|Tornquist, S - OR ST.UNIV.,CORVALLIS, OR|
|Gerros, T - OR.ST.UNIV.,CORVALLIS, OR|
|Topper, M - WALTER REED,WASHINGTON,DC|
Submitted to: Veterinary Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 23, 1998
Publication Date: N/A
Interpretive Summary: In North America, equine protozoal myeloencephalitis (EPM) is considered one of the most common disease that affects the spinal cord and the brain of horses. The cause of this disease is a parasitic organism called Sarcocystis neurona. Recently another parasite, Neospora caninum has been reported in 2 horses with neurological signs resembling EPM. We describe here an additional case of EPM associated with Neospora caninum. The affected horse was a 20-year-old gelding with severe nervous signs. Lesions were present in the spinal cord and the brain of this horse. Laboratory examination of tissues of this horse revealed lesions with parasites which were identified as Neospora caninum by a special laboratory technique (immunohistochemistry). We remind veterinarians and horse owners that they should be aware of increasing prevalence of Neospora caninum as another parasitic agent responsible for EPM.
Technical Abstract: Equine protozoal myeloencephalitis (EPM) was clinically diagnosed in a 20-y ld horse with severe ataxia. The cerebrospinal fluid was positive for Sarcocystis neurona antibodies by western blot. The horse was administered corticosteroids to facilitate invitro culture of S. neurona from its spinal cord following necropsy. Microscopic lesions of EPM were present in the brain and the spinal cord, including multifocal inflammatory cellular infiltrates and several large groups of protozoa. Immunohistochemical, and light and electron microscopic examinations revealed that the protozoa was Neospora caninum and not S. neurona. The protozoa divided by endodyogeny, tachyzoites had rhoptries, and organisms reacted specifically to N. caninum antibodies. Veterinarians should be aware of increasing prevalence of N. caninum as another etiological agent responsible for the lesions of EPM.