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Summer 2002 Newsletter

Intestinal Giardiasis
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West Nile Encephalitis In Horses

West Nile Virus (WNV) encephalitis is a viral disease that is relatively new to the United States.  The disease gets its name from the West Nile District of Uganda in Africa where it was first recognized in humans in 1937.  The first cases of WNV infection in horses were recognized in France and Egypt in the early 1960’s.  WNV infection was known to occur in Africa, the Middle East and parts of southern Europe, but the virus was not isolated in the U.S. until 1999, when an epidemic of WNV encephalitis and aseptic meningitis was diagnosed in New York City.  Concurrent epizootics occurred in horses on Long Island and in birds.  The close genetic relationship between WNV isolates from Israel and New York suggests that the virus was imported into North America from the Middle East.  It is not known how the virus came to the U.S. but, given the location of the first outbreak, it is likely that it arrived via airline or boat in an infected bird or mosquito.

  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 U.S., the complex has two other representatives, Powassan and St. Louis Encephalitis viruses, both of which cause encephalitis in humans.  In 1999, 9 of 25 (36.0%) horses from Long Island, NY with clinical signs of the disease died or were euthanized.  In 2000, 60 cases of WNV were reported in horses from 7 states, and 23 (38.3%) horses either died or were subjected to euthanasia.  In 2001, 640 confirmed cases of WNV infection in horses were reported from 20 states, and 156 (24.4%) horses either died or were euthanized.

  Wild birds of many different species are the reservoir for WNV.  The virus is transmitted by mosquitoes who acquire it from infected birds.  Horses and humans are considered accidental or dead-end hosts.  A mosquito that has fed on an infected bird can bite people or horses (or other mammals) and transmit WNV to them.  Infected birds may die from the disease though most avian species are resistant.  Consequently, birds may have the virus circulating in their bloodstream for some time (viremic stage) allowing further infection of other mosquitoes, but they do not develop symptoms of illness.  Horses and humans only develop a low-level and transient viremia, thereby diminishing the importance of their role in the transmission cycle of the virus.

  Persistence of the virus in migrating birds is considered to be one of the main factors in the spread of the disease.  At least 17 species were affected in 1999 and 76 in 2000, particularly the American crow.  The signs of illness in these birds include convulsions, tremors, head tilt, wing drop, paralysis, loss of balance, and circling.  Less specific signs, such as weakness and lying on the chest, may also be observed.  Although as many as 40 species of mosquitoes are potential hosts and 14 different species were identified as carriers of the virus in the U.S., the primary species involved are Culexpipiens and Aedesvexans.

  The incubation period of WNV infection is usually 5-22 days.  Clinical signs in affected horses may include both central and peripheral nervous system signs, consisting most frequently of ataxia, lack of interest in surroundings, weakness of limbs, muscle fasciculation, and loss of appetite.  Horses may become recumbent and may be unable to get up without help.  Some horses may develop fever. The target organ of the virus is the brain and spinal cord where it causes inflammatory reaction (encephalitis), manifested by variable neurological signs.  Affected horses, which show no progression of gait abnormalities, usually recover completely with no consequences within 5-15 days.

  The clinical signs of the disease may be indistinguishable from other equine encephalitides including rabies, equine herpes virus-1, equine protozoalmyeloencephalitis, and Eastern, Western, or Venezuelan equine encephalomyelitides.  Therefore, diagnostic tests are necessary for a definitive diagnosis.  Whole blood, serum, and cerebrospinal fluid (CSF) should be submitted to the National Veterinary Services Laboratory, through Purdue ADDL, with a complete history of the case.  If the animal presented rapidly progressive neurologic signs including recumbency, it should be submitted to ADDL requesting rabies and WNV testing.  Field postmortem analysis should follow USDA guidelines.

  There is no specific treatment for WNV encephalitis.  General supportive care should be provided.  Regardless of the treatment, horses that survive usually recover quickly.  A new vaccine is available for prevention of WNV infection in horses.  It is a killed vaccine which must be given in two doses initially, with an interval of three to six weeks.  Both doses should be completed at least three weeks prior to mosquito season.  Efficacy data of the vaccine are not available at this time; however, the vaccine is considered to be safe.

  Since mosquitoes are associated with WNV transmission, the key for preventing or controlling future outbreaks of WNV among horses is to control mosquito populations and prevent horses from being exposed to these insects.  Recommendations include reducing mosquito breeding sites, providing screened housing, using insect repellants, and reducing outside exposure of the animals.  Horse owners also need to watch for dead birds, particularly crows, on their property.   Presence of the virus in a given area may be first indicated by seeing dead birds in the vicinity.  Crows are particularly susceptible.  Diagnosis of WNV can be determined by submitting dead birds to the ADDL or the Indiana Department of Health.

  Testing at this time is limited to crows,blue jays or raptors as these are the species most susceptible to the disease

-by Rajeev Nair, ECFVG Student

-edited by Dr. Ingeborg Langohr, ADDL Graduate student


1.  Cantile C. et al: 2000.  Clinical and neuropathological features of West Nile Virus equine encephalomyelitis in Italy.  Equine Vet J 32: 31-35.

2.  Ostund, EN et al: 2001.  Equine West NileEncephalitis, United States.  Emerg Infect Dis 7: 665-669.

3. Ostlund EN et al: 2001.  West Nile Encephalitis.  Vet Clin North Am Equine Pract 16: 427-441.

4. Petersen LR : 2001.  West Nile Virus: A reemerging global pathogen.  Emerg Infect Dis 7: 611-615.

5. Trock, SC: 1999, 2000.  West Nile Virus Outbreak among Horses in New YorkState Emerg Infect Dis 7:745-747.


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