Since the outbreak of neurological Equine Herpes Virus-1 (EHV-1) disease at the University of Findlay four years ago, which took the lives of 12 horses and produced symptoms in 85% of the horses affected, further sporadic outbreaks of the neurological form of the disease have appeared at racetracks, training centers and most recently in the show-horse population, including an outbreak in Wellington, Fla. These outbreaks have caused concern, if not panic, throughout the equine industry.
EHV (aka the Rhinopneumonitis virus) exists in two forms. EVH-1 and EHV-4. EHV-1 is the most prevalent form. It can cause upper-respiratory disease (usually in animals under two years of age), abortion in pregnant mares, or neurological disease. Estimates are that from 60 to as many as 90% of adult horses are asymptomatic carriers of Herpes virus. These viruses are found in horses worldwide, with little variation between strains of virus around the world.
Until recently, the Herpes virus would manifest itself in outbreaks of respiratory virus in young horses (e.g., at weaning), or as abortion storms in mares. Rare instances of horses developing neurological disease following an EHV upper-respiratory infection have been known to occur for a very long time.
The typical history would be that there was an outbreak of the respiratory disease (or an abortion storm), followed by the development of typical neurological signs of difficulty with passing manure and urinating as well as weakness and ataxia behind, with ”dog sitting.” Symptoms were confined to the hind end, were slow to develop and with adequate nursing the horses could recover, although severe cases may be euthanized. In recent years, we’re experiencing a syndrome that appears to be different.
Instead of isolated cases of neurological involvement of the terminal end of the spinal cord following a respiratory or abortion outbreak, we’re seeing adult horses rapidly coming down with neurological symptoms that involve all levels of the nervous system with few, if any, respiratory symptoms. Higher percentages of exposed horses are becoming infected, more are neurological and the death toll is much higher.
Thanks to work of an international research project, we now know that most outbreaks of neurological disease involve a specific mutation of the Herpes virus. This mutation influences how rapidly the virus multiplies and results in circulating levels of virus that are 10 times higher than with other strains. This higher level of virus is believed to account for both high levels of spread (from 20 to 50% of exposed horses become infected) and the much higher risk that the nervous system can be involved, at all levels from brain to spinal cord.
A characteristic of the neuropathogenic strain of virus is that the immunity produced by currently available vaccines (with the possible exception of Rhinomune) is not effective in controlling this virus. Although detailed information on vaccination history isn’t available for all outbreaks, there are several instances, including at Findlay and in racehorses, where infected horses were confirmed to have been aggressively vaccinated (e.g., every three months) and were current in their vaccinations.
Despite this, it’s still commonly recommended to vaccinate when an outbreak of neurological Herpes occurs. This ”can’t hurt, might help” approach may be worse than simply ineffective. Many researchers are concerned that heavy vaccination schedules may have helped force the mutation that resulted in the more virulent neuropathogenic strain.
Even with respiratory disease and abortion, vaccination with current killed virus vaccines is little more than a public service. They don’t provide reliable protection from disease for the individual animal. They do decrease the amount of virus shed in respiratory secretions or placental fluids, so decrease the risk that any given infected animal poses to those around it. However, the decrease in shedding doesn’t seem to apply to the neuropathogenic strain and high infection rates in adult horses, normally resistant to other strains, are common.
Research into the development of a vaccine that specifically protects again the neuropathogenic strain of EHV-1 is ongoing under the direction of researchers such as Dr. Klaus Osterrieder at Cornell University.
In the meantime, there is one study that suggests the use of the modified-live EHV vaccine, Pfizer’s Rhinomune, may offer some protection against the neuropathogenic strain of the virus.
A 2006 study performed at Cornell University divided horses up into three groups of five. One group was vaccinated with a killed-virus vaccine, one with the modified-live virus vaccine from Pfizer and one group unvaccinated controls. These horses were then all exposed to a known neuropathogenic strain of virus. The duration of fever was shorter in the live-vaccine group. Three horses from each of the unvaccinated and killed-virus vaccine groups developed neurological signs, none in the modified-live group.
Although circulating virus was found in all three groups, the duration was much shorter in the live-vaccine group and virus shedding was also almost undetectable and significantly lower in the live-vaccine group. So, while the modified-live vaccine wasn’t completely effective in preventing the virus from infecting the horses, it did protect them from neurological disease developing, hastened clearance of virus and fever, and resulted in low levels of virus shedding for a shortened period of time. Whether these findings are repeatable, and how much protection the vaccine really offers under ”real life” circumstances, remains to be seen.
For any given outbreak involving this neuropathogic EHV-1 strain, from 20 to 85% of exposed horses will pick up the virus, and 20 to 50% that become infected will go on to show neurological disease. What influences these numbers’
• The health of the individual horse’s immune system. Immune responses weakened by age (both very young and very old), disease, immunosuppression (Cushing’s disease or use of corticosteroids), suboptimal nutrition, or a concurrent infection will increase risk of both infection and development of symptoms.
• Stress is also an important suppressor of immune responses. Recent travel or heavy exercise are often involved in these outbreaks.
• The dose. The risk of an infection taking hold depends on how many organisms are in the exposure. A horse in close contact with an actively shedding animal is at higher risk than one at the other end of the barn. Ventilation has an important role to play here also. The number of viruses and irritant dust particles in the air rises dramatically when barns are closed up tightly. Keep air moving freely.
Like all other Herpes viruses, EHV can and usually does go into a latent, asymptomatic stage after a horse’s initial infection. These horses carry the virus, possibly for life. Herpes viruses are not prone to frequent major mutations, so a peaceful coexistence develops between the horse’s immune system and the virus. The immune system keeps it in check and localized to the lymph nodes of the upper-respiratory tract. These carrier horses don’t normally shed virus, but they may do so if they are under stress or fighting another infection.
It’s currently unknown how these neuropathogenic virus outbreaks get started. How did the firs t case in the series get the virus’ In some cases, it may be that there was another case the horse came in contact with before becoming ill that was never reported. It’s also possible the Herpes virus the horse himself was carrying mutated to the more dangerous form, or that another horse carrying the neuropathogenic strain was shedding but not showing symptoms.
The case at a veterinary hospital in Connecticut was likely the result of a latent infection in a carrier being activated by the stress of surgery. Work is underway at the Gluck Equine Research Center to attempt to get some idea of how many horses may be carriers of this strain. We have a long way to go in finding out how many horses may be carriers, what threat they may pose and what, if anything, can be done about it.