TABLE 1.

Questions and main conclusions in the 2009 EHV‐1 consensus statement.

Question	Main conclusions
How and why does equine herpesvirus‐1 (EHV‐1) infection target the pregnant uterus and CNS? Why do some horses but not others develop neurological disease?	Primary EHV‐1 infection occurs in epithelial cells of the upper respiratory tract (URT), with cell‐to‐cell spread leading to infection of URT lymph nodes within 24 to 48 hours. A mononuclear cell–associated viremia follows and can last up to 14 days. Nasal viral shedding typically ends by 10 to 14 days after infection. The viremia can infect endothelial cells of both the spinal cord resulting in equine herpesvirus myeloencephalopathy (EHM) or the pregnant uterus, resulting in abortion in the third trimester. The underlying pathogenesis is similar for both EHM and abortion. Incidence rates of EHM and abortion in infected horses are approximately 10% and ≥50%, respectively. The factors that lead to development of EHM are poorly understood, but in experimental infection studies, it occurs at much higher rates in old horses (18 years+).
What are the clinical implications of the DNApol single‐nucleotide polymorphism (SNP) (D752 versus N752)?	There is evidence of an association between a SNP in the DNA polymerase (DNApol) gene, leading to D752 and N752 biovars, which have been more often associated with EHM, and abortion, respectively. However, this association is not absolute and may be influenced by the relative prevalence of each strain in different populations. As a result, DNApol genotype is not relevant to the management and prevention of EHV‐1 disease outbreaks.
What does the most current data tell us about EHV‐1 epidemiology, and the prevalence of strain variants?	Reactivation from latency, with shedding and transmission to susceptible hosts are critical features of the epidemiology of EHV‐1 infection. Primary EHV‐1 infection occurs in the early months of life and may occur because of viral reactivation in latently infected mares. When horses are first infected, latency is established in both the lymphoreticular system and in the trigeminal ganglion. Clinicians should presume that most horses are latently infected with EHV‐1. Subclinical shedding of EHV‐1 is relatively infrequent.
What are the risk factors for horses for respiratory, abortigenic, or neurologic disease caused by EHV‐1?	Risk factors that influence the size and clinical presentation of EHV‐1 disease outbreaks include viral, host, and environmental factors. The presence of both EHV‐1 (eg, from an infected shedding horse) and susceptible horses is a prerequisite. Host factors also include breed, sex, reproductive status, and age. Younger horses (<2 years old) are at increased risk of developing respiratory disease, whereas older horses at increased risk of developing EHM. Abortion is largely restricted to the last trimester of pregnancy. Weaning, commingling, transportation, concurrent infections, and other stressors may increase infection rates. The role of immunity and EHM risk remains uncertain. Environmental factors include season with most EHM outbreaks occurring in late autumn, winter, and spring. Geographical region also appears to be associated with the development of EHM.
What kinds of viral detection tests should I select for diagnosis, prognosis, and screening of horses for EHV‐1 and its strains?	General recommendations for documenting an active EHV‐1 infection include the use of uncoagulated blood and nasal swab samples for quantitative real‐time PCR assays. These samples can be used for virus isolation of EHV‐1 when clinical signs and PCR results are suggestive of infection. Paired‐serum samples collected 15 to 21 days apart for serology—VN assay and ELISA for specific virus antigen, can provide presumptive evidence of EHV‐1 infection. In the absence of clinical signs consistent EHV‐1 infection, use of current diagnostic methods, including real‐time PCR, as a screening test is not recommended.
How and when should I use current commercially available vaccines to control EHV‐1 infection and disease?	Protection against EHV‐1 may require a combination of mucosal and systemic immune responses including both neutralizing antibody and CTL responses. Vaccination remains the optimal means to prevent infectious diseases; however, there is no evidence that vaccines prevent EHM, although there is some evidence for protection against abortion. Vaccination can be expected to reduce nasopharyngeal virus shedding during an outbreak and thereby limit the spread of infection.
What are the key factors to consider in controlling disease caused by EHV‐1?	Control measures include those designed to prevent or reduce the likelihood of outbreaks, and those designed to limit the spread of disease when an outbreak occurs. For example, measures used to prevent abortion or neurologic disease in pregnant mares include segregation of pregnant mares from other horses, isolation of all mares entering a stud facility for at least 3 weeks, subdivision of pregnant mares into small physically separated groups for the duration of gestation, maximize herd immunity through vaccination, and stress reduction. Similar measures can be applied to other horse populations.
What are the key things I need to know as I plan for, and respond to, an outbreak of clinical EHV‐1 infection?	The priorities for management of an outbreak of EHV‐1 are early diagnosis, prevention of further viral spread including disinfection of contaminated areas, isolation of infected horses and enhanced biosecurity to reduce the spread of infection, and management of clinical cases. Air‐borne, direct contact, and fomite transmission and contact with aborted fetuses, fetal membranes, and infected neonates are important modes of transmission. In the face of an EHV‐1 outbreak, vaccination can be used in horses at increased risk of exposure in the hope it may reduce spread of infectious virus. A period of 28 days after the occurrence of any new cases of EHV‐1 infection is recommended for the lifting of quarantine. Alternative strategies such as a 14‐day quarantine period followed by testing all horses by real‐time PCR analysis of nasal swabs for 2 to 4 consecutive days, along with twice daily monitoring of rectal temperatures has also been used. Horses that are dispersed to other stables should be quarantined on arrival and their health monitored. Virus in the environment is very unlikely to survive in an infectious form 21 days after depopulation of horses.
What therapeutic modalities are useful for treating EHM, beyond supportive and symptomatic care?	The treatment of horses with EHM involves empiric supportive care. The use of corticosteroids is reserved for EHM cases presenting in recumbency or with severe ataxia, in which the prognosis is guarded for survival. There is limited scientific rationale for the use of immunomodulators. Some antiviral drugs including the thymidine kinase inhibitor acyclovir have demonstrated in vitro efficacy against EHV‐1. However, evidence‐based studies of the value of antiviral drugs in the prevention and treatment of EHV‐1 infection are lacking. Acyclovir after a single oral administration to adult horses is associated with high variability in serum acyclovir‐time profiles and poor bioavailability. Bioavailability of valacyclovir is higher, although its impact on treatment outcome is unknown.