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in Journal of the American Veterinary Medical Association

Objective

To identify intrinsic, management, nutritional, and environmental risk factors associated with equine motor neuron disease (EMND) and to determine whether epidemiologic evidence supports oxidative stress as a risk factor for developing EMND.

Design

Case-control study.

Animals

87 horses with EMND and 259 control horses.

Procedure

Information concerning each horse’s history of exposure to multiple environmental factors prior to developing EMND was obtained by means of a questionnaire or personal interview. Exposure histories of horses with EMND and control horses were compared, and the association of each risk factor with EMND was evaluated, using logistic regression analysis.

Results

Factors significantly associated with risk of developing EMND included age, breed of horse, duration of residence at the farm, not vaccinating against rabies, and certain feeding practices. Horses that were exercised on green pasture or in grass paddocks were less likely to develop EMND, compared with horses that were exercised in dirt paddocks. Feeding complete pelleted feed as the only source of concentrate or combined with sweet feed was associated with a significant increase in the risk of EMND. Supplementary feeding of vitamin and mineral mixtures not formulated to provide vitamin E or selenium was associated with increased risk of EMND. Horses with a history of cribbing or coprophagia were also at higher risk of developing EMND.

Clinical Implications

Several husbandry practices and intrinsic characteristics of horses appear to modify the risk of EMND. The relationship of specific nutritional factors to EMND supports the hypothesis that a deficiency of vitamin E contributes to the disease. (J Am Vet Med Assoc 1997;211:1261–1267)

Free access
in Journal of the American Veterinary Medical Association

Abstract

Objective

To examine the regional variations in the distribution of equine motor neuron disease (emnd) in the United States and the factors that might explain those variations.

Design

Cluster investigation and case-control study.

Sample population

The study population consisted of 97 horses with histopathologically confirmed emnd and 698 controls with diagnosis of other spinal cord disorders at 21 US veterinary teaching hospitals participating in the Veterinary Medical Data Base.

Procedure

The total horse population of the United States was divided into 21 regions, and the regional incidence rates of emnd from January 1985 through January 1995 were estimated. Moran's index of spatial autocorrelation was calculated to test for spatial clustering of the disease. The 21 regions were then joined in broader areas according to the similarity of their emnd rates by means of the cluster analysis statistical technique. Finally, the role of potential confounding factors (age at diagnosis, month of diagnosis, breed, and sex) in the present distribution of emnd was assessed, using logistic regression analysis.

Results

Differences in estimated rates across the 21 regions resulted in a strong pattern of spatial clustering of emnd in the United States. The geographic units were grouped into 5 risk regions, with the gradient of emnd incidence rates increasing from the western states (almost 0 cases/1,000,000 horse-years) toward New England (20.78 cases/1,000,000 horse-years). Reported risk factors of emnd (age, breed) and other extraneous factors (sex, month of diagnosis) could not explain the observed geographic variations of disease rates. Nevertheless, there is evidence of some confounding attributable to age and breed.

Conclusions

Although the mechanism responsible for the clustering of emnd in northeastern states is still unexplained, it is not an epiphenomenon caused by regional differences in the distribution of the factors investigated.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To develop a method to experimentally induce Borrelia burgdorferi infection in young adult dogs.

Animals—22 healthy Beagles.

Procedure—All dogs were verified to be free of borreliosis. Twenty 6-month-old dogs were exposed to Borrelia burgdorferi-infected adult ticks and treated with dexamethasone for 5 consecutive days. Two dogs not exposed to ticks were treated with dexamethasone and served as negative-control dogs. Clinical signs, results of microbial culture and polymerase chain reaction (PCR) testing, immunologic responses, and gross and histologic lesions were evaluated 9 months after tick exposure.

Results—Predominant clinical signs were episodic pyrexia and lameness in 12 of 20 dogs. Infection with B burgdorferi was detected in microbial cultures of skin biopsy specimens and various tissues obtained during necropsy in 19 of 20 dogs and in all 20 dogs by use of a PCR assay. All 20 exposed dogs seroconverted and developed chronic nonsuppurative arthritis. Three dogs also developed mild focal meningitis, 1 dog developed mild focal encephalitis, and 18 dogs developed perineuritis or rare neuritis. Control dogs were seronegative, had negative results for microbial culture and PCR testing, and did not develop lesions.

Conclusions and Clinical Relevance—Use of this technique successfully induced borreliosis in young dogs. Dogs with experimentally induced borreliosis may be useful in evaluating vaccines, chemotherapeutic agents, and the pathogenesis of borreliosisinduced arthritis. (Am J Vet Res 2001;62:1104–1112)

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in American Journal of Veterinary Research