The equid herpesviruses (EHV) are highly prevalent pathogens in all global equid populations, with infection prevalence rates of up to 100%. They are responsible for considerable economic losses in the equine industry, and can also readily adapt to infecting new (non-equid) host species. In these novel hosts, EHV infections are typically more severe than in equids and often fatal. Herpesviruses typically remain in their hosts as a latent, lifelong infection in the host’s neural tissue and lymphoid cells and can reactivate during times of acute stress or reduced immunocompetence. So far, the triggers causing EHV reactivation in equids are not comprehensively understood. Following viral recrudescence and viraemia, EHVs are typically shed in nasal discharge and transmitted via a naso-nasal infection route. Therefore, EHV monitoring in wildlife has mostly been performed employing invasive methods, including capture and immobilization. These approaches, however, involve various risks for the target animal and for the people involved in the procedures. Furthermore, due to intense time and financial effort, invasive measures are usually limited to very few individuals. In contrast, non-invasive sampling relies on collecting sample material which is shed from the target organism into its environment, thereby circumventing the need for direct contact with the animal. In chapter 2 I established a non-invasive, indirect sampling method to collect nasal discharge and saliva of captive zebras. This method was tested on three different zebra species, and I successful isolated DNA of sporadically reactivated EHVs as well as host DNA from an enrichment toy which was provided to the study animals for certain periods of time. A similar approach might be tested on wild equids in their natural habitats to facilitate non-invasive EHV screening in situ with a time- and cost-efficient approach. In chapter 3 I used non-invasive sampling methods to screen EHV shedding in captive zebras in order to investigate the effect of presumed environmental stressors on the probability of EHV reactivation and transmission. In addition, I measured faecal glucocorticoid metabolite (fGCM) concentrations to assess a potential physiological stress response to a translocation event and subsequent social group re-structuring. Both fGCM concentrations and EHV shedding frequencies increased significantly after the translocation event and group re-structuring, compared to control periods, in the 108 translocated and in the non-translocated animals. This indicates that environmental stressors, including potential social conflict, may play a crucial role for reactivation and transmission of EHV infections in wild equids. In chapter 4 I examined whether ex situ captivity and its inherent deviations from natural living conditions of zebras (e.g. differences in climate, diet, movement space, social structure, and infection pressure) and acute EHV infections would had an effect on selected markers of the innate and adaptive immune system. Moreover, I also examined the effect of lactation on these markers, as it is known from other species that energy re- allocation may lead to a down-regulation of certain immune functions, while other immune markers are up-regulated for passive immunisation of nursing offspring. I found that constitutive innate markers were significantly higher in the natural, than in the captive environment, whereas induced immune markers were significantly higher in the wild. Lactating zebras also showed significantly higher constitutive immune functions than non-lactating mares, which may be a result of passive immunization of the offspring, but also of increased activity of this branch of immunity. Acute EHV infections, however, did not affect the measured immune markers. In chapter 5 I aimed to identify the factors which contribute to an increase of the allostatic load of free-ranging plains zebras in the Serengeti ecosystem. For this, I measured fGCM concentrations of zebras at different life history stages and under different (socio-)ecological conditions. I found significantly higher fGCM levels in zebras during times of large aggregations, compared to medium-sized and small aggregations. Furthermore, family group stallions produced higher fGCM concentrations than bachelors. Lactation and season, however, had no effect on fGCM concentrations. This indicates that EHV recrudescence is most likely when zebras are in large aggregations, and is presumably more frequent in family group stallions than in bachelors. Taken together, my results indicate that social cues seem to be important factors contributing to perceived stress, and thereby, to the probability of EHV reactivation, in zebras. Non-invasive methods for VH screening should be evaluated in the future to facilitate large-scale screening of free-ranging equid populations, in order to identify the factors which promote reactivation and transmission of latent infections such as EHV.