Introduction

Sarcina is a gram-positive, anaerobic, but aerotolerant, nonmotile, and packet-forming coccoid bacterial organism within the family Clostridiaceae.^1–8 Sarcina can survive in a wide range of pH environments (from 1 to 9.8) utilizing carbohydrate fermentative metabolism as its sole source of energy to produce large amounts of gas.^4–11 Sarcina bacteria are spherical, 1.8 to 3 microns in diameter, and form characteristic tetrads or packets of eight or more cells, a diagnostic feature of mucosal colonization by histological examination.^5,7,8 An association between gastric colonization with Sarcina and gastric outflow obstruction, delayed gastric emptying, and gastritis leading to perforation and peritonitis has been proposed in human patients.^5,7,11,12 While the pathogenic contribution of Sarcina in human disease is incompletely known, in veterinary medicine, an association between Sarcina and spontaneous disease and experimentally-induced gastric dilatation (GD) and abomasal tympany leading to fatal emphysematous abomasitis is well established in young ruminants, including calves, lambs, and goat kids (Table 1).^4,6,10,13 In monogastric animals, an association between the presence of Sarcina and GD volvulus has been reported in dogs and in a horse with unresponsive acute colic and gastric reflux (Table 1).⁹ This case report presents the clinical and pathological findings and response to therapy in an adult cat with chronic enteritis that was presented with an acute onset of vomiting, GD, and confirmed gastric colonization by Sarcina-like bacteria.

TABLE 1 Reports of Gastric Colonization by Sarcina in Various Animal Species

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Case Report

An 11 yr old spayed female domestic longhair cat (5.1 kg) was referred after a sudden onset of vomiting and severe gastric distention on abdominal radiographs of 2 days duration. The cat lived indoors in New York City and had no recent travel history or contact with other animals, including farm animals. The cat was fed a commercial adult maintenance diet consisting of canned and dry food and had no history of prior medical problems. The cat had been seen by a primary care veterinarian the day prior to referral and the complete blood count, serum biochemistry profile, and serum thyroxine concentration were all within normal reference intervals (RIs).

On initial examination, the cat exhibited ptyalism and was mildly tense on abdominal palpation. The remainder of the physical examination and vital parameters were unremarkable. An abdominal ultrasound revealed a severely gas- and fluid-distended stomach without obvious signs of a gastric foreign body. A SNAP fPL^a was normal and nonsupportive of pancreatitis. A presumptive diagnosis of gastroparesis secondary to acute gastroenteritis was made, and the cat was treated with IV fluid^b, dolasetron^c (3 mg/kg IV q 24 hr), pantoprazole^d (1 mg/kg IV q 24 hr), cisapride^e (2.5 mg per cat by mouth q 8 hr), and mirtazapine^f (1.8 mg per cat by mouth q 24 hr). A nasogastric (NG) tube was placed to allow continuous gastric decompression.

During the initial 24 hr after presentation, 200 mL of gas and 30 mL of bile-tinged, turbid fluid were removed via the NG tube, and repeated abdominal ultrasounds revealed persistent GD. The decision to pursue esophagogastroduodenoscopy to evaluate the upper gastrointestinal tract was made. The esophagogastroduodenoscopy revealed small amounts of bile-tinged fluid within the gastric fundus. The gastric mucosa including the pyloric outflow tract were grossly normal and without notable mucosal ulceration or masses. The duodenal mucosa was mildly erythematous. Mucosal pinch biopsy specimens of the stomach (4 fundic and 7 pyloric) and duodenum (13 biopsies) were harvested and submitted for histopathological evaluation (Cornell University, Animal Health Diagnostic Center, Ithaca, New York). A serum sample was submitted for cobalamin and folate determination (Antech Diagnostics, Irvine, California). Continuous rate infusion of metoclopramide^g (2 mg/kg/day), maropitant^h (1 mg/kg IV q 24 hr), and ampicillin sodium-sulbactam sodiumⁱ (30 mg/kg IV q 8 hr) were added to the existing treatment plan to further assist with gastrointestinal motility, nausea, and potential underlying gastrointestinal bacterial infection, respectively. In addition, a continuous rate infusion of elemental enteral liquid feeding^j was initiated via the NG tube to provide adequate nutrition. After 24 hr, 6 mL of gas and 30 mL of brown fluid consistent with liquid nutrition medium were removed from the NG tube, and ultrasound examination confirmed reduced GD. Despite ongoing anorexia, the cat remained bright and comfortable, and vomiting stopped. The cat was subsequently discharged with the following oral medications: amoxicillin-clavulanic acid^k (62.5 mg per cat q 12 hr), ranitidine^l (1 mg/kg q 12 hr), metoclopramide^m (0.5 mg/kg q 8 hr), cisapride, and mirtazapine. The owner was instructed on home administration of elemental enteral liquid feeding (40 mL q 6 hr) via a NG tube.

The results of serum analysis indicated a low-normal cobalamin level (323 pg/mL, RI 290–1500 pg/mL) and low folate level (7.79 ng/mL, RI 9.7–21.6 ng/mL), suggesting ongoing underlying mid-to-distal small intestinal disease.¹⁴ Histopathological examination of routine hematoxylin and eosin–stained gastric biopsies revealed colonization of the superficial gastric mucosa by large numbers of Sarcina-like bacteria along with a few mixed bacterial rods without associated gastric mucosal inflammation (Figure 1). A modified Steiner’s silver histochemical stain and a tissue Gram stain of the gastric mucosal biopsies confirmed the presence of large numbers of gram-positive Sarcina-like bacteria along with a few gram-positive bacterial rods within the surface mucin and occasional gram-negative, spiral-shaped bacteria with a morphology consistent with Helicobacter-like organisms (HLOs) along the surface and extending for a short distance into gastric glands. The duodenal biopsies showed moderate numbers of lymphocytes and plasma cells together with occasional eosinophils and neutrophils within the villous and crypt lamina propria (Figure 2). A Masson’s trichrome histochemical stain of the duodenal biopsies revealed a band of fibrillar collagen within the lamina propria along the villus-crypt junction bridging adjacent villus-crypt units, a change consistent with chronic inflammation.¹⁵

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On reexamination 1 wk later, the patient showed remarkable clinical improvement with resolution of vomiting, increased appetite, and increased activity levels. No gastric changes including GD were found on an abdominal ultrasound. Ranitidine and cisapride were discontinued, and the NG tube was removed. Consistent with a recent case report of Sarcina gastritis in a human being, the amoxicillin-clavulanic acid therapy was also stopped.⁸ The dosage of metoclopramide was reduced to 0.5 mg/kg q 12 hr. A cyanocobalamin injectionⁿ (250 mcg) was administered subcutaneously, and the owner was instructed to continue with the cyanocobalamin once weekly for an additional 5 wk, then taper to once monthly. Oral supplementation with folic acid was recommended, but the owner was not compliant because of difficulty with administration. The owner was also instructed to start a hypoallergenic diet trial. At the 1-mo recheck examination, the owner reported recurrence of vomiting at a rate of once or twice a wk despite the cat having a good appetite and activity level. No evidence of GD was found on repeated abdominal radiographs and ultrasound examination. The decision was made to initiate treatment for chronic enteritis with oral prednisolone^o (1 mg/kg q 24 hr). At the 2-mo follow-up examination, the owner reported resolution of vomiting, and an abdominal ultrasound revealed a normal gastric profile. The owner was advised to continue with prednisolone and cyanocobalamin as previously directed. The metoclopramide was discontinued. The cat remained in good health on prednisolone and cyanocobalamin at the 3-, 4-, and 5-mo follow-up evaluations.

Discussion

To the authors’ knowledge, this is the first documented report of an association between the gastric colonization with Sarcina-like bacteria and GD and vomiting in an adult cat with chronic enteritis. Gastric dilatation is a condition typically seen in dogs with or without concomitant volvulus. Although the cause of GD is not completely understood, delayed gastric emptying, pyloric obstruction, aerophagia, and engorgement have been implicated alone or in combinations as contributing factors.¹⁶ Gastric dilatation is a rare condition in cats, and there have been only a few cases reported in the veterinary literature. Diaphragmatic hernia has been reported as the most common predisposing condition in cats with GD.¹⁷ In our case, GD was noted in a cat without evidence of foreign body, gastric outflow obstruction, or diaphragmatic hernia. Histopathological evidence of chronic intestinal inflammation together with the clinical response to steroid therapy suggested underlying inflammatory bowel disease in this cat.¹⁸ The only significant finding beside chronic enteritis was gastric mucosal colonization by large numbers of Sarcina-like bacteria in endoscopic gastric biopsies. It is suspected that chronic enteritis might have contributed to delayed gastric emptying, resulting in stasis and an environment favorable to Sarcina-like bacteria overgrowth and massive gas production from fermentation of gastric ingesta.¹⁹ Delayed gastric emptying leading to overgrowth of Sarcina has been suggested in humans presented with GD.^7,8,12 However, further experimental confirmation would be necessary in order to confirm an association between Sarcina-like bacteria and GD in cats.

There is a paucity of information regarding normal gastric microflora in cats. The only report of normal feline gastric microflora reveals Clostridium cluster I as the only clone identified by using comparative 16S ribosomal ribonucleic acid gene analysis of a stomach specimen taken from a specific pathogen-free cat.²⁰ Interestingly, it was noted that one of the clones identified in the small intestine of that study corresponded to Sarcina ventriculi (Clostridium subcluster Ia), confirming that Sarcina bacteria are part of the normal small intestinal microflora in cats.²⁰ Sarcina are ubiquitous bacteria that are widely distributed in the soil and thus can be ingested with plant material contaminated with soil particles.⁵ We speculate that colonization of the gastric mucosa by Sarcina-like bacteria in our cat might have been acquired by ingestion from the environment or resulted from translocation of small intestinal Sarcina-like bacteria by duodenal reflux associated with vomiting. Further studies are needed in order to determine the prevalence and extent of Sarcina colonization in the gastrointestinal tract of cats.

The currently published veterinary literature describing GD and abomasal tympany associated with the Sarcina organism is summarized in Table 1. In the only report of GD associated with Sarcina in a monogastric carnivore, large numbers of S. ventriculi were found within the mucus and gastric contents of two young adult dogs, both dying of GD volvulus.⁹ Conversely, the common occurrence of HLOs in the gastric mucosa of cats argues against these bacteria playing a role in the GD seen in our cat.^21,22 Consistent with a previous report in two human pediatric patients with Sarcina, and given the absence of significant inflammation of the gastric mucosa in our cat, the contribution of coinfection by HLOs in the pathogenesis of GD appears unlikely.¹²

Although specific therapies to control Sarcina have not been previously reported, oral administration of an antibiotic effective against anaerobes and antiulcer therapy have been recommended in humans with GD associated with Sarcina.^8,11 Of the reported human cases of GD associated with Sarcina, treatment with imipenem and combination therapy of metronidazole and ciprofloxacin was effective.^8,11 Further studies to determine the antimicrobial sensitivity pattern of Sarcina would assist with selection of specific antimicrobials effective against Sarcina. In our case, GD appeared to resolve when antibiotics were given; however, given that other medications were also administered, the resolution of GD might not be attributable to Sarcina antimicrobial therapy alone.

Conclusion

This case report presents clinicopathological findings in a mature cat with gastric colonization by Sarcina-like bacteria and an acute onset of vomiting and GD. Future controlled, prospective studies assessing colonization of the gastric mucosa of cats presented with vomiting and GD with Sarcina-like bacteria will provide additional insights into this newly identified and potentially significant disease association. Fulfilling Koch’s postulates by oral inoculation of specific pathogen-free cats with Sarcina-like bacteria followed by reisolation of the bacteria from the gastric mucosa of cats with clinical signs of GD would confirm the role of this agent in disease.