Absence of Equid Herpesvirus‐1 Reactivation and Viremia in Hospitalized Critically Ill Horses

Abstract

Background: Equid herpesvirus-1 (EHV-1) reactivation and shedding can occur in latently infected, asymptomatic animals. Risk factors for reactivation include stress and illness. The risk of asymptomatic shedding in hospitalized, critically ill horses with acute abdominal disease is unknown. This information is important to assess the need for additional biosecurity protocols to prevent spread of EHV-1 in hospitalized critically ill horses with acute abdominal disorders.Objectives: To determine the frequency of reactivation and nasal shedding of EHV-1 in hospitalized critically ill horses. Animals: One hundred twenty-four client-owned horses admitted to the Veterinary Teaching Hospital with acute abdominal disorders were included in the study.Methods: Cross-sectional study examining the risk of reactivation of EHV-1 in horses admitted with acute, severe, gastrointestinal disease. Whole blood and nasal secretions were collected throughout hospitalization. In addition, mandibular lymph nodes were collected from 9 study horses and 26 other Michigan horses. All samples were tested for the presence of EHV-1 nucleic acid by real-time PCR assays targeting the glycoprotein B gene and the polymerase (ORF 30) gene.Results: One hundred and twenty-four horses met the inclusion criteria. None of the samples were positive for EHV-1 DNA.Conclusion and Clinical Importance: These results suggest that nasal shedding and viremia of EHV-1 in hospitalized critically ill horses with acute abdominal disorder is extremely rare. Implementation of additional biosecurity protocols to limit aerosol spread of EHV-1 among horses with acute abdominal disease and other hospitalized horses is not necessary.

Prevalence of equine herpesvirus type 1 in trigeminal ganglia and submandibular lymph nodes of equids examined postmortem

“…Differences in horse populations, geographical origin and management practices may have accounted for the apparent differences in prevalence. The low prevalence of latent infection in the present study is compatible with previous observations that EHV-1 viral shedding and/or viraemia were uncommon in critically ill horses hospitalised in the William R. Pritchard Veterinary Medical Teaching Hospital (VMTH) at the University of California, Davis (Carr and others 2008). Together, these studies suggest that the prevalence of latent EHV-1 is low in the population of horses admitted to the VMTH.…”

Failure to detect equid herpesvirus types 1 and 4 DNA in placentae and healthy new-born Thoroughbred foals

“…A recent study found a low rate of detection of EHV-1 in adult horses, even among those showing pyrexia and respiratory signs (Pusterla et al 2016). In another study of 124 hospitalised critically ill horses, no evidence of EHV-1 shedding was detected, although low levels of latency could not be excluded (Carr, Schott & Pusterla 2011). Sonis and Goehring (2013) concluded from a study of hospitalised febrile horses that nasal shedding of EHV-1 and EHV-4 was a rare event, as only one of the 64 febrile horses was PCR positive for EHV-4 and none were positive for EHV-1.…”

Nasal Shedding of Equid Herpesvirus Type 1 and Type 4 in Hospitalized, Febrile Horses

“…Following long-distance transportation, the number of horses detected with EHV-1 nasal shedding was low in adult horses (1% [3 of 302 horses]) [10], and nasal swabs from 17 of 451 horses were either positive for EHV-1 or -4 in juvenile horses upon arrival at show grounds or sales [11]. Horses hospitalized with acute gastrointestinal disease requiring an emergency celiotomy or horses with acute colitis all tested negative for cell-associated viremia or for the presence of EHV-1 in nasal secretions on one sample collected on admission and two more swabs between days 2 and 12 [12]. These findings indicate that there is probably a low frequency of EHV recrudescence from its latent location, and stressors like transportation and physical stress resulting from concurrent disease may not be the correct stressors that cause recrudescence with detectable virus replication in the upper respiratory tract.…”