Medical management of
inflammatory bowel disease in a
Spider Monkey



Reference: Journal of the American Veterinary Medical Association

Ramiro Isaza,  DVM; Barbara Baker, DVM; Freeland Dunker, DVM

A 3-year-old, captive-born, hand raised, female spider monkey (Ateles geoffroyi) was evaluated because of severe intermittent enteritis.  The monkey was housed with 2 other spider monkeys in an outdoor moated enclosure with an adjoining indoor area.  Their diet consisted of commercial monkey food and a mixture of fresh fruits and vegetables fed twice daily.  Review of medical records from the institution at which the monkey was born indicated that the monkey's first episode of enteritis was at 3 months of age.

During an 18-month period at our facility, 5 episodes of enteritis were documented at 1 - to 5- month intervals.  Between these episodes, the monkey appeared clinically normal, with behavior and appetite similar to her unaffected cagemates.  The typical clinical episode of enteritis began with signs of depression, anorexia, and apparent abdominal tenderness.  This often progressed to bloody diarrhea and vomiting lasting between 4 and 12 days.  These episodes of enteritis varied from mild self-limiting to severe, which often required treatment with bland diet, oral administration of electrolyte solutions, and empirical treatment with antibiotics (amoxicillin, gentamicin, tetracycline, trimethoprim-sulfamethoxazole, and metronidazole).

Results of 3 CBC counts and 2 serum biochemical analyses performed during separate clinical episodes were all within normal limits for spider monkeys.   Repeated direct fecal smears and fecal flotation examinations failed to reveal nematode parasites, but motile flagellates were observed in several direct fecal smears.   In one fecal sample, cysts morphologically similar to Giardia were seen, but trichrome staining of smears from the same sample failed to reveal any parasites.   Leukocytes and evidence of pathogenic organisms were not seen in fecal smears stained with modified Wright-Giemsa.  Gram-stained fecal samples were considered to have normal bacterial flora.  Two fecal samples were submitted for aerobic bacteriologic culture, using media selective for Salmonella, Shigella, Campylobacter, and Yersinia.  Escherichia coli was isolated from both samples.  Positive contrast radiography performed after oral administration of barium sulfate during a clinical episode revealed diffuse ulceration of the colonic mucosa.

Because of the severe and episode nature of the enteritis, endoscopy was performed to establish a diagnosis.  Colonoscopy was undertaken during a period of disease quiescence to limit the anesthetic risks and the possibility of colonic perforation.  A pediatric gastoscope was used; however, it could be advanced only to the hepatic flexture of the transverse colon.  The mucosa appeared edematous, granular, hyperemic, and friable.  Esophago-gastroduedenoscopy, performed with the same gastroscope, failed to reveal abnormalities.  Multiple biopsy specimens were taken from the colon, rectum, and duodenum and placed in buffered 10% formalin solution.

Biopsy specimens were sectioned and stained with hematoxylin and eosin.  Microscopic examination of the colon specimens revealed areas of mucosal hemorrhage.  A moderate chronic inflammatory infiltrate consisting of lymphocytes and plasma cells was seen in the lamina propria of the colon and duodenum.  Infective agents were not seen in any of the specimens.  The rectal biopsy specimens were considered clinically normal.  A presumptive diagnosis of inflammatory bowel disease was made.

The next episode of enteritis was 3 months after the endoscopic examination.  Treatment consisted of administration of prednisone (1 mg/kg of body weight, PO; q 12h for 5 days, then q 24 h for 5 days and finally q 48 h for 10 days) and sulfasalazine (30 mg/kg, PO; q 12 h for 21 days).  A flavored pediatric suspension of trimethoprim-sulfamethoxazole (15 mg/kg, PO; 12 h for 14 days) as a palatable vehicle for the other medications.  A bland diet and an electrolyte solution were given free choice until the vomiting and diarrhea resolved.  Response to treatment was seen within 24 hours, and recurrence of clinical signs was not observed during the first 3 weeks of treatment.

When the sulfasalazine dose was maintained at 30 mg/kg, PO; q 12 h, and prednisone was eliminated, a mild episode of vomiting and diarrhea was observed.   The clinical signs resolved when the prednisone (0.5 mg/kg, PO, q 48 h) was given concurrently with the sulfasalazine (30 mg/kg, PO; q 12 h).  Medication was stopped after 60 consecutive days in which clinical signs were not observed.  All subsequent episodes of enteritis were treated as described with the exception of trimethoprim-sulfamethoxazole.

Bacterial enteritis has been reported in primates and was strongly suspected in this monkey.  Normal fecal smears and normal CBC results did not support this diagnosis.  Although E coli was isolated twice from the feces, the organism was considered a nonpathogenic isolate of normal flora.  Infection with Mycobacterium sp, amoebae, or anaerobic bacteria could not be ruled out, but the biopsy results did not indicate any organisms or lesions suggestive of these types of infections.   Flagellates can cause diarrhea and were identified in the feces.  Generally, these organisms are considered normal flora that tend to increase in numbers during diarrheal episodes.  Infection with Giardia lamblia had been associated with inflammatory changes in human beings.  During the first few episodes, giardiasis was the presumptive diagnosis, because cysts morphologically similar to Giardia sp were seen in a fecal smear.  The inability to detect Giardia sp in subsequent fecal examinations, combined with lack of duodenal lesions eliminated giardiasis as the primary cause of the enteritis.  The role of a primary immunosuppressive disease, social stress, or genetic factors as causes of the enteritis were not investigated.  An environmental or dietary allergen stimulating the enteritis was considered, but no efforts were taken to isolate such an agent.

A histologic diagnosis of inflammatory bowel disease is a subjective assessment, particularly from the species in which normal microscopic intestinal microanatomy has not been described.  The fact that only moderate intestinal inflammation was seen in this monkey most likely was attributable to collection of biopsy specimens during a period of disease quiescence.  Because of the limitations of an endoscopic examination, inflammation was seen only in the descending colon and the proximal portion of the duodenum, leaving possible involvement of the ascending colon, ileum, and jejunum undetermined.

Inflammatory bowel disease has been well described in human and veterinary medical literature.  In human beings, the typical clinical presentation of inflammatory bowel disease is intermittent episodes of bloody diarrhea with abdominal pain, nausea, and anorexia.  A single definitive cause of this disease has not been identified, but suggested causes include infective agents ( bacterial, viral, fungal, and helminthic), genetic predisposition, and nonspecific allergic reaction leading to inflammation of the gastrointestinal tract.  As is common in other species, a primary cause for the intestinal inflammation could not be identified in this monkey.

Treatment of inflammatory bowel disease is designed to give initial supportive care and to control the inflammation in the gastrointestinal tract.   In the case reported here, prednisone was used to alleviate some of the clinical signs and reduce the gastrointestinal inflammation.  Because of the side effects associated with long-term use of prednisone, the dosage was tapered to an alternate day treatment schedule.  Sulfasalazine is a conjugate of 5-aminosalicylic component is a nonsteroidal anti-inflammatory drug that is primarily responsible for the therapeutic effect.

Our diagnosis was made on the basis of clinical signs, positive-contrast radiographic series, endoscopy, histologic appearance of intestinal biopsy specimens, and response to treatment.  Several reports have described inflammatory bowel disease in primate species but, to our knowledge, this is the first report of this disease in a spider monkey.  This case illustrates that recurrent enteritis in primates may be noninfectious and may respond to anti-inflammatory agents.

Intermittent treatment was chosen to limit potential side effects of continuous long-term corticosteroid treatment and to monitor the duration of remission between treatments.  Two years following the writing of this manuscript, the monkey has had multiple relapses of enteritis that have responded to the treatment described in this report.  This monkey's long-term prognosis for a normal social and reproductive life in a zoo exhibit remains guarded.


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