Fatal Genetic Quarter Horse Disease Identified

Glycogen branching enzyme deficiency in Quarter Horses might cause unexplained stillbirths/deaths of foals.
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An inherited disorder called glycogen branching enzyme deficiency (GBED) in American Quarter Horses and related breeds that appears to be the cause for many unexplained stillbirths and deaths of young foals was identified by the University of Minnesota’s Stephanie Valberg, DVM, PhD, Department of Clinical and Population Sciences, and Jim Mickelson, PhD, associate professor veterinary pathobiology, both in the College of Veterinary Medicine. The disease was found to be an autosomal recessive trait, meaning each normal parent carries one allele that is defective and passes that "mutant" along to the foal, which ends up with a pair of defective alleles and expression of the disease.

This discovery means GBED could be prevented prior to breeding if parents are tested and carriers are not mated. (This type of recessive gene passage is similar to HC/HERDA found in Quarter Horses, but there isn’t a genetic test available to identify carriers of HC/HERDA.)

GBED-affected foals are either born dead or are weak at birth with a low body temperature, according to Valberg. With assistance to nurse and intense nurturing, such foals often become stronger and nurse on their own. However, their activity level is typically less than that of healthy foals; they might have flexural deformities of the lower limbs, show a more rapid rate of breathing, and have intermittent seizures or signs easily interpreted as sepsis or infection. Most foals with GBED die suddenly by eight weeks of age due to a fatal drop in blood glucose levels or sudden heart failure. Some foals are euthanized because they become progressively weaker and are unable to rise without assistance.

A new type of equine disease was first suspected when muscle biopsies from a foal at Kansas State University were submitted to Valberg’s Neuromuscular Diagnostic Laboratory. She found that this foal–as well as muscles from other affected foals–had a lower-than-expected amount of glycogen (the intracellular storage form of glucose) and an abundance of abnormal polysaccharide that formed both crystalline rods and large globules within the cells. This histopathological picture was very similar to human glycogen storage disease type IV that is due to a deficiency in the glycogen branching enzyme (GBE)

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Written by:

Kimberly S. Brown is the editor of EquiManagement/EquiManagement.com and the group publisher of the Equine Health Network at Equine Network LLC.

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