Diagnosis and Management of Endocrine Pancreatic Aplasia in a Juvenile Bengal Tiger (Panthera tigris tigris)
American Association of Zoo Veterinarians Conference 2003
Ray L. Ball1, DVM; Tamara Gardner2, DVM; Mike Garner3, DVM, DACVP; Mike Burton1, VMD; Genny Dumonceaux1, DVM; John H. Olsen1, DVM
1Busch Gardens, Tampa, FL, USA; 2Midway Animal Hospital, Homosassa, FL, USA; 3Northwest ZooPath, Snohomish, WA, USA


A 6-month-old female intact white Bengal tiger (Panthera tigris tigris) started developing clinical signs consistent with exocrine pancreatic insufficiency (EPI) soon after it was weaned from a hand-raising formula to a meat diet (Dallas Crown). Voluminous, greasy stools, poor hair coat, abdominal distension, polyphagia, and poor rate of gain compared to age and sex matched conspecifics were noted. Flatulence and borborygmus were also noted. Prior to the onset of clinical signs the cub had showed a normal development and had been vaccinated routinely with a commercial feline vaccine for rhinovirus, calicvirus, and panleukopenia, (Fel-O-Vax, PCT, Fort Dodge®, Fort Dodge Laboratories, Inc, Fort Dodge, IA 50501 USA) and rabies (Rabdomun®, Pfizer Animal Health, Exton, PA 19341 USA). The cub had two negative ELISAs to feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV). A slight titer to canine distemper was found on quarantine exam but this did not persist. Empirical therapy for EPI was started and included a commercial porcine pancreolipase supplement (Pancreazyme Plus Powder®, Butler) at 1500 IU of lipase per kg of body weight. This product was chosen due to the added vitamin A, D3, and E. Some improvement in stool quality was noted but the cub continued to have a suboptimal weight gain, was ravenous, and was generally uncomfortable. The cub allowed blood sampling via a squeeze cage by means of operant conditioning. Cobalamine (<100 ng/L) and folate (7.9 µg/L) were found to be abnormal based on domestic cats’ values (290–1500 ng/L and 9.7–21.6 µg/L respectively). The tiger was hand reared and leash trained which allowed a limited physical exam by age of 10 months. The cub weighed 54 kg, had a taunt abdomen, was moderately thin with a scruffy coat and an overall stunted appearance. Abdominal palpation revealed a mid-abdominal mass that was immediately painful. Standing radiographs demonstrated a soft tissue mass in the mid-abdomen. The films were not diagnostic enough to delineate which organ was involved. The cub was anesthetized with medetomidine (18 µg/kg, Domitor®, Pfizer Animal Health, Exton, PA 19341 USA) and ketamine (2.94 mg/kg, Ketaset®, Fort Dodge®, Fort Dodge Laboratories, Inc, Fort Dodge, IA 50501 USA) IM, intubated and maintained on isoflurane for diagnostic evaluation. Abdominal palpation and ultrasound evaluation revealed mesenteric lymphadenopathy and thickened small intestinal loops. Radiographs suggested primary lymph node involvement as all other organ systems appeared normal and suggested thickened small intestinal walls as well. Exploratory laparotomy was elected. Significant finding included grossly enlarged lymph nodes associated with the mesentery and small intestine. One node at the root of the mesentery measured 10 cm across. The small intestine was diffusely thickened and felt heavy. The most notable finding was the sparse condition of the pancreas. The pancreatic mass was greatly reduced, and only small blushes of tissue were found in the mesentery in both arms of the pancreas. There was, however, no evidence of inflammation nor necrosis in the organ. Biopsies of the small intestine, lymph nodes, and pancreas were taken. The cub recovered uneventfully.

Histopathology revealed severe acinar cell hypoplasia/aplasia of the pancreas, mild chronic enteritis, and marked reactive lymphoid hyperplasia. Special staining for viral induced pancreatic disease, feline parvovirus and canine distemper virus, were negative. No growth was obtained on tissue culture form surgery. The pathologist gave a grave prognosis and the clinical staff concurred. The cub was managed with 4–5 feedings daily, each treated with the pancreolipase supplement. Cyanocobalamin was given every 21–28 days SC and monitored based on the serum levels of cobalamin and folate levels. Simethicone (Gas Relief®, Rugby Laboratories, Inc., Duluth, GA 30097 USA) 125 mg PO SID was also given to manage the condition. The cub began to stabilize and gain weight. Hair coat improved; attitude became much more relaxed. Appetite was still ravenous and while stool quality improved overall there was still occasional episodes of steatorrhea. Initial feeding consisted of only meat product other items such as ribs and whole prey on an occasional basis were added. One year later it was decided that the young tigress should be permanently sterilized. The tiger now weighed 104 kg and was again anesthetized with medetomidine (20 µg/kg) and ketamine (2.11 mg/kg) IM and prepped for ovariohysterectomy and laparotomy. The small intestine was thickened still but not nearly as severe as the original surgery. The lymph nodes were generally enlarged and edematous but again not as severe. The pancreas was, however, much reduced. Biopsies of all three were taken and the ovariohysterectomy performed. The tigress recovered uneventfully. Histopathology was essentially identical to the original biopsies. The tigress continues to thrive with four other conspecifics and is maintained on the feeding regime with routine blood draws to taper the cyanocobalamin therapy. Pancreolipase dosing has been increased to 1800 IU lipase per kg of body weight to prevent steatorrhea.

The clinical picture in this tiger most closely resembled juvenile pancreatic hypoplasia in German shepherds3 both clinically and on the initial histopathology. This condition is believed to be an autosomal recessive trait. Given the early onset of this condition in this tiger, a congenital etiology was likely and therefore this condition is most appropriately called exocrine pancreatic aplasia. The absence of viral particles on special staining also supported this diagnosis. The likelihood of a congenital problem prompted the decision for elective sterilization. This provided an opportunity to evaluate the condition of the pancreas firsthand after 1 year of therapy. In felids, chronic pancreatic insufficiency has been found in a pair of Indian lions.1 The lions in this case were not able to be maintained on a commercial pancreolipase supplement and were euthanatized. The authors concluded in their case that the disease process was a degenerative one and believed that pancreatic exocrine atrophy is most appropriate term for the condition they documented. Most cats with EPI become severely cobalamin deficient and also require tocopherol and folate supplementation.2 Folate and cobalamin are useful measures of small intestinal health and can be useful in the diagnosis and management of EPI like diseases.2,4 In this tigress, folate levels returned to normal without specific folate supplementation. Utilizing a laboratory with specific diagnostics for domestic cats (GI Lab, Department of Small Animal Medicine and Surgery, Texas A&M University, College Station Texas, 77843-4474) proved essential for this case. Reference values for cobalamin and folate proved adequate for the management of this tiger.


I would like to thank the Animal Care Staff at Busch Gardens, especially Jody Hackman, Kendal Duncan, Deb Smith, and Jason Green for their technical and academic input in this case. Their care and dedication have far exceeded any contributions the authors had in the successful management of this tiger.

Literature Cited

1.  Port, C.D., E.R. Maschgan, J. Pond, B. Kirschner, S. Poticha, and D.G. Scarpelli. 1981. Chronic exocrine pancreatic insufficiency in two Indian lions (Panthera leo persica). J. Comp. Pathol. 91: 483–491.

2.  Steiner, J.M., and D.A. 1999. Williams. Feline exocrine pancreatic disorders. Vet. Clin. North Am. 29: 551–575.

3.  Thomson, R.J. ed. 1988. Special Veterinary Pathology. B.C. Decker Inc., Philadelphia, PA. p. 261.

4.  Williams, D.A. May 2000. Treating dogs and cats with exocrine pancreatic insufficiency. Proc. 18th ACVIM, Seattle, WA. Pp. 531–533.


Speaker Information
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Ray L. Ball, DVM
Busch Gardens
Tampa, FL, USA

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