Full Text

Brief communications
b. Dr. Victor Nettles, College of Veterinary Medicine, University
of Georgia, Athens, GA.
c. Sigma Chemical Co., St. Louis, MO.
d. Jackson ImmunoResearch Laboratories, West Grove, PA.
e. Dr. Geoff Gard, formerly with the Department of Primary Production, Darwin, Northern Territory, Australia, and Dr. Bill
Taylor, formerly with the Institute for Animal Health, Pirbright
Laboratory, Working, Surrey, UK.
8.
9.
10.
References
1. Afshar A, Thomas FC, Wright PF, et al.: 1987, Comparison
of competitive and indirect enzyme-linked immunosorbent assay for detection of bluetongue virus antibodies in serum and
whole blood. J Clin Microbiol 25:1705-1710.
2. Afshar A, Thomas FC, Wright PF, et al.: 1989, Comparison
of competitive ELISA, indirect ELISA and standard AGID test
for detecting bluetongue virus antibodies in cattle and sheep.
Vet Rec 124:136-141.
3. Afshar A, Wright PF, Taylor LA, et al.: 1992, Development
and evaluation of an enzyme-linked immunosorbent assay for
detection of bovine antibodies to epizootic hemorrhagic disease
of deer viruses. Can J Vet Res 56:154-160.
4. Borden EC, Shope RE, Murphy FA: 1971, Physiochemical and
morphological relationships of some arthropod-borne viruses
to bluetongue virus -a new taxonomic group, physiochemical
and serological studies. J Gen Virol 13:261-271.
5. Bowen RA: 1987, Serologic responses of calves to sequential
infections with epizootic hemorrhagic disease virus serotypes.
Am J Vet Res 48:1449-1452.
6. Della-Porta AJ, Parsonson IM, McPhee DA: 1985, Problems
in the interpretation of diagnostic tests due to cross-reactions
between orbiviruses and broad serological responses in animals.
Prog Clin Biol Res 178:445-453.
7. Dulac GC, Dubuc C, Afshar A, et al.: 1988, Consecutive out-
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Gibbs EPJ, Greiner EC: 1988, Bluetongue and epizootic hemorrhagic disease. In: The orbivirus: epidemiology and ecology,
ed. Monath TP, vol. 2, pp. 39-70. CRC Press, Boca Raton, FL.
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Adv Vet Sci Comp Med 22:111-132.
Metcalf HE, Luedke AJ, Jochim MM: 1992, Epizootic hemorrhagic disease virus infection in cattle. In: Bluetongue, African
horse sickness, and related orbiviruses, ed. Walton TE, Osburn
BI, pp. 222-237. CRC Press, Boca Raton, FL.
Nettles VF, Hylton SA, Stallknecht DE, et al.: 1992, Epidemiology of epizootic hemorrhagic disease viruses in wildlife in
the USA. In: Bluetongue, African horse sickness, and related
orbiviruses, ed. Walton TE, Osburn BI, pp. 238-248. CRC Press,
Boca Raton, FL.
Pearson JE, Gustafson GA, Shafer AL, et al.: 1992, Diagnosis
of bluetongue virus and epizootic hemorrhagic disease. In: Bluetongue, African horse sickness, and related orbiviruses, ed. Walton TE, Osburn BI, pp. 533-546. CRC Press, Boca Raton, FL.
Thevasagayam JA, Woolhouse TR, Mertens PPC, et al.: 1996,
Monoclonal antibody based competitive ELISA for the detection of antibodies against epizootic hemorrhagic disease of deer
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J Vet Diagn Invest 9:311-313 (1997)
Equine gastric impaction, ulceration, and perforation due to persimmon
(Diospyros virginiana) ingestion
Connie A. Cummings, Karen J. Copedge, Anthony W. Confer
Overeating of ripe persimmons is a common occurrence
in the fall for many birds and mammals. However, only 2
cases of persimmon consumption in horses leading to gastric
abnormalities have been reported.2,8 In neither of the cases
were persimmons confirmed as the actual cause of the lesions.
Persimmons are well known for their sour taste that turns
sweet when the fruit matures in the cool temperatures of the
fall. The sour taste results from tannic acid, an astringent
compound, found under the persimmon skin and around the
From The Departments of Anatomy, Pathology, and Pharmacology (Cummings, Confer) and Equine Medicine and Surgery (Copedge), Oklahoma State University, College of Veterinary Medicine,
Stillwater, OK 74078.
Received for publication August 19, 1996.
calyx.1 The concentration of water-soluble tannin contained
within the fruit’s tannin cells varies with season, fruit development, and fruit maturation. These tannins reach maximum concentrations by mid-October, when the concentrations decline as the temperature decreases. In humans, tannic
acid polymerizes to a coagulum in the stomach that can
entrap cellulose, hemicellulose, and protein. This coagulum
forms the basis for a gastric phytobezoar.1 In addition, tannic
acid reacts with mucin, thereby decreasing the cytoprotective
mechanism of the gastric mucosa.3
Animals may gorge themselves on persimmons, especially
after the first frost of the season. In horses, overconsumption
of persimmons can result in colic and impaction.2,8 In the
case reported here, overconsumption resulted in gastric ulceration, impaction, and perforation.
312
Brief communications
Figure 1. Persimmon phytobezoar in the stomach.
In October 1995, an 8-year-old female Quarter Horse with
a 9-day history of colic was admitted to the Boren Veterinary
Medical Teaching Hospital at Oklahoma State University.
The referring veterinarian had treated the horse for mild colic
possibly due to persimmon or acorn toxicity. Results of a
complete blood count indicated leukopenia (4,500) and a
degenerative left shift. A chemistry profile indicated hyponatremia (127 mmol/liter, reference range: 132-144 mmol/
liter), hypochloremia (82 mmol/liter, reference range: 94103 mmol/liter), mild azotemia (34 mg/dl, reference range:
8-27 mg/dl), hypocalcemia (7.4 mg/dl, reference range: 10.713.4 mg/dl), hypoalbuminemia (2.2 g/dl, reference range:
2.5-8.8 g/dl), and hyperbilirubinemia (3.9 mg/dl, reference
range: 0.1-2.6 mg/dl). Cytologic examination of the peritoneal fluid revealed a marked leukocytosis with > 90% degenerative neutrophils, mixed bacteria, and feedstuff. Abdominal ultrasound indicated a fluid line up to the level of
the point of the shoulder and a floating liver. The horse died
during the early morning, and a complete necropsy was done.
At necropsy, lesions were confined to the peritoneal cavity.
The cavity contained 45-60 liters of a dark red to brownish
gray thick, foamy, cloudy fluid, which contained free-floating
fibrin clots and plant material. In addition, there was an
unusually distinct strong pungent fermenting acrid odor. The
omentum was friable and necrotic. In numerous areas, the
omentum adhered to both the small and large intestines. The
most severe lesions were the fibrinous adhesions on the peritoneal surface of the diaphragm and serosa of the stomach.
Along the greater curvature of the stomach, where the
greater omentum attaches, there was a 1.5-cm-diameter hole
with brownish gray edges and hemorrhage on the serosal
surface. This hole penetrated through from the mucosal surface of the glandular portion of the stomach and corresponded to a 4.5-cm depressed, dull gray 5-mm-deep ulcer found
on the mucosal surface. Within the stomach, the unusually
distinct fermenting acrid odor was associated with an ovalshaped firm, dry, crumbling phytobezoar approximately 20
cm long x 16 cm in diameter composed of persimmon seeds,
persimmon pulp, and other plant material (Fig. 1). By volume, the bezoar was composed of 85-90% persimmon seeds,
both whole and cracked. In addition to the perforated ulcer,
8 other ulcers were found in the glandular portion and ranged
from 0.5 to 4 cm in diameter and were 0.5-3 mm deep. The
nonglandular portion of the stomach contained 3 large ulcers:
1 was white/tan, firm, and 2 x 10 x 0.5 cm deep, and the
other 2 were 2 x 8.5 cm and 2.2 x 12 cm, respectively, and
both were 1.0 mm deep. The remaining intestinal tract had
a diffusely reddened mucosa and contained ingesta with whole
and cracked persimmon seeds. All other organ systems were
unremarkable.
Microscopic examination confirmed a fibrinous, necrotizing, subacute peritonitis with congestion of multiple organs.
Throughout the gastrointestinal tract, there was edema of the
mucosal and submucosal walls, congestion, and moderate to
severe inflammation consisting of lymphocytes, neutrophils,
and macrophages. Lining the lower villous epithelium and
within the crypts of the mucosal layer in numerous intestinal
tract sections there was a dark purple-staining, irregularly
shaped amorphous material, which failed to polarize or stain
with special stains. This material probably was persimmon
pulp.
Persimmons are a depressed-spherical or egg-shaped fruit
with a rounded or pointed apex and a tough, puckered skin
that is initially green and matures to a purplish black. The
pulp is yellow and astringent until overly ripe. The seeds are
oblong (1-1.5 x 0.5 cm) and flat, with 1 edge straight and
the other rounded and a pale brown, hard, wrinkled coat. In
the fall, ruminants and horses will eat persimmons. However,
few documented cases have been found implicating persimmons as directly producing gastrointestinal mucosal damage
or impactions in animals. 2,8 Ingestion of persimmons is considered the most common cause of phytobezoars in humans
worldwide.4 A persimmon bezoar probably forms from soluble tannin (shibuol), which becomes coagulated in the course
Brief communications
of ripening.4 These tannins are found around the calyx and
under the skin and are at highest concentration in unripe
fruit. One property of soluble shibuol is the ability to coagulate in the presence of acids. In 1 study, soluble shibuol
precipitated in the presence of gastric juices, and at body
temperature, the shibuol precipitated quickly to form a sticky
mass that progressed to a cemented ball.4 A horse ingesting
whole persimmons is at a higher risk of developing a gastric
phytobezoar based on the amount of skin and pulp consumed.
Persimmon seeds do not contain soluble shibuol and thus
do not contribute to the primary formation of a phytobezoar.4
However, because of the seeds’ hard outer coat, they can
easily be cemented into the phytobezoar. When the persimmon seed becomes cemented into the phytobezoar, it functions as an instrument of mechanical damage, abrading the
mucosal lining of the stomach. In this horse the phytobezoar
was composed primarily of persimmon seeds, mixed with
persimmon pulp, persimmon skin, and a little hay, indicating
that seeds were a primary contributor to the gastric mucosal
damage.
Human impactions due to phytobezoars occur frequently
and commonly in the stomach.1 In humans with history of
peptic ulcers, ingestion of unpeeled persimmons predisposed
them to develop phytobezoars.1 In horses, gastric impactions
are difficult to diagnose and surgically treat2,6 and can be due
to intrinsic and/or extrinsic causes.6 Intrinsic causes include
defective gastric secretions, stomach atony, or pyloric strictures. Extrinsic causes are related to water intake, the types
of food ingested, improperly masticated food, or eating behavior. Extrinsic factors can cause impactions and can influence gastric acidity and secretion of digestive enzymes.2.6
Gastric ulcers may result from either an imbalance in gastric acid and pepsin release or inability of the mucosal lining
to maintain integrity when exposed to damaging agents. Gastric ulcers in adult horses occur most often in the squamous
epithelium of the stomach and are considered to be due to
excess acidity. Ulcers in the glandular mucosa, however, are
due to decreased mucosal protection.9 Often, treatment with
nonsteroidal anti-inflammatory drugs (NSAID) is associated
with gastric ulcers. In this horse, however, there was no history of NSAID use. Damage to the gastric mucosal cells
through a direct corrosive effect due to tannic acid released
from persimmons has been documented.3 Tannic acid reacts
with mucin. a protein present in the mucous coating of the
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stomach. With mucin precipitated, the cytoprotective mechanism of the gastric mucosa is decreased, thereby exposing
the mucosal lining to the acidic gastric juices. So strong is
the effect of tannic acid, it could be used as an ulcer inducer
in an animal model.3 In the horse in the report, both the
glandular and squamous portions of the stomach contained
ulcers. Although some ulcers could have been preexisting,
they probably resulted from a combination of mechanical
damage caused by the persimmon seeds and decrease cytoprotection from mucus lacking in mucin.
Gastric perforations are rare in horses. When they do occur, the cause can be parasitism, neoplasia, or gastric ulceration. The perforation in this horse resulted from the gastric
ulcer along the greater curvature of the stomach. Most likely,
the cause of the perforation was weakening of the stomach
lining due to ulceration and stress exerted from the massive
size and weight of the phytobezoar.
The pathogenesis of persimmon-induced impactions in animals is almost certainly due to the physical and chemical
composition of the persimmon fruit.
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a pony. J Am Vet Med Assoc 187:501-502.
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