Equine protozoal myeloencephalitis (EPM) is a syndrome that includes neuroinflammation. Recognizing the inflammatory component of the syndrome may make EPM a treatable disease, of course supporting a presumptive diagnosis requires a clinical examination and ruling out other causes of disease. Ruling out other diseases begins with a physical and neurological exam. Diagnostic tests can include radiographs and immunodiagnostics. Primary complaints that are related to an abnormal gait indicate a standard lameness exam (that includes nerve and joint blocks) should be performed. After routine diagnostic procedures, some veterinarians use a response to treatment to support a diagnosis.
When ataxia is apparent, ruling in/out the location of the problem is useful. Localizing the lesion is an achievable art. In early S. neurona infections vestibular disease is recognizable and can involve the peripheral or central vestibular system, brainstem, or cervical vertebrae. When localizing a lesion to the clinical signs an important consideration-- is it one lesion or a multifocal issue? The onset of signs can be sudden and indicate trauma, infections, inflammation, toxicity, or idiopathic causes. Chronic and non-progressive disease make trauma or infections more likely. A thorough examination and diagnostic testing can rule out or point to an etiology.
Induced EPM infections cause ataxia in horses. Prior to ataxia, central vestibular disease is apparent. Since publication of Early Signs of Equine Protozoal myeloencephalitis (Ellison, Kennedy, Brown, 2003. Journal of Applied Research in Veterinary Medicine p.272-278) the observations in 44 ataxic horses were documented. The determination of disease in horses in these blinded, placebo controlled studies was by a grade 2 ataxia. Observing the signs indicated in the chart below suggested central lesions quickly after S. neurona challenge.
The focus of EPM research is on the pathogenesis of protozoal encephalomyelitis. Vestibular disease is part of the disease process, as shown by documenting signs in challenged horses. In field cases, the most common causes of vestibular disease are trauma or infection. The clinical signs in horses are often acute. Management and treatment of these cases can be difficult. Central and peripheral lesions are treated differently with different prognosis and that makes differentiation between these two conditions important. Central vestibular disease (affecting the brainstem or ventral portion of the cerebellum) often results in severe signs including trouble eating, ataxia, and paresis in multiple limbs, or even recumbence. Central vestibular disease is often observed in cases of EPM. Early recognition of central vestibular disease associated with EPM combined with effective treatment can resolve clinical signs returning a horse to use.
The location of the protozoa in active EPM cases is currently under debate. Some practitioners argue that protozoa must be in the CNS to cause the observed inflammatory signs of disease. We argue that protozoa can occupy the CNS, breaching the blood brain barrier inside white blood cells (Trojan Horse model), but assert that this scenario is rare. Undoubtedly there are cases in which protozoa are found post mortem in horse with a diagnosis of EPM. The far more common condition is that protozoa are not found in histological samples. Histological specimens are rife with inflammatory lesions, considered evidence of protozoal infection. However, these lesions are not described as pathopneumonic. The term is idiopathic if a definitive diagnosis is not made.
The basis for our opinion is that protozoa are not found in the majority cases of suspect EPM that undergo post mortem examination. Even in the stress model used to induce EPM (Saville et al 2001. Veterinary Parasitology 211-222) the researchers were unable to demonstrate protozoa in the CNS of the challenged horses. Alleviation of signs can occur rapidly with treatment. Should necrotic lesions (due to parasites) be present in the CNS one would expect a long period for recovery including an aftermath of signs that could not be resolved. A rapid response to treatment and return to use in suspect EPM cases is our goal. Our goal is facilitated by an early recognition of central vestibular signs. No doubt EPM is a difficult disease to identify, treat, and manage. Our view is based on available literature, experiment, and clinical observations made by veterinarians. The optimistic view is that EPM is treatable because a large part of the disease syndrome is inflammation. Until scientific evidence shows us an alternative, defensible view, we will continue suggesting treating neuroinflammation as a practical approach to treating EPM.