With several recent outbreaks of neurological herpesvirus infections in the US and Canada, much attention has been turned to this common disease. The virus is not new, and is considered endemic in most regions of the world. Although some aspects of the disease have been understood for decades, there is still much to be learned about the virus and its effects on horses.
What clinical signs does herpesvirus infection cause?
Herpesvirus most commonly causes respiratory tract infections in young horses, marked by fever, lethargy, nasal discharge, lack of appetite, and a cough. Most foals are exposed to the virus in the first weeks of months of life, and the respiratory infections are most commonly seen in weanlings, yearlings, or young horses entering training, especially when horses from different sources are brought together. Because the virus is so common in our horse populations, most mature horses have been exposed many times and develop some immunity to the virus, so show little signs of respiratory disease when infected. However, the virus can also cause outbreaks of abortion in late term mares, or the birth of weak, non-viable foals. Sporadically, the virus can cause paralytic neurological disease. For reasons not understood, older horses do not become immune to the abortion and neurological forms of the disease even with repeated exposure, and in fact, older horses are more prone to neurological disease caused by herpesvirus than are younger horses. The reasons for the increased rate of neurological disease in older horses have not been completely defined, but it may be related to changes in how the immune system responds to the virus as the horse ages.
The neurological form of herpesvirus infection can be devastating. The virus tends to attack the spinal cord, resulting in incoordination and weakness, especially in the hind end. Horses can also commonly lose the ability to void their bladder and their rectum. This hind end weakness can also progress to paralysis, and the prognosis decreases if the horse becomes recumbent. Because it is a viral infection, antibiotics do not address the infection, and most treatments are supportive and can be very intensive and expensive. Anti-viral medications have been tried in neurological cases, but their efficacy has not been proven.
The virus is shed in nasal secretions, and is typically spread by direct or indirect contact with aerosolized droplets given off when an infected horse coughs. Alternately, the virus can be transmitted by contact with aborted infected fetuses, fetal fluids, or placentae. Once the virus enters the horse, the immune system fights off the active infection, but the virus can go into hiding for long periods of time, only to become reactivated and cause clinical disease or shedding of the virus later on, usually during periods of stress. This is similar to the human herpesvirus that causes chicken pox in young children, of which the infection is never completely cleared and can go on to cause Shingles in older adults. In an outbreak of neurological disease, the number of exposed horses that develop neurological symptoms is typically about 10%; in herpesvirus induced “abortion storms,” it is not unusual to have 50% of exposed mares abort. Because of the highly contagious nature of the disease and the devastating effects the neurological form can have, identification of neurological disease results in prompt and strict quarantine and movement restrictions, disrupting breeding or training schedules, shutting down shows or races until the threat as passed. This can have major economic impacts on the equine industry.
The Tale of Two Strains
Recently, a genetic variation of Equine Herpesvirus Type I was identified that is more common in cases of neurological disease. This is a single point mutation in the DNA polymerase at position 752, with one form having the amino acid aspartic acid (D) at this position and the other form having asparagine (N) at this site. Therefore, the two forms are referred to as D752 or N752. With the apparent recent increase in neurological herpesvirus infections, it is tempting to believe that this variation is a new genetic mutation that has made the virus more virulent and thus responsible for the increased rate of neurological disease. This does not appear to be the case, however. It appears that the D752 strain may be the original strain of the virus, not a new mutation. Further, although the D752 strain is responsible for a majority of the outbreaks of EHV-induced neurological disease (potentially as high as 80-90% of neurological cases), both D752 and N752 can and do cause neurological disease. N752 is not innocuous, however. It is estimated to be responsible for 95-98% of abortion outbreaks in addition to the minority of neurological outbreaks. It must also be noted that the presence of D752 strain does not mean that a horse will become neurological—it is possible to 5-10% of all horses normally carry the D752 virus with no outward effects, and some horses may be infected with both the D752 and N752 strains. For now, since both strains can cause neurological disease, the identifying D752 or N752 within a herd with a herpesvirus outbreak has little implications for how the outbreak should be managed, except potentially for the concern that neurological disease might be a little more likely. Quarantine and biosecurity protocols should remain the same, however, regardless of the strain detected.
So what about vaccination?
With the devastating effects the neurological disease can have, an effective vaccine would be comforting. Unfortunately, no vaccine currently on the market carries a claim of preventing neurological disease. So why vaccinate? There are two vaccines currently on the market that do carry a claim of decreasing the risk of herpesvirus induced abortion in pregnant broodmares. Available vaccinations can also help decrease the symptoms and transmission of the respiratory form of the disease in young horses and high-risk performance and show horses. It is hoped that by decreasing the transmission of the respiratory forms of the virus, the incidence of the neurological form could also be reduced. Vaccinal protection, however, is short-lived—booster vaccination can be resumed as little as 6 months after a clinical case of herpesvirus has been cleared.
Control measures
So how can we control the spread of clinical disease caused by equine herpesvirus? Eradication of the virus is impossible, so control is aimed at preventing clinical disease or, failing that, limiting its severity, impact, and transmission.
Control of the spread of the disease in pregnant broodmares relies largely on minimizing contact with other horses, in addition to vaccination at 5, 7, and 9 months of gestation. It is recommended that pregnant mares be segregated from other horses on the property, especially from show horses or equines that are otherwise travelling to other venues and returning home again. When a new broodmare arrives on the property, they should be isolated from other pregnant mares for not less than 3 weeks. If there are many pregnant mares located on a given premises, it is likely wise to subdivide the mares into small, physically separated groups for the entire period of their pregnancy. And lastly, avoidance of stress (iincluding social stresses, prolonged transport, poor nutrition, etc) may help decrease the impact of the disease.
In the remainder of the horse population, three key principles can similarly be employed to reduce the impact of clinical disease: subdivision of horses into smaller, isolated groups, minimizing stresses, and vaccination. If an outbreak of neurological disease is encountered, prompt recognition of the disease, isolation of affected animals, effective quarantine and an immediate halt to all equine traffic onto and off of the affected premises are crucial components of the response. Affected horses may shed the virus for as long as 21 or even up to 28 days, so quarantine must be maintain for at least 3-4 weeks after resolution of all clinical cases on the farm. Diligent biosecurity practices and disinfection of any contaminated premises are critical.
Although there are many aspects of equine herpesvirus that are not well understood, the virus is nonetheless ubiquitous and control must be approached with a thorough, rationale plan. It is not completely known what causes the virus to cause neurological disease rather than the respiratory or abortogenic forms, however it is well recognized that rigorous biosecurity protocols are crucial to minimizing the effects of all forms of herpesvirus clinical disease.