The discovery of West Nile virus (WNV) in the Northeast United States in 1999 and its subsequent successful establishment
on the North American continent over the last three years has had an impact on human and animal populations nationwide.
West Nile virus continues to spread across the country affecting both people and animals. Although the virus has been predominately
found in humans, horses and birds, there are now cases confirmed in companion animals.
While primarily an infection of birds and mosquitoes, the continental United States has seen an ever-widening epizootic involving
avians, mammals and even reptiles. Each successive year of active transmission has seen an explosive increase in morbidity
and mortality in birds, humans and horses as well as a widening list of other mammalian species identified with WNV-associated
illness as the virus gained new territory.
In the initial year of its discovery, WNV encephalitis was identified in a cat by the Centers for Disease Control and Prevention
(CDC). During the years 2000 and 2001, WNV infections in squirrels, rabbits and bats were identified as a consequence of public
health surveillance efforts. No additional confirmed cases of WNV encephalitis were reported in small domestic companion animals
until the summer of 2002.
WNV is one of the oldest known flaviviruses with an extensive historical geographic distribution in Africa and Asia. Previous
experimental and serosurvey data suggested the WNV had an extremely broad host range that included amphibians, mosquitoes,
ticks, birds and mammals but caused clinical illness in only a small percentage of avian species and of mammals, mainly humans
and horses. This is generally consistent with the extensive surveillance data collected in the Northeast and Southeast United
States during the first two years of the expanding epizootic and with more recent experimental infection data in dogs and
Table 1: Reported Clinical Signs in Dogs with Positive IgM and Virus Neutralizing WNV Antibody
A serosurvey was done by the CDC in stray and owned dogs and cats in New York City after the 1999 epizootic to determine the
level of exposure of these animals to WNV. Samples of 189 dogs and 12 feline samples were tested for neutralizing antibody
by plaque reduction neutralization against WNV and St. Louis encephalitis virus. Five percent of the dogs had neutralizing
antibody titers to WNV ranging from 1:80 to >/= 1:320 while none of the cats had neutralizing antibody.
More recent data presented by the CDC at the 2003 WNV Planning Meeting sponsored by the CDC and the American Society of Microbiology
in February provided additional support for the conclusion that cats and dogs are susceptible to WNV infection, but that infection
does not cause overt clinical signs in infected animals. The experiments also demonstrated that ingestion of infected mice
by cats led to productive infection of the cats and suggested that exposure by consumption was an efficient route of infection.
Infected animals developed only low virus titers and are considered to be incapable of transmitting virus to mosquitoes or
Table 2: Testing options for west nile virus
What happened in 2002?
The summer of 2002 was an explosive year for WNV in the United States and Canada. Virus expansion across the country continued
at a rapid rate. Morbidity and mortality in birds, humans and horses increased exponentially over 2001 figures, and several
new species were identified as having WNV-associated morbidity and mortality. These included llama, sheep, reindeer and a
mountain goat. The toll WNV took on wildlife in Central and Southern regions of the country has largely been unquantified,
but was substantial.
Additional firsts included a confirmed diagnosis of WNV encephalitis/myocarditis was made in an 8-year-old Golden Retriever
and a wolf cub was confirmed to have died of WNV infection in Illinois. The Animal Health Diagnostic Laboratory at Cornell
began identifying WNV neutralizing antibody positive serum samples from dogs and cats in the Midwest, Central west and Southeast
in mid to late summer with clinical histories of an acute onset neurological illness. Of the 461 dogs tested during 2002,
60 had high serum neutralizing antibody titers to WNV. One dog showed a >/=four-fold rise in titer on paired serum samples
and one 4-month-old puppy had a high SN antibody titer in serum and CSF.
A good correlation was also established between IgM positive dogs tested at the University of Nebraska and positive serum
neutralizing titers obtained from the same samples at the Cornell lab (Galeota and Glaser, unpublished data). We have follow-up
information for about 30 percent of the WNV positive dogs tested at Cornell for which histories were provided, all of which
recovered. Samples were received from 45 cats, including a cougar. Four of the cats, including the cougar were SN antibody
positive for WNV with high titers demonstrated. The cougar and one domestic cat died with no further diagnostic testing performed.
Clinical signs in WNV antibody positive dogs reported on forms or during telephone interviews with veterinarians included
weakness, ataxia, flaccid paralysis, decreased or absent patellar reflexes, inability to stand, muscle tremors, depression,
hyperesthesia, seizures and fever. Most dogs were reported to be bright, alert and able to eat and drink. Clinical signs in
the cats included seizures, ataxia, nystagmus and hyperesthesia. These signs did not differ significantly from signs reported
for animals with no detectable WNV SN titers.