CHAPTER 39 Equine Herpesvirus Myeloencephalopathy
Equine herpesvirus myeloencephalopathy (EHM) is an infrequent but serious outcome of equine herpesvirus type 1 (EHV-1) infection. It is well established that EHV-1 infection is highly prevalent in horses throughout the world, and its most common clinical manifestations are pyrexia and respiratory tract disease, particularly in weanlings and young adults, and abortion in mares in late pregnancy. Subclinical spread of infection is also common, and the epidemiologic features of EHV-1 infection in horses are dependent on the ability of the virus to establish latent infection in the majority of exposed horses. Sporadically, and in the course of conventional outbreaks of EHV-1 infection, EHM can develop, typically affecting 10% to 50% of infected, viremic horses. This percentage can fluctuate substantially among horse operations, and it depends strongly on the demographics of a specific horse operation. It is widely believed that there has been an increase in EHM outbreaks in recent years in North America, and in 2007 EHM was declared to be a potentially emerging disease by the United States Department of Agriculture-Animal and Plant Health Inspection Service. Our understanding of what precipitates an EHM case or outbreak remains rudimentary, although key scientific advances have been made during the last decade (Box 39-1).
Box 39-1 Key Findings about Equine Herpesvirus-1 and Developments during the Last Decade
PATHOGENESIS
Viremia typically persists for 5 to 7 days, although reports of viremic periods lasting for 21 days exist. Viremia is a prerequisite for EHM, as it allows for transport of virus to the vasculature of the central nervous system (CNS), where endothelial infection occurs. This results in damage to the microvasculature of the CNS secondary to initiation of an inflammatory cascade, vasculitis, microthrombosis, and extravasation of mononuclear cells with perivascular cuffing and local hemorrhage. Although viremia is a common sequel to EHV-1 infection, transfer of virus to the CNS endothelium and development of EHM are not. The mechanism underlying CNS endothelial infection is unknown. The typical result is disseminated ischemic necrosis of the spinal cord. The gray matter and white matter of the spinal cord are most commonly affected, with the brainstem being infrequently affected. The forebrain is usually unaffected. This can result in a wide range of neurologic signs, but in many instances, EHM can lead to profound weakness, ataxia, and recumbency, which often makes euthanasia necessary.
