Approximately 1 week after eating live trout from a northern California hatchery, two sun bears (Helarctos malayanus) at The Oakland Zoo developed vomiting, anorexia, diarrhea, and lethargy. A 25-year-old, 83-kg, male sun bear exhibited a sudden onset of clinical signs, and a 20-year-old, 47-kg, female bear that shared his enclosure was consistently 24–48 hours behind him in exhibiting clinical signs. A fecal flotation performed on loose stool from the male bear on the first day abnormal clinical signs were observed was negative for ova and parasites. Abdominal ultrasound of the male bear revealed mild ascites, mesenteric lymphadenopathy, and gastric dilation. Cytology of an aspirate of the abdominal fluid revealed a modified transudate with an increased number of eosinophils. Gastroduodenoscopy of the male bear revealed patchy erythema of the gastric mucosa and a large volume of green fluid in the stomach. The duodenum appeared thickened and pale. Gastrointestinal biopsies revealed severe lymphoplasmacytic and eosinophilic gastritis and enterocolitis, and erosive enteritis of the duodenal mucosa.
Subsequent flotation performed on a fecal specimen from the female on day 4 revealed multiple large, gold-colored, operculated trematode ova. The diagnosis of salmon poisoning was made after a UC Davis parasitologist identified the ova as those of Nanophyetus salmincola. Both bears were treated with oxytetracycline (Oxybiotic 200, The Butler Company, Columbus, OH, USA) at 10 mg/kg IM SID for 12 days, followed by doxycycline (IVAX Pharmaceuticals, Miami, FL, USA) at 10 mg/kg PO BID for 21 days. They also received praziquantel (Droncit, Bayer, Shawnee Mission, KS, USA) at 4 mg/kg IM SID for 3 days, followed by praziquantel at 12 mg/kg PO once, 5 days later. Both bears also received famotidine (Pepcid, Merck, Fort Washington, PA, USA) at 0.5 mg/kg PO BID for 7 days. Appetite began to gradually return within 2 days of the initiation of treatment, and stools slowly returned to normal consistency within 7 days. Fecal ova shedding began on day 4 after onset of clinical signs and ceased approximately 9 days later.
Salmon poisoning disease is caused by a rickettsial organism (Neorickettsia helminthoeca) which infects a trematode, N. salmincola. This fluke requires two intermediate hosts: a snail (Juga silicula) and a fish (usually a salmonid). The definitive host, a fish-eating mammal or bird, becomes infected when it consumes trematode-infected fish. Wild black bears native to the endemic region of this parasite have been found to be infected with the fluke but appear to be resistant to development of clinical disease. Zoo bears fed raw or improperly frozen fish have contracted the disease, but the species most affected have been bears not native to the Northwest coastal areas (polar, sloth, Himalayan, and European brown). Fish hatcheries are providing potentially infected fish for sport fishing to a geographic range far wider than the parasite’s known range, which is defined by the habitat of the intermediate host snail. With ever-increasing emphasis being placed on environmental and behavioral enrichment for captive wildlife, many zoos have adopted the practice of feeding live prey. The potential for this disease should be considered whenever fish are fed to bears. This is the first published report of salmon poisoning disease in captive sun bears.