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EQUINE herpesvirus type 1 (EHV-1) infection can be subclinical or lead to a number of clinical presentations including abortions, neonatal death, respiratory disease or neurological disease. The apparent recent increase in the numbers of reported cases of equine herpesvirus myeloencephalopathy (EHM) in the USA and Europe (Kydd and others 2012) have caused concerns among veterinarians regarding possible transmission of EHV-1 among hospitalised horses, with the subsequent risk of nosocomial EHM cases. One of the key questions central to such concerns is ‘how common is it for hospitalised horses to shed EHV-1?’ According to the results of a paper by Pusterla and others (2015) summarised on page 70 of this issue of Veterinary Record, only 2.7 per cent of 4228 horses from 139 veterinary practices throughout the USA tested positive for EHV-1 DNA in their nasal secretions or blood. The strength of the study includes availability of a large data set from a wide geographical area, with sampling spanning a five-year period. While this relatively low EHV-1 detection rate may be reassuring to equine veterinarians, the data should be interpreted with consideration of the complexity of the relationship between EHV-1 and its equine host.
The hallmark of EHV-1 biology is its ability to establish latency following primary infection. Based on serological evidence from studies conducted in New Zealand and Australia, EHV-1 infection often occurs within the first few months of the foal's life, which may or may not be accompanied by signs of respiratory disease (Gilkerson and others 1997, Dunowska and others 2002). This feature constitutes an important epidemiological advantage for the virus, as it establishes a population of latently infected animals (presumably for life). Such animals harbour EHV-1 in trigeminal ganglia or in lymphoid cells (Slater and others 1994, Allen 2006). The virus can periodically reactivate from …
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