall thickening, luminal narrowing, and proximal dilatation. When no obstruction is found, functional gastroparesis should be considered, and gastric emptying scintigraphy is the next appropriate step.

SV and upper gastrointestinal neoplasia

A recurring and clinically important observation is the codetection of SV in patients with upper gastrointestinal neoplasia. Multiple reported cases (Table 1) associate gastric adenocarcinoma with SV, usually in the setting of gastric outlet obstruction or delayed gastric emptying. Endoscopically, lesions ranged from pyloric ulcers to obstructive masses. SV was identified in these cases, sometimes with concurrent H pylori infection, suggesting that identification of SV in gastric biopsies should prompt careful evaluation for an underlying neoplastic process, particularly when imaging shows profound gastric retention [2,[8], [9], [10], [11], [12]]. Causality between SV and carcinogenesis is unproven, and the most parsimonious explanation is that SV behaves as an opportunistic organism thriving in a stasis-prone environment created by mechanical obstruction or dysmotility [1,2,4]. Nevertheless, several reports emphasize an important practical implication: SV may act as a “red flag” histologic clue prompting renewed suspicion of an underlying malignancy or obstructive process when symptoms suggest retention or when initial endoscopic sampling is suboptimal [11,12]. From an anatomic pathology perspective, explicitly documenting SV in the report is clinically useful because it can trigger reassessment of gastric emptying, reinforce the need for adequate and repeated sampling when warranted, and sharpen the clinician’s focus on obstruction-related complications [3,4,11,12].

Table 1.

Published reports of SV detected with upper gastrointestinal neoplasia.

Source	Neoplasia context	Endoscopic context	Histology/ microbiology	Treatment	Follow-up/outcome
Bhagat et al. [9]	Gastric adenocarcinoma	Pyloric ulcer (obstructive context)	Adenocarcinoma + SV	NR	NR
Darch et al. [8]	Adenocarcinoma causing obstruction	Obstructive context; stomach/duodenum sampled	SV in stomach/duodenum samples	NR	NR
Marampudi et al. [10]	Gastric adenocarcinoma	Case abstract	SV with gastric adenocarcinoma	NR	NR
Ugarte Bilbao et al. [11]	Underlying neoplasia (2 patients)	Persistent retention; repeat endoscopy	Gastritis + SV	Antibiotics reported	Triggered further work-up
Skowronek et al. [12]	Gastric carcinoma	SV framed as a warning sign	SV + gastric carcinoma	NR	NR
Our case, 2025	Poorly differentiated infiltrating gastric adenocarcinoma with metastases	Ulcerated budding antral lesion extending to the greater curvature	Poorly differentiated adenocarcinoma with Hp + SV on H&E	Hp eradication + supportive/palliative orientation	Unfavourable course driven by metastatic disease

NR, not reported.

Treatment: Prioritising the underlying cause

Across reviews and case reports, the most consistent principle for managing SV is that treatment should prioritize correction or palliation of the underlying cause of delayed gastric emptying or obstruction, with rapid escalation only if severe mucosal injury or emphysematous change is suspected [2,[4], [5], [6]]. In our patient, the dominant clinical driver was the malignant antro-pyloric obstruction. Given metastatic dissemination, management was palliative from the outset.

What remains less certain is whether relieving stasis alone—without antibiotics—consistently eradicates SV. The available evidence is mixed. In a 2020 case by Heidinger et al. [13] a patient with delayed gastric emptying and SV was treated with a proton pump inhibitor and the prokinetic agent domperidone. Symptoms improved, gastric emptying normalized, yet follow-up biopsy 15 months later still demonstrated persistent SV colonization [13]. This case demonstrates that improving stasis does not guarantee microbial clearance. Conversely, a 2023 report by Mohamed et al. [14] described a patient with gastric outlet obstruction and SV in whom antibiotics (ciprofloxacin and metronidazole) failed to improve symptoms. However, a subsequent distal gastrectomy with Roux-en-Y reconstruction led to clinical resolution [14]. The authors concluded that surgical relief of mechanical obstruction was the definitive intervention.

Taken together, these reports support a nuanced conclusion: relieving stasis is the therapeutic priority, but it should not be assumed to clear SV. In most cases, SV represents colonization rather than true infection, and no specific antimicrobials are required in the absence of severe mucosal injury or emphysematous change [2,5,6]. When dangerous complications are present—deep ulceration, emphysematous gastritis, perforation risk—broad-spectrum antibiotics with robust anaerobic coverage (e.g., metronidazole-based regimens) are warranted regardless of the underlying stasis cause [2,5,6].

In our patient, as detailed in the case report, symptomatic support, acid suppression, and H pylori eradication were provided. No specific anti-Sarcina therapy was intentionally prescribed, consistent with the view that SV represents colonization rather than true infection in the absence of severe mucosal injury [2,5,6]. The patient died 2 months later from metastatic disease. SV’s independent contribution to his symptoms could not be isolated—but its presence served its most important function: as a histologic red flag pointing toward the underlying malignancy.

Conclusion

SV is an uncommon finding on gastric biopsies and should be interpreted primarily as a marker of delayed gastric emptying or mechanical obstruction rather than an independent pathogen. Its presence likely reflects an underlying stasis-prone environment and should prompt clinicians to actively search for the precipitating cause, including malignancy, while also evaluating for complications such as deep ulceration or emphysematous gastritis. Management should primarily focus on treatment of the underlying condition; antibiotics may be considered on a case-by-case basis in symptomatic or complicated presentations, and concomitant H pylori infection, when present, should be treated according to standard guideline-based eradication regimens. In our patient, SV did not cause the disease, but it correctly pointed toward it.

Patient consent

Written informed consent for publication of this case report and accompanying images was obtained from the patient.