Introduction

Gastrointestinal infections caused by uncommon organisms can present with subtle or misleading clinical findings, often mimicking more common diseases such as malignancies or inflammatory conditions.

Among these, Sarcina ventriculi and mucormycosis represent two rare but clinically significant pathogens. Sarcina ventriculi, a gram-positive, obligate anaerobic coccus, is typically identified histologically by its distinctive tetrad or octet morphology. Though it may be a commensal in some individuals, it has been increasingly recognized in association with delayed gastric emptying, gastric ulcers, emphysematous gastritis, and perforation.[1], [2]

Mucormycosis, a life-threatening fungal infection caused by Mucorales species, is most frequently observed in immunocompromised hosts.[6],[7] Gastrointestinal involvement is particularly rare, often presenting with nonspecific symptoms and overlapping radiological features that simulate malignancy. This report presents two cases: Gastric Sarcina infection and Colonic Mucormycosis, highlighting the pivotal role of histopathology in identifying these rare entities and guiding optimal therapeutic intervention.

Case Report: 1

A 39-year-old male presented with persistent abdominal pain and discomfort of one year's duration. Esophagogastroduodenoscopy revealed duodenal and antral ulcers. Multiple grey-white mucosal biopsies were obtained and submitted for histopathological examination.

Microscopy revealed areas of ulceration with necrotic debris and dense neutrophilic infiltrates. The granulation tissue beneath showed reactive nuclear changes in stromal cells, accompanied by lymphocytic and neutrophilic infiltration. Within the inflammatory exudate, small, basophilic, spherical microorganisms arranged in tetrads were identified, morphologically consistent with Sarcina ventriculi. The organisms exhibited the characteristic refractile appearance with a cuboid structure and size approximating that of red blood cells. Coexistent colonization by Helicobacter pylori was noted. No features of malignancy were identified.

Figure 1: (a) & (b): Esophagogastroduodenoscopy of gastric body & antrum shows multiple 0.25-0.5cm slough-covered ulcers. (c) Basophilic-stained and spherical-shaped sarcina organisms arranged in tetrad packs adjacent to ulcer bed[ H&E stain, 10x magnification] (d) Small spherical microorganisms arranged in tetrads within inflammatory exudate, with flattened thick cell walls at points of contact with adjacent cells [ H&E stain, 40x magnification]

Discussion

Sarcina ventriculi was first described in 1842 by Goodsir and can be identified on hematoxylin and eosin (H&E) stained sections as cuboid basophilic cells in tetrad or octet formations. It ferments carbohydrates to produce acetaldehyde, ethanol, hydrogen, and carbon dioxide.[2], [3]

The organism thrives in acidic, anaerobic environments and is often found in patients with delayed gastric emptying due to diabetic gastroparesis, gastric surgery, or pyloric stenosis. It is typically located on the mucosal surface, embedded within gastric mucin or necrotic debris, without invading underlying glands.[2], [3]

Although Sarcina is occasionally found incidentally, its association with severe gastric complications such as emphysematous gastritis, food bezoars, and perforation necessitates its reporting when observed histologically.[2],[4],[5] Historically, the presence of sarcinous vomiting, persistent, frothy emesis was associated with Sarcina overgrowth.[4], [5]

In the present case, the tetrad arrangement, flattened cell walls, and basophilic staining supported the diagnosis of Sarcina ventriculi. Co-infection with Helicobacter pylori may exacerbate mucosal damage.[4] Despite its distinct morphology, Sarcina is often confused with Micrococcus species; however, the latter are smaller, catalase-positive, and aerobic. Sarcina maxima lacks the thick extracellular cellulose layer found in S. ventriculi.[4] Molecular identification through 16S rRNA and pyruvate decarboxylase gene sequencing offers definitive confirmation but remains largely unavailable in routine settings.[1], [3], [5]

Mucormycosis, caused by Mucorales such as Rhizopus, Mucor, Lichtheimia, and Rhizomucor, is an angioinvasive fungal infection with a high mortality rate.[6], [7], [9]While rhinocerebral and pulmonary forms are more prevalent, gastrointestinal mucormycosis constitutes only about 7% of cases.[7,8]Among GI cases, the stomach is the most frequently affected site (57.5%), followed by the colon (32.3%) and ileum (6.9%).[7] The disease is most often seen in immunocompromised individuals, particularly those with uncontrolled diabetes, hematologic mali-gnancies, or post-transplant immunosuppression.[6], [7],[8], [9]