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Sarcina ventriculi: Review of the Literature.

Sarcina ventriculi is a gram-positive, anaerobic coccus that can grow in acidic environments, (1) with a carbohydrate fermentative metabolism as its sole energy source. (2) It was first identified as a human pathogen by Goodsir (3) in 1842, which was followed by a few early reports of its presence in the human stomach. (4) However, since then, there have been only 19 cases of S ventriculi (Table 1) reported in the English literature, to our knowledge, and almost all of those cases were reported within the past 5 years. Importantly, S ventriculi accompanies delayed gastric emptying (5,6) and is thought to cause emphysematous gastritis (7) and perforation. (8) This review of the literature discusses the clinical features, endoscopic findings, histopathology, ancillary studies, microbiology, pathogenesis, differential diagnosis, treatment, and prognosis of this rare, but increasingly common, bacterium based on 19 published cases.


Sarcina ventriculi occurs mainly in adults (Table 2) but has been identified in an age range from 3 to 73 years. It occurs more often in women than it does in men, with 13 of the reported 19 cases (68%) in women, resulting in a female to male ratio of slightly more than 2:1. Although the race of the patient was not documented in most articles, there is at least one report identifying patients as Hispanic, (8) white, (9) and African American. (10) More than one-half of the patients (11 of 19; 58%) had a history of gastrointestinal surgery, gastroparesis, and/or gastric outlet obstruction. S ventriculi is also reported to present in association with acute, life-threatening complications, such as gastric perforation8 and emphysematous gastritis. (7) In addition, it has been identified in the stomach of patients with gastric adenocarcinoma and pancreatic adenocarcinoma. (5)

The earliest clinical observations of patients with this organism led to the term sarcinous vomit, which described a characteristic, obstinate, frothy vomit in patients with chronic disease of the stomach. (6) Clinically, as shown in Table 2, most patients present with gastrointestinal symptoms, such as nausea, vomiting, and/or abdominal pain. (5,11) However, the patients may be asymptomatic, and the bacterium may present as an incidental finding in a gastric biopsy (12) or with more worrying symptoms, such as melena (3 cases; 15.8%), hematemesis (2 cases; 10.5%), and weight loss. During endoscopy, the most consistent feature is the presence of food bezoar (9 cases; 47.4%) because of the delayed gastric emptying, which is often accompanied by an inflamed and/or ulcerated gastric mucosa (12 cases; 63.2%).


Classically, S ventriculi is identified by light microscopy in a gastric biopsy specimen with the following characteristic morphologic features: (1) basophilic staining with hematoxylin-eosin (11,12); (2) cuboid shape13; (3) 1.8 to 3 [micro]m individual size, (5) or packets approximately the size of a red blood cell11; (4) a tetrad packet arrangement (14) (Figure, A), which is a result of the replication occurring in at least 2 planes of growth (5); (5) flattening of the cell walls in areas of contact with adjacent cells (8); and (6) its refractile nature, which can mimic vegetable matter. (5)

The organisms are generally located near the mucosal surface in the gastric mucin (Figure, B), rather than in the gastric pits, and are not invasive. (11) The histologic features of the gastric mucosa can vary, ranging from being fairly unremarkable (3 cases, 15.8%) in some patients (15,16) to displaying diffuse, acute hemorrhagic gastritis with ulceration in others. (8) Given that there are no consistently associated histologic features in the gastric mucosa, a high level of suspicion is necessary, particularly when examining gastric biopsies from patients with a history of gastrointestinal surgery or delayed gastric emptying.

Regarding its relationship to Helicobacter pylori, only Sauter et al (11) identified the concurrent presence of H pylori and S ventriculi in the same specimen, whereas Haroon Al Rasheed et al (12) reported the presence of S ventriculi after treatment of H pylori, raising the interesting possibility of S ventriculi and H pylori being mutually exclusive. However, case reports have identified S ventriculi as occurring concurrent with other organisms, particularly Candida spp (2 cases, 10.5%). (7)


Sarcina ventriculi is typically diagnosed with a hematoxylineosin stain and, if needed, with a Gram stain, which stains strongly positive. However, the organism can also be confirmed at a molecular level by polymerase chain reaction and sequencing of the 16S ribosomal RNA (rRNA) gene and pyruvate decarboxylase gene. The 16S rRNA gene is highly conserved within the different species of bacteria and is, therefore, commonly used to classify and identify organisms. The 16S rRNA gene of each bacterial species is unique, so once it is sequenced, the 16S rRNA gene can be compared with validated gene-sequence databases to identify the specific bacterium. In addition, the pyruvate decarboxylase protein is involved in a rare metabolic pathway present in only a few bacterial species, including S ventriculi. (5)

These findings were demonstrated by Lam-Himlin et al, (5) who designed 2 sets of primers using sequence data from GenBank to target proximal, mid, and terminal regions of the 16S rRNA gene (AF110272.1) and the pyruvate decarboxylase gene (AF354297.1) of S ventriculi. According to the article, (5) S ventriculi was identified as present only with histologic evidence, a positive polymerase chain reaction result, and sequencing for both regions of pyruvate decarboxylase and at least one region of 16S rRNA. (5) Similarly, polymerase chain reaction and DNA sequencing for the pyruvate decarboxylase gene was used by Sauter et al (11) for positive identification of S ventriculi. Both studies successfully provided molecular confirmation in nearly all the histologically suspected cases and provided support for an accurate diagnosis being based on histology alone.


Sarcina ventriculi is a gram-positive, nonmotile, chemoorganotrophic, anaerobic coccus with an exclusive carbohydrate fermentative metabolism. The main products of carbohydrate fermentation are ethanol, acetaldehyde, carbon dioxide, and hydrogen. (8)

Sarcina ventriculi was first isolated in pure culture from the stomach in 1911, using strict anaerobic techniques. (17) Sarcina ventriculi has also been reported in the feces of healthy humans, particularly those with vegetarian diets. (18) The organism can normally be found in the soil and air, where it can survive for years by forming spores at alkaline pH. (1) Sarcina species, whose natural habitat is the soil, is probably ingested with soil particles present in the food. (13) Various reports in veterinary literature have implicated the Sarcina species in the development of gastric dilatation (19) and death in livestock, cats, and horses. (20-22)

There are conflicting reports on whether this organism is found in healthy human stomachs. Some authors favored this theory, (23) whereas others, such as Canale-Parola, (13) suggest that, although it was originally observed in stomach contents, this organism is not found in the healthy human stomach. Growth of S ventriculi takes place in the human stomach because of delayed gastric emptying from pathologic conditions such as diabetic gastroparesis, gastric surgeries, scarring, pyloric stenosis, (13) or an obstructing mass. With these diseases, the acidic pH of the stomach, and the presence of carbohydrates and other growth nutrients contained in food, S ventriculi thrives and multiplies rapidly. (13) Only 2 cases (10.5%) had severe complications, such as emphysematous gastritis and peritonitis, and both patients had underlying ulcers. Therefore, Lam-Himlin et al (5) suggested that a preexisting mucosal defect provided the nidus for emphysematous gastritis to develop, rather than direct invasion of Sarcina species into the gastric wall. Although the role of S ventriculi as the mechanism of mucosal injuries in these cases is not clear, the local accumulation of acetaldehyde and ethanol formed from carbohydrate fermentation by the organism could induce stomach and duodenal injuries, similar to the acetaldehyde-induced mucosal injuries in acute alcohol ingestion. Furthermore, the carbon dioxide production from glucose fermentation and pyruvate metabolism results in abdominal distention in some of these patients. (8)


The tetrad or packet-forming arrangement is not unique to Sarcina organisms, and the main differential diagnosis upon light microscopy is with Micrococcus species, which is also a gram-positive coccus that occurs in tetrads or packets. (13) However, a few features are helpful in differentiating the 2 organisms: histologically, at 0.5 [micro]m, the Micrococcus species are considerably smaller than the Sarcina bacterium and, unlike the Sarcina species, the Micrococcus species tends to form tightly packed clusters. (5) In addition, Micrococcus bacterium yields positive catalase results, (24) is aerobic, and does not form spores, in contrast to S ventriculi, which is catalase-negative, anaerobic, and spore forming. (13)

Other differential diagnoses for S ventriculi are Sarcina maxima and Staphylococcus species. The most helpful feature in light microscopy to differentiate S ventriculi from S maxima is the thick extracellular layer present on the outer surface wall of S ventriculi, which is not observed in S maxima. This layer generally measures 150 to 200 nm in thickness and is composed of mostly of cellulose or a closely related compound. (13) The thick layer is the result of the refractile nature of the cell wall, which has caused S ventriculi to be mistaken for a fungus or vegetable matter.10 Sarcina bacteria can be differentiated from Staphylococcus species, even though both organisms are gram positive, because Staphylococcus bacteria, at approximately 1 [micro]m in diameter, is much smaller and is arranged in characteristic grapelike clusters, rather than a tetrad pattern. (25)


The recent increase in reports of Sarcina organisms supports the observation by Sopha et al (10) underscoring the need to define a standard regimen for its treatment. Current reports indicate successful eradication of the organism, with treatment usually consisting of metronidazole in combination with another antibiotic (8,16) and/or a gastrointestinal agent. (22,26) However, as evident in Table 1, there is no consensus on the type and duration of treatment. Medlicott and Adams (26) outlined a treatment approach based on the clinical status of the patient. If the patient is clinically stable and healthy, they suggested it was reasonable to forego treatment because the organism can occur commensally. If, however, the patient is symptomatic, particularly with prominent dysphagia or substernal burning, treatment with a proton pump inhibitor and a prokinetic was indicated. If there is evidence of associated gastric erosion or similar acute conditions, eradication of the organism with antibiotics was recommended. (26) However, there is little to no data on the efficacy of the various treatment regimens. The treatment provided in the few reports with follow-up data (n = 12; 63%) are listed in Table 1, with subsequent improvement in symptoms and histology, (5,22) and the organism was never reidentified in any of the cases.


In conclusion, S ventriculi is an increasingly common, gram-positive bacterium, seen predominantly in patients with delayed gastric emptying. Presence of S ventriculi has been associated with cases of gastric perforation and emphysematous gastritis, and although the pathogenicity of this organism is not entirely certain, its recognition in an endoscopic biopsy raises important diagnostic and therapeutic considerations. (27) Because Sarcina organisms are difficult to grow on cultures in general laboratories and molecular methods of confirmation are not available in many parts of the world, histopathologic examination for the classic morphologic features remains a key to the diagnosis until specific microbiologic diagnostic methods become available.

Mohamed Rizwan Haroon Al Rasheed, MBBS; Carmencita G. Senseng, MD

Accepted for publication April 6, 2016.

From the Department of Pathology, University of Illinois, Chicago (Dr Haroon Al Rasheed); and the Department of Pathology, John H. Stroger Jr Hospital of Cook County, Chicago (Dr Senseng).

The authors have no relevant financial interest in the products or companies described in this article.

Reprints: Mohamed Rizwan Haroon Al Rasheed, MBBS, Department of Pathology, University of Illinois, 840 S Wood St, Ste 130 CSN, Chicago, IL 60612 (email: or


(1.) LoweSE, Pankratz HS, Zeikus JG. Influence of pH extremes on sporulation and ultrastructure of Sarcina ventriculi. J Bacteriol. 1989;171(7):3775-3781.

(2.) Claus D, Wilmanns H. Enrichment and selective isolation of Sarcina maxima Lindner. Arch Microbiol. 1974;96(3):201-204.

(3.) Goodsir J. XXIII: history of a case in which a fluid periodically ejected from the stomach contained vegetable organisms of an undescribed form. J Nat Hist. 1843;11(68):125-126.

(4.) Burget GE. Note on the flora of the stomach. J Bacteriol. 1920;5(3):299-303.

(5.) Lam-Himlin D, Tsiatis AC, Montgomery E, et al. Sarcina organisms in the gastrointestinal tract: a clinicopathologic and molecular study. Am J Surg Pathol. 2011;35(11):1700-1705.

(6.) Ferrier D. The constant occurrence of Sarcina ventriculi (Goodsir) in the blood of man and the lower animals: with remarks on the nature of sarcinous vomiting. Br Med J. 1872;1(578):98-99.

(7.) Laass MW, Pargac N, Fischer R, Bernhardt H, Knoke M, Henker J. Emphysematous gastritis caused by Sarcina ventriculi. Gastrointest Endosc. 2010; 72(5):1101-1103.

(8.) Tolentino LF, Kallichanda N, Javier B, Yoshimori R, French SW. A case report of gastric perforation and peritonitis associated with opportunistic infection by Sarcina ventriculi. Lab Med. 2003;34(7):535-537.

(9.) Berry AC, Mann S, Nakshabendi R, Kanar O, Cruz L. Gastric Sarcina ventriculi: incidental or pathologic? Ann Gastroenterol. 2015;28(4):495.

(10.) Sopha SC, Manejwala A, Boutros CN. Sarcina, a new threat in the bariatric era. Hum Pathol. 2015;46(9):1405-1407.

(11.) Sauter JL, Nayar SK, Anders PD, D'Amico M, Butnor KJ, Wilcox RL. Coexistence of Sarcina organisms and Helicobacter pylori gastritis/duodenitis in pediatric siblings. J Clin Anat Pathol (JCAP). 2013;1(1):1-3.

(12.) Haroon Al Rasheed MR, Kim GJ, Senseng C. A rare case of Sarcina ventriculi of the stomach in an asymptomatic patient. Int J Surg Pathol. 2016; 24(2):142-145. doi:10.1177/1066896915610196.

(13.) Canale-Parola E. Biology of the sugar-fermenting Sarcinae. Bacteriol Rev. 1970;34(1):82-97.

(14.) Canale-Parola E, Wolfe RS. Studies on Sarcina ventriculi, I: stock culture method. J Bacteriol. 1960;79(6):857-859.

(15.) Kumar M, Bhagat P, Bal A, Lal S. Co-infection of Sarcina and Giardia in a child. Oxf Med Case Reports. 2014;2014(7):118-119.

(16.) Kulkarni G, Shen B, Gordon I. Sarcina spp infection of the stomach [poster P018]. Inflamm Bowel Dis. 2013;19(suppl 1):S30-S31.

(17.) Beijerinck MW. An experiment with Sarcina ventriculi. In: Proceedings of the Royal Netherlands Academy of Arts and Sciences. Vol 13. Amsterdam, the Netherlands: Johannes Muller;1911:1234-1240. Translated April 28, 1911.

(18.) Crowther JS. Sarcina ventriculi in human faeces. J Med Microbiol. 1971; 4(3):343-350.

(19.) Edwards GT, Woodger NG, Barlow AM, et al. Sarcina-like bacteria associated with bloat in young lambs and calves. Vet Rec. 2008;163(13):391-393.

(20.) DeBey BM, Blanchard PC, Durfee PT. Abomasal bloat associated with Sarcina-like bacteria in goat kids. J Am Vet Med Assoc. 1996;209(8):1468-1469.

(21.) Vatn S, Gunnes G, Nyb K, Juul HM. Possible involvement of Sarcina ventriculi in canine and equine acute gastric dilatation. Acta Vet Scand. 2000; 41(3):333-337.

(22.) Ratuapli SK, Lam-Himlin DM, Heigh RI. Sarcina ventriculi of the stomach: a case report. World J Gastroenterol. 2013;19(14):2282-2285.

(23.) Ali MA, Arnold CA, Singhi AD, Voltaggio L. Clues to uncommon and easily overlooked infectious diagnoses affecting the GI tract and distinction from their clinicopathologic mimics. Gastrointest Endosc. 2014;80(4):689-706.

(24.) Baker JS. Comparison of various methods for differentiation of staphylococci and micrococci. J Clin Microbiol. 1984;19(6):875-879.

(25.) Ananthanaryan R, Paniker CKJ, eds. Staphylococcus. In: Textbook of Microbiology. 6th ed. Hyderabad, India: Orient Longman;2002:178.

(26.) Medlicott SA, Adams F. Sarcina ventricularis complicating a patient status post vertical banded gastroplasty, a case. J Gastroenterol Hepatol Res. 2015;4(2): 1481-1484.

(27.) DiMaio MA, Park WG, Longacre TA. Gastric Sarcina organisms in a patient with cystic fibrosis. Hum Pathol (N Y). 2014;1(3):45-48.

(28.) Bhagat P, Gupta N, Kumar M, Radotra BD, Sinha SK. A rare association of Sarcina with gastric adenocarcinoma diagnosed on fine-needle aspiration. J Cytol. 2015;32(1):50-52.

Caption: A, Sarcina organisms arranged in tetrad packets in the background of gastric mucin and inflammatory cells in a patient with gastric outlet obstruction secondary to recurrent gastric ulcers. B, Basophilic-stained and cuboid-shaped Sarcina organisms adjacent to normal-appearing foveolar gastric mucosa in a patient with diabetic gastroparesis (hematoxylin-eosin, original magnification X400 [A and B]).
Table 1. Clinical Features, Endoscopic Findings, Histopathology,
Treatment, and Follow-up of 19 Cases of Sarcina ventriculi
Reported in the Literature

Source, y              y/Sex   Clinical

Tolentino et al,       14/M    Abd pain, distension,
(8) 2003                       gastric perforation,
                               peritonitis, and necrosis;
                               PMH: bowel resection

                       50/M    N, V, hematemesis, melena,
                               weight loss

Laass et al, (7)        3/F    Anorexia, V, hematemesis, abd
2010                           distension;x-ray: dilated
                               stomach with intramural air,

Lam-Himlin et al,      58/F    Abd pain, V; PMH: GOO
(5) 2011
                       44/F    Postprandial dyspepsia; PMH:
                               type I DM with GP

                       36/M    N, V, with epigastric pain;
                               PMH: narcotic-related
                               GP and GOO

                       12/F    Dysphagia;PMH: esophageal
                               atresia after gastric pull-
                               through with anastomotic

                       46/F    Painful epigastric spasms;h/o
                               pylorus-sparing pancreatico-
                               duodenectomy for pancreatic

Ratuapli et al, (22)   73/M    Chronic iron deficiency
2013                           anemia; PMH: refractory
                               gastric ulcers treated by
                               Billroth II antrectomy and
                               truncal vagotomy

Sauter et al, (11)     12/M    V, epigastric pain refractory
2013                           to PPIs; serum positive
                               for H pylori

                       16/F    V, epigastric pain;PMH: GERD

Kulkarni et al, (16)   34/F    Veterinarian with epigastric
2013                           pain, chronic intermittent

DiMaio et al, (27)     37/F    Intermittent epigastric pain,
2014                           N, anorexia x 2 wk, abdominal
                               distension;PMH: cystic

Kumar et al, (15)       3/M    V, chronic diarrhea;
2014                           PMH: hep A

Bhagat et al, (28)     55/F    V, abd pain;CT: diffuse
2015                           thickening of pyloric antrum

Medlicott and          53/F    Epigastric pain,
Adams, (26) 2015               regurgitation, V; PMH:
                               gastric banding, gastric
                               ulcer, GERD, DM, hiatus

Berry et al, (9)       65/F    Melena, diarrhea, weakness;
2015                           PMH: laparoscopic banding

Sopha et al, (10)      32/F    Headache, dyspnea, melena;
2015                           PMH: gastric banding

Haroon al Rasheed      57/F    Asymptomatic;PMH: type 2 DM,
et al, (12) 2016               H pylori, chronic active
                               gastritis, multiple ulcers

Source, y              y/Sex   Endoscopy

Tolentino et al,       14/M    N/A
(8) 2003

                       50/M    Esophagitis, hiatal hernia,
                               duodenal mass

Laass et al, (7)        3/F    Necrotic stomach distended
2010                           by blood and air

Lam-Himlin et al,      58/F    Gastritis, pyloric mass with
(5) 2011                       obstruction and bezoar

                       44/F    Gastric ulcer, pyloric
                               polyps, and food bezoar

                       36/M    Food bezoar

                       12/F    Stricture at anastomosis,
                               food bezoar

                       46/F    Bile, food bezoar

Ratuapli et al, (22)   73/M    Diffuse gastric erythema, 2
2013                           polyps at anastomosis site,
                               food bezoar

Sauter et al, (11)     12/M    Erosive esophagitis,
2013                           gastritis, edematous
                               and tight pylorus

                       16/F    Erosive esophagitis,
                               gastritis, edematous
                               pylorus, food bezoar

Kulkarni et al, (16)   34/F    Normal esophagus, stomach,
2013                           and duodenum

DiMaio et al, (27)     37/F    Severe erythema, linear
2014                           erosions in posterior wall
                               of gastric antrum

Kumar et al, (15)       3/M    Normal gastric mucosa, mild
2014                           grooving in D2

Bhagat et al, (28)     55/F    Deep ulcer in pylorus

Medlicott and          53/F    Food bezoar, polyps,
Adams, (26) 2015               healed ulcer

Berry et al, (9)       65/F    Pouch, restriction
2015                           with ulcers

Sopha et al, (10)      32/F    Ulcer at gastric cardia

Haroon al Rasheed      57/F    Scarred and eroded before
et al, (12) 2016               prepyloric ulcer, food bezoar

Source, y              y/Sex   Histopathology

Tolentino et al,       14/M    Diffuse, acute, hemorrhagic
(8) 2003                       gastritis with perforation,
                               ulceration, necrosis,
                               and Sarcina

                       50/M    Chronic, superficial
                               gastritis and ulcer
                               with Sarcina

Laass et al, (7)        3/F    Chronic, active gastritis,
2010                           Sarcina, and intramural air

Lam-Himlin et al,      58/F    Chronic, active gastritis
(5) 2011                       and Sarcina

                       44/F    Nonmalignant gastric ulcer
                               with Sarcina, gastric
                               hyperplastic polyps

                       36/M    Normal gastric
                               mucosa and Sarcina

                       12/F    Reflux esophagitis and

                       46/F    Chronic active
                               duodenitis and Sarcina

Ratuapli et al, (22)   73/M    Diffuse gastritis,
2013                           gastric ulcer, and
                               Sarcina; no H pylori

Sauter et al, (11)     12/M    Active erosive esophagitis
2013                           and ulcer bed; chronic,
                               active H pylori gastritis
                               and duodenitis; Sarcina
                               in esophagus and stomach


Kulkarni et al, (16)   34/F    Normal gastric mucosa with
2013                           Sarcina; intraepithelial
                               eosinophils in esophagus
                               and lymphocytosis with
                               villous blunting in

DiMaio et al, (27)     37/F    Moderate chronic gastritis
2014                           and superficial mucosal
                               hemorrhage with Sarcina
                               and Candida

Kumar et al, (15)       3/M    Normal duodenal mucosa with
2014                           Sarcina and Giardia

Bhagat et al, (28)     55/F    Gastric adenocarcinoma,
2015                           ulcer, and Sarcina

Medlicott and          53/F    Mild, chronic gastritis
Adams, (26) 2015               with Sarcina

Berry et al, (9)       65/F    Sarcina

Sopha et al, (10)      32/F    Sarcina

Haroon al Rasheed      57/F    Sarcina, ulcer bed, and
et al, (12) 2016               reactive gastropathy

Source, y              y/Sex   Treatment

Tolentino et al,       14/M    Gentamicin and
(8) 2003                       metronidazole x 12 d

                       50/M    N/A

Laass et al, (7)        3/F    Imipenem and fluconazole x
2010                           2 wk and omeprazole

Lam-Himlin et al,      58/F    Partial gastrectomy.
(5) 2011

                       44/F    Omeprazole, ranitidine,
                               metoclopramide x 5 mo

                       36/M    Jejunostomy tube for

                       12/F    N/A

                       46/F    N/A

Ratuapli et al, (22)   73/M    Metronidazole and
2013                           ciprofloxacin x 1 wk
                               and sucralfate

Sauter et al, (11)     12/M    N/A

                       16/F    N/A

Kulkarni et al, (16)   34/F    Ciprofloxacin and
2013                           metronidazole x 1 wk

DiMaio et al, (27)     37/F    Omeprazole.

Kumar et al, (15)       3/M    N/A

Bhagat et al, (28)     55/F    N/A

Medlicott and          53/F    Motilium and metronidazole
Adams, (26) 2015

Berry et al, (9)       65/F    PPIs

Sopha et al, (10)      32/F    Metronidazole,
2015                           fluoroquinolone, and
                               PPI x 4 wk

Haroon al Rasheed      57/F    N/A
et al, (12) 2016

Source, y              y/Sex   Follow-up

Tolentino et al,       14/M    Symptomatic improvement
(8) 2003

                       50/M    N/A

Laass et al, (7)        3/F    Fully recovered; normal
2010                           mucosa and no Sarcina

Lam-Himlin et al,      58/F    Treated for gastric
(5) 2011                       adenocarcinoma

                       44/F    Symptomatic improvement

                       36/M    No Sarcina

                       12/F    N/A

                       46/F    Continued spasms

Ratuapli et al, (22)   73/M    Improved gastric erythema;
2013                           no food bezoar or Sarcina

Sauter et al, (11)     12/M    N/A

                       16/F    N/A

Kulkarni et al, (16)   34/F    Identical histology
2013                           but no Sarcina

DiMaio et al, (27)     37/F    Symptomatic improvement

Kumar et al, (15)       3/M    N/A

Bhagat et al, (28)     55/F    N/A

Medlicott and          53/F    Persistent polyps and
Adams, (26) 2015               reactive gastropathy;
                               no Sarcina

Berry et al, (9)       65/F    Stable

Sopha et al, (10)      32/F    Persistent ulcer with
2015                           perforation during endoscopy

Haroon al Rasheed      57/F    N/A
et al, (12) 2016

Abbreviations: Abd, abdominal; CT, computed tomography;
D2, second part of the duodenum; DM, diabetes mellitus;
GERD, gastroesophageal reflux disease; GOO, gastric outlet
obstruction; GP, gastroplasty; hep A, hepatitis A; h/o, history
of; H pylori, Helicobacter pylori; N, nausea; N/A, not applicable;
PMH, past medical history; PPI, proton pump inhibitor; V, vomiting.

Table 2. Clinical and Histologic Presentation
of Sarcina ventriculi in the Literature

  Characteristics                    Cases, No. (%), n = 19

  F                                        13 (68.4)
  M                                         6 (31.6)

Age, y
  0-10                                      2 (10.5)
  11-17                                      4 (21)
  18-64                                    11 (57.9)
  [greater than or equal to] 65             2 (10.5)

Clinical presentation
  Abdominal pain                           11 (57.9)
  Nausea and vomiting                       9 (47.4)
  Abdominal distension,                  3 (15.8) each
    diarrhea, melena
  Asymptomatic, dysphagia, or            2 (10.5) each
  Other (weight loss, anorexia,             6 (31.6)
    regurgitation, weakness)

  Delayed gastric emptying                 11 (57.9)
  Gastrointestinal surgery or            7 (36.8) each
    gastric outlet obstruction
  Gastroparesis                              4 (21)

  Food bezoar                               9 (47.4)
  Gastric ulcer, gastritis                4 (21) each
  Esophagitis                               3 (15.8)
  Edematous/tight pylorus,               2 (10.5) each
    gastric perforation, healed/
    scarred gastric ulcer, mass,
    necrosis, or normal
  Other (hiatal hernia, polyp,              6 (31.6)
    duodenal groove, bile, or

Histopathology, in addition to
Sarcina organisms

  Gastric ulcer                              8 (42)
  Chronic active gastritis                  5 (26.3)
  Chronic inactive gastritis                 4 (21)
  Duodenitis, esophagitis                 4 (21) each
  Unspecified gastric findings              5 (26.3)
  Normal                                    3 (15.8)
  Gastric adenocarcinoma                    2 (10.5)
  Hyperplastic polyp,                     1 (5.3) each
    intramural air, necrosis,
    reactive gastropathy

Other concurrent organisms                  6 (31.6)
  Candida                                   2 (10.5)
  Giardia, Helicobacter pylori,           1 (5.3) each
    Staphylococcus, or mixed
    gram-positive and gram-
    negative flora
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Author:Rasheed, Mohamed Rizwan Haroon Al; Senseng, Carmencita G.
Publication:Archives of Pathology & Laboratory Medicine
Date:Dec 1, 2016
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