Lessons Learned from the West Nile Virus Outbreak of 1999: A Pathologist’s Perspective
American Association of Zoo Veterinarians Conference 2000
Tracey McNamara, DVM, DACVP
Wildlife Health Sciences Department of Pathology, Wildlife Conservation Society, Bronx, NY, USA



By the time this meeting takes place, the medical and veterinary community will already have weathered the second summer of potential West Nile virus cases. Many veterinarians in the audience will have read the description of the gross, histopathologic, ultrastructural, and immunohistochemical features of this viral infection in birds, as the article was published in May 2000.1 Even those without access to the journal may have reviewed the article on our website (Available: http://www.wcs.org/science/wildlifehealthsci/, then follow links to pathology) (VIN editor: Link not accessible). Therefore, the purpose of this presentation is not to rehash what has been made publicly available. Instead, as the veterinary pathologist who was on the front line during the outbreak, I would like to share some thoughts and observations about the events that led up to the unprecedented diagnosis of West Nile virus, what went right, what went wrong, and what lessons were learned for the future.

“You Are Just Dealing With a Veterinary Thing”

When the Centers for Disease Control and Prevention (CDC) was contacted in early September about the suspected link between the human deaths and the birds, the theory was dismissed with skepticism. The patients in New York City had been diagnosed as having St. Louis encephalitis (SLE), a mosquito-borne disease. According to the textbooks, birds have always served as reservoirs for the known arboviruses of the Western hemisphere. The bottom line was that birds were not supposed to die from SLE. And yet, birds were dying with encephalitis, and in large numbers.

At the zoo, antennae were raised when neurologic crows began showing up on zoo grounds. Concerned about the possibility these birds could introduce a disease to the collection, samples were submitted to the Department of Environmental Conservation (DEC), which has jurisdiction over free ranging wildlife. In the absence of a diagnosis and in the face of increasing crow mortalities, an in-house investigation was launched.

Then, when a cluster of zoo birds died with symptoms and gross and histopathologic findings similar to those seen in the crows, we shifted into emergency mode.

By 9 September, when the National Veterinary Services Laboratories (NVSL) and the CDC were contacted and sent samples, this is what they were told.

The Logic

In the face of a sudden die-off of birds, a list of possible differentials had to be considered, and quickly. What could cause high mortality in both captive and free-ranging birds? Could it be due to a bacterial infection? The birds did not have flaccid paralysis, so botulism was unlikely. Fifty-seven bacterial cultures had been performed since 1 August, and none were positive for Pasteurella multocida, the agent of fowl cholera, nor were bacteria seen on histopathologic review. Neither of these diagnoses were consistent with our findings.

Pesticides had been suspected in the crow deaths but, toxicologic analysis of several zoo cases were negative for pesticides as well.

The character of the inflammatory infiltrate and distribution of lesions were most compatible with a viral infection. But, which one? Exotic Newcastle’s disease (VVND) was a possibility due to the lymphoplasmacytic encephalitis and the presence of hemorrhage at the proventricular-ventricular junction in one flamingo. Highly pathogenic avian influenza (HPAI) was another possibility. However, having had the opportunity to participate in the Professors Course on the Recognition of Foreign Animal Diseases at the Foreign Animal Disease Laboratory (FADL) at Plum Island many years ago, I had seen experimentally induced VVND and HPAI. There were simply too many differences in the presentation of our birds, such as the lack of conjunctivitis, chemosis, shank hemorrhages, or respiratory lesions, to be comfortable with either one of those diagnoses. Besides, the chickens and turkeys in our collections were healthy. Logically, if we had been dealing with any of the known poultry diseases, those birds would have been the first to go. Hmmmm?

What if it were a mosquito-borne disease? SLE had never before been diagnosed in New York City. The human outbreak was an extraordinary event in and of itself. If, as everyone insisted, the birds could not be dying from SLE because they have co-evolved with the virus and serve as its reservoir in nature, what then, did they have?

Eastern equine encephalitis (EEE) was a reasonable possibility. EEE does occur in this region and it can be fatal to exotic birds. But that was the problem. EEE is known to be virulent in emus and, the fact was, our emus were doing just fine. Would they not have acted as sentinels in the face of an EEE outbreak? Hmmmm...

Finally, there was another puzzling fact. North and South American species of birds were dying. Chilean flamingos, Guanay cormorants, a bald eagle, and a snowy owl. If we were dealing with a mosquito-borne disease in the avian population, logic dictated it would have to be either a variation on the known or, something entirely new.

The Outcome

Ultimately, the virus that killed New Yorkers, wild crows, and our collection birds was found to be one and the same. What came as a shock to the medical community did not, however, come as a great surprise to those in the field of zoo and wildlife comparative pathology. We are accustomed to working at the edge of a frontier. We routinely expect the unexpected. This mindset and outlook is the reason we campaign for complete necropsies on every animal, on the preservation of samples from each and every organ for histopathologic review, for the creation of archival tissue, slide, and paraffin block libraries, for readily accessed computerized databases, for routine bacteriologic cultures, impression smears, preservation of samples for ultrastructural studies, and virus isolation. All of these played a critical role in the recognition, diagnosis, and understanding of the pathogenesis of West Nile virus in birds. Ironically, more complete pathology data are available on the bird than on human cases from this outbreak. This, in spite of the fact that zoological institutions are generally underfunded, underequipped, and understaffed when compared to the domestic veterinary or medical community. We did everything right. Now, if only we could get the funding to allow us to do more of it!

Literature Cited

1.  Steele KE, Linn MJ, Schoepp RJ, Komar N, Geisbert TW, Manduca RM, et al. Pathology of fatal West Nile virus infections in native and exotic birds during the 1999 outbreak in New York City, New York. Vet Pathol. 2000;37(3):208–224.


Speaker Information
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Tracey McNamara, DVM, DACVP
Wildlife Health Sciences Department of Pathology
Wildlife Conservation Society
Bronx, NY, USA

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