HISTORY DIAGNOSIS AND TREATMENT OF
EQUINE PROTOZOAL MYELOENCEPHALITIS.
Equine Protozoal Myeloencepalitis is a serious neurological disease in horses caused by a parasite protozoa thought to be sarcosystis neurona. The disease was first identified in the 1960’s when lesions and inflammation were seen in the brain and spinal cords of horses that had died of severe neurologic disease. Protozoa were discovered on the lesions in 1974, however the vector was unknown and the disease considered rare. Recently the opossum has been isolated as the probable vector and the likely parasite organism identified as Sarcosystis falcatula. (Fenger, 1996)
The Sarcosystis protozoan parasites have a complicated life cycle. They exist in two distinct forms. One in the definitive host (a carnivore like the opossum) and one in a secondary or intermediate host (wild birds that the opossum feeds on). It reproduces in the digestive tract of the definitive host and passes infective sporocysts in the feces, which are then taken in by the secondary host. There the sporocysts migrate to the muscles and can persist for years until the secondary host is eaten by the definitive host. The protozoa are usually very host specific (requiring a specific carnivore to reproduce), and most likely neither host show any clinical signs of disease. (U. Missouri… 1999)
The horse is an unfortunate casualty in this cycle; it is infected when feces of the opossum are ingested with their food material. The horse is a dead-end host, meaning it is not required in the parasite’s life cycle and therefore the disease cannot be transmitted from horse to horse. Several interesting facts put forth by the University of Missouri: EPM is seen only in parts of the world that are inhabited by opossum specifically the Americas. It has been estimated that seroprevalence (indicating exposure) in Pennsylvania, Ohio, and Kentucky is as high as 50%, however only a small percentage (2-3%) of those exposed will become ill with symptoms. Native wild birds infected are not likely to show any symptoms, however non-native birds become acutely ill and die from S. falcatula exposure. (U. Missouri… 1999)
Primary clinical signs of EPM occur from swelling and nerve death in the central nervous system as a result of the replicating protozoa. Neurologic signs can be directly referable to the site or sites of infection. The spinal cord is most often affected resulting in the “three A” symptoms of asymmetric ataxia and focal muscle atrophy. (Fenger, 1996) Ataxia affects the horse’s sense of position in space. When the nerves in the inner ear are damaged the horse loses unconscious proprioception which is the directional sense of up and down. When the conscious proprioception tracts from the joints and muscles of the legs are damaged the animal loses its sense of limb position in space. (Fenger, 1995) Ataxia is associated with the staggering “drunken sailor” gait used to describe animals with neurological dysfunction, and can be rated on a scale of one to five. Five being a horse which cannot stand up and one being a horse which is unlikely to fall and looks normal walking strait but can be made to show deficit when turning, or going up and down an incline. Horses with EPM can exhibit any level of ataxia from mild to severe however often horses’ symptoms will be asymmetric (more severe on one side) and be combined with focal muscle atrophy (wasting and weakness) especially in the hindquarters. (Fenger, 1995) It is important to note that often the only signs of EPM may be a slight gait asymmetry or apparent lameness that fails to block out in a comprehensive lameness exam. Therefore the disease may not be apparent to the lay person in its early stages. (Fenger, 1996) EPM is often overlooked in the ten percent of horses that experience airway problems as a result of cranial nerve dysfunction. Because most horses that have airway problems do not have EPM it is often missed in its early stages, the astute observer may notice signs of ‘quidding’ (food material in the nostrils) and atrophy of the temporalis and/or masseter muscles. (Fenger, 1996)
Secondary clinical signs are the result of injury to other structures such as muscles, tendons, and ligaments due to ataxia and nerve dysfunction. Upward fixation of the patella is common, probably because of quadriceps weakness. Other problems such as bucked shins, splints and bowed tendons can occur due to the tendency for these animals to travel very heavily on the forehand. Another common side effect is back soreness-often severe-resulting from the asymmetric use of the limbs. (Fenger, 1996)
EPM can often be seen by observing horses during training however, it may easily be overlooked or attributed to a number of other ailments. Early signs may include evident discomfort and weakness in the rear limbs. Frequent bucking, head tossing or excessively high head carriage. Minimal forward extension at the gallop and difficulty maintaining a specific lead, and negotiating turns are all symptoms; the horse may cross-canter or frequently change leads. The front limbs may seem to “float” at the trot, or the horse may drag one or all of its feet. Racehorses frequently have trouble breaking from the starting gate, and/or maintaining position in the turns. An important sign of EPM that is probably most often overlooked is many horses with the disease develop a bad attitude towards training, due to a lack of confidence, or pain associated with secondary problems. (Fenger, 1996) Horses that exhibit these problems should be evaluated by a vet for other neurological abnormalities.
EPM can mimic any other neurological disease and therefore can be very difficult to diagnose effectively. The clinical signs can range from very mild to severe and the progression of the disease slow or sometimes not at all. Meaning that many horses with mild cases will never be diagnosed at all. A Western blot test can be used to test blood serum for anti-bodies indicating exposure, however a positive serum result does not mean that the horse is infected with the disease. Because EPM can present itself like a number of other diseases it is necessary to use further tests to definitively diagnose. For most animals this means an analysis of the cerebral spinal fluid (CSF) which when abnormal will show in increased level of proteins and inflammation. (Fenger, 1996) The CSF can be extracted either from the Allanto-occipital space (where the head meets the neck) or from the Lumbo-sacral space (above the hindquarters.) However since the CSF flows in a caudal (towards the back) direction the Lumbo-sacral space is preferred as it will be more likely to show inflammation. Also important to consider is that testing the Allanto-occipital space requires that the horse be anesthetized and laid down, which can be dangerous in a horse that has neurological problems. (Levine, 1999)
The University of Missouri-Columbia’s current recommendations for treatment include a course of oral anti-protozoal drugs combined with sulfa drugs for a minimum of 12-16 weeks, and the horse should remain on the medication for 4 weeks after neurological symptoms disappear. The relapse rate after treatment is about 40%, however the majority of those cases occur because treatment was discontinued after less than three months. (Fenger, 1996) The current medicine of choice is Sulfadiazine and Pyremethamine used together, they should be administered once a day orally on an empty stomach to achieve peak drug levels. (U. Missouri… 1999) About 10% of horses experience a ‘treatment crisis’ where the symptoms actually worsen while on the medication, this may be caused by the dying parasites and the resulting inflammation. Usually these horses respond to anti-inflammatory drugs such as Banamine. (Levine, 1999) About one third of horses will respond to treatment in the first 10-14 days, however sometimes permanent damage has occurred to the Central Nervous System and the horse may not fully recover. If improvement is not noted within 4-6 weeks then the prognosis for recovery is relatively poor. (U. Missouri… 1999)
Pyremethamine and Sulfdiazine may cause folic acid deficiency in treated animals and previously supplementation was recommended. New research indicates that oral folic acid supplements can actually interfere with folic acid absorption making the situation worse, especially in pregnant mares and foals. Supplementation with Folinic acid appears to be safer and is routinely administered to human patients with CNS Toxoplasmosis to prevent anemia during treatment. It should be noted that Pyremethamine cause birth defects in humans and therefore foals born to treated mares may be abnormal and often die. (U. Missouri… 1999) Vitamin E supplements have also been recommended due to its antioxidant and mild anti-inflammatory properties.
There is no vaccine for EPM and treatment does not always result in success therefore prevention is the only method of management for this disease. Currently the only way to prevent EPM is to be vigilant about keeping opossums and wild birds out of the barn. Big dogs will deter the animals and barn cats are useful in keeping birds away, however dog and cat food must be minimized because that will attract the opossum. Trapping and removal of opossum is possible however the best method of prevention is to eliminate food sources. Grain should be stored in a sealed airtight container, any spills should be cleaned up immediately and excess should not accumulate in the stalls. If possible horses should not be permitted to drink from stagnant ponds or slow moving streams that may be contaminated. Mice and rats should also be minimized in the barn because they may play a role in dispersing the opossum’s feces. (U. Missouri… 1999)