Davis, California, the College of Veterinary Medicine (Reed), Ohio. State University ... All that is known about the disease is from natural infections. Typically ...
Epidemiology of Equine Protozoal Myeloencephalitis in North America Based on Histologically Confirmed Cases A Report R. Fayer, PhD, I. G. Mayhew, BVSc, PhD, J. D. Baird, BVSc, PhD, S. G. Dill, DVM, J. H. Foreman, DVM, MS, J. C. Fox, PhD, R. J. Higgins, BVSc, MS, PhD, S. M. Reed, DVM, W. W. Ruoff, DVM, MS, R. W. Sweeney, VMD, and P. Tuttle, DVM
Following a workshop on equine protozoal myeloencephalitis (EPM) convened at the Veterinary Medical Forum of the American College of Veterinary Internal Medicine in 1988, this survey of EPM in North America was developed. It is based upon 364 histologically confirmed case records from California, Florida, Illinois, Kentucky, New York, Ohio, Oklahoma, Ontario, Pennsylvania, and Texas up to 1988. The highest rate of infection was found in young Thoroughbred, Standardbred, and quarter horses. Differences in geographic location, sex, and month (season) of infection were not discernible. This report, the first comprehensive survey of EPM in North America, is intended to serve as a basis for evaluating future changes in prevalence and spread of EPM. (Journal of Veterinary Internal Medicine 1990; 454-57)
SEVERAL equine diseases designated as focal myelitisencephalitis, segmented myelitis-encephalitis, equine spinal ataxia, and equine protozoal myelitis have similar
clinical signs, gross and histopathologic findings, and associated protozoan parasites. ' These diseases are now considered to be the same disease and are referred to now as equine protozoa1 myeloencephalitis (EPM).2 All that is known about the disease is from natural infections. Typically, there is central nervous system (CNS) involvement. Although almost any neurologic syndrome can result, the more common signs are falling, stumbling, recumbency, ataxia, spasticity, and pares ~ s Other .~ signs might include lameness, weakness, asymmetrical hypermetria, asymmetrical facial paralysis, partial paralysis of the tongue, or atrophy of various muscle group^.^ The disease has been seen as peracute, acute, and chronic forms but once clinical signs appear the disease most often is progressive and usually necessitates euthanasia if untreated. Because the accuracy of diagnosis based on clinical signs alone is recognized as imperfect it is impossible to tell how many of the horses originally diagnosed as EPM and then successfully treated (with the antifolate, antiprotozoal drugs pyrimethamine and sulfonamides) actually are EPM. Lesions are confined to the CNS, most often the spinal cord. They frequently are (multi-) focal and range from microscopic to several centimeters in size and are
From the Zoonotic Diseases Laboratory (Fayer), Agricultural Research Service, United States Department of Agriculture. Beltsville. Maryland, the College of Veterinary Medicine (Mayhew), University of Florida, Gainesville, Ronda, the Department of Clinical Studies (Baird), Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada, the New York State Veterinary College (Dill), Cornell University, Ithaca, New York, the Department of Veterinary Clinical Medicine (Foreman). College of Veterinary Medicine, University of Illinois, Urbana, Illinois, the Department of Veterinary Parasitology (Fox), Microbiology and Public Health, College of Veterinary Medicine, Oklahoma State University, Stillwater, Oklahoma, the School of Veterinary Medicine (Higgins), University of California, Davis, California, the College of Veterinary Medicine (Reed), Ohio State University, Columbus, Ohio, the Department of Large Animal Medicine and Surgery (Ruoff), College of Veterinary Medicine, Texas A&M University, College Station, Texas, the School of Veterinary Medicine (Sweeney), The University of Pennsylvania, Kennett Square, Pennsylvania, and the Livestock Disease Diagnostic Center (Tuttle), Department of Veterinary Science College of Agriculture, University of Kentucky, Lexington, Kentucky. Dr. Mayhew's present address is the Animal Health Trust, Balaton Lodge, P.O. Box 5 , Newmarket, Suffolk, England CB87DW. Reprint requests: Dr. R. Fayer, Zoonotic Diseases Laboratory, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, MD 20705.
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Vol. 4
. NO.2
55
EPIDEMIOLOGY OF EPM
found in all portions of the gray and white matter. The most accurate diagnosis is based on histologic findings of necrosis and mild to severe, nonsuppurative myeloencephalitis with infiltration of neural tissue by mononuclear cells, and sometimes giant cells, neutrophils and eosinophils, and infiltration of perivascular tissue by mononuclear cells including lymphocytes and plasma cells. The putative organism causing EPM is a coccidian that is differentiated from those in the genera Besnoitia, Eimeria, Hammondia, Isospora, Neospora, and Toxoplasma. It most strongly resembles those in the genus Sarcocystis. It has been found in neurons, mononuclear cells, intravascular polymorphonuclear leukocytes (one neutrophil and one eosinophil), and vascular endothelium in the CNS. The organism is found in the cytoplasm, not within an intracellular parasitophorous vacuole. Individual parasites are banana-shaped, resembling the motile stages of coccidia: sporozoites, merozoites, tachyzoites, and bradyzoites. Multinucleate stages resemble immature schizonts and others resemble mature schizonts with merozoites in rosettes or in random arrangements. The method of schizogony, endopolygeny, resembles that used by Sarcocystis. The first cases of EPM were reported in the 1960s in Kentucky and Penn~ylvania.~-~ Subsequent cases were reported in New York, Illinois, Ohio, Oklahoma, Missouri, New Jersey, Florida, Texas, California, Saskatch- ' ~ was found in a pony in ewan, and in B r a ~ i l . ~ - 'EPM Maryland." The only cases of EPM outside America were in England in horses originally from the United States (K. Whitwell, personal communication). Materials and Methods
tribution. To obtain recent, quantitative data on EPM a workshop was convened at the Veterinary Medical Forum of the American College of Veterinary Internal Medicine in Washington, DC on May 26, 1988, with representatives from veterinary medical establishments throughout North America. Data on histologically confirmed cases of EPM from clinical files have been summarized and tabulated in this report to show at specific geographic locations the number of horses, the monthly or seasonal prevalence of disease, and the age, sex, and breed of horses with EPM. The data are from California (1983-1987), Florida (1979-1987), Illinois (19831987), Kentucky (1984-1987), New York (1976-1987), Ohio (1983-1988), Oklahoma (1985-1988), Ontario (1983-1987), Pennsylvania (1983-1987), and Texas ( 1983- 1987). Such data should provide a baseline for assessing the prevalence and distribution of EPM and might provide some insight into the nature of the organism responsible for the disease. In addition, future comparable data will assist in determining changes in prevalence and spread of disease. Although total suspected cases were presented at the workshop, it was decided to include only those putative cases of EPM based on clinical signs that were confirmed histologically by the presence of organisms and/ or typical lesions (Tables 1-3). It was recognized that diagnosis based on identification of the organism was ideal and that diagnosis based on interpretation of lesions might be subject to error. Because of the retrospective nature of the study and the need to obtain a perspective of the prevalence and distribution of the disease, this possibility for error was accepted and must be recognized in interpreting the data. Data from these cases form the basis for the present survey.
Although EPM is recognized as an emerging disease of considerable economic importance by equine practitioners and clinicians, except for a few case reports there is no literature to document either its prevalence or dis-
Results Of 364 confirmed cases of EPM (Tables 1-3), most have been recognized in Florida (94), New York (82).
TABLE1. Number of Horses With Histologically Confirmed Equine Protozoal Myeloencephalitis by Month and Location Location Month
CA
FLA
ILL
KY
NY
OH
OK
JAN FEB MAR APR MAY JUNE JULY AUG SEPT OCT NOV DEC Unknown Total/location
2 0
6 10
2 0 0 0 2 2 2 0 2
2
10 9
0 3 2 2 4 4 4 3 2 3 2 2 0 31
2
4
3 2 0
0 0 2 I 2 I 0 0 2 0 14
2 10 3 10
9 6 10 5 4 94
1
I
2 3 3 4 I 1
1
0
22
3 6 8 I1 9 10 8 7 5 4 4
5 82
1
2 2 0 16
0 3 6 0 4 3 0 0 I 4 0 0 23
ONT CAN
0 0 1
0 0 I 0
PA
TX
3 0 5 6 3
3
0 0 0
8 8 5 5 5 5
1
4
0 4
0 57
1
1
0 4 3 0 2 3 0 1
I 3 0 21
Total Number of Horses/Month 23 19 31 36 26 42 36 35 30 23 29 24 9 364
56
Journal of Veterinary internal Medicine
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Vol. 4
. NO. 2
57
EPIDEMIOLOGY OF EPM
and Pennsylvania (74). However, these figures might not accurately reflect the incidence of infection because of the uneven period of time reflected by the data base: Florida, eight years; New York, 1 1 years: and Pennsylvania, four years. There was no apparent trend regarding the month or season when EPM was diagnosed in a specific location (Table I), nor was there an apparent trend regarding the month or season when EPM was diagnosed in the total group of locations representing North America (Table 1). More Thoroughbreds were found to have EPM than any other breed examined (Table 2). In rank order thereafter were Standardbreds then quarter horses (Table 2). Although Appaloosa, Arabian, Morgan, Paint, Belgian, Crossbred, and other breeds had histologically confirmed EPM, there were relatively few infected horses of those breeds. No apparent difference was found in the number of EPM-infected males compared with females of any breed or at any age (Tables 2 and 3 ) . Nearly one third of the horses with histologically confirmed EPM were two years old or younger and more than 60% were four years old or younger (Table 3). However, some horses at virtually every age from two months to more than 19 years of age were found to have EPM. The following suggestions are provided for the prospective collection of data to assist in determining future changes in prevalence and spread of EPM. It is recommended that Tables 1 to 3 be used as guides for specific data to be collected from each case. To standardize the age and the month of infection, this information should reflect the onset of signs as opposed to the time of diag-
nosis. Definitive diagnosis should be based on identification of the organism in tissue sections, by isolation of organisms via cultivation or other procedures, or by serology using a defined, noncrossreactive antigen. In the present survey, none of the tabular data was subjected to statistical analysis. In designing future surveys, demographic records of age, breed, and sex for horses in a specific geographic location (state or province) will be needed in addition to the clinical information for such statistical purposes. References I . Mayhew IG, de Lahunta A, Whitlock RH. Krook L. Tasker JB. Spinal cord disease in the horse. Cornell Vet 1978: (Suppl 6)68:1-207. 2. Fayer R, Dubey JP. Comparative epidemiology ofcoccidia: Clues to the etiology of equine protozoal myelo-encephalitis. In: Parasitology-Quo Vadit. Canberra: Austral Acad Sci. 1986; 6 15-620. 3. Mayhew IG, Greiner EC. Protozoal diseases. Vet Clin North Am [Equine Pract] 1986; 439-459. 4. McGrath JT. Some nervous disorders of the horse. Proc 8th Ann Conv Am Assoc Eq Pract 1962: 157-163. 5. Prickett ME. Equinespinal ataxia. Proc 1 Ith Ann Conv Am Assoc Equine Pract 1968; 147-158. 6. Rooney JR, Prickett ME, Delaney FM. Crow FW. Focal myelitisencephalitis in horses. Cornell Vet 1970; 60:494-50 I . 7. Brown TT, Patton CS. Protozoan encephalomyelitis in horses. J Am Vet Med Assoc 1977: 171:492. 8. Clark EG, Townsend HGG, McKenzie NT. Equine protozoal myeloencephalitis: A report of two cases from Western Canada. Can Vet J 1981; I1:140-144. 9. Dorr TE, Higgins RJ, Sangler CA. Madigan JE. Endemic protozoal encephalomyelitis in horses in California. J Am Vet Med Assoc 1984; 185:801-802. 10. Madigan JE, Higgins RJ. Equine protozoal myelitis. Vet Clin North Am [Equine Pract] 1987: 397-402. I I . Dubey JP. Miller S. Equine protozoal myelitis in a pony. J Am Vet Med Assoc 1986: 188:1311-1313.
