Equine infectious neurologic disease (Proceedings)

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Equine infectious neurologic disease (Proceedings)

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Apr 01, 2009

Equine infections neurologic diseases are important individual horse disease but can also occur in significant epizootics and outbreaks with substantial economic loss. The horse often serves as a sentinel for human disease making testing and reporting practices important.

Arboviral diseases account for significant enzootics of equine and human disease. St. Louis encephalitis and West Nile Virus encephalitis are flaviviruses, Eastern, Western, and Venezuelan Equine encephalitis are the alphaviruses, and California encephalitis is a bunyavirus. The numbers of human cases of encephalitis have increased since 2000 with St. Louis encephalitis, West Nile Virus encephalitis, and Eastern Equine encephalitis accounting for the majority of these cases. The horse has served as an important sentinel in these epizootics. Eastern encephalitis and West Nile virus causes 5 to 15 % mortality in people, while the mortality in horses is 90% and 30 to 40%, respectively. Although euthanasia accounts for some of the increased mortality in horses, this disparity largely results from increased sensitivity of horses to these viruses. The higher susceptibility of horses makes them an important sentinel for human disease. Seroconversion to St. Louis encephalitis in horses has not been demonstrated.

In some states equine neurologic diseases are reportable. Suspect cases of arboviral encephalitis are defined as neurologic signs accompanied by febrile illness. Suspect cases of herpes encephalitis should be isolated. Confirmation of arboviral encephalitis is usually performed by identification of IgM antibody in a serum sample or by immunohistochemistry of brain tissue sections. A fourfold or greater increase in IgG antibody is used in absence of IgM testing.

West Nile Virus in horses can cause a variable clinical response. In the majority of cases, there is an acute onset with progression of signs for 48 to 72 hours followed by stabilization. However, in some cases progression or recrudescence after improvement occurs 4 to 14 days later. These cases are heart breaking after stabilization and some improvement. The most common clinical signs are fever, ataxia and paresis involving 1-4 limbs, hyperesthesia and excitability and muscle fasciculations. Other less common clinical signs include brain stem signs (facial paresis, tongue paralysis, dysphagia), blindness, altered mentation, seizures and coma. Complete blood count is generally normal but may reveal a lymphopenia. Serum biochemistry is usually normal but may reflect dehydration. Cerebrospinal fluid tap reveals a mononuclear pleocytosis.

Many cases recover in three to five days. Many of these are left with residual deficits that last several months or are permanent. The mortality rate is 30 to 40% comprised of those that are die and those that are euthanized for humane reasons due to severe neurologic signs.

Treatment involves supportive therapy including fluid support when dehydration occurs and nursing care. Anti-inflammatory therapy is considered pivotal and may include one or more of the following: 1 g/kg DMSO (10%) intravenously once daily, 1.1 mg/kg Flunixin meglumine intravenously one daily, or Dexamethasone. Hyperimmune plasma and interferon are available and may stop progression early in the disease. Antiviral therapy (ribavarin) has been used in some horses.

West Nile virus is harbored and amplified in various species of birds with some avian mortality. The disease is transmitted by many species of mosquitoes and culicoides. Horses and humans typically have a low viremia and are dead end hosts. One hundred seventy cases of WNV were reported to the USDA in 2008 in horses.

Eastern equine encephalitis is also maintained in birds and is transmitted by various species of mosquitoes. The disease constantly cycles between mosquitoes and birds in the Eastern United States. The reasons for break out of these cycles causing epizootics in humans and horses are unknown. There were 158 cases of Eastern equine encephalitis in horses in the United State in 2008 in Alabama, Louisiana, Florida and Georgia. Epizootics tend to occur in mid to late summer but have been reported as early as March.

There are three clinical forms in horses that are highly dependent on vaccination status. The unapparent form occurs in adequately vaccinated (every 4 to 5 months in most cases). There is a febrile illness without neurologic signs that occurs in partially vaccinated horses (interval > 5 months). Febrile illness with neurologic disease occurs in horses that are not vaccinated or that are grossly undervaccinated. The first signs occur approximately 5 days after infection and progress to death within 2-3 days. The fatality rate is 90%. Cerebral signs do predominate including: obtundation that may progress to somnolence or coma, blindness, ataxia, and proprioceptive deficits. Cerebrospinal fluid analysis reveals a mononuclear pleocytosis. A lymphopenia and neutropenia may accompany clinical signs. Diagnosis occurs via IgM testing of serum or fluorescent antibody testing of brain tissue.

Treatment involves supportive care with control of seizures and dementia via sedation. Anti-inflammatory drugs as listed above for West Nile Virus are used. The prognosis is poor due to high mortality rate.