Abstract

In August 2004, a 24 year-old, male harbor seal (Phoca vitulina) displayed an acute onset of an abnormal swimming pattern accompanied by muscle fasciculations and head tremors. This seal shared an outdoor exhibit with two other harbor seals, two gray seals (Halichoerus grypus), and five California sea lions (Zalophus californianus). The seal appeared to be positively buoyant and unable to dive, with its back abnormally arched. When offered food, the seal would mouth the fish but appeared unable to swallow. The seal was moved to inside holding where radiographs were negative for abnormal gastrointestinal gas as a cause of the abnormal buoyancy. Blood work at this time was unremarkable. Medical treatment was initiated with trimethoprim sulfadiazine and flunixine meglumine, which was changed to carprofen after two days. Clinical signs were unchanged after five days. Repeat blood work showed elevated BUN, total protein, magnesium and phosphorus suggesting the seal was becoming dehydrated from being held out of water. A plaque reduction neutralization test (PRNT) for West Nile virus (WNV) was submitted at this time; this test assays for WNV-specific antibodies, IgG specifically. The next day, the seal displayed hematuria and the trimethoprim sulfadiazine, which had been stopped, was restarted. The next day, the seal displayed melena and subsequently died. Histopathology found a hemorrhagic colitis, most likely stress-related, to be the proximate cause of death; brain was not submitted. That same day, the WNV PRNT results were returned as positive.

A second, 27 year-old male harbor seal began to display the same clinical signs within a few days of the first, including anorexia, muscle twitching, and abnormal swimming pattern. Blood work showed moderate elevations in AST (200 IU/L) and ALT (100 IU/L). However, after one week of medical treatment with parenteral trimethoprim sulfadiazine, the neurologic signs abated and the seal began to eat. To minimize the stress of being held off-exhibit, the seal was returned to exhibit and the medical treatment changed to oral trimethoprim sulfadiazine, with sucralfate, a gastrointestinal protectant, added. For five days the seal ate well enough to be successfully medicated orally, but not much more. The seal died after two subsequent days of complete anorexia. This seal was also positive for WNV by PRNT. Histopathology found meningitis and myocarditis consistent with WNV infection.

Four days after the death of the second harbor seal, a 31 year-old, male grey seal became acutely anorexic and lethargic, refusing all food and training commands. After one week, recovery was spontaneous and the clinical signs have not returned. Diagnostics were not able to be performed on this seal. Two days before the onset of the clinical signs in the first harbor seal, a thick-billed parrot (Rhynchopsitta pachyrhynca) and an Impeyan pheasant (Lophophorus impeyanus) died and were both diagnosed with WNV by polymerase chain reaction (PCR) performed on kidney samples postmortem. A second pheasant and a rainbow lory (Trichoglossus haemotodus) also subsequently died and were diagnosed with WNV during this outbreak at our zoo.

The current epizootic of WNV, which primarily affects birds and horses, started in the area surrounding New York City in 1999. It has since spread slowly but steadily westward. In 2002, two other harbor seals and a grey seal held in three different institutions east of New Mexico were reported with clinical signs remarkably similar to those seen in our seals in Albuquerque; all three were diagnosed with WNV and all three succumbed to either primary or secondary infections associated with the virus.¹ It would not be surprising to see other marine mammals soon affected in California and along the Pacific coast as WNV continues its western movement.

References

1.  Duncan AE, DW Stremme, SZ Murray, AL Glaser, CK Stadler. 2003. Proceedings of the American Association of Zoo Veterinarians: 202-203.