Equine Herpesviruses (EHV) are common and often latent pathogens of equids which can cause fatalities when transmitted to non-equids. Stress and elevated glucocorticoids have been associated with EHV reactivation in domestic horses, but little is known about the correlation between stress and viral reactivation in wild equids. We investigated the effect of an environmental stressor (social group restructuring following a translocation event) on EHV reactivation in captive Grévy's zebras (Equus grevyi). A mare was translocated by road transport from Zoo Mulhouse, France, to join a resident group of three mares in Tierpark Berlin, Germany. We used an indirect sampling method to assess the frequency of EHV shedding for 14 days immediately after the translocation event (termed the 'experimental period'). The results were compared with those from two control periods, one preceding and one subsequent to the experimental period. In addition, we measured fecal glucocorticoid metabolite (fGCM) concentrations daily in all individuals from 6 days before, to 14 days after translocation. We found significantly higher EHV shedding frequencies during the experimental period, compared to each of the two control periods. All animals showed significantly elevated fGCM concentrations, compared to fGCM levels before translocation. Finally, we found that an increase in fGCM concentration was significantly associated with an increased likelihood of EHV shedding. Although the small number of animals in the study limits the conclusions that can be drawn from the study, taken together, our results support the hypothesis that environmental stressors induce viral reactivation in wild equids. Our results suggest that potentials stressors such as group restructuring and translocation should be considered in the management of zoological collections to reduce the risk of fatal EHV infections in novel hosts. Moreover, environmental stressors may play an important role in EHV reactivation and spread in wild equid populations.
Keywords: EHV; Fecal glucocorticoids; Latent infection; Reactivation.