INTRODUCTION

Both acute and chronic gastritis is a significant health problem in captive cheetahs. Chronic gastritis is commonly identified in the captive cheetah, of which the majority (95%) of cases are associated with gastric spiral bacteria. In captive cheetahs with chronic vomition histological examination of gastric mucosal biopsies can vary from mild to severe gastric changes characterized by infiltration of lymphocytes and plasma cells, epithelial erosions and the presence of spiral shaped bacteria. Two bacteria that have been identified namely, gastrospirillum-like organism (GLO) referred to as Helicobacter heilmannii and H. acinonyx. Gastritis in cheetahs is similar to gastritis caused by H. pylori in man. In the cheetah it appears that Helicobacter sp. (possibly H. acinonyx) may be the more pathogenic organism as severe gastritis and clinical signs are more pronounced than in animals infected with GLO. Spiral bacteria have been most commonly detected in the gastric fundic mucosa, but can colonize all parts of the stomach, occurring in the surface mucus, glandular lumina, and intracellular canaliculi of parietal cells. Helicobacter species have been isolated from the stomach of various mammals including dogs, cats, ferrets, pigs, monkeys, and cheetahs, all of which are associated with various degrees of gastritis in their hosts.

Although Koch's postulates have been fulfilled for human gastritis caused by H. pylori, they have not been fulfilled in cheetahs, thus it cannot be categorically stated that H. acinonyx causes gastritis in the cheetah. Although the presence of spiral bacteria is highly associated with gastritis, the development of gastritis is likely multifactorial. At the Columbus Zoo in Ohio, USA, bacterial gastritis in their cheetah population seemed to be aggravated by highly stressful conditions, including large numbers of cheetahs in small enclosures, exposure to severe weather, and adult males housed in adjacent enclosures. Reduction of these stressors appeared to aid in stopping the incidence of gastritis.

CLINICAL SIGNS

Cheetahs with gastritis may show one or more of the following clinical signs: vomition, salivation, weight loss, varying degrees of anorexia, and poor hair coat. The vomition is often associated with eating. Haematemesis and melaenia are infrequently seen.

DIFFERENTIAL DIAGNOSES

Although helicobacter gastritis is a common cause of vomition and gastritis, other aetiologies need to be considered and ruled out. These include: foreign bodies, parasites, renal disease, hepatic disease, and neoplasia.

DIAGNOSTIC TESTING

In an animal that is showing acute clinical signs this is not necessary, however, in animals that show chronic vomition and/or systemic signs diagnostic testing is always indicated. It is imperative that a complete clinical examination must precede any further diagnostic testing.

Blood testing

To rule out underlying primary or secondary organ dysfunction a routine haematology and chemistry panel including serum electrolytes, urea, creatinine, proteins, and liver enzymes should be performed.

Diagnostic imaging

Depending on availability, survey and contrast radiographs and abdominal ultrasonography may be useful to rule out foreign bodies, obstructions, or masses.

ENDOSCOPY

Endoscopy is a rapid method to evaluate the gastric mucosa as well as to collect samples for analysis. The cheetah is anaesthetised, placed on left lateral recumbency and a flexible fiberoptic scope is advanced into the stomach. After all the regions of the stomach are evaluated, multiple biopsy specimens should be taken from 3 sites in the stomach: cardia, fundus, and pyloric antrum. The biopsies are taken with a biopsy forceps inserted through the endoscope.

Impression smear cytology

Gastric biopsies can be touched onto a sterile glass slide, air-dried, heat-fixed, and stained with Gram's stain or Diff Quik^® to detect the presence of Gram-negative curved to spiral bacteria, parasites, or neoplasia.

Urease test

This is done by placing a few pieces of biopsy material and gastric mucous into a tube containing urease indicator broth, sealed and incubated at 37°C for up to twenty-four hours. A colour change from deep orange to cherry red within twenty-four hours will indicate the presence of urease and thus bacteria.

Culture of gram-negative spiral bacteria

Gastric biopsies are plated immediately onto fresh brain heart infusion (BHI) agar containing horse blood containing antibiotics, and incubated at 37°C, with lid uppermost in an anaerobic jar. The presence of smooth, transparent, glistening colonies, which spread as a film over the agar, can be considered indicative of Helicobacter sp. All suspect colonies can be stained with Gram's stain to detect the presence of Gram-negative curved to spiral bacteria.

Histopathology

Gastric biopsies are fixed in 10% neutral buffered formalin, embedded in paraffin wax, cut at a thickness of 5 µm, and stained with haematoxylin and eosin (H&E). The sections are scored according to the presence of lymphocytes and plasma cells:

 Grade 0--none present.

 Grade 1--mild, multifocal or mild widespread infiltration.

 Grade 2--moderate, widespread or severe multifocal infiltration.

 Grade 3--severe, widespread infiltration and epithelial necrosis.

THERAPY

Therapy is based on basic principles that include: correcting fluid and electrolyte imbalances, deworming for intestinal parasites, reducing vomition with anti-emetics, and the surgical removal of obstructions.

Although the therapy for helicobacter gastritis is straightforward the eradication of gastric spiral organisms is difficult. Combination therapy using amoxicillin (20 mg/kg bid), metronidazole (20 mg/kg bid), and omeprazole (20 mg oid) has been used. Other drugs that that have been used are tetracyclines, sucralfate, and Pepto-Bismol. In a recent study were combination triple therapy (amoxicillin, metronidazole, and omeprazole) was used, histological gastritis was not eradicated, but gastritis improved both macroscopically and histologically by 3 months after treatment. In some cheetahs the therapy resulted in improved appetite, reduced passage of undigested meat in the faeces, improved coat quality, and a gain in body weight.

References

1.  Eaton, K.A., Radon, M J., Kramer, L., Wack, R., Shredding, R., Krakow, S., Fox, JIG. & Morgan, DRY. 1993. Epizootic gastritis associated with gastric spiral bacilli in cheetahs (Acinonyx jubatus). Vet. Pathol. 30: 55-63.

2.  Eaton, K.A., Radin, M.J., Kramer, L., Wack, R., Sherding, R., Krakwoka, S. & Morgan, D.R. 1991. Gastric spiral bacilli in captive cheetahs. Scand. J. Gastenterol. 81: 38-42.

3.  Eaton, K.A., Dewhirst, F.E., Radin, M.J., Fox, J.G., Paster, B.J., Krakwoka, S. & Morgan, D.R. 1993. Helicobacter acinonyx sp. nov. isolated from cheetahs with gastritis.. Int. J. Syst. Bacteriol. 43: 99-106.

4.  Jenkins, C.C. & Basset, J.R. 1997. Helicobacter infections. Comp. Contin. Educ. Pract. Vet. 19: 267-279.

5.  Johnson, J.H., Wolf, A.M., Jemsen, J.M., Fossum, T., Rohn, D., Green, R.W & Willard, M. 1997. Duodenal perforation in a cheetah (Acinonyx jubatus). J. Zoo Wild. Med. 28: 481-484.

6.  Lobetti, R., Kriek, N., Picard, J. & Rogers, P. 1999. Prevalence of helicobacteriosis and gastritis in semi-captive cheetahs (Acinonyx jubatus). J. Zoo Wildl. Med. 30: 492-496.

7.  Munsun, L. 1993. Diseases of captive cheetahs (Acinonyx jubatus): Results of the Cheetah Research Council Pathology Survey, 1989-1992. Zoo Biol. 12: 105-124.

8.  Radin, M.J., Eaton, K.A., Kramer, L.W., Wack, R.F., Sherding, R., Krakowka, S. & Morgan, D.R. 1990. Diagnosis of gastric spiral bacteria in the cheetah. Vet. Clin. Pathol. 20: 17.

9.  Wack, R.F., Eaton, K.A. & Kramer, L.W. 1997. Treatment of gastritis in cheetahs (Acinonyx jubatus). J. Zoo Wild. Med. 28: 260-266.

10. Wack, R.F. 1999. Gastritis in cheetahs. In: Fowler ME & Miller RE (Eds) Zoo and Wild Animal Medicine, Current therapy 4 pp 458-460.