Equine Protozoal Myeloencephalitis

 by Philip J Johnson Veterinary Medical Teaching Hospital
College of Veterinary Medicine    University of Missouri
Equine Internal Medicine: Updated January l0th 2000

PART ONE:

Equine protozoal myeloencephalitis or "EPM" is an infectious disease of horses caused by a microscopic protozoan parasite, which as been name Sarcocystis neurona. Incidence of this disease might be increasing in the mid-west. It represents one of the most common diagnoses made in our teaching hospital at the present time.   Certainly, from the perspective of horses presented to our college, EPM is the most common cause of neurological disease in Missouri. It seems that everything that is known about this disease is re-evaluated every week.  Recommendations regarding diagnostic test, specific treatment, and how to determine when to stop treatment, certainly change rather frequently; this is a function of all the new information being learned about EPM.

Hopefully, increased awareness of EPM will lead to earlier disease recognition and treatment: treatment will likely be more successful when instituted early in the course of the disease.

Introduction to EPM Part One

Although, at that time, it was not appreciated that the symptoms were due to a protozoan parasite, it is well documented that horses in North American were affected with EPM in the l960s. The disease was then known as "focal or segmental myelitis/encephalitis" {the cause was unknown-a pathologist's diagnosis}.   Judging from the literature, EPM may not have been as common in those days.

In the l970s, a protozoan parasite was seen in affected neural tissues obtained from EPM-affected horses, the disease was then described as Equine protozoal myeloencephalitis for the first time, but the actual protozoan parasite was not identified. It was (incorrectly) thought that the protozoan was Toxoplasma gondii (leading to the incorrect name-"equine toxoplasmosis").  Probably most (if not all) of the literature about neurological disease associated with toxoplasmosis in horses actually relates to EPM. In the late l970s and the early l980s, evidence was accumulating to suggest that the EPM protozoan parasite belonged to the Sarcocystis group.   In the late l980s the causative organism of EPM was isolated in the laboratory and determined to be a previously undescribed species of Sarcocystis; it was named Sarcocystis neurona. After it had been isolated in the lab, it was possible to develop some accurate diagnostic tests for EPM. 

One of the persisting mysteries about Sarcocystis neurona had been its life cycle.  After it had been determined that the causative parasite was Sarcocystis, a search for possible definitive hosts was undertaken.  logical candidate species included the raccoon, the opossum, and the skunk.  These animals were considered because they are not found beyond the Americas and EPM has only ever been described in North and South American where these particular mammalian species exist.   EPM has only been described outside of the America's in horses which had previously been living in American. In North American, the distribution of the majority of cases of EPM almost exactly follows the population distribution of the opossum.

There is now much convincing evidence that the definitive parasite host ( for Sarcocystis neurona) is the opossum.  Like other Sarcocystis spp, in order to complete its life cycle-the parasite cycles between the opossum and wild birds (intermediate hosts).  The horse is a dead-end or aberrant host!  Recently, there has been reports that  cats may be an intermediate host, it might not be a bird, as originally been thought. (interesting!)

Once the actual parasite (Sarcocystis neurona) was identified as being a natural parasite of the opossum, it was possible to go back in the literature regarding the zoology of the opossum and look at previously-described Sarcocystis spp for that animal.  There was some speculation hat the newly described Sarcocystis neurona might be the same as  Sarcocystis falcatula, which had been described in the late l9th century.  However, it currently appears that the causative organism of equine protozoal myeloencephalitis Sarcocystis neurona is probably not the same protozoan parasite as Sarcocystis falcatula.

Recently, in a small number of horses, equine protozoal myeloencephalitis has been attributed to infection by  Neospora caninum (in California) whether Neospora agents are epidemiological important as Sarcoystis neurona has not been determined yet. In some parts of the USA where the opossum is not found-such as Arizona-horses which have always lived there may develop EPM and may have a positive blood test for EPM. It is possible that, in those cases, the disease may be associated with Neospora agents.

Life cycle of Sarcocystis neurona


Sarcocystis protozoan parasites follow a relatively complicated life cycle.  They exist in two distinct forms. In one form, the parasite lives in the lining of the intestine of a carnivore (the definitive host) and it reproduces at that location and passes infective SPOROCYSTS in the feces of the carnivore. Sarcocystis parasites are usually very host specific meaning the parasite requires a specific carnivore host for reproduction. In order to successfully complete its life cycle, the infective sporocysts must be ingested by a secondary host (intermediate host). In the intermediate host, the sporocysts migrates to the skeletal muscles and can persist there as a sarcocyst for many years. The definitive carnivore host becomes infected (in its intestinal lining) by eating the skeletal muscles of the secondary host. Obviously, the secondary host has either been killed by the carnivore or has died for other reasons. Of the two classic Sarcocyst hosts, one is a predator, the other is prey.

Recently, the carnivore host in North American has been identified as the opossum (Didelphis virginiana) . EPM is virtually only seen in those parts of the world which are inhabited by the opossum. There are many more cases of EPM in horses in the eastern states of the USA than the western states because the opossum is present in greater numbers in these states.  EPM is also seen in South American ( a different opossum species). EPM is only seen in the Old World in those horses which have been imported from the USA.  Opossums eat almost anything: dead birds, insects, etc.  It is not surprising that the feces of the opossum represent a rich source of nutrition for wild birds.  By eating dead birds, the opossum enables the Sarcocystis parasite to complete its life-cycle. Wild birds ingest sporocysts by eating opossum feces.  Whether a bird is the intermediate host or not has recently fallen into dispute.

Horses may be infected with EPM by eating food material (grain, hay, grass) or drinking water (ponds, streams, water troughs, etc) which have been contaminated by the feces of the opossum. The horse is infected in the he same way as birds are infect-by ingesting the infective sporocysts. But unlike birds, in the horse the infective sporocysts migrate into the CNS (central nervous system).  Even when the infected horse dies it is unlikely that its brain or spine will be ingested by an opossum or anything else-therefore the horse is a dead-end host for this parasite; the horse is not needed for the parasite's life cycle. Sarcocystis neurona parasites cannot be transmitted from the horse to other animals (including other horses). EPM is not contagious!

If particular interest is the recent observation that Sarcocystis neurona has been identified as an incidental finding in horses not exhibiting CNS signs at necropsy. It appears that, although horses may be infected with this parasite, even thought the parasite enters the brain/spine, it does not necessarily give rise to neurological symptoms (at least they are not recognized by the horse owner)

Probably, neither the opossum nor the intermediate bird hosts are clinically affected in any way by the presence of a few Sarcocystis parasites- at least not seriously.

It is important to note that not all the sporocysts that are eaten by birds are converted to sarcocysts in the birds musculature. Some sporocysts may also be passed in the birds feces unchanged.  Therefore, bird droppings are also potentially infective to horses.  If this is true, birds can act as mechanical vectors for dispersion of the infective sporocysts.!!

How Horses become infected with EPM
Symptoms of EPM

Horses become infected with EPM by ingesting food material (grain, hay, grass) or drinking water which has been contaminated by the feces of the opossum.  Bird droppings may also be an important source for the infective sporocysts.  In the horse, the Sarcocystis neurona parasites migrate to the central nervous system (CNS, brain and spine).

***Not all infected horses develop recognized symptoms of neurological disease****

Recent  epidemiological surveys suggest that approximately 50-60% of all horses in the mid-west have been infected by or exposed to Sarcocystis neurona. Only a relatively small number of those horses will actually develop neurological disease due to the parasite damage in  the CNS.   Unfortunately, we do not presently know which exposed horses are likely to actually develop signs of EPM.

Sarcocystis neurona parasites set up tiny colonies in the CNS.   The actual signs of abnormality depend on the location and the extent of these colonies.  The disease may be "encephalitis" when effects of damage are seen in The brain; it may be "myelitis" when effects of damage are seen in the spine.  Many infected horses exhibit abnormal signs associated with both the brain and the spine "encephalomyelitis" or "myeloencephalitis".  The symptoms of EPM may be attributed to either the body's inflammatory reaction to the parasites (swelling in the tissues) or to actual destruction of nerve structures within the CNS.

Essentially, EPM causes signs of neurological dysfunction.   EPM may cause any neurological sing or combination of signs; any neurological sign or combination of signs could be due to EPM.


Behavioral abnormalities are also sometimes reported in conjunction with other signs. 

It is important to recognize that EPM can cause any neurological abnormality or combination of abnormalities; therefore, EPM must be considered by the veterinary diagnostician whenever he/she is presented with equine neurological problems. It is also important to consider EPM because it is so common.
 

Mild lethargy Poor bodily condition Attitude change
Reduced exercise tolerance Difficulty with complex gaits Slight incoordination

Alternatively, EPM may cause some rather striking and clear cut neurological abnormalities as well, such as the following:

In coordination Inability to stand Lameness Blindness
head tilt Inability to chew Inability to swallow Facial paralysis
Abnormal eye control Stumbling/falling Seizures/convulsions Headshaking
Muscle tremors Inappropriate patchy sweating Collapse Discrete loss of specific muscle groups

Many EPM-affected horses exhibit signs of multifocal neurological disease (often one lesion affects the spine and another affects part of the brain). The multifocal nature of EPM is important in distinguishing it from other CNS diseases.

EPM often affects one side of the brain/spine to a greater extent than the other (asymmetry)
EPM sometimes leads to focal skeletal muscle atrophy (lower motor neuron lesion)

However, it has been currently stated that focal skeletal muscle atrophy and brain involvement, are relatively uncommon.
The most common clinical manifestation of EPM is simple spinal ataxia/weakness.
EPM- affected horses are commonly presented to veterinarians for diagnosis of "lameness".

But, a diagnosis of EPM as a cause for lameness should not be made with out first undertaking both a thorough lameness examination and a thorough neurological examination!

 In coordination (associated with EPM or other causes of spinal dysfunction) might predispose to lameness because the affected horse (ataxia and weakness) is prone to falling or spraining joints. It might be difficult to determine whether "lameness" is due to musculoskeletal pain, neurological dysfunction, or a combination of both. In horses, which are lame as a consequence of musculoskeletal pain, the lameness should be less pronounced during treatment with pain relieving drugs such as phenylbutazone. Veterinarians may use a short course of treatment with phenylbutazone to determine whether the observed problem is associated with pain. If treatment with phenylbutazone causes a reduction in the severity of the lameness it is less likely that the major problem is a neurological disease (such as EPM)- signs of limb dysfunction associated with EPM do not typically change during treatment with phenylbutazone.
 

Other Disease with Similar symptoms to EPM
What determines whether a horse will develop symptoms of infections?

Important other causes of Brain Disease in Horses:

Trauma Moldy Corn Poisoning Rabies
Stereotypic behavior Polyneuritis equi Abscess
Bacterial meningoencephalitis Viral Encephalitis Tetanus
Botulism Head-shaking syndrome Neoplasia

What determines whether a horse will develop symptoms of infection? There is not yet a good answer for this question. There is much active research to try to provide a scientific answer. There is little evidence yet, that there are significant differences between strains of Sarcocystis neurona; all isolates of the parasite have been exactly the same so far.  Infected horses do produce antibodies against the parasite (which are used in the diagnostic testing for EPM). Unfortunately, producing antibodies does not appear to be protective!  Probably, two important factors are involved in  determining whether infection will  lead to disease (these same factors are important in most infectious diseases).  The first factor is the number of infective sporocysts with which the horse is challenged in a given period of time.  Horses challenged with large numbers are more likely to develop symptoms than horses challenged with a smaller number of infective sporocysts.  The second factor is the level of the horses general immune system;  horses which are immunocompromised are more likely to develop symptoms of EPM following infection!

Important other causes of Spinal Disease in Horses:

Trauma

Cervical vertebral malformation (wobbles)

Degenerative myeloencephalopathy

Equine Herpes virus One

Polyneuritis equi

Rabies

Important factors which may adversely affect a horse's ability to fight infection include the follow:

Certain drugs(especially steroids) Inclement weather (especially very hot weather) Foaling/dystocia
Management changes New ownership Long journeys
Stress Intercurrent Disease Excessive workloads
Intensive Training Programs Surgical Procedures General Anesthesia
Pain Cushings Disease Trailering


Although at least 50% of horses in the Midwest have been exposed to EPM, only a relatively small number of those horses actually develop the disease symptoms. Possibly many horses have been infected with EPM for many months.  Only when the immune system is compromised will neurological signs associated with active parasite damage be seen. Very often, the earliest signs are missed because they are so insidious, the horse is not being monitored/observed very closely, or because they are attributed to something else (commonly a mild lameness).

EPM PART TWO

How is EPM Diagnosed


This disease should be suspected whenever horses develops signs of neurological disease which cannot be readily explained by other obvious events. It must be remembered that EPM can produce any neurological abnormality or combination of abnormalities.

The blood test for EPM is not very useful because approximately 50% of horses in the Midwest have been exposed to EPM and will have a positive blood test.  A negative blood text provides evidence that the horse may not have been exposed to EPM (but it is not a guarantee!) And a positive blood test result does not confirm a diagnosis of EPM either.

It is necessary to make a thorough effect to rule-out other causes of neurological disease in horses in order to support a diagnosis of EPM (especially to rule out cervical vertebral malformation in young male horses- wobbler syndrome).

The best test involves the collection of a spinal fluid sample which is tested for antibodies against Sarcocystis neurona; this test is the western immunoblot.   This test relies on the fact that, during active EPM, antibodies are being produced against Sarcocystis neurona within the spine and brain.  Effort must be made to prove that the spinal fluid is not blood-contaminated (see below). It is becoming evident that a substantial number of horses which do not exhibit signs of neurological disease may also have a positive spinal fluid blot reaction.

NOTE: A positive spinal fluid western immunoblot test is strong evidence that EPM may be the problem IF THE TESTED HORSE IS TRULY DEMONSTRATING SIGNS OF NEUROLOGICAL DYSFUNCTION!  A positive spinal fluid western immunoblot test result is not evidence that EPM is present in horses in which neurological dysfunction can NOT be demonstrated.

All too commonly, neurological symptoms are contrived in order to support the diagnosis of EPM in the face of a positive spinal test result!!  Although EPM is common in specific locations, the diagnosis must be supported by proper interpretation of the horse's clinical situation and the diagnostic tests which are currently available.

There are no logical reasons at the current time to test spinal fluid for EPM in horses which are not demonstrating signs of neurological dysfunction.

A positive spinal test in a non-neurological horse is meaningless.

Collection of spinal fluid can be done at two locations: the lumbosacral tap is done in the standing horse at a point just behind where the saddle is located.  This procedure requires a specific technique for which veterinarians have been trained.   alternatively, the horse can be anesthetized and a spinal fluid sample obtained from the cisterna magna (atlantooccipital tap) which is close to the head.  The general anesthetic is stressful and may cause worsening of EPM, therefore, the lumbosacral tap is recommended whenever possible.  The spinal fluid must be stored carefully and submitted to a laboratory in Lexington, KY.  The fluid should arrive in the lab at the beginning of the week when it can be processed fresh- it should not be mail-delayed as it can deteriorate.  The cost of the western immunoblot spinal fluid is currently $60.

As noted above, greater than half the horses in the Midwest contain antibodies against EPM in the blood.  Therefore, the blood test for antibodies is not very useful on its own.

Other diseases of the brain and spine can sometimes cause antibodies from the blood to leak from the blood into the spinal fluid.  A good example of this situation is when signs of neurological dysfunction have occurred as a consequence of trauma.   In order to help to differentiate actual EPM disease from other causes of disease which are associated with simple transfer of antibodies from the blood into spinal fluid, we also sometimes run two extra tests (albumin quotient and antibody index) on the spinal fluid.  These two tests are also helpful in determining whether accidental blood contamination of spinal fluid has occurred during collection of the sample (if the horse moved, for example)-which would lead to a false positive result.

Sometimes, though uncommon, we recommend also testing spinal fluid for the actual presence of the Sarcocystis neurona antigen in a test known as a PCR (which can also be done on blood and tissues).  This test is more expensive and is not always necessary.  We use the PCR test when we are trying to interpret unusual cases of EPM.   A negative PCR test does not rule-out EPM-most cases that we test using PCR are negative. A positive PCR test (in a clean spinal fluid sample) is very strong evidence for EPM.

In very acute (sudden) onset cases of EPM, the antibody response (as assessed by the western immunoblot test) is negative in both blood and spinal fluid.  The parasite can cause damage very quickly before an antibody response has occurred, it is in these cases that the PCR test is particularly helpful.

If expense to the client is not a problem, it is recommended that the serum should be tested using the western immunoblot (for antibodies) and the CSF should be tested using both the western immunoblot and the PCR. Also both the albumin quotient and the immunoglobulin index should be done. The CSF should also be tested in the clinical pathology lab, routinely for protein concentration and cell counts, etc. Remember the CSF should be analyzed very quickly after collection-call the clinical pathology lab ahead of time so that they will anticipate receiving the sample.

The minimal laboratory test protocol which should be recommended (when the cost of diagnostic tests is critical ) is:

SPINAL FLUID WESTERN IMMUNOBLOT AND SPINAL FLUID ALBUMIN QUOTIENT (also need a blood sample for this test)

Statistical analysis of preliminary data with respect to value of the serum and CSF tests:

Serum and CSF test results from 295 horses necropsied from 1991 to 1996 were compared to postmortem diagnoses. Spinal fluid samples with obvious blood contamination were excluded. The positive predictive value for CSF test results among this group of neuralgic horses was 85%. The negative predictive value was 92%. The sensitivity and specificity were approximately 89%.  The negative predictive value of serum testing was 88%. Therefore, the probability that a horse with a negative serum test would also be negative for EPM at postmortem was 88%.

The laboratory in which these tests are done is

Equine  Biodiagnostics, Inc
Coldstream  Research Campus/University of Kentucky
1505 Bull Lea Road/Suite 104
Lexington KY  40511~~~~~ Telephone:859-514-4994     Fax: 859-514-4999

Cost:  The laboratory undertakes both the spinal fluid western immunoblot and the albumin quotient for a total cost of less than $100.00

Another important aspect to establishing the diagnosis includes ruling out other possible causes of similar neurological sings. It should also be remembered that EPM can occur at the same time as other neurological diseases.  A full physical and neurological examination should be done in order to be as accurate as possible regarding both the horses general health and the neurological status.   Careful notes/video recording should e prepared so that follow up examinations can be done reasonably objectively.  Sometimes other blood tests or special radiography are also recommended.

The other important aspect of the establishment of the diagnosis is done by evaluating the effect of treatment. Most , but not all horses affect with EPM will respond to treatment for Sarcocystis neurona. The response to treatment can represent an important aspect of the diagnostic procedure.  It should be remembered that for all laboratory tests, there exist false positives and false negatives.

Ultimately, the diagnosis of EPM can often be made after an affected horse has died.  The pathologist is able to examine the spine and the brain under the microscope and identify either the protozoal parasites or the characteristic effects of parasite damage.  Sometimes, the parasite colonies are so tiny that the pathologist cannot find them-in which case the pathologist also relies on the western immunoblot test on spinal fluid.  Following the death of a horse, the CNS deteriorates very quickly; it is important in order to secure a diagnosis, to remove the brain and the spine very soon after death. If the brain and the spine are not quickly removed, they deteriorate to such an extent that the pathologist is not able to establish a diagnosis.  When collecting spinal fluid at point of death, it is essential to obtain the specimen within a few minuets (10 minutes) . A good neurological evaluation will help the pathologist determine where is the most likely site to find a lesion within the CNS.

Treatment for EPM
 Length of Treatment

Rest/minimize stress-walking exercise with light trotting is helpful-under supervision
Sulfadiazine: 15-25 mg/kg of body weight, orally,e very 24 hours for at least 4 months
Pyrimethamine(Daraprim): 1.0 mg/kg orally, every 24 hours for at least 4 months
Consider vitamin E: 5,000 units twice daily
Consider treatment with thiamin and other B-vitamins

Please note: do not use trimethoprim at the same time as pyrimethamine (pyrimethamine is better than trimethoprim).  We sometimes also us anti-inflammatory agents such as dimethyl sulfoxide and flunixin meglumine (banamine). We recommend treatment of EPM diagnosed pregnant mares with the same drugs, but we use only half the pyrimethamine dose.

It is important to not use glucocorticold steriods unless absolutely necessary. We sometimes use steroids in severe cases of EPM for short periods in conjunction with the standard treatment.

How Successful if Treatment?

Unfortunately, we are not able to answer this question very accurately.  Most horses respond to treatment-but, based on our observations, relatively few make a complete recovery. Some horses do not respond to treatment whatsoever. Without treatment, many horses progressively deteriorate to the point that they are unable to stand up.  A significant number of horses eventually relapse and develop further active EPM.   Currently, we generally advise that approximately l0% of treated horses might make a  full recovery; 20% of treated horses do not respond and are euthanatized; the remainder (70%) make various degrees of partial recovery. If treated horses do respond favorably, it appears that they are at risk for recurrence of EPM.

Early diagnosis and prompt therapy help to ensure a favorable response.

If the horse does not respond to treatment, it is appropriate to also reconsider other possible neurological diseases.

Both sulfa drugs and pyrimethamine must be used for the duration of therapy since resistance can development to pyrimethamine alone.  Supplementation with folic acid has been recommended-but currently there has been some suggestion that supplementation may be detrimental-we currently do not recommend concomitant folic acid supplementation.

If improvement is not noted after four to six weeks of therapy, the prognosis for recovery is poor.  The prognosis for horses with EPM is variable.   Early diagnosis and prompt therapy help to ensure a good response.   irreversible damage to the brain or spinalcord is more likely to occur if the parasite has been present for long periods of time.

There are a few adverse effects of treatment.  Orally administered sulfadiazine may increase the risk of diarrhea.  Risk of diarrhea may be increased by stress factors or the presence of concurrent intestinal disease. Treatment should be discontinued if diarrhea occurs.

Both sulfadiazine and pyrimethamine are folic acid antagonist. These drugs might cause a folic acid deficient state for the horse (but this is not common). Folic acid deficiency leads to pancytopenia (inhibited bone marrow); anemia, leukopenia and thrombocytopenia.  We recommend monitoring for pancytopenia using a CBC every 2-4 weeks during treatment (or sooner if needed). If folic acid deficiency problems are suspected, the sulfadiazine and pyrimethamine treatment should be discontinued and the patient might be treated using folic acid supplement.  The blood should be monitored (once weekly) and treatment resumed when the cell counts normalize.

New information suggests that concomitant supplementation with folic acid potentates the toxic action and reduces efficacy of pyrimethamine-especially with foals or foals prior to birth.

There may be an increased incidence of abortions in pregnant mares.

Foals born from mares treated with EPM may be abnormal.

Folic acid supplements for the mare does not appear to reduce the risk of newborn foal problems. Newborn foal problems include: anemia, thrombocytopenia, decrease white blood cells (neutrophilis, and lymphocytes), immunosuppression, kidney malformations and abnormal skin/haircoat. These foals usually die.

What can be done to prevent EPM? It has been recently reported that evidence of EPM can be seen in  approximately l0% of Thoroughbreds going through the Thoroughbred sales (horses which are being sold as "normal"). Be ware of the clinical signs-know what to look for.

  • The opossum and wild birds should not be tolerated in close proximity to horses

  • Opossums should be trapped and removed to distant locations. It is very easy to catch opossums in live traps.

  • Special electrical fencing can be used to inhibit the movement of opossums onto the farm-low fencing requires that grass and vegetation will be kept very low adjacent to the fence.

  • Birds are difficult to control but should kept out of barns (cats may help)

  • Big dogs will discourage opossums from entering horse premises

  • An Important point in controlling opossums is eliminating food sources. Store all grain in tightly closed containers, dog and cat food should not be left outside.  Dead animals should be disposed of expeditiously and not allow to rot in situ. Food material should not be available to the opossum in areas where horses are kept.

Opossum management will be a constant problem for horse owners in the mid-west. It is not advisable nor is it like to be successful for horse owners to attempt opossum eradication, but it is possible to decrease the contact horses have with opossums.

Prevention of EPM

In order for horses to develop signs of neurological disease attributable to equine protozoal myeloencephalitis (EPM), they must be infected by the protozoan parasite, Sarcocystis neurona (although, for reasons which are currently unknown, most infected horses appear to develop a protective immunological response and do not actually develop neurological symptoms). Infection occurs when the horses ingest food or water which  have been contaminated by the infective sporocysts of the parasite. It should be emphasized that horses can not acquire EPM by exposure to other horses in which EPM has been diagnosed.

In light of the fact that opossum (Didelphis virginiana) feces represent the most significant source of environmental contamination by the infective sporocysts of Sarcocystis neurona, the most effective and practical recommendations for prevention of EPM pertain to minimizing the chances that horses might eat feedstuff which has been tainted by opossum feces. Every effort should be made to lessen the chances that opossums might interact closely with horses. Certainly, opossums should never be tolerated inside barns, in places where horse feed is stored, and especially at locations where horses are fed.   Keeping big dogs in or around the horse barn has been suggested to be a useful method for frightening off opossums. It is also recommended that stored hay should be securely covered in a manner to prevent contamination by opossums. It has been our experience that horses on certain farms are at particular risk for problems associated with EPM when those farms are located in particularly close proximity to woodlands. It might be prudent to consider not allowing horses to graze pastures which are adjacent to extensive woodland in areas in which the opossum is found.

In those areas in which it is found, the opossum is an abundant nocturnal marsupial which is rarely seen during daylight hours (and is therefore often underestimated). The opossum, an omnivore with a ravenous and undiscriminating appetite, is attracted to many different potential food materials, including horse feed, pet dog and cat food, fallen fruit, carrion, and discarded human food (in trashcans). In order to reduce the number of opossums which might be attracted to a horse farm or barn, all uneaten and discarded animal feed should be picked up and cleaned away, spilled grain should not be allowed to accumulate, animal cadavers should be disposed of in an expeditious manner, and fallen fruit should be picked up quickly. Grain, sweet feed and pelleted feed intended for horses should be thoroughly inspected for possible contamination by opossum feces and stored in air tight containers. Heat treated (60-166C) commercial horse rations (such as steam-flaked, pelleted or extruded feeds) represent a safe source of feed because the infective sporocysts are destroyed by the high temperature (unless they have been contaminated subsequent to packaging and shipment).  It has not been determined if cold processed commercial horse feed is/are  free of sporocysts.

The horse owner should develop vigilance for opossum feces in the horse barn (commonly found along the top of wooden struts and beams) which should signify a need to increase surveillance for opossums, improve the general level of hygienic in the barn, and to reconsider the extent to which preventive measures have been undertaken.

If possible, horses should not be allowed to drink from slow running streams or stagnant ponds (especially in wooded areas). Fresh water should be provided in clean containers or through automatic waterier. Watering sources for horses in paddocks or at pasture should be inspected periodically to ensure that fecal contamination by wild animals and birds is no occurring.

If necessary, opossums may be trapped and removed from the farm. It is strongly recommended that, if a capture and relocation strategy is attempted, specific guidance should be sought from the local state Department of Conservation.  We have found that the wildlife experts in our Missouri Dept of Conservation have been very helpful.  In conjunction with trapping and removal of opossums, the use of a partially buried 5cm x 10cm mesh fence and electric topline may further prevent entry of opossums into the horse paddocks.

Other small wild mammals (rats and mice), certain birds and insects might also play a role in the mechanical dispersion of infective sporocysts from opossum feces into the horse's environment; for this reason, preventive measures should also include strategies to minimize the numbers of rats and mice in barns and in places where horse feed is stored.  Wild birds should not be tolerated in horse barns and mesh net screens may be used to impede bird access into the barns.  Bird feeders should be eliminated. Regular treatments of the equine environment by an insect exterminator should be considered as part of any EPM prevention strategy.  Allowing cats to live in the horse barn might deter wild birds.

It is fortunate that, although a majority of horses are exposed to Sarcocystis neurona in certain parts of the United States and Canada (leading to a positive blood test for EPM), only a small number of exposed horses actually develop neurological signs.   At this time, highly effective preventive measure (such as vaccination) have not been designed and the strategies suggested here are simply logical approaches to management which are largely based on what little we know about the natural history of this parasite and the opossum.

Any specific questions or comments mail to:

johnsonpj@missouri.edu
 
 

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