User:SkipDiggy14/Equine protozoal myeloencephalitis

Equine protozoal myeloencephalitis (EPM) is a disease that affects the central nervous system of horses. It is caused by a protozoal infection that is brought about by the apicomplexan parasite Sarcocystis neurona or Neospora hughsei however most cases are caused by Sarcocystis neurona as the lifecycle along with the transmission of Neospora hughsei is not well understood. The parasites create lesions in both the brain and spinal cord of the affected horses leading to neurological issues.

History
EPM was first discovered in the 1960s by American biologist Dr. Jim Rooney. The disease is considered rare, though recently, increasing numbers of cases have been reported.[ citation needed] Previous research identified the "barn cat" as the definitive host of the disease. Since that time, though, the definitive host has been found to be the opossum, while any of a number of mammals can serve as intermediate hosts in the disease's two-host lifecycle. In a test conducted by Clara K, Fenger, Sarcocystos sporocytes were taken from opossum feces which were then the DNA was amplified in order to create a clinical diagnosis for EPM. It was found that opossums are hosts for several other Sarcocystis species.

The term EPM refers to the clinical neurologic symptoms caused by the parasite, not infection itself. The parasite S. neurona was named by J.P. Dubey due to the morphological characteristics of the parasite. With that, through cultivation, this parasite detailing strategy allowed for better diagnostic testing, genome characterization, morphological definition, and host identification. Most horses infected with S. neurona do not exhibit neurological symptoms consistent with EPM. Six subspecies of S. neurona can be identified by surface antigens (SAG). Equine EPM is caused by the parasites that exhibit SAG1, SAG5, and SAG6. SAG1 and SAG5 are responsible for the majority of EPM cases in horses. Horses produce antibodies to these surface antigens. Serum antibody testing is available that measures levels of these antibodies in the blood of horses, which is helpful in diagnosing EPM in an ataxic horse. Serial blood levels are helpful in guiding treatment. In experimentally infected horses it takes 14 days from infection to positive antibody tests. 80% of horses with EPM have positive antibody tests. A negative antibody test in the presence of EPM results if testing is done before 17 days or if the horse has been treated with antiprotozoal drugs which delays antibody production.

Causes
EPM is caused primarily by the parasite Sarcocystis neurona. The lifecycle of S. neurona is well described. To complete its lifecycle, this parasite needs two hosts, a definitive and an intermediate. In the laboratory, raccoons, cats, armadillos, skunks, and sea otters have been shown to be intermediate hosts. The opossum is the definitive host of the disease, passing the parasite through feces. Horses contract EPM from contaminated feed or water. Horses cannot pass the disease among themselves; that is, one horse cannot contract the disease from another infected horse. The horse is a dead-end, or aberrant, host of the parasite. undefinedAlthough all horses are believed to be susceptible to EPM the disease is usually found in younger horses typically around three to six years of age. With that, the disease does not typically correlate with other factors such as poor nutrition or other diseases. In a study done by Ronald Fayer, he found that there was no correlation to the genders of the horses infected nor was there a correlation with the time of year. His study also found that out of 364 horses approximately 62% of these horses were under the age of four.

Symptoms
The onset of EPM can come on suddenly or gradually however once the lesion is created it is extremely hard to reverse the damage. The most common symptoms of EPM are ataxia, general weakness with muscle spasticity. However, this is not specific to EPM and is common in many other neurological disorders. Clinical signs among horses with EPM include a wide array of symptoms that may result from primary or secondary problems. Apparent lameness, particularly atypical lameness or slight gait asymmetry of the rear limbs are commonly caused by EPM. Focal muscle atrophy, or even generalized muscle atrophy or loss of condition may occur. Secondary signs also occur with neurologic disease. Airway abnormalities, such as laryngeal hemiplegia, snoring, or airway noise of undetermined origin may result from damage to the nerves which control the throat, although this is quite uncommon.

In experimentally infected horses, very early signs included loss of appetite, decreased tongue tone, facial paresis, altered mental status, generalized weakness, and lameness.

Diagnosis
Diagnosing EPM can be challenging because the signs can vary significantly from horse to horse, and the symptoms can be similar to those of other CNS diseases. The only way to definitively diagnose EPM is through postmortem testing, but there are ways to exclude other diseases and establish a basis for the EPM diagnosis. One method is a neurological examination that assesses the CNS function of the horse. Another option is a cervical radiograph, which can identify any compression in the spinal cord that may cause a horse to lose coordination. A veterinarian can also draw blood and spinal fluid and send it to a lab to confirm if a horse has been exposed to opossum feces. Labs can perform immunodiagnostic testing on spinal fluid to evaluate the production of antibodies that fight against these parasites.

Treatment and prevention
EPM is treatable, but irreversible damage to the nervous system is possible. Identifying the disease as early as possible and beginning treatment with antiprotozoal drugs is important. Currently, three FDA approved treatments are available in the US: ReBalance (sulfadiazine and pyrimethamine), Marquis (ponazuril), and Protazil (diclazuril). These drugs minimize the infection, but do not kill the parasite. The use of anti-inflammatory agents such as banamine, corticosteroids, or phenylbutazone are often used to help reduce inflammation and limit further damage to the CNS. Antioxidants, such as vitamin E, may help promote the restoration of nervous tissue. Response to treatment is often variable, and treatment may be expensive. Recently, antiprotozoal treatments that kill the parasite and clear the infection have shown promise. The inflammatory component is thought responsible for the symptoms of EPM;  anti-inflammatory drugs that target the IL-6 pathway have been particularly effective at reversing symptoms. However it is important to note that there is no vaccine to cure EPM. There are several ways that horse owners can potentially lessen the chances of their horse(s) getting EPM. Some of these preventative measure include proper storage of hay and feed, if possible, not feeding on the ground, “” reducing wildlife access to stalls and pastures, thoroughly cleaning the horse’s water source often, and prompt disposal of animal carcasses.