Cats and Birds information on net.

Domestic dogs and cats were infected by mosquito bite and evaluated as hosts for West Nile virus (WNV). Viremia of low magnitude and short duration developed in four dogs but they did not display signs of disease. Four cats became viremic, with peak titers ranging from [10.sup.3.0] to [10.sup.4.0] PFU/mL. Three of the cats showed mild, non-neurologic signs of disease. WNV was net isolated from saliva of either dogs or cats during the period of viremia. An additional group of four cats were exposed to WNV orally, through ingestion of infected mice. Two cats consumed an infected mouse on three consecutive days, and two cats ate a single infected mouse. Viremia developed in all of these cats with a magnitude and duration similar to that seen in cats infected by mosquito bite, but none of the four showed clinical signs. These results suggest that dogs and cats are readily infected by WNV. The high efficiency of oral transmission observed with cats suggests that infected prey animals may serve as an important source of infection to carnivores. Neither species is likely to function as an epidemiologically important amplifying host, although the peak viremia observed in cats may be high enough to infect mosquitoes at low efficiency.
The appearance of the West Nile virus (WNV) in New York in 1999 and the subsequent establishment and spread of the virus have aroused public anxiety about the potential of companion animals to become infected, show illness and die, and transmit WNV to other species, including humans. Little information is available concerning the susceptibility of dogs and cats to WNV infection. Approximately one third of a large sample of dogs from a WNV-endemic region of South Africa had neutralizing antibody to WNV, and viremia was detected in one of three dogs inoculated with a large dose of WNV (1). Recently, WNV was isolated from the brain of a cat with "neurologic disease" (2), but nothing is known about the natural history of WNV infection in this species. Most dogs and cats spend at least some time out of doors and thus risk exposure from hematophagous insect vectors. Also, as carnivores, they may be exposed to WNV through ingestion of infected small mammals and birds, which are known to have large quantities of WNV in blood and tissue during the course of infection (2,3). Since there are an estimated 68 million companion dogs and 73 million pet cats in the United States alone (4), evaluating their response to WNV infection, assessing their potential to serve as amplifying hosts for tiffs virus, and obtaining some estimate of the clinical consequences of infection are important concerns.

Four young adult female, crossbred hounds (Harlan, Indianapolis, IN) and eight adult, female domestic, crossbred cats (Liberty Laboratories, Waverly, NY) were used. All were purchased as specific pathogen-tree animals. Each cat was negative for antibodies to feline immunodeficiency virus and negative for feline leukemia virus antigen in serum. Animals were gang housed by species under animal biosafety level three conditions with ad libitum access to food and water. They were examined clinically by a veterinarian twice daily for the duration of the study but did not receive formal neurologic evaluations. Body temperature and general appearance were recorded twice daily from days -0.5 to 7 or 9 (day 0 being the day of infection). With few exceptions, blood was collected twice daily from days -1 (dogs) or 0 (cats) to 9, at 2 and 3 weeks postinfection, and at the time of euthanasia. For the animals exposed to WNV through mosquito bites, blood was collected into EDTA tubes for hematology once daily from days -1 (dogs) or 0 (cats) to 10, and on days 14 and 21. Hematologic parameters (erythrocyte and leukocyte counts, platelet counts, plus relative and absolute mononuclear and granulocyte counts) were evaluated by using a QBC-V analyzer (Clay-Adams, Parsippany, NJ). Saliva was collected from mosquito-inoculated animals once daily from days 0 to 7 by swabbing the oral cavity with a cotton swab premoistened with BA-1 medium (M-199 salts, 1% bovine serum albumin, 250 mg/L sodium bicarbonate, 100 U penicillin G/mL, 100 [micro]g/mL streptomycin, 1 [micro]g/mL amphotericin B in 50 mM Tris, pH 7.6). All animals were euthanized between days 22 and 50 after infection by pentobarbital overdose and necropsied; their carcasses were incinerated within the containment facility.

Hematologic and body temperature data were analyzed by repeated measures analysis of variance and compared to a baseline by using the differences of least squares means statistical test (Proc Mixed, SAS Statistical Software, SAS Institute, Cary, NC). Baseline values were obtained on day 0 (body temperature) or represent the mean of values obtained on days 0 and 21 (hematologic data