Andrés Diaz-Méndez, Laurent Viel
Equine Rhinitis Virus Infection
Respiratory viral infections play an important role in commonly diagnosed equine respiratory diseases. These infections are recognized worldwide and affect the athletic performance of the horse, resulting in extended recovery periods and delays in training schedules.
Equine rhinitis A virus (ERAV) and equine rhinitis B virus (ERBV), formerly known as equine rhinoviruses, have been considered to be of relatively low importance among respiratory viruses and were believed to cause only mild upper respiratory disease in the horse. Previous nomenclature has caused confusion between the terms “rhinopneumonitis” and “rhinovirus infection.” Rhinopneumonitis, which is caused by equine herpesvirus infection, is not the same as equine “rhinovirus” infection. Equine rhinitis viruses (ERVs) are single-stranded RNA viruses in the family Picornaviridae. So far, only two genera (ERAV and ERBV) and four serotypes have been identified: ERAV (formerly known as equine rhinovirus 1), ERBV1 (formerly known as equine rhinovirus 2), ERBV2 (formerly known as equine rhinovirus 3), and ERBV3 (formerly known as acid-stable picornavirus). Although the ERAV group has been allocated to the genus Aphthovirus, ERBV1, ERBV2, and ERBV3 have recently been included in genus Erbovirus in family Picornaviridae.
Recent worldwide surveillance and seroprevalence investigations have demonstrated that these viruses are highly prevalent in the horse population (with prevalence ranging from 20% to 70%) and are actively associated with clinical respiratory disease. Nevertheless, ERVs have not been well characterized, and their role as an active entity in clinical respiratory disease is ill defined. ERAV, the most seroprevalent serotype among horses, was first documented in 1962 in the United Kingdom and was subsequently recognized globally. There is sufficient evidence that ERVs have circulated within the horse population for decades, and viral coinfection may play an important role in viral respiratory outbreaks. Importantly, the presence of an ERAV noncytopathic strain has been reported in recent years. This strain was implicated in clinical respiratory disease when no other viral agents could be identified. Therefore clinical respiratory disease from primary ERV infection may have been underestimated. Interestingly, a recent genome-sequencing study has revealed that ERAV may be evolving at a slow rate, compared with other equine respiratory viruses, making ERVs good candidates for vaccine development.
Clinical Signs
The clinical significance of ERVs as primary or concomitant agents in equine respiratory infections has been controversial. Studies by Plummer in 1962 demonstrated that experimental intranasal infection of horses with ERAV induced clinical respiratory signs characterized by nasal discharge, pyrexia, and viremia that lasted 4 to 5 days. No other clinical signs were recorded at the time; however, the virus was isolated in very small quantities from the feces of infected animals and was initially named “equine respiratory enterovirus.” A recent experimental infection study in horses has confirmed field observations indicating that ERAV induces not only clinical upper respiratory disease, but also compromises the lower airways. In that experimental study, infected horses developed increased body temperature, submandibular lymphadenopathy, abnormal lung sounds, tracheal and bronchial mucoid secretions, nasal discharge, and hyperemia in the lower trachea and large bronchi. Increased body temperature was detected 24 hours after infection in the experimentally infected animals, and was significantly higher than in control horses from day 2 to day 6. The submandibular lymph nodes became painful on palpation on day 2 after infection, a finding that persisted for up to 2 weeks in all infected animals. Additionally, tracheal and bronchial mucoid secretions were endoscopically detectable on day 1 after infection and persisted for up to 21 days. Bronchoalveolar lavage cytology revealed an increase in the neutrophil percentage by days 7 to 14 after infection. Contrary to other reports, the ERAV was recovered not only from the upper airways but also from the lower airways from day 1 to day 7, when a serum antibody response was first detected. This antibody response detected by viral neutralization (VN) testing peaked by postinfection day 14, with antibody titers ranging from 1 : 1024 to 1 : 2048. In respiratory outbreaks in which the ERV titers have had a four-fold increase, veterinarians have reported occasional edema of the lower limbs. These findings require further confirmation.
Viral Shedding
Even though ERAV was originally recovered from feces, the virus has commonly been isolated from equine respiratory samples and, on rare occasions, recovered from saliva, peritoneal fluid, urine, and plasma. Interestingly, only ERAV has been recovered from samples other than respiratory secretions, whereas ERBV1 seems to be recovered solely from respiratory samples. It is debatable whether ERAV replicates only in the upper airways because there are limited studies on this subject. Studies in 1992 and 2010 suggested that ERAV may replicate and persist in the urinary tract; however, the evidence is inconclusive. As previously reported, the viral load in fecal samples may be minimal, and current field and experimental investigations have not further characterized and explored viral replication or shedding in the urinary and gastrointestinal tracts. Recovery and detection of ERAV from urinary and fecal samples does not confirm viral replication at those sites.
