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Background: Equine herpesvirus type 1 (EHV-1) infection causes neurologic disease in horses. However, risk factors for the disease and long-term prognosis are poorly characterized.Hypothesis: There are identifiable risk factors for equine herpes-1 myeloencephalopathy. Animals: The entire population of 135 horses housed within the equestrian facility. Methods: A descriptive study investigated the clinical, serologic, virologic, and management aspects of an outbreak of EHV-1 myeloencephalopathy.Results: Out of 135 horses at the facility, 117 displayed signs of EHV-1 infection. Forty-six horses developed neurologic deficits characterized by symmetrical hind limb ataxia and weakness. Twelve horses that developed neurologic deficits became recumbent and did not survive. The development of severe neurologic deficits during the outbreak was associated with the presence of residual deficits at the 6-month examination. Within 1 year of the outbreak onset, all horses that survived had returned to an exercise level comparable to that experienced before the outbreak. Factors associated with the development of neurologic disease included age of .5 years, location in the south or arena stall areas, and highest rectal temperature on day 3 or later of the febrile period.Conclusions and clinical importance: Being .5 years of age, having had a rectal temperature of .103.5uF, and highest rectal temperature occurring on or after the 3rd day of the febrile period were the factors most predictive of the development of neurologic disease and death. Data obtained during this outbreak substantiate previous findings relating to clinical aspects and diagnosis of EHV-1 myeloencephalopathy. The prophylactic and therapeutic use of acyclovir during this outbreak is described.

Nontoxigenic and bacteriophage-sensitive bacterial cultures have been isolated from toxigenic Clostridium botulinum type C, strain 468C, after treatment with either ultraviolet light or acridine orange. Two bacteriophages, designated CEbeta and CE(gamma), were isolated from toxigenic strain 468C. Both of these bacteriophages were capable of infecting the nontoxigenic type C cultures, but only bacteriophage CEbeta was involved in the change from nontoxigenicity to toxigenicity.

Summary The cervical spines of 6 horses with cervical stenotic myelopathy (CSM) were examined using myelography and contrast‐enhanced computed tomography (CECT). Histopathology of the spinal cord of these horses identified 10 neurologically significant compressive lesions. Myelography and CECT were both able to demonstrate all 10 spinal cord compressive lesions, but myelography falsely identified 2 sites and CECT falsely identified 1 site as compressive lesions of the spinal cord which were not supported by histopathology. Additional qualitative information was obtained by CECT regarding the source, severity and location of spinal cord compression. Computed tomography identified stenosis of the vertebral canal with circumferential loss of contrast agent and documented lateral compressive lesions of the spinal cord due to malformed articular facets. Compression of the peripheral nerve roots by malformed articular facets encroaching on the intervertebral foramen was easily identified by CECT in the axial plane. No compressive lesions were identified in 3 unaffected horses by either method. Minimum sagittal diameter (MSD) values obtained from CECT images were strongly correlated with necropsy measurements, validating CECT as an accurate method of obtaining MSD values. The MSD values in the CSM‐affected horses were significantly narrowed (P<0.05) from C3C6 regardless of the site of spinal cord compression, when compared with the unaffected controls. This finding supports previous reports suggesting that generalised stenosis of the vertebral canal is an important feature in the pathogenesis of cervical stenotic myelopathy.

Equine protozoal myeloencephalitis (EPM) is a serious disease of horses, and its management continues to be a challenge for veterinarians. The protozoan Sarcocystis neurona is most commonly associated with EPM. S. neurona has emerged as a common cause of mortality in marine mammals, especially sea otters (Enhydra lutris). EPM-like illness has also been recorded in several other mammals, including domestic dogs and cats. This paper updates S. neurona and EPM information from the last 15 years on the advances regarding life cycle, molecular biology, epidemiology, clinical signs, diagnosis, treatment and control.

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Equine protozoal myeloencephalitis (EPM) remains an important neurologic disease of horses. There are no pathognomonic clinical signs for the disease. Affected horses can have focal or multifocal central nervous system (CNS) disease. EPM can be difficult to diagnose antemortem. It is caused by either of 2 parasites, Sarcocystis neurona and Neospora hughesi, with much less known about N. hughesi. Although risk factors such as transport stress and breed and age correlations have been identified, biologic factors such as genetic predispositions of individual animals, and parasite‐specific factors such as strain differences in virulence, remain largely undetermined. This consensus statement update presents current published knowledge of the parasite biology, host immune response, disease pathogenesis, epidemiology, and risk factors. Importantly, the statement provides recommendations for EPM diagnosis, treatment, and prevention.