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Ohio State University Extension


West Nile Virus Fact Sheet for Veterinarians

William J. A. Saville, DVM, PhD, Dipl ACVIM, Chair, Veterinary Preventive Medicine
Jeffrey D. Workman, PhD, Extension Program Coordinator, Veterinary Preventive Medicine

West Nile virus (WNV) had never been seen in the Western Hemisphere prior to 1999. It has a geographic range greater than any other known arbovirus. It is found throughout Africa and north to central Europe and eastern Asia. The earliest epidemic of West Nile (WN) fever occurred in Israel in 1951 and 1952, and involved more than 500 hospitalized patients from several small outbreaks. The largest epidemic of WN fever on record occurred in South Africa during 1974. This epidemic involved an area of about 2,500 square kilometers in the Karoo and southern Cape provinces and resulted in thousands of human infections. More recently, epidemics of WN fever have occurred in Romania (1996–97), Czechland (1997), Italy (1998), Russia (1999) and Israel (2000) so that it is considered a reemerging mosquitoborne disease. How WNV managed to be introduced into the United States and precisely when it first entered is unknown. There is speculation that it was through the importation of birds, or possibly by a mosquito transported to the United States by ship or airplane.

WNV is a member of the Japanese encephalitis virus complex of the genus Flavivirus, family Flaviviridae. This genus includes nine viruses distributed around the world. In the United States, the complex has two other representatives: Powassan and St. Louis encephalitis (SLE) viruses, both of which cause encephalitis in humans. The epidemiology of WNV is nearly identical to that of SLE virus. Both are principally carried by species of Culex mosquitoes and have birds as the reservoir. They differ in that WNV causes disease and mortality in humans, wildlife (birds, particularly crows and blue jays) and domestic animals, particularly horses. St. Louis encephalitis does not cause any remarkable disease in wildlife or mammals other than man.


Early outbreaks of WNV in horses occurred in 1962 in France, and 1963 in Egypt. Much later outbreaks occurred in 1996 in Morocco, 1998 in Italy, 2000 in France and Israel, and since 1999, the United States. In France, they recorded a 10 percent morbidity with a 30 percent mortality rate. In Morocco, the case fatality rate was 44.7 percent (42/94), and in Italy it was 42 percent (6/14). In the United States in 1999, 9 of 25 (36 percent) horses with clinical signs of the disease died or were euthanized. In 2000, there were 60 cases of WNV reported in horses from seven states, and 23 horses either died or were euthanized (38 percent). During 2001, there were 738 confirmed horses that developed clinical signs of WNV infection in 19 states with ~25 percent fatalities. In 2002, there were >14,000 confirmed equine cases of WNV from 40 states; however, no mortality data is available.

Since 1999, WNV has become endemic to the United States and continues to infect horses. WNV in equine is not on the list of reportable diseases; therefore, the number of annual cases reported is probably significantly lower than the actual number of infected horses.

WNV continues to be a serious threat to humans. The following table presents the number of human cases and fatalities in both the United States and Ohio.

WNV—Human Cases/Deaths
Year United States Ohio
Cases Deaths Cases Deaths
1999 62 7 0 0
2000 21 2 0 0
2001 66 10 0 0
2002 4,156 284 441 31
2003 9,862 264 108 8
2004 2,539 100 12 2
2005 3,000 119 61 2
2006 4,269 177 48 4
2007 3,630 124 23 3
2008 1,356 44 15 1
2009 720 32 2 0
2010 1,021 57 5 0
2011 712 43 21 1
2012 5,674 286 122 7
2013 2,469 119 24 4
2014 2,122 85 11 1

Clinical Signs

In the Italian outbreak, all cases exhibited varying degrees of ataxia and weakness in the hind limbs. Asymmetric weakness was detected in the rear limbs of some horses. Some cases also had involvement of one or both forelimbs. In six cases, there was progression of clinical signs with ascending paresis leading to tetraplegia and recumbency within nine days. Depressed mental state and tremors were noted in a few cases; however, there were no behavioral or head posture abnormalities or cranial nerve involvement. In the U.S. cases, similar clinical signs were seen; however, more brainstem signs were present in some cases. For the horses that died or were euthanized, death usually occurred within five days.


No gross pathologic lesions were detected. Histologically, all animals exhibited slight to moderate nonsuppurative encephalomyelitis, primarily in the spinal cord and lower brainstem, affecting both grey and white matter. The most severe lesions were in the thoracic and lumbar spinal cord.

Differential Diagnosis

Rabies, botulism, EPM, CVM, EHV1, EDM and other encephalitis such as WEE, EEE and VEE, would all have to be considered. Many of the cases have looked similar to commonly diagnosed neurologic diseases, particularly EPM. Considering the ascending paralysis, mentation changes and hyperesthesia in some cases, all horses that die or are euthanized should be sent for rabies diagnostics. Diagnostic rule-outs are necessary. See for aids in differential diagnosis.


Due to the zoonotic potential of WNV, all horses that develop neurologic signs from June to October should be considered WNV suspects, particularly if the virus has been detected in Ohio close to the animal you are examining. If the animal is demonstrating rapidly progressive neurologic signs with recumbency, the animal can be submitted to the ODA Animal Disease Diagnostic Laboratory in Reynoldsburg, Ohio, for rabies and WNV testing. Other diagnostics include PCR of CNS tissues and immunohistochemistry. If you decide to perform a postmortem in the field, please refer to USDA guidelines. (See


In the Italian outbreak, no treatments were effective. Similar findings occurred in the U.S. cases, as well. Regardless of the treatment, horses that survive at 6-month follow-up, ~40 percent were still exhibiting neurologic deficits. Supportive care is the only therapeutic alternative.


There are four USDA-licensed vaccines available for prevention of WNV infection in horses. A killed vaccine must be given in two doses initially, 3–6 weeks apart. Both doses should be completed at least 4 weeks prior to mosquito season. If the horse has already had the initial two doses, the first yearly booster should be given in early April. Horses that are stressed, such as show and race horses, should be given another booster in late July. Efficacy data from Ohio would suggest that <6 percent of horses that are properly vaccinated may die from WNV infection. The vaccine is considered very safe. A canarypox-vectored vaccine must be administered in two doses initially followed by annual boosters. In addition, a DNA vaccine has been released, which has demonstrated 100 percent efficacy in preventing clinical signs in foals. A WNV-chimera vaccine was also 95 percent efficacious in preventing clinical signs using a challenge model. Reduce mosquito breeding sites; decrease exposure to adult mosquitoes; provide screened housing; use insect repellents; and reduce outdoor exposure. Local mosquito control authorities may be able to help in assessing the mosquito breeding risks associated with a specific property.

Contact V​eterinarian

William J. A. Saville, DVM, PhD, DACVIM
Professor and Chair
Extension Epidemiologist/Internal Medicine
Department of Veterinary Preventive Medicine
The Ohio State University
Telephone: 614-292-9453; Fax 614-292-4142

The Status of WNV in Ohio

WNV has been confirmed in Ohio every year since 2001. Infected mosquitoes, birds, horses and humans have been found in all Ohio counties. Therefore, the virus can be present throughout the state.


For the current status of WNV in Ohio and for more information, you can visit the following websites or contact your local health department.

Program Area(s): 
Originally posted May 8, 2015.