In 2013, the horse industry received a huge reality check when an outbreak of the neurological form of equine herpesvirus-1 in Florida left major showgrounds temporarily quarantined and the rest of the season in doubt. With two cases of EHV currently in Ocala, Florida, and much of Europe’s competition halted due to the disease, equestrians worldwide fear what might be coming next.

So what do we know about equine herpesvirus?

There are nine types of EHV, but only EHV-1, -2 and -3 are of primary concern as disease-causing agents. EHV-4 typically causes upper respiratory disease in young horses with older horses developing natural immunity. EHV-3 causes a rare but disruptive venereal disease, characterized by genital lesions, which has the potential to bring breeding programs to a halt.

EHV-1 is the real bad-boy and can spawn a spectrum of problems. It used to be responsible for terrible clusters of “abortion storms” and stillbirths on farms before it was identified as the causative agent, and vaccinations against “rhino” became standard practice.

It also presents in a generally mild respiratory form, as well as a rare, rapidly fatal lung infection that can kill an animal overnight with no warning. The latter syndrome, which resembles African Horse Sickness, was identified by researchers at the Pennsylvania School of Veterinary Medicine’s New Bolton Center.

Behind the recent EHV-1 headlines and the focus of most current research efforts is its sometimes-fatal neurological syndrome, referred to as equine herpesvirus myeloencephalopathy. These cases can begin with non-specific clinical signs, including a fever of 102 degrees or greater, and sometimes, but not always, respiratory symptoms such as nasal discharge and cough, reddish mucous membranes, swollen legs and puffy, red eyes.

How Does The Virus Operate?

EHV-1 is everywhere. Some studies estimate that 80 percent or more of the general horse population are latently infected, which means they carry an inactive form of the virus.

The virus isn’t spread in this form, but when it is reactivated, most commonly thought to be in response to environmental or immune system stress, it begins to multiply inside the horse. A horse may or may not show clinical signs of illness while carrying the reactivated virus, but they are now capable of spreading it.

The active virus is shed via the respiratory tract through the horse’s nose and can be spread to other horses by nose-to-nose contact; by contact with contaminated people and equipment, such as trailers, tack, feed tubs, water buckets, grooming equipment, etc.; and via airborne contact, though the virus doesn’t persist very long in the environment.

Stressors that might encourage such reactivation, shedding and potential development of disease may include travel, weaning, breeding, foaling, training or competition—activities that often place horses in contact with lots of other new horses (often soon to be returning to their own farms), the perfect conditions for viral spread.

In a survey of horses judged to be at high-risk for infection at several show and sale facilities, a research team from Colorado State University’s College of Veterinary Medicine and Biomedical Sciences, led by Paul Lunn, BVSc, Ph.D., found that as many as 4 percent were actively shedding EHV-1 into the environment upon arrival.

Researchers don’t fully understand EHV’s mechanisms for latency and infection or precisely why some infected horses develop the potentially fatal neurological form of the disease, while others get a fever and a head cold, and some appear perfectly fine yet proceed to spread virus. Natural age-related immune system decline has been associated with a higher risk for older horses to develop the neurological form of the disease.

A major area of current research interest concerning EVM deals with the identification of variant strains of EHV-1, characterized by one small difference in the virus’ genetic code that makes it multiply more effectively and makes it more selective for causing neurological disease.

“It replicates more efficiently in the horse, achieving 10-fold higher levels of virus within the blood and vasculature of the central nervous system,” wrote George Allen, Ph.D., head of the Office International des Epizooties reference laboratory for EHV, located at the University of Kentucky’s Gluck Equine Research Center, in a research coordination paper for the AAEP. “Of singular importance is its enhanced virulence for the nervous system with greater morbidity, higher mortality and increased potential for causing an epidemic.”

“Dr. Allen’s work with experimentally infected foals suggest a five-fold higher risk of a horse developing neurological disease when infected with the form of EHV-1 containing the neuropathogenic marker,” noted the University of California Davis Center for Equine Health’s online EHV-1 reference resource.

Utilizing a diagnostic test he developed to differentiate between the neuropathogenic and non-neuropathogenic strains, in another study Allen detected latent EHV-1 infection in 54 percent of 132 Thoroughbred mares. Eight percent of the mares were carriers of the neuro-specific variation of the virus. He explained that “these preliminary results indicate that the neuropathogenic strain of EHV-1 may have already established a significant latent reservoir (carriers of the virus) within some of the nation’s horse populations.”

Prevention

Vaccination against EHV-1 is a controversial subject, and there are few concrete answers.

A regular vaccination protocol for pregnant mares and other horses on breeding farms is clearly recommended for reducing the risk of EHV-1-induced abortion, but beyond that there are conflicting opinions and data. None of the currently available vaccines are marketed as an effective preventative against neurological EHV-1, though there has been some experimentally demonstrated reduction in severity of non-neurological clinical signs, virus load and post-infection nasal shedding of virus, which could potentially reduce the spread of infection within a group of horses.

There are major hurdles in the development of more effective vaccines. After a horse recovers from a naturally occurring EHV-1 infection, his immune system’s resistance to re-infection is short-lived—a few months at most.

“For most diseases, the best vaccines stimulate immune responses that closely mimic those that result from recovery from natural infection. Thus, the maximum possible degree and duration of protection induced by a particular vaccine can usually be predicted based on the effectiveness of the immune response resulting from natural infection,” wrote David Wilson, BVMS, of the University of California Davis Veterinary Medical Teaching Hospital, in “Vaccination for Equine Herpesvirus-1 Myeloencephalopathy: The Dilemma.”

One reason why it’s hard for the horse’s immune system to knock out the virus is that once it infects the horse, EHV-1 takes up residence inside cells in the horse’s body. The virus doesn’t spend time hanging around outside cells, where it could be more easily attacked and eradicated by the immune system. That means that even if a vaccine effectively primes a horse’s immune system against EHV-1, the antibodies may not be able to get at the virus to kill it.

If another animal at your facility becomes sick with EHV-1, it’s probably a good idea to boost your horse’s vaccination if he’s not up to date or close to needing it. If your horse hasn’t been previously vaccinated, however, one dose to a “naïve” immune system probably won’t do them any good.

If a horse is sick with EHV-1, some experts recommend boosting in hopes of reducing the shedding of virus to other horses.

Treatment of equine herpesvirus myeloencephalopathy consists primarily of supportive/nursing care, though some antiviral medications show some potential usefulness.

Valacyclovir, which was marketed as the genital herpes drug Valtrex for humans, is a more bioavailable form of the generic herpes-specific drug acyclovir. A study published in 2017 with 18 aged mares showed that valacyclovir treatment significantly decreased viral replication and signs of disease in EHV-1–infected horses. The treatment was most effective when given as a prophylactic, i.e. right before the test subjects were exposed to the disease.

While debate surrounds many aspects of EHV-1, there is no argument against the value of biosecurity in preventing the spread of the disease. Whether keeping a single case from becoming an outbreak or containing an outbreak that’s already underway, prompt isolation of definitively infected horses—as well as those with undiagnosed fevers, respiratory or neurological signs—and careful management to prevent cross-contamination within a population via equipment and handlers are the most powerful weapons we have against EHV-1.