BEN BUCHANAN, DVM, DACVIM, DACVECC
BRAZOS VALLEY EQUINE HOSPITAL
*last updated May 16, 2011*
An outbreak of Equine Herpes Myeloencephalopathy (EHM) (neurological form of EHV-1) has been traced to horses who attended the NCHA’s Western National Championships in Odgen, Utah on April 30 – May 8, 2011. Affected horses have been publicly identified in California, Colorado, and Washington. The University of Washington has voluntarily closed their large animal clinic due to identification of a positive horse. Additional states have possible cases pending and/or are looking for animals that attended the event and returned home. Texas does not currently have any confirmed positives and the state veterinary office is working on identifying all the horses that attended the show in Utah and then traveled to the state. If your clients were at that event the possibility exists that they could have been exposed to this virus. Additionally horses returning from Utah were exposed to horses that subsequently traveled to the Breeders Invitational in Tulsa, Oklahoma and likely other weekend events. On May 14, 2011 in a precautionary move to ensure the health and safety of horses, the Breeder’s Invitational Board of Directors cancelled the BI Aged Event and the NCHA cancelled the Mercuria World Series of Cutting event that had been scheduled to be conducted in from May 14-28.
BACKGROUND on Equine Herpes Viruses – Five different herpes virus are commonly found in domestic horses. Equine Herpes Virus (EHV) infection is ubiquitous in the equine population and most horses are infected in the first few months of life. Following infection with an EHV, the virus is able to essentially hide from the immune system in the lymphoid or neurologic tissues; horses are then said to have a “latent infection.” Once infected with EHV, horses are thought to be permanently infected. A latent viral infection can become reactivated via currently unknown mechanisms often during times of stress. Horses with re-activated latent infections are a source of infection for other horses. EHV-1 was one of the first equine herpes viruses to be described. EHV-1 is termed an “alpha herpes virus” that can cause severe pneumonia in newborn foals, mild respiratory disease in young horses and abortion in pregnant mares. The neurologic form of disease is a consequence of vasculitis and endothelial damage leading to thrombi formation, ischemia, interrupted function and neuronal death. Depending on what part of the neurologic system is affected (i.e., the spinal cord and brain) clinical signs will vary. The neurologic form of EHV-1 infection is generally referred to as Equine Herpes Myeoloencephalopathy (EHM) as both the brain and spinal cord can be involved. This form of herpes virus infection can cause clinical signs in any age, breed, or gender of horse. In many outbreaks (~80%) of the neurologic disease a specific mutatation of the DNA polymerase gene can be identified.
TRANSMISSION: Horse to horse transmission of the herpes viruses is significant when horses are kept in close contact. Contaminated equipment (e.g., water buckets, water hose handles, cleaning and grooming equipment etc) can also be a source of infection and people can transmit the virus on their hands or clothes. An infected horse will excrete and aerosolize the virus in respiratory secretions. All horses with clinical signs are expected to be contagious, although horses not showing any clinical signs can shed EHV. Neurologic horses shed large quantities of EHV-1 and should be securely isolated. The virus is estimated to be viable for up to 7 days in the environment under normal circumstances but may remain viable for a maximum of one month under perfect experimental conditions. The virus is easily killed in the environment by most disinfectants.
DIAGNOSIS: Once exposed and infected with EHV-1 the virus may be detected in blood and nasal swabs for 21 and 14 days respectively in laboratory settings. Horses can develop clinical signs as early as 1 day after exposure to the virus, although clinical signs can be delayed up to 10 days after exposure. Typically EHM develops 5 to 6 days after the primary infection. Infection usually develops following exposure to a horse shedding the virus but in a small percentage of cases, infection occurs by reactivation of latent virus. EHV-1 typically causes a biphasic fever peaking on day 1 or 2 and again on day 6 or 7. With respiratory infections there is often significant nasal and ocular discharge, but not a lot of coughing. There may be some persistent enlargement of submandibular lymph nodes. With the neurologic form there is typically minimal respiratory signs, with fever (rectal temperature greater than 102ÔøΩ?F) being the only warning. Neurologic disease appears suddenly and is rapidly progressive reaching its peak intensity within 24 to 48 hours. In horses infected with the neurologic strain of EHV-1, clinical signs may include: nasal discharge, incoordination, hind end weakness, recumbency / paralysis, lethargy, urine dribbling, decreased tail tone, and/or head tilt. CSF collection from horses with EHM shows evidence of vasculopathy with a normal cell count, increased protein and xanthochromia.
Horses that show a fever and any of these signs should be isolated and immediately. Diagnosis of EHM is based on clinical signs and isolation of the virus or detection of viral DNA by PCR. Samples should be collected from the nasal passages and whole blood and submitted for PCR to evaluate for shedding in the respiratory tract and viremia.
PREVENTION: For all of the equine herpes viruses, vaccination is not fully protective. An effective immune response requires a local mucosal response, systemic antibody production, and a cell mediated immune response. No current vaccine achieves all of these measures. Current EHV vaccines may reduce the amount of the virus shed in secretions of the respiratory tract, but do not protect against the neurologic form. Unfortunately, boostering well vaccinated horses during an outbreak is not helpful. Vaccinations 14 days prior to exposure is not likely to be harmful, and may help limit the spread of the disease.
BIOSECURITY: Horses with confirmed equine herpes myeoloencephalopathy should be isolated and the farm quarantined. Strict hygiene and biosecurity measures should be implemented because the virus can be aerosolized. A secondary containment should be setup for exposed horses to control the spread of the virus. Based on a analysis of a recent outbreak at Colorado State, the authors concluded: “horses with active nasal EHV-1 shedding should be isolated in an airspace that is separate from other horses by strictly enforced biosecurity and isolation procedures.
If it is necessary to admit a horse to a farm with ongoing cases, they should be current on EHV-1 vaccination and isolated away from the resident population. The neuropathic strain of EHV-1 can also cause abortion and location of pregnant mares should be considered during an outbreak.
Veterinary care for suspect horses should be performed on the farm as much as possible to prevent spread of the disease. A detailed history should be provided on the movement of the patient, as well as, movement of other horses at the facility. Knowledge of the vaccination history (type and date) is also important. If a horse is showing any clinical signs or has a unexplained fever, do not move the horse prior to an examination or testing.
TREATMENT: The prognosis after infection is dependent on the severity of the neurologic symptoms and the duration of recumbency. The disease spreads quickly and can have high morbidity and mortality. There is little scientific evidence to support specific therapies and treatment is mostly empirical. Most cases are treated symptomatically, although some practitioners have used antiviral therapy. Symptomatic therapy includes NSAIDs, DMSO, aspirin, L-lyseine, vitamin E and/or corticosteroids, along with nursing care. Neurologic or recumbent horses can be maintained in a sling for a short period of time in referral facilities or in custom setups on the farm. Acyclovir, Valcyclovir and Ganciclovir are drugs that have been studied in horses.
PROGNOSIS: A recent outbreak in a stable in Findlay Ohio has been described. Of the 135 horses exposed, 117 (86%) had some clinical signs. Neurologic deficits were identified in 46 (39%) of the affected horses. 12 horses did not survive. The authors concluded being > 5 years of age, having had a rectal temperature of > 103.5 degrees F, and highest rectal temperature occurring on or after the 3rd day of the febrile period were the factors most predictive of the development of neurologic disease and death. Horses that remain standing have a good prognosis for recovery and improvement is generally seen in a few days. However it may takes months to over a year before a horse is completely recovered and returned to its previous level of performance. Some horses may be left with permanent residual neurologic deficits.