Equine infectious neurologic disease (Proceedings)

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.

Western Equine encephalitis harbors in birds and is transmitted by mosquitoes similar to Eastern encephalitis. This virus causes much less morbidity and mortality than Eastern encephalitis. Only a little over 100 equine cases have been reported in the US since 1994.

The clinical manifestation of Venezuelan equine encephalitis is similar to that for Eastern encephalitis. The mortality and morbidity is higher than with Western Equine encephalitis but lower than that for Eastern encephalitis. The last epizootic occurred in Venezuela in 1971 and spread to Texas where it killed 1500 horses. The main host for this virus is probably rodents. The horse IS a powerful amplifying host for Venezuelan Equine encephalitis and the disease can be maintained in a population of susceptible horses with sufficient mosquitoes. Vaccination of horses is an important part of control of the virus. Horses in Texas are vaccinated for VEE if transport to South America is planned. However, export of horses to other countries requires negative testing for VEE and vaccination is avoided in these horses.

Arboviral control involves surveillance to target vector control. Equine serology, equine cases, serotesting of sentinel chickens, and PCR testing of collected mosquitoes are important parts of surveillance. Control involves mosquito sprays (trucks and planes), larvacidal treatment of mosquito pools, and elimination of standing water. Individual control includes vaccination (horses) and protective clothing.

Equine herpes-1 encephalitis results from a viral induced vasculitis of the nervous system. Two similar but genetically distinct types of Equine herpesvirus-1 are the wild type virus and the neurotropic virus. Either type can cause neurologic signs. The wild type virus is more commonly accompanied by respiratory and reproductive abnormalities and the rate of shedding by affected horses is lower. The wild type virus has a high propensity to cause neurologic signs and is shed in large amounts resulting in more rapid spread in outbreaks.

Neurologic signs most commonly include peracute ataxia with ascending paralysis (lower motor neuron disease). Urinary incontinence and/or brain stem signs can occur. However, any neurologic signs including seizures are possible. Cerebrospinal fluid commonly reflects a vasculitis with dramatically elevated protein and a normal or mildly elevated cell count. PCR testing of nasal swabs and buffy coat for herpes virus is a helpful diagnostic test. Paired serology can provide retrospective confirmation. Single serologic tests are not helpful as vaccinal titer are exceedingly high.

Treatment of Equine herpes virus-1 encephalitis includes anti-inflammatory therapy as listed above and antiviral therapy. Acyclovir and Valcyclovir have been used in horses at a cost of $80 to $170 dollars per day. Supportive care is essential and may include urinary catheterization and antimicrobials if incontinence develops.

It is recommended that congregated horses be vaccinated every 4 months to reduce the susceptibility of the population to infection in outbreak. This practice will not eliminate infection in all horses or outbreak but will reduce viral shedding, severity of cases, and severity of outbreak. The protection afforded in neurotropic outbreaks may be less. Vaccination of exposed horses in an outbreak is likely to be too late and is not advocated.

Outbreak control involves a 3-tier approach with horses with clinical signs and/or positive tests in the primary isolation group. The secondary group includes horses that were exposed to primary horses but do not have clinical signs and test negative. The tertiary group is nonexposed horses. Each group should be kept at least 3 stalls distance from other group and people should not move between the three groups without precautions designed to prevent transfer of virus. Each group should have their own supplies to prevent transmission on fomites. Body temperatures should be monitored twice daily and horses developing fever, respiratory, or neurologic signs should be quarantined and tested. Quarantine is continued for 21 days and positive tests on additional horses restart the 21 day quarantine. Outbreaks with significant losses have recently occurred in Florida, Georgia, Pennsylvania, Colorado, California, University of Findlay and other locations. In the University of Findlay outbreak, the incidence of fever was 88% 118/135 horses, Neurologic signs occurred in 34% and mortality occurred in 12%. All deaths were related to neurologic disease.