Sarcinaventriculi (S. ventriculi) are gram-positive, obligate anaerobic
bacteria first documented in the human gastrointestinal
tract in 1842 [1-4]. Latin for "package" or "bundle,"Sarcinacocci
undergo fission in three planes, perpendicular to one another,
resulting in theircharacteristicpacketed morphology, often in
tetrads but occasionally in cubes of eight [3,5,6]. In addition,
S. ventriculi has a thick (150 to 200 nm) fibrous layer on the
outer surface of its cell wall composed mostly of cellulose [1,3].
Given these unique conjoining features-tetrad packets with a
thick cellulose-dominant wall-it is not surprising that these
organisms were initially thought to be vegetable matter .
The purpose of this article is to report an unusual occurrence
of pediatric siblings with metachronous presentations of severe
Helicobacter pylori (H. pylori) gastritis/duodenitiswith coexisting
Sarcina. Only rare pediatric cases of human disease
associated with Sarcina organisms have been documented . To our knowledge, these are the first cases of Sarcina organisms
co-existing with H. pylori.
Report of a Case
A previously healthy 12-year old male underwent esophagogastroduodenoscopy
(EGD) following a 3-month history of
emesis and epigastric pain, which did not respond to standard
dose proton pump inhibitor. Endoscopy revealed erosive
esophagitis in the distal third of the esophagus (Figure 1A),
erythematous gastric mucosa and a highly edematous, tight
pylorus (Figure 1B).At the time, serum antibodies for H.pylori
were positive, and four months later, the patient's 16-year old
sister presented with similar symptoms. She had a history of
medication-controlled gastroesophageal reflux disease with a
normal EGD one-year prior; however, her current endoscopy
was significant for severe erosive esophagitis and a highly
edematous pylorus. In addition, the stomach was markedly
inflamed and full of food debris. Endoscopic biopsies were
Histologic features of the sibling's biopsies were nearly identical:
active erosive esophagitis with Sarcina present in ulcer bed
debris; chronic active H. pylori gastritis with Sarcina and H.
pylori organisms admixed in overlying mucin as well as in areas
of erosion; and H. pylori duodenitis also with both organisms
admixed in areas of erosion (Figure 1C-Figure 1F). Classic tetrad
packets of Sarcina organisms were present in both patients
(Figure 1E). Although H. Pylori was present in surface mucin
and gastric pits, Sarcina organisms were identified only in surface
exudate and remained non-invasive in both patients.
Polymerase chain reaction (PCR); DNA sequencing
Areas containing Sarcina organisms, present in formalin-fixed,
paraffin-embedded tissue from biopsies of the brother's esophagus
and stomach and the sister's esophageal biopsies were
isolated through microdissection. The pyruvate decarboxylase
(PDC) gene, present in only a few bacterial species, including S.
ventriculi, allows bacteria to convert pyruvate to acetaldehyde and carbon dioxide, and was therefore used as positive identification.
Exploiting this unique metabolic feature,primerswere
designed (forward: 5'-AGCGGTTGCAGCGACAATAGGA-
3'; reverse: 5'-CTGCAACCAGCGCTGCACCT-3') to
target the PDC gene of S.ventriculi (AF354297.1), yielding a
149 base-pair amplicon. The PCR and DNA sequencing techniques
used in this study follow the protocol outlined previously
Findings by DNA sequencing and alignment
Amplification of the PDC gene was present in DNA isolated
from the brother's esophagus and stomach biopsies, with a
96% blast match rate to S.ventriculi. Both of these samples,
esophageal and stomach, matched to each other with 100%
identity. Multiple attempts to amplify DNA isolated from the
sister's esophageal biopsy yielded no reaction. As positive control
tissue produced expected results, the DNA from the sister's
sample was assumed to be non-viable.
The natural habitat of Sarcina is the soil, yet its presence has
also been well documented in stagnant water, on the surface
of cereal seeds, and interestingly as one of the major bacterial
contaminants isolated from commercially available children's
soap bubbles [2-4,9].It has been postulated that when Sarcina
is present in the human GI tract,the organisms are likely ingested
with soil particles associated with food . Further,
Sarcina has been identified in the feces of healthy human
adults, particularly vegetarians .
Although Sarcina is well-recognized in the veterinarian literature
as a cause of abomasal gas and bloating in ruminants [10-
13], its role as a causative agent of gastrointestinal disease versus
bystander in humans remains uncertain. There have been a
few reports of Sarcina causing acute emphysematous gastritis,
a rare potentially fatal condition resulting from invasion of the
gastric wall by gas-forming bacteria, including a three yearold
child who recovered following antibiotic therapy against
Sarcina is not generally present in the normal healthy human
stomach; however, it has been reported in the setting of pyloric
ulceration and stenosis . Indeed, when Dr. Ferrier of King's
College first documented the presence of Sarcina within the
human stomach in 1842, he used the term "Sarcinous vomiting,"
as he generally found the organisms in patients "with
chronic diseases of the stomach associated with obstinate
vomiting of acid, frothy, yeasty matters' . In the setting of
gastric obstruction, the presence of carbohydrates and other
nutrients in food provide fermentative substrates for Sarcina
. Sarcina thrives under these conditions since they are able
to tolerate the strongly acidic environment of the stomach
[3,11,14,15], while the growth of other microorganisms is
inhibited at this low pH.In their recent review of endoscopic
biopsies, Lam-Himlin and colleagues identified Sarcina most
commonly in patients with a history of gastric outlet obstruction
or delayed gastric emptying .
We describe pediatric siblings with identical presentations of
active H. pylori gastritis/duodenitis with the co-existence of
Sarcina occurring four months apart. Given their relationship,
these two patients are assumed to have had similar exposures.
The degree of gastric and duodenal inflammation and edema
in both cases were marked enough to cause secondary gastric
outlet obstruction including retained food and difficulty passing
the endoscope through the pylorus. This presentation is in
keeping with the documented association of the presence of
Sarcina with gastric outlet obstruction.
In addition to the histologic evidence of Sarcina organisms,
the brother's esophagus and stomach biopsies showed the
distinct 149 base-pair ampliconfrom the PDC gene of S.
ventriculi. Subsequent sequencing showed a 96% homology
(NCBI reference sequence AF354297.1) providing molecular
confirmation of the morphologic impression of S. ventriculi.
Sarcina's characteristic histomorphology of basophilic tetrads
or cubes of eight, measuring approximately the size of
a red blood cell, make them quite distinct once recognized.
Our experience with respect to these cases emphasizes that
Sarcina organisms can be easily and accurately identified on
H & E-stained sections. We speculate that these organisms are
present in more cases of active esophagitis/gastritis than are
currently documented and that increased awareness will lead
to greater recognition.