Abstract

A 48 kg, male, banded wobbegong shark (Orectolobus ornatus) presented with a history of having prolapsed its stomach through one of its gill slits 48 hours previously. The shark had been successfully kept in a 1.25×106 L mixed species oceanarium for several years prior to this.

On examination, 20–30 cm of brown-purple tissue was protruding from the shark’s right caudal external gill slit. The animal was resting on the floor of the aquarium and there appeared to have been minor bleeding from the everted tissue.

The wobbegong was anesthetized with 1,750 mg ketamine (36.5 mg/kg) (ketamine HCl, 1 g powder; Parke Davis, North Caringbah, NSW, Australia) combined with 500 mg xylazine (10.4 mg/kg) (Rompun Dry, 500 mg base; Bayer, Pymble, NSW, Australia) administered intramuscularly by a scuba diver using a pole syringe.

Loss of righting reflex occurred after 12 minutes. Surgical anesthesia occurred after approximately 20 minutes and lasted about 50 minutes. The shark was placed in an isolation tank in 15 cm of water, allowing the gills to be covered. An oxygen cylinder, regulator, and aerator pump bubbled oxygenated water into the shark’s mouth. Spontaneous respiratory movements continued throughout the anesthetic period, at a similar rate to pre-induction (12–18 gill slit movements/minute) although at a shallower amplitude.

The prolapse consisted of a mass of swollen tissue 15×25 cm, thought to be the stomach protruding from the right caudal external gill slit. An area of more dense tissue, with an outlet tract inverting towards the oral cavity was presumed to be the pylorus. There were areas of abrasion and superficial necrosis of the gastric mucosa, but the tissue bled easily and appeared viable.

The prolapse was reduced with difficulty by traction from within the oral cavity by an arm inserted through a length of PVC piping to provide protection from the shark’s teeth. Concurrently, a second person repulsed the tissue externally whilst manually stretching the external gill slit. Once the stomach was retracted into the shark’s mouth, a single “swallowing” movement occurred, and the organ rapidly disappeared. It was assumed to have been repositioned.

Dexamethasone, 20 mg (Dexason; Ilium Veterinary Products, Smithfield, NSW, Australia), 100 ml of 5% glucose (5% Glucose Intravenous Infusion; Baxter Healthcare, Old Toongabbie, NSW, Australia) and 500 ml of Hartmann’s solution (Compound Sodium Lactate Intravenous Infusion; Baxter Healthcare, Old Toongabbie, NSW, Australia) were administered IV into the ventral caudal vein in an attempt to decrease the effects of shock and metabolic acidosis. Six daily doses of 600 mg oxytetracycline IM (Oxytet-200 LA; Ilium Veterinary Products, Smithfield, NSW, Australia) were given prophylactically as the gastric mucosal barrier was compromised.

Respiratory amplitude and rate increased to 25–30 gill movements/minute after Doxapram 100 mg IV (Dopram-V; Bomac Laboratories, Castle Hill, NSW, Australia). Yohimbine 20 mg IV (Reverzine; Parnell, Silverwater, NSW, Australia) was given to reverse xylazine induced anesthesia. Anesthetic recovery was prolonged but uneventful, and the shark was behaving and swimming normally 36 hours after chemical immobilization.

Blood was collected from the ventral caudal vein at the time of surgery and two days later (Table 1). The shark continued to behave normally over the following two weeks although it refused food. Fourteen days after replacement of the prolapsed stomach, the animal was found dead.

Table 1. Hematology and plasma biochemistry from an adult male wobbegong shark

^aThe first sample was taken 48 hours after the stomach prolapsed.
^bThe second sample was taken approximately four days after the prolapse.
^cRange of values for serum from wild and captive animals (n<20, up to eight different species)¹ converted to SI units.²

At postmortem examination, the wobbegong weighed 47 kg. The stomach was correctly positioned and was empty. There was no discernable esophago-gastric sphincter, and the mucosa was discolored red-brown in several places. Histologically, there was focal hemorrhagic necrosis of the right caudal gill lamellae with surface necrosis and deeper congestion of the surrounding gill slit area. In the stomach, there was edema and focal, hemorrhagic, mucosal necrosis with extensive submucosal necrosis. The liver showed intense, foamy vacuolation of hepatocytes, probably due to fat accumulation.

There was no evidence of bacterial infection, and microbiological culture of brown-tinged fluid from the coelomic cavity failed to grow any organisms. Heart blood was not cultured. There are no blood reference values published for the banded wobbegong shark, hence values were compared with those of other sharks.¹

No references were found to gastric prolapse in sharks, although there are anecdotal reports from fishermen of temporary stomach eversions through the mouth on capture of several shark species. The anesthetic regime used for this procedure provided surgical anesthesia of sufficient duration without the need for supplemental doses, although this was at the expense of a prolonged recovery period.

The patches of gastric mucosal and submucosal necrosis may have contributed to the death of the wobbegong but were not considered severe enough to have caused death in the apparent absence of bacterial infection. The cause of the gastric prolapse and the death of the shark two weeks after replacement remain unknown.

Acknowledgments

The authors wish to thank the staff of Sydney Aquarium, Darling Harbour, Sydney, for referring this case and for the care of the wobbegong.

Literature Cited

1.  Stoskopf MK. Clinical pathology of sharks, skates, and rays. In: Stoskopf MK, ed. Fish Medicine. Philadelphia, PA; WB Saunders & Co; 1993:754–757.

2.  Lehman HP. Metrication of clinical laboratory data in SI units. Am J Clin Path. 1976;65:2–18.