Clinical Illness in Two Harbor Seals (Phoca vitulina) and One Grey Seal (Halichoerus grypus) Caused by the West Nile Virus
American Association of Zoo Veterinarians Conference 2003
Ann E. Duncan1, DVM; Donald W. Stremme2, DVM; Suzan Z. Murray3, DVM, DACZM; Amy L. Glaser4, DVM, PhD; Cynthia K. Stadler1, DVM
1Detroit Zoological Institute, Royal Oak, MI, USA; 2New Jersey State Aquarium, Camden, NJ, USA; 3National Zoological Park, Washington, DC, USA; 4Animal Health Diagnostic Laboratory, Cornell University, Ithaca, NY, USA


The West Nile virus (WNV) caused clinical illness in three seals housed at different institutions during the summer of 2002. The course of illness varied among the three, but all eventually succumbed to the virus or other illness thought to be secondary or concurrent with the virus. The cases described are the first known incidences of clinical illness due to WNV in marine mammals.

Clinical signs in each included twitching of the face, head/neck and body, reluctance to move, increased respiratory rate and effort, and anorexia. The tremors were evident when the seals were at rest but were more pronounced when they moved or reached for food items. The seals also sometimes demonstrated violent twitching in response to noises or touch. The first harbor seal (Phoca vitulina) began improving after a few days of illness and was nearly normal after day 5 with only occasional, mild tremors. He developed sneezing and epistaxis on day 12 of illness, which appeared to be resolving. He then developed dyspnea on day 23 and died on day 25. Gross and histologic exam determined the cause of death to be bronchopneumonia, possibly secondary to WNV. The second harbor seal had similar clinical signs and also had difficulty manipulating feed items. When force-fed, he gagged and appeared to be unable to swallow. The anorexia and twitching were progressive, and his motor abilities deteriorated. He died on day 10. The primary cause of death was judged to be WNV encephalitis. The grey seal (Halichoerus grypus) presented with facial twitching, lethargy, anorexia and an increased respiratory rate. Ultrasound revealed an enlarged, globoid heart. She succumbed after 3 days· of increasing respiratory distress and neurologic signs. The cause of death was determined to be dilative cardiomyopathy. In all three cases the histopathologic lesions in the brain and spinal cord were mild and alone not useful to identify affected seals.

All three seals tested positive for WNV with the plaque reduction neutralization test (PRNT) at a titer of 1:640 and were negative for St. Louis encephalitis virus (SLE) at a screening titer of 1:20. Both serum samples and pooled tissue samples from all three seals tested positive on RT-PCR. Two of the three were also positive on immunohistochemistry for WNV; one was focally positive only in the cerebrum and one was strongly positive in the spinal cord. Virus isolation was performed on the grey seal and WNV was isolated.

A second harbor seal at the first facility had very mild tremors of the head and neck on the third day of seal #1’s illness but appeared completely normal the next day. Serum was collected on day 2 and was positive for WNV on PRNT at a titer of 1:8192 and negative on RT-PCR.


I would like to thank Mike Garner, James Raymond, Dan Bradway, Donald Nichols and Ann Manharth for their knowledge and assistance with this case. Also, I would like to acknowledge the veterinary technicians and keepers at DZI and the other institutions for their dedication to the animals in our care.


Speaker Information
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Ann E. Duncan, DVM
Detroit Zoological Institute
Royal Oak, MI, USA

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