Equine protozoal myeloencephalitis: Etiology, diagnosis and treatment - DVM
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Equine protozoal myeloencephalitis: Etiology, diagnosis and treatment
Early identification is key in this widespread neurologic disease


DVM360 MAGAZINE


"The second advantage of the UC Davis-developed test is that it tests for antibodies to both S. neurona and N. hughesi," Pusterela continues. "If you use only the SnSAG 2,3,4 ELISA test, if the disease is caused by N. hughesi, you're not going to pick it up. So, you're going to falsely determine the animal does not have EPM. You're not going to treat him, and this horse will not improve."

MacKay says that, although several tests are available, none are "terribly satisfactory." "They're good at identifying horses that don't have any kind of infection," he says. "They've not been good at discriminating between the types of infection—the one with neurologic signs and the one without."

Whichever blood test is used, the information is still available, says Morrow. The presence of antibodies can support an EPM diagnosis in the presence of clinical signs. "But the diagnostic value is better if you add the CSF component, especially with the SAG 2,3,4 ELISAs," she notes.

Reed adds, "It's certainly easier if a practitioner only had to take a blood sample, but as EPM is a neurologic disease, there's CNS involvement, and it's logical that CSF would be an important diagnostic specimen. I realize how important it is to most veterinarians in the field if we could develop a test where you could dependably determine the disease probability from blood alone. That would sure make life easier for most practitioners. To really increase the accuracy of diagnosis, the ratio of antibody in blood to CSF is the best. And if you become used to tapping CSF from every horse, it doesn't become an enormous challenge."

Treatment

Newer antiprotozoal drugs are available to help diagnose and treat EPM. Without treatment, the progression of EPM is somewhat unpredictable, as the neurologic signs in untreated horses usually get worse—from the more mild signs to ataxia, recumbency or death in hours to years, with periods of severe exacerbations possible after prolonged periods of quiescence.

"Most of the cases of EPM are progressive," says Pusterela. "And we know that the more severely affected horses may improve with treatment, but the chance for full remission in the severely affected animal is significantly worse. If the same animal is treated early on, the signs may be fairly mild to moderate."

Four drugs have been approved by the FDA for treatment of EPM: pyrimethamine, sulfadiazine, ponazuril and diclazuril. Approved by the FDA in 2003, nitazoxanide was recently withdrawn because of potentially serious side effects such as enterocolitis, laminitis, anorexia, fever and lethargy. Several other drugs are considered for treating EPM, but none of them are FDA-approved.

Pyrimethamine and sulfadiazine

According to scientists at UC Davis, pyrimethamine and sulfadiazine, previously thought to cure EPM, only provide temporary relief of the condition. Apparently they're effective only in depressing the viability of the causative parasites S. neurona and N. hughesi. The drugs enable the horse's immune system to kick in—to control the infection temporarily during the treatment period. When treatment is curtailed and the horse returns to work or is stressed, the disease often recurs.

The pyrimethamine-sulfadiazine combination is of limited effectiveness, and its treatment period is three to four months, or longer. It also requires supplemental folate, since these drugs counter folate metabolism, which is especially critical to pregnant mares.

"In the compounded form of pyrimethamine-sulfadiazine, there's very little problem with toxicity," says MacKay.


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Source: DVM360 MAGAZINE,
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