Equine arboviral encephalomyelitis is due to infection with arthropod-borne viruses typically belonging to the families Togaviridae (genus Alphavirus) or Flaviviridae (genus Flavivirus). Initial clinical findings are nonspecific and include fever, anorexia, and stiffness. Subsequent diffuse encephalomyelitis causes clinical signs consistent with forebrain and cranial nerve dysfunction. In endemic areas, a presumptive diagnosis is based on vaccination history, clinical presentation, and case progression; however, serologic testing and necropsy are required for definitive diagnosis of viral infection and subsequent encephalomyelitis.
Equine encephalitides can be clinically similar between viral etiologies; they are usually characterized by diffuse encephalomyelitis or meningoencephalomyelitis, signs of CNS dysfunction, and moderate to high mortality rates. Arboviruses are the most common cause of equine encephalitis; however, rabies virus, Sarcocystis neurona , Neospora hughesi, equine herpesviruses, and several bacteria and nematodes may also cause encephalitis.
Arboviruses are transmitted by mosquitoes or other hematophagous insects, can infect a variety of vertebrate hosts (including humans), and may cause serious disease. Most pathogenic arboviruses use a mosquito-to-bird or mosquito-to-rodent cycle. Tickborne encephalitides are also a differential cause in the eastern hemisphere. Arboviral diseases are ever-emerging, and there are arboviruses pathogenic to horses on virtually every continent.
Etiology and Epidemiology of Equine Arboviral Encephalomyelitis
Alphaviruses
Togaviridae species endemic to North, Central, or South America include Eastern equine encephalitis virus (EEEV), Western equine encephalitis virus (WEEV), Highlands J virus, Venezuelan equine encephalitis virus (VEEV), Everglades virus, and Una virus ( see Table: Equine Encephalomyelitis: Causative Arboviruses). Other alphaviruses associated with equine encephalitis are Semliki Forest virus in Africa and Ross River virus in Australia and the South Pacific.
EEEV has two distinct antigenic variants that are separated geographically. The North American variant is the most pathogenic and is found in eastern Canada, all US states east of the Mississippi River, Arkansas, Minnesota, South Dakota, Texas; and in the Caribbean islands. The South American variant, now called Madariaga virus (MADV), is less pathogenic and is confined to Central and South America.
The general life cycle of alphaviruses involves transmission between birds and/or rodents and mosquitoes. In North America, theoretically, EEEV is perpetuated in a sylvatic cycle between avian hosts (passerine birds) and mosquitoes, with primary transmission in this cycle via Culiseta melanura. Birds do not develop disease but develop sufficient viremia for transmission to mosquitoes. Fieldwork in Alabama indicates that the northern cardinal is the primary target for C melanura feeding; however, other mosquitoes (eg, C erraticus) are capable of feeding on a wider variety of birds, including robins, chickadees, owls, and mockingbirds. Mammalian reservoirs such as the cotton rat may also be important during years of high EEEV transmission. Horses and humans are clinically affected but do not develop sufficiently high viral loads to transmit virus to mosquitoes, and so are considered “dead-end” hosts. During epizootics, alpacas, llamas, sheep, cattle, swine, cats, and dogs can develop disease. Snakes have been identified as a possible reservoir.
Freshwater hardwood swamps are the most associated enzootic niche for EEEV. In the southern US, which has the highest number of reported annual cases, reemergence within mammalian hosts is associated with “tree farms” that often function as inland freshwater swamps. However, EEEV disease occurs frequently in naive horses in southeastern habitats not associated with sylvatic field ecology, so a full understanding of the epizootic cycle still remains to be elucidated. Intense focal activity has also been reported in northern states, including Michigan, Wisconsin, Ohio, Massachusetts, and New Hampshire. In 2005, Massachusetts experienced a human case rate more than five times that of the preceding 10 years; those affected resided within half a mile of a cranberry bog or swamp associated with forest habitat.
In Central and South America, the principal vectors of MADV are Culex (Melanoconion) spp. These vectors feed on birds, rodents, marsupials, and reptiles, with rodent reservoirs possibly featuring more importantly in this life cycle. Before the year 2000, comparatively few epizootics of disease due to MADV in horses were recorded in South America, with minimal disease reported in humans. However, in 2008, 2009, and 2019, larger outbreaks occurred in Central and South America. In northeastern Brazil, 229 horses were affected in 2009, with a case fatality rate of 73%.
Equine Encephalomyelitis: Causative Arboviruses
Virus Species or Variant | Geographic Location | Most Important Reservoir |
|---|---|---|
Alphaviruses | ||
EEEV | Eastern North America, primarily east of Mississippi River | Birds |
Madariaga virus | South America, Caribbean | Rodents |
Western equine encephalitis virus | Western North America, Central and South America | Birds, rabbits, and snakes |
Highlands J virus | Eastern North America (as for EEEV) | Birds |
Venezuelan equine encephalitis virus | Central and South America, Caribbean | Cotton rat and other rodents |
Everglades virus | South Florida (US) | Rodents |
Ross River virus | Australia, Papua New Guinea | Marsupial and placental mammals |
Semliki Forest virus | East and West Africa | Unknown |
Una virus | South America | Birds |
Flaviviruses | ||
Japanese encephalitis | Asia: particularly India and Russia; Western Pacific | Birds, swine |
Murray Valley | Australia, Papua New Guinea | Birds, marsupials, and foxes |
Kunjin virus | Australia | Birds (herons and ibis) |
St. Louis encephalitis | North, Central, and South America | Birds |
Usutu virus | Europe, Africa | Birds |
West Nile virus | Africa; Middle East; Europe; North, Central, and South America; Australia | Passerine birds |
Louping ill virus | Iberian Peninsula, UK | Sheep, grouse |
Powassan virus | North America, Russia | Lagomorphs, rodents, mice, skunks |
Tickborne encephalitis | Asia, Europe: particularly Finland and Russia | Small rodents |
EEEV, eastern equine encephalitis virus. | ||
As the name implies, WEEV is found in western regions of North America, and also in Mexico and South America. WEEV has several other subtypes: Highlands J virus, Sindbis, Aura, Ft. Morgan, and Y 62–33. WEEV previously isolated in the southern and eastern US has been shown to belong to the Highlands J virus serogroup. WEEV is transmitted primarily by Culex tarsalis, which is found just west of the Mississippi River and throughout the West. This mosquito breeds in sunlit marshes and in pools of irrigation water in pastures. WEEV can also be transmitted by the tick Dermacentor andersoni. Epizootics of WEE are associated with increased rainfall in early spring followed by warmer than normal temperatures.
VEEV has six antigenically related subtypes: subtype I, Everglades, Mucambo, Pixuna, Cabassou, and AG80–663. Subtype II (Everglades) has been isolated from humans and mosquitoes in Florida; subtype III has been isolated in the Rocky Mountains and northern plains states. Sylvatic VEE viruses are found throughout North, Central, and South America in jungle or swampy areas. The mosquitoes that serve as the primary vectors for the bird- or rodent-mosquito life cycle are members of the subgenus Melanoconion (eg, Culex cedecci). Both enzootic and epizootic cycles exist. Epizootics (outbreaks) are associated with viral mutation to a subtype I (AB, C, and possibly E), a change in mammalian pathogenesis, and a change to several bridge vectors (mosquitoes capable of feeding on animals of multiple species).
The enzootic (endemic) cycle centers around sylvatic rodents such as spiny and cotton rats, who develop a high-titer viremia and transmit VEEV to mosquitoes. Opossums, bats, and shorebirds likely contribute to dispersal of the enzootic virus. When epizootics of VEEV occur with viral mutation and the aforementioned change in mosquito vectors, equine infection perpetuates the outbreak: although all mammalian hosts are capable of developing a high-titer viremia, the horse appears to be the most important mammalian host for vector transmission.
Flaviviruses
In general, viruses belonging to the Flaviviridae and Bunyaviridae families are less pathogenic than the Togaviridae; however, viral encephalomyelitis due to any of these pathogens is a potentially catastrophic illness for any vertebrate host. There are 53 species of flavivirus, and many are clinical pathogens for horses, including Japanese encephalitis, West Nile virus (WNV) encephalitis, Kunjin virus (KUN), and Murray Valley encephalitis virus.
Overall, the diseases due to the Japanese encephalitis serogroup are similar ( see Table: Equine Encephalomyelitis: Causative Arboviruses). All of these viruses are transmitted by a mosquito vector, with Culex spp usually the most efficient transmitter. KUN is actually a strain of WNV and is found in Australia, some southeast Asia countries, and New Guinea. Disease in horses due to Murray Valley fever is geographically restricted to the South Pacific and occurs sporadically.
Most equine-associated flaviviruses are maintained in an enzootic transmission cycle between wild birds and mosquitoes, although tickborne encephalitis found in Eurasia can also cause disease in horses. Many species of mosquitoes can transmit the equine virulent viruses, although Culex spp are principal vectors to maintain enzootic activity. Culex pipiens complex and C tarsalis are thought to play the largest role in natural transmission in North America. In the eastern and Midwestern regions of the US, C pipiens is one of the major vectors, whereas in the western regions of the US, C tarsalis is thought to be one of the most efficient vectors.
West Nile virus has the widest geographic distribution of all of the flaviviruses. Prior to 1999, WNV was recognized in Africa, the Middle East, Asia, and occasionally in European countries. In 1999, WNV infection was first recognized in North America. Since then, the virus has spread throughout the US and parts of Canada and Mexico.
Both wetland and terrestrial birds may be involved in the natural cycle of WNV, with migratory birds thought to introduce the virus into a geographic region. WNV isolated from the outbreak in New York in 1999 appears to be closely related to an isolate recovered from geese in Israel in 1998. Although fatal infections among corvids (eg, crows, blue jays, and magpies) were the hallmark of the initial WNV outbreak in the US, a wide range of infected birds (~326) have high, sustained viremia but little or no clinical disease (eg, passerines). Ticks have been demonstrated to be infected with WNV, but their role in natural transmission is unknown. In addition to birds, only alligators have consistently demonstrated high enough viremia to amplify virus, serve as reservoir hosts, and transmit WNV back to mosquitoes. Sporadic WNV infections and illness have also occurred in several other mammalian species besides horses, including dogs, cats, camelids, sheep, and squirrels. In humans, other non-vector routes of infection include blood transfusions, organ donation, breast milk, and across the placenta.
Bunyaviruses
Miscellaneous bunyaviruses, such as Cache Valley virus, Main Drain virus and snowshoe hare virus, have all been identified as infrequent causes of encephalitis in horses.
Zoonotic Risk of Equine Arboviral Encephalomyelitis
Humans may be infected by most of the arboviruses that commonly cause viral encephalitis in horses. Clinical signs in humans vary from mild flu-like symptoms to death. Children, the elderly, and those who are immunosuppressed are the most susceptible. Humans with neurologic disease due to arboviruses usually have permanent neurologic impairment after recovery. Human disease is reported infrequently and generally follows equine infections by ~2 weeks.
Veterinarians should be aware of the possibility of human infection and use repellents and other procedures to protect themselves from hematophagous insects when working in sylvatic virus habitats or handling viremic horses. In addition, waterproof clothing (gown, boots, gloves), respirator (N95 or N99 mask), face shield, and hair covering are recommended during all necropsies performed on horses suspected of having encephalomyelitis.
The reporting of equine arboviral encephalomyelitis (or suspicion of such) on an international and national basis is a basic duty of all veterinarians to ensure the health and safety of horses and humans. As such, a thorough diagnostic investigation to confirm these infections is imperative.
Clinical Findings of Equine Arboviral Encephalomyelitis
The initial clinical signs of equine encephalomyelitis are similar among the arboviruses; progression of clinical signs and severity of disease are the differentiating features. Initially, horses are quiet and somnolent, with neurologic clinical signs generally occurring 9–11 days after infection.
Clinical signs of EEE and VEE include altered mentation, impaired vision, aimless wandering, head pressing, circling, inability to swallow, ataxia, paresis and paralysis, seizures, and death; these features are less commonly found in WEE and WNV cases. Spinal ataxia is often symmetric in all limbs, rapidly progressing to quadriparesis, along with intensification of forebrain signs. Many horses progress to recumbency within 12–18 hours of onset of neurologic abnormalities. Most deaths occur within 2–3 days after the onset of clinical signs.
The clinical signs and course of disease are highly variable with WNV and other flavivirus encephalomyelitis. Cases typically present with neurologic dysfunction; other initial complaints include colic, lameness, and systemic clinical signs such as fever, anorexia, and lethargy. Neurologic clinical signs are highly variable, but spinal cord disease and moderate mental aberrations are most consistent. Spinal cord disease manifests as asymmetric, multifocal, or diffuse ataxia and paresis. Severe manifestations of WNV may occur independently in the fore- or hindlimbs, unilaterally, or in a single limb.
In all clinical studies published to date, for WNV, > 90% of affected horses developed some type of spinal cord clinical signs, whereas 40%–60% displayed behavioral changes characterized by periods of hyperesthesia, ranging from mild apprehension to overt hyperexcitability, with fractious reactions to aural, visual, and tactile stimuli. Fine and coarse tremors of the face and neck muscles are common, described in 60%–90% of horses. Some horses have periods of cataplexy or narcolepsy that may render them temporarily or permanently recumbent.
Cranial nerve deficits can be seen in all arbovirus infections of horses. Weakness and/or paralysis of the face and tongue are most frequent. Horses with facial and tongue paresis can be dysphagic, and overt clinical signs of quidding or even esophageal choke can develop. Many horses with severe obtundation and facial paresis will keep their heads low, resulting in marked facial edema. Occasionally, a head tilt may be seen.
Infrequently in WNV disease, urinary dysfunction ranging from mild straining to stranguria has been reported; when present, these signs make differentiation from equine herpesvirus 1 (EHV-1) myeloencephalopathy more challenging.
Secondary effects of neurologic deficits can themselves be life-threatening in horses with encephalomyelitis. During the neurologic phase, horses frequently thrash and cause self-trauma. Prolonged recumbency leads to pulmonary infections, especially in foals. The use of slings or recumbency itself can cause serious decubital sores; corneal injury, myopathy or neuropathy may also occur. Dysphagia leads to decreased water and food intake, with potential for renal injury due to concurrent use of anti-inflammatory drugs.
Lesions on Post-mortem Examination
All necropsies on horses suspected of viral encephalitis should be performed with all participants wearing personal protective gear (ie, waterproof gown, boots, gloves, N95 or N99 mask, face shield, and hair covering). Gross lesions are most common with EEE and severe VEE and are characterized by widespread and prominent congestion of the meninges. In other infections, gross lesions are rarer, and are limited to small multifocal areas of discoloration and hemorrhage throughout the brain and spinal cord. The brain should be examined microscopically for the presence of meningoencephalitis.
In EEEV infection, a severe gliosis with necrosis of the neuropil occurs in the cerebrum and extends through the hindbrain into the cervical spinal cord. Although mononuclear cells are present, neutrophils are predominant and are diffusely distributed. The gliosis is less nodular than in WNV, and when there are accumulations of cells, there is extensive necrosis and often frank microscopic hemorrhage within and around lesions. In milder cases of EEE and in WNV infections, a non-necrotizing lymphohistiocytic encephalitis of the gray matter is seen on histology. In more severe cases of EEE, there can be extravasation of fluid and red blood cells from vessels. The most severe gliosis and perivascular cuffing is often in the midbrain and hindbrain (pons and medulla), extending into the cerebellum. Lesions can be multifocal in the spinal cord and can be more severe in the lumbar cord.
Diagnosis of Equine Arboviral Encephalomyelitis
Clinical presentation (including epidemiology and vaccination status)
Serologic testing (IgM capture ELISA)
Exclusion of other differentials (eg, equine protozoal myeloencephalitis)
Viral detection (postmortem)
No consistent changes in clinical pathology have been found in equine arboviral encephalomyelitis, and no pathognomonic signs distinguish these infections from other CNS diseases of horses; as such, a full diagnostic evaluation should be performed. Confirmation of viral encephalitis in horses begins with assessment of whether the horse:
meets the case definition based on clinical signs
resides in an area in which arbovirus has been detected in the current calendar year in mosquitoes, birds, humans, or horses
has received appropriate vaccination
In terms of antemortem diagnostic testing, analysis of CSF can be a valuable adjunct to presumptive clinical assessment. CSF from horses with acute EEEV infection typically shows a neutrophilic pleocytosis with markedly increased protein concentration. Horses infected with EEEV that are partially immune may have predominantly mononuclear cells; however, nondegenerate neutrophils are still present. WNV-infected horses can have normal CSF, but if the CSF is abnormal, there is a mononuclear pleocytosis with moderately to markedly increased protein. In a few horses with acute infections, virus may be isolated from the CSF; since viremia ends before neurologic signs develop, the virus cannot be detected in plasma.
Serology is the key to antemortem diagnosis of recent alphavirus and flavivirus infection in horses showing clinical signs. Paired serum samples are essential to detect recent exposure and differentiate antibody response due to field infection from vaccine responses. IgM antibody rises sharply and is increased in 85%–90% of horses with clinical arboviral encephalitis. Thus, the IgM capture ELISA is the test of choice to detect recent exposure to these viruses. Neutralizing antibody titers (primarily IgG) develop slowly during this time and stay increased for several months. Neutralizing antibody tests will differentiate between subtypes of these viruses and are considered the gold standard for confirmatory serology; the most common neutralizing antibody test formats are the classic plaque reduction neutralization test and a microwell format test.
Because virus-neutralizing antibodies appear at the end of viremia and may precede appearance of neurologic clinical signs, paired samples may not show a 4-fold increase in horses with neurologic signs. In horses that succumb without antemortem and postmortem testing, paired samples from febrile herdmates may be necessary to confirm presence of arbovirus activity within a locale. Maternal antibodies may interfere with neutralizing responses in young foals, and this response is also confounded by recent vaccination.
Several postmortem diagnostic assays are available, and, although specific, they vary in sensitivity, depending on the virus. The brainstem has the highest concentrations of encephalitic viruses, including rabies virus. Immunohistochemistry and PCR assay testing for EEEV and EHV-1 are relatively straightforward compared with that for WNV.
Because of the low viral load in WNV infection, viral detection is unreliable as a diagnostic. Often, only a single neuron in one or two sections may yield positive virus staining in the horse by immunohistochemistry. When tested by PCR assay, the limited viral load requires testing of samples from several locations, including the thalamus, hypothalamus, rostral colliculus, pons, medulla, and spinal cord.
Infectious and noninfectious causes of brain and spinal cord diseases should be considered as differential diagnoses. Infectious causes include alphaviruses, rabies, equine protozoal myeloencephalitis, and EHV-1; less likely causes are botulism, bacterial meningoencephalitis and verminous meningoencephalomyelitis (eg, Halicephalobus gingivalis, Setaria spp, Strongylus vulgaris, ). Hendra virus infection is an important differential in Australia. Noninfectious causes include hypocalcemia, various toxicities, hepatoencephalopathy, head trauma, and equine leukoencephalomalacia.
Treatment of Equine Arboviral Encephalomyelitis
No specific antiviral treatment
Supportive care (especially if recumbent)
Sedation, anti-inflammatories, and antimicrobials
Treatment of equine arboviral encephalomyelitis is supportive because there are no specific antiviral therapies. Management is focused on controlling pain and inflammation, preventing injuries associated with ataxia or recumbency, and supporting bodily functions as needed by hydration, nutrition and rotational positioning. Intervention does not appear to greatly affect the outcome of most fulminant EEEV infections. For WNV, flunixin meglumine (1.1 mg/kg, IV, every 12 hours up to 5 days) early in the course of the disease decreases the severity of muscle tremors and fasciculations within a few hours of administration. Until equine protozoal myeloencephalitis is excluded, antiprotozoal medications may be instituted. Broad-spectrum antimicrobials should be administered for treatment of wounds, cellulitis, and pneumonia.
Recumbent horses that are mentally alert frequently thrash, causing self-inflicted wounds and posing a risk to personnel. Responses to tranquilizers and anticonvulsant medications are variable, depending on the virus and severity of disease. A sling and hoist may be used to assist horses that are recumbent and have difficulty rising; however, recumbent horses with EEEV generally are too neurologically compromised to sling. Horses with intermittent or focal neuropathies have a better prognosis than those with complete flaccid paralysis or that appear comatose.
Prognosis of Equine Arboviral Encephalomyelitis
Mortality of horses showing clinical signs from equine arboviral encephalomyelitis is 50%–90%, from WEEV 20%–50%, from VEEV 50%–75%, and from flavivirus infections 35%-45%. In EEEV infection, death is frequently spontaneous. With WNV disease, horses are more often euthanized for humane reasons, but spontaneous death does occur.
In WNV disease, clinical signs can last from 1 day to several weeks in horses that survive; improvement usually occurs within 7 days of onset of clinical signs. Although 80%–90% of owners report that the horse returns to normal function 1–6 months after disease, at least 10% of owners report longterm deficits that limit athletic potential and resale value. Deficits include residual weakness or ataxia in one or more limbs, fatigue with exercise, focal or generalized muscle atrophy, and changes in personality and behavioral aberrations. In contrast to WNV, horses that recover from alphavirus infection have a high incidence of residual neurologic deficits.
Prevention of Equine Arboviral Encephalomyelitis
Protection against the viruses linked to equine arboviral encephalomyelitis is essential. Vaccination against alphaviruses and flaviviruses with core annual vaccines is considered the standard of care for all horses in the US as endorsed by the American Association of Equine Practitioners. Formalin-inactivated whole viral vaccines for EEEV, WEEV, and VEEV are commercially available in bi- and trivalent forms, usually formulated with tetanus toxoid; several now include WNV.
Nonvaccinated adult horses require an initial two-injection series. For adult horses in temperate climates, an annual booster within 1 month before the start of the arbovirus season is recommended. However, for horses that travel between northern and southern areas affected by the virus, boosters should be administered two or even three times yearly in active arbovirus seasons. Mares should be vaccinated 1 month before foaling to induce colostral antibody. If a pregnant mare has not previously been vaccinated, the full priming series starting 2 months before foaling is recommended. However, some mares do not produce colostral antibody if vaccinated for the first time during gestation.
Foals that have received adequate colostrum from vaccinated dams should be vaccinated at 4–6 months old and administered booster vaccines 30 and 90 days later. It is unclear whether maternal antibody interferes with vaccine responses in foals. Epidemiologic evidence strongly indicates that horses between 4 months and 4 years old are highly susceptible to EEEV. If there is early spring (March) arboviral activity in the southeastern US, horses may require three injections throughout the year, especially in horses < 5 years old and in horses that have recently arrived in the region. In foals born to nonvaccinated or minimally vaccinated mares, maternal immunity may wane, and a 4-series vaccination protocol should be started at 3 months old. The second and third doses should be administered 4 weeks apart, and the fourth dose at 10 months old, prior to the onset of the vector season.
In Florida, where the highest numbers of EEEV cases occur, horses of all ages should be vaccinated in January and again in April before the peak of the season. A third vaccination should be administered late in the summer if the season is particularly active. The frequency of vaccination may be minimized to once or twice per year in climates that have short mosquito seasons and in which limited activity has historically been reported.
Currently, several whole inactivated virion vaccines, one recombinant inactivated vaccine, one killed, adjuvanted vaccine and a canarypox-vectored vaccine are licensed for prevention of WNV viremia in most of the Americas, including the US and Canada, and in Europe. There is experimental evidence that the canarypox WNV lineage 1 vaccine provides cross-protection against WNV lineage 2 infection. WNV challenge studies indicate that ~10% of properly immunized horses do not produce neutralizing antibodies to WNV and that 2.3%–3% of equine WNV cases seen in the field are in fully vaccinated horses. The duration of immunity from vaccination with the killed, adjuvanted WNV vaccine is unknown.
Protection of horses from arboviruses must also include efforts to manage the environment and minimize exposure to infected mosquitoes, such as:
applying insect repellent containing permethrin on the horses at least daily during vector season, especially at times of day when mosquitoes may be most active
keeping barn area, paddocks, and pastures cleared of weeds and organic material, such as feces, that might harbor adult mosquitoes
cleaning water tanks and buckets at least weekly to decrease mosquito breeding areas
removing stagnant water from the property
Options for control of arbovirus infection in other animals emphasize decreasing exposure. Few arbovirus infections have been documented in dogs and cats; however, exposure to EEEV and WNV is detected in both species during arbovirus seasons. In active years, young dogs have been reported to be susceptible to EEEV infection. Keeping dogs and cats indoors or in a screened area, especially during the time when mosquitoes are most active, decreases exposure. Disposal of dead birds or other small prey that might be eaten may decrease oral exposure.
Clinical cases of EEEV and WNV have also been recorded in other domestic and exotic animals during active seasons. Emus are exceptionally susceptible to EEEV. These animals are used for the commercial food industry, and infection results in high viremia and high amounts of virus shedding rectally, orally, and in regurgitated material. Vaccination will prevent viremia, shedding, and disease. Camelids are susceptible to WNV, and numerous reports of disease and pathology were recorded as the virus spread across North America. The killed, adjuvanted virus vaccine marketed for use in horses has been administered in camelids without any reports of major adverse effects, and animals have demonstrated production of neutralizing antibody.
Key Points
Pathogenic arboviruses are found worldwide and mostly rely on a mosquito-to-bird or mosquito-to-rodent life cycle.
Infected horses initially show nonspecific clinical signs during viremia; neurologic deficits become evident approximately 10 days after infection. Disease is associated with moderate to high mortality.
A presumptive diagnosis is often made in endemic areas based on clinical presentation, case progression, lack of appropriate vaccination, and serological evidence of acute viral infection. A definitive diagnosis is typically only made postmortem.
Most of the arboviruses that commonly cause viral encephalitis in horses are zoonotic, thus can cause disease in humans.
For More Information
West Nile virus 2022 provisional multi-mode data. CDC ArboNET. Published online August 23, 2022.
Core vaccination guidelines. American Association of Equine Practitioners. Published online 2020.
