In recent years there has been an increasing incidence of outbreaks throughout North America of Equine Herpes Myelitis (EHM) caused by Equine Herpesvirus 1(EHV 1). Why are we seeing this disease with increased frequency, we don't really know. What we do know is that it's a virus that been around for decades. The effects of EHV-1 on the equine population are 3 fold. It has the ability to cause mild respiratory disease and fever, abortion, typically in the 3rd trimester, neonatal foal death, and outbreaks of neurologic disease or EHM.
EHV's 1&4 are what we refer to as alpha herpesviruses. One of the key features of these alpha herpesviruses is latency and reactivation. Once infected the virus has the ability to reside in the lymphoreticular system and trigeminal nerve, and in times of stress the dormant virus can become re-activated (stress of transport, weaning, handling, experimental induction with corticosteroids) leading to virus shedding and transmission. The frequency of reactivation is generally unknown, but what we do know is that these horses are general asymptomatic.
With respect to latency, this is actually established during the first weeks to months of life. It is thought that viral reactivation in in latently infected mares leads to the foal becoming infected at this stage. The prevalence of latency in the equine population ranges from 60-88% based on necropsy studies where testing for the virus has been performed in bronchial and retropharyngeal lymph nodes. So it's safe to assume that the majority of horses are latently affected with EHV 1. Given the high prevalence of latency, and the size of the equine population outbreaks of EHM are still considered rare.
The best analogy is to compare EHV 1 with the Human Herpes Simplex 1 virus, where 67% of people around the world under the age of 50 are affected with the virus. Like EHV 1 this virus also establishes itself during childhood and the infection is life long. Stressors in life may also precipitate the development of disease.
Back to EHV 1. There are two strains of the virus, the D 752 strain referred to as the neurolologic or neuropathic strain. This strain is more commonly isolated from horse with EHM (85%) than the N752 strain or non neuropathic strain. Now the nomenclature can be somewhat confusing, since the non neurologic strain can account for a minority of neurologic outbreaks (15-25%). The Non neurologic starin is however responsible for 95% of the abortion outbreaks. With respect to latency, the good news is that approximately only 5-20% of the equine population is latently affected with this strain. So latency likely plays a significant role in these outbreaks, with the source being either a latently infected horse with the D variant becoming re-activated or spontaneous mutation from the N variant to the D variant.
Risk / protective Factors
The presence of an infected/shedding horse in the herd along with other susceptible horses in the herd. Data suggests that older horses >5yrs are at an increased risk of developing EHM. May be related to the immunological status of older horses.
Season: The majority of EHM outbreaks occur in late autumn, winter and spring.
Introduction of horses into a herd is a commonly reported before the development of EHM outbreaks.
Breed and sex: In one epidemiological survey, ponies and smaller breeds were les likely affected and females more commonly affected.
Stressors: Weaning, Commingling, transportation and concurrent infections
Treatment with anti-viral drugs may decrease the chance of developing EHM in horses with a high risk of exposure. IV acyclovir or gangciclovir are preferable, followed by oral acyclovir.
Immunity: Past exposure produces a limited period of immunity which may last only 3-6 months.
Vaccination: EHM has been observed in horse vaccinated against EHV 1 at 3-4 month intervals. No evidence that the vaccines that are currently available have the ability to prevent naturally occurring cases of EHM. The current goal with vaccination against EHV 1 is to stimulate the immune response with the hope of reducing or eliminating the viremia that develops with infection.
Incubation period: 2-8 days. Once a fever occurs, neurologic signs may develop within the next week.
Shedding: Shedding in horses with EHM may occur for as long as 28 days. The virus does not survive outside of the host for very long in the environment. Dies within hours on a smooth dry surface and if exposed to sunlight. Same goes for clothing and dry hands. Can be easily killed by washing hands and using hand sanitizer.
Transmission: Direct contact or fomites most common mode. Coughing is not a common feature of EHM, so aerosol transmission is not a common feature of the disease.
Mules, donkeys and zebras can be infected with EHV1 and can shed the virus, as well as develop neurologic disease.
Recurrence of disease: There have been no confirmed cases of recurrence of disease in horses that have been previously affected with EHM