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in Journal of the American Veterinary Medical Association



To trace pedigrees from affected horses, identify likely contributing founder horses, and determine the conditional probability of founder genotypes.


Muscle biopsy records from the Neuromuscular Disease Laboratory at the University of California-Davis and the University of Minnesota were searched to identify horses with a polysaccharide storage myopathy and exercise intolerance/rhabdomyolysis. Pedigrees containing 5 to 6 generations were obtained where possible.


13 Quarter Horses, 4 American Paint Horses, 3 Appaloosas, and 3 Quarter Horse crossbreds (16 mares, 4 geldings, and 3 stallions) were identified with polysaccharide storage myopathy. Pedigrees were available for 18 horses.


Inbreeding coefficients, founder contributions, and conditional probability of founder genotypes were calculated.


Three stallions (A, B, and C) were featured prominently in the pedigrees. Stallions A and B descended from a common sire. On average, A contributed 8.8% (range, 0 to 23%) of the genes in affected horses, B contributed 4.2% (range, 0 to 14%), and C contributed 3.0% (range, 0 to 14%). The sire and dam of 4 horses were descendants of stallion A, the sire and dam of 1 horse were descendants of stallion B, and the sire and dam of 11 horses were descendants of a combination of stallions A and B. The pattern of inheritance resembled an autosomal recessive disorder. Assuming this pattern of inheritance, the conditional probability that these founders were carriers or recessive for the trait was > 99.29% for stallions A and B and 92% for stallion C.


Results support a familial basis for polysaccharide storage myopathy and associated exertional rhabdomyolysis in Quarter Horse-related breeds. The strong contribution of particular founder stallions to the gene pool in some lines of Quarter Horses may explain the high incidence of exertional rhabdomyolysis in these horses.(Am J Vet Res 1996; 57: 286-290)

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in American Journal of Veterinary Research


To investigate the relationship between pelvic muscle mass and development and expression of canine hip dysplasia (CHD).


Prospective study.


5 Greyhounds with anatomically normal hip joints, 59 German Shepherd Dogs (23 with CHD, 24 with near-normal hip joints, and 12 with normal hip joints), and 18 German Shepherd Dog-Greyhound crossbreeds (7 with CHD, 6 with near-normal hip joints, and 5 with normal hip joints) between 12 and 47 months old in which pelvic muscle mass was evaluated. Pectineal muscle and hip joint development were evaluated in 25 German Shepherd Dogs at 8 and 16 or 24 weeks of age.


For evaluation of pelvic muscle mass, individual pelvic muscles were weighed and hip joints were assigned a score on the basis of severity of degenerative changes, For evaluation of pectineal muscle development, muscle sections were stained and examined.


Pelvic muscle mass was greatest in Greyhounds, intermediate in crossbred dogs, and smallest in German Shepherd Dogs. Differences in pelvic muscle mass among breeds were attributable to differences in weights of individual muscles. Hip score was negatively correlated with pelvic muscle mass and weights of selected pelvic muscles. Dogs with pectineal hypotrophy at 8 weeks of age had type-2 muscle fiber paucity or muscle fiber-type grouping at 16 or 24 weeks of age. At 8 weeks of age, hip joints were composed of multiple centers of ossification, and the acetabulum was largely cartilaginous. By 24 weeks of age, the pelvic bones were largely, although incompletely, fused.

Clinical Implications—

Diminished pelvic muscle mass in dogs with CHD and altered muscle fiber size and composition in 8-week-old dogs that subsequently develop CHD strongly suggest that abnormalities of pelvic musculature are associated with development of CHD. The complex development of the hip joint from multiple centers of ossification may make the joint susceptible to abnormal modeling forces that would result from abnormalities in pelvic muscle mass. (J Am Vet Med Assoc 1997;210:1466–1473)

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in Journal of the American Veterinary Medical Association


Eleven horses (3 mares, 7 stallions, 1 gelding) with clinical and biochemical evidence of hyperkalemic periodic paralysis were studied. Each horse had history of episodic weakness, muscular tremors, or collapse, which lasted for periods of a few minutes to hours. Diagnosis was based on hyperkalemia in association with a spontaneous episode of paralysis or by precipitation of an episode by oral administration of potassium chloride. Clinical and biochemical events were documented during spontaneous and induced episodes of muscular weakness. During episodes, electrocardiographic findings were consistent with hyperkalemia. Electromyography performed between episodes revealed fibrillation potentials and positive sharp waves, complex repetitive discharges, and myotonic discharges. Histologic changes in muscle biopsy specimens varied from no overt changes in some horses to vacuolation in type-2B fibers with mild degenerative changes in other horses. Electron microscopy of myofibers revealed dilatations of the sarcoplasmic reticulum.

Analysis of blood samples taken serially during induced attacks in 5 horses revealed marked hyperkalemia (5.5 to 9.0 mEq/L), with normal acid-base status, hemoconcentration, and modest changes in muscle-derived enzymes. Close correlation (r 2 = 0.882) between total plasma protein and plasma potassium concentrations was observed and indicated a shift of fluid out of the extracellular fluid compartment. Treatment of either spontaneous or induced episodes by iv administration of calcium, glucose, or bicarbonate resulted in rapid recovery. Dietary management or daily administration of acetazolamide effectively controlled episodes.

An affected mare was bred to an affected stallion, and 3 affected offspring were produced by embryo transfer. Blood samples from another extended family of affected horses were analyzed for identification of a genetic marker. Blood typing, including 22 loci, revealed no linkage with erythrocytic or serum markers. Lymphocyte typing for equine lymphocytic antigen markers also failed to reveal any linkage.

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in Journal of the American Veterinary Medical Association