Neurologic diseases can be deceiving, presenting as subtly as an extremely mild lameness or as plainly as a suddenly staggering, dogsitting, or recumbent (down and unable to get up) horse. And while a large number of conditions can cause neurologic signs in horses, some are much more likely to than others. Our experts report the following as three conditions all horse owners need to be aware of:
- Equine protozoal myeloencephalitis (EPM) – Inflammation of the spinal cord and brain caused by protozoa (single-celled parasites);
- Equine herpesvirus myeloencephalopathy (EHM) – A disease affecting the brain and spinal cord as a result of equine herpesvirus-1 (EHV-1) infection; and
- Wobbler syndrome (cervical vertebral compressive myelopathy, CVCM) – Compression of the spinal cord in the cervical, or neck, region by the vertebrae and associated soft tissues.
Here’s an in-depth look at what we know about these conditions. Call your veterinarian immediately if you think your horse might be neurologic. Such horses lack balance and coordination, making them unpredictable to ride and handle.
Equine Protozoal Myeloencephalitis
Two distinct protozoa cause EPM: Sarcocystis neurona and Neospora hughesi. Most of what we know about EPM involves S. neurona. Opossums, which are definitive hosts for EPM, ingest muscle of S. neurona-infected intermediate hosts (cats, skunks, raccoons, and armadillos) and, in turn, shed sporocysts in their feces. Horses consume food and water contaminated by these feces and are considered accidental or aberrant hosts because S. neurona’s natural life cycle does not involve them. Next, the parasites spread throughout the horse’s body.
“We believe the parasite can be found in muscle and perhaps other tissues in horses but is then cleared by the horse’s immune response,” explains Martin Furr, DVM, MA Ed, PhD, Dipl. ACVIM, head of the Department of Physiological Sciences at Oklahoma State University College of Veterinary Medicine, in Stillwater. “The parasite does not ‘target’ the nervous system but, rather, appears to be an accidental infection which the horse then cannot clear from the nervous system as it does in other tissues.”
“To the best of my knowledge, the definitive and intermediate hosts are still not known for N. hughesi, but we believe that the parasite migrates to the CNS (central nervous system) the same way as S. neurona,” says Amy Johnson, DVM, Dipl. ACVIM, section chief of internal medicine and ophthalmology at the University of Pennsylvania School of Veterinary Medicine, in Kennett Square.
Our lack of knowledge pertaining to N. hughesi could, at least in part, be because it causes infection far less commonly than S. neurona. Up to 89% of U.S. horses have antibodies against S. neurona, depending on location. Studies show only about 3-10% of horses, and possibly up to 34%, have antibodies against N. hughesi (James et al., 2017).
The presence of S. neurona or N. hughesi antibodies in a horse’s blood, however, doesn’t necessarily mean the horse is actively infected and suffers from EPM. Instead, antibodies simply reveal a horse has been exposed to them at some point. Only a small number of exposed horses develop neurologic disease; most fight off the parasite without showing signs.
“Both parasites cause similar neurologic deficits because they both cause similar types of damage to the brain and spinal cord,” says Johnson, though the signs are highly
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