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Summary

Serial sections of bone and soft tissue from the metacarpophalangeal joints of 2 mature and 2 immature horses were evaluated for substance P immunoreactive sensory nerve fibers. Formalin-fixed specimens were sectioned, either nondemineralized or demineralized with formic acid or edta. Rabbit antiserum to substance P (sp) was used in the streptavidin-biotin-peroxidase complex method for immunolocalization of sp antigen, and staining with 3,3′- diaminobenzidine was used for permanent identification of sp fibers. Abundant sensory nerve fibers were identified in the joint capsule, synovial membrane subintimal layers, collateral ligaments, suspensory ligament and distal sesamoidean ligament attachments to the sesamoid bones, and the periarticular periosteal layers. Sparse sp-immunoreactive nerve fibers were found in subchondral bone plates of the metacarpus, proximal first phalanx, and dorsal articular surface of the sesamoid bones. Most sp fibers were associated with blood vessels in the small cancellous spaces and haversian canals of the subchondral bone. The deeper marrow spaces contained increased numbers of sp sensory fibers; a few appeared in small groups and as several sp-immunoreactive fibers in a larger nerve. Cortical bone contained only a few sp fibers in the haversian canals. Substance P fibers were not identified in the osteocytic lacunae, canaliculi, or the bony lamellae of the haversian systems of the subchondral bone plate, and its extension to the metaphyseal and diaphyseal cortical bone. Equine metacarpophalangeal joint soft tissues have an abundant sensory nerve supply, similar to that of other species. However, the subchondral bone plate also has sparse sensory nerve fibers, which is a unique finding, and may help explain signs of bone pain associated with disease states of the fetlock.

Free access
in American Journal of Veterinary Research

Summary

Four German Shepherd Dogs from a litter of 10 were evaluated because of postnatal onset of proportionate growth stunting that clinically resembled well-documented hypopituitary dwarfism in that breed. Although 2 pups had histologic evidence of hypopituitarism, the remaining 2 pups had normal serum growth hormone concentration and adrenocorticotropin secretory capability, and normal adrenal function test and thyroid function study results. Furthermore, the initially stunted German Shepherd Dogs grew at a steady rate until at 1 year, body weight and shoulder height approximated normal measurements. Seemingly, delayed growth in these pups may represent one end of a clinical spectrum associated with hypopituitarism in German Shepherd Dogs.

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

Expiants were prepared from skeletal muscle tissue from 5 nondystrophic pups and from 5 pups with X-linked muscular dystrophy; pups were 2 to 17 weeks old. A serial reexplant method resulted in optimal cell density with minimal fibroblast growth. Cultures were examined daily by use of phase-contrast microscopy; differentiated (post-fusion) cultures were examined by electron microscopy. Moderate nuclear pleomorphism and cell clustering were observed in cultures of normal and dystrophic muscle cells. Cultures were maintained to 27 days after plating. Minimal myofilament synthesis was observed in multinucleate cells from nondystrophic and dystrophic pups, but spontaneous contraction of myotubes was not observed during this period. Differences in growth, fusion, or differentiation of myogenic cells into multinucleate cells and myotubes were not found between dystrophic and normal muscle.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To compare concentrations of trace minerals in the spinal cord of horses with equine motor neuron disease (EMND) with those of horses without neurologic disease (control horses).

Animals—24 horses with EMND and 22 control horses.

Procedure—Spinal cord trace mineral concentrations in horses with EMND and control horses were analyzed by use of inductively coupled plasma atomic emission spectroscopy (calcium, phosphorus, sodium, potassium, magnesium, copper, iron, manganese, nickel, zinc, aluminum, cobalt, and chromium), atomic absorption spectrophotometry (lead and cadmium), flameless atomic absorption (mercury), and fluorometry (selenium).

Results—Copper concentration was significantly higher in the spinal cord of horses with EMND, compared with control horses; spinal cord concentrations of all other trace minerals were similar between groups.

Conclusion and Clinical Relevance—Among spinal cord trace minerals investigated in the study, only copper concentrations were significantly different between horses with EMND and horses without neurologic disease, which suggests that copper may be involved in the pathogenesis of EMND. An hypothesis of oxidative injury in this disease is supported by the finding of increased copper concentrations in the spinal cord and by low vitamin E concentrations reported by other researchers. (Am J Vet Res 2000; 61:609–611)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine whether equine motor neuron disease (EMND) could be induced in adult horses fed a diet low in vitamin E and high in copper and iron.

Animals—59 healthy adult horses.

Procedure—Horses in the experimental group (n = 8) were confined to a dirt lot and fed a concentrate low in vitamin E and high in iron and copper in addition to free-choice grass hay that had been stored for 1 year. Control horses (n = 51) were fed a concentrate containing National Research Council–recommended amounts of copper, iron, and vitamin E. The hay fed to control horses was the same as that fed to experimental horses, but it had not been subjected to prolonged storage. Control horses had seasonal access to pasture, whereas experimental horses had no access to pasture. Horses that developed clinical signs of EMND were euthanatized along with an age-matched control horse to determine differences in hepatic concentrations of vitamin E, vitamin A, copper, iron, and selenium.

Results—4 experimental horses developed clinical signs of EMND. Plasma concentrations of vitamin E decreased in all 8 experimental horses. There were no significant changes in plasma concentrations of vitamin A, selenium, and copper or serum concentrations of ferritin. There were no significant differences in those analytes between experimental horses with EMND and experimental horses that did not develop EMND. No control horses developed EMND.

Conclusions and Clinical Relevance—Results suggest that lack of access to pasture, dietary deficiency of vitamin E, or excessive dietary copper are likely risk factors for EMND.

Full access
in American Journal of Veterinary Research

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 investigate risk factors for the development of pasture- and endocrinopathy-associated laminitis (PEAL) in horses and ponies in North America.

DESIGN Case-control study.

ANIMALS 199 horses with incident cases of PEAL and 351 horses from 2 control populations (healthy horses [n = 198] and horses with lameness not caused by laminitis [153]) that were evaluated in North America between January 2012 and December 2015 by veterinarian members of the American Association of Equine Practitioners.

PROCEDURES North American members of the American Association of Equine Practitioners were contacted to participate in the study, and participating veterinarians provided historical data on incident cases of PEAL, each matched with a healthy control and a lameness control. Conditional logistic regression analysis was used to compare data on PEAL-affected horses with data on horses from each set of controls.

RESULTS Horses with an obese body condition (ie, body condition score ≥ 7), generalized or regional adiposity (alone or in combination), preexisting endocrinopathy, or recent (within 30 days) glucocorticoid administration had increased odds of developing PEAL, compared with horses that did not have these findings.

CONCLUSIONS AND CLINICAL RELEVANCE The present study identified several risk factors for PEAL that may assist not only in managing and preventing this form of laminitis, but also in guiding future research into its pathogenesis.

Full access
in Journal of the American Veterinary Medical Association