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There are several genetic diseases that are devastating to Quarter Horses, Paints and/or Arabians. Since we breed Paints (which are nothing more than spotted Quarter Horses) Arabians, and Paint/Arab crosses, I've wanted to do more for our prospective buyers along this line.
If you're planning to acquire a horse, you will want to get one that is clear of these major genetic disorders. You definitely don't want to spend money on a horse, just to experience the heart wrenching loss of your pal, if you can help it! Thus, you will want to purchase your horse through a reputable seller...one who pays attention to these disorders, and, if a breeder, gets their breeding stock genetically tested to be sure they don't have these problems.
If you are interested in getting your own mare bred, you need to know the risks involved with breeding to a horse that is a carrier of these diseases, as well.
Here at WisCountry Dreams Farm we take the health of our horses seriously. We test our breeding stock for these diseases, and know, when we breed, that we can expect healthy, sound foals. We also can discuss these factors with you if you were to choose to use one of our stallions for breeding your mare.
Below is a list of six of the major hereditary diseases affecting the QH, Paint and Arabian breeds. Click on the name of the source of the information to see more info and/or photos.
With the exception of Lethal White Overo (LWO), we do not recommend breeding any horse that is a carrier of these diseases. Because the LWO is is the result of breeding two horses which carry the Frame Overo color pattern gene, it is impossible to eliminate the disease without eliminating the color pattern, too. So, in this case, we recommend having any Paint/Pinto horses tested for the Frame Overo gene before breeding. This way, if the horse carries a Frame Overo gene it can be bred to a non-carrier, and still have the chance for the beautiful pattern, without the danger of producing a foal that will die. In the case of all of the other listed diseases, they could be totally wiped out if all breeders would refuse to breed any horse that was a carrier. But, sadly, not all breeders are willing to do this. Others may not even be aware of the diseases, or the ability to test for them.
Hereditary Equine Regional Dermal Asthenia (HERDA)
Hereditary Equine Regional Dermal Asthenia (HERDA) also known as Hyperelastosis Cutis (HC) is a genetic skin disease predominately found in the American Quarter Horse. Researchers at Mississippi State University and Cornell University believe that the origin of this genetic disorder may be the Poco Bueno's sire line. Symptoms of this disorder is a lack of adhesion within the layers of skin due to a genetic defect in the collagen that holds the skin in place. This defect causes the outer layer of skin to split or separate from the deeper layers sometimes tearing off completely. Areas under saddle seem to be most prone to these lesions often leaving permanent scares, preventing the horse from being ridden. The disorder is recessive, which means that a horse must be homozygous positive or have two copies of the defective gene to suffer from the disease. Consequently both the sire and the dam must possess at least one copy of the mutated gene in order for the offspring to be afflicted. Offspring born with one copy of the defective gene and one non-defective copy are considered a carrier and have a 50% chance of passing the defective gene on.
Lethal White Overo (LWO)
(NOTE: This is not a "disease", per se, but a condition that occurs 25% of the time when two Frame Overo horses are bred, producing a foal that is homozygous for Frame Overo, called Lethal White.)
Lethal White Overo (LWO) syndrome occurs when a horse is homozygous (OO) for the frame overo gene. This genetic disorder causes the intestinal system not to develop properly (involving aganglionosis of the bowel). The foal will die within the first 72 hours after birth when its first meals cannot be digested properly. The lethal white foal will be born almost pure white.
Since frame overo is a desirable quality and requires one frame overo copy, proper mating must be done to avoid possible loss due to lethal white overo while still achieving a high probability for the frame overo pattern. The way to avoid this problem is to avoid breeding frame overo to frame overo. Identification of frame overo can only be definitively done by genetic testing since the frame overo pattern is not always expressed and can be masked by other genetic traits. The gene has been associated with Paints, Thoroughbreds, Quarter Horses as well as Miniature Horses.
Hyperkalemic Periodic Paralysis Disease (HYPP)
Hyperkalemic Periodic Paralysis Disease (HYPP) is a muscular disease that affects both horses and humans. In horses, HYPP has been traced back to one horse named Impressive and has the alternative name, Impressive Syndrome, named after this horse. Symptoms of HYPP may include muscle twitching, unpredictable paralysis attacks which can lead to sudden death, and respiratory noises. Severity of attacks varies from unnoticeable to collapse or sudden death. The cause of death is usually respiratory failure and/or cardiac arrest. The HYPP gene is dominant so both homozygous positive (HH) and heterozygous (nH) will cause this muscular disorder. Only homozygous negative (nn) has no HYPP effect. Since HYPP is dominant, the effects of it can also be transposed to other species of horses when intermixing occurs. This makes the recognition and elimination of this disorder very important in preserving the inherited health of all horses.
Severe Combined Immunodeficiency (SCID)
An affected foal is born with a severely weakened immune system. Because the foal’s natural defense system against infection is not functioning properly, by the time they are five months or so of age, they generally die of an opportunistic infection (such as pneumonia) or they are euthanized.
SCID is known to be an autosomal recessive trait. "Autosomal" means the trait is not sex linked, and "recessive" means that in order for a foal to be affected, it must have 2 copies of the mutated allele, receiving one copy from both the sire and the dam. In 1997, a genetic test became commercially available to determine both SCID affected foals and SCID carrier horses. The use of this test allows people to avoid ever breeding an affected animal, and it also allows breeders the opportunity to make an informed choice to breed or not breed a carrier, as they may choose.
Cerebellar Abiotrophy (CA)
Cerebellar abiotrophy (CA), also referred to as cerebellar cortical abiotrophy (CCA), is a genetic neurological disease in animals best known to affect the Arabian horse and over a dozen breeds of dog. In addition to dogs and horses, there also have been cases of
cerebellar abiotrophy in Siamese and Domestic Shorthair cats; in Angus, Polled Hereford, Charolais and Holstein Friesian cattle; Merino and Wiltshire sheep; and Yorkshire pigs.
CA is believed to follow a monogenic autosomal recessive inheritance. This means it is not sex-linked, and the mutant allele has to be carried and passed on by both parents in order for an affected animal to be born. Horses that only carry one copy of the allele may
pass it on to their offspring, but themselves are perfectly healthy--without clinical signs of the disease.
CA cannot be prevented, other than by selective breeding to avoid the concurrence of two alleles for CA, and it cannot be cured. In horses, the condition is most commonly seen in Arabian and part-Arabians, but a few cases have been observed in the Miniature Horse, the Gotland Pony, and possibly the Oldenburg. Most foals appear normal at birth, with clinical signs noticeable at an average age of four months, though there have been cases where the condition is first seen shortly after birth and other cases where the onset is gradual and clinical signs are first recognized in horses over one year of age.
The condition develops when a set of neurons located in the cerebellum of the brain, known as Purkinje cells, begin to degenerate. These cells affect balance and coordination. They have a critical role to play in the brain. The Purkinje layer allows communication between the granular and molecular cortical layers in the cerebellum. Put simply, without Purkinje cells, an animal loses its sense of space and distance,
making balance and coordination difficult.
Clinical signs of cerebellar abiotrophy include ataxia or lack of balance, an awkward wide-legged stance, a head tremor (intention tremor), hyperreactivity, lack of menace reflex or blink response, a stiff, excessively high-stepping gait in the forelimbs known as hypermetric action, a stiff, abrupt, bursty quality of the gait in all limbs, coarse or jerky head bob when in motion (or in very young animals, when attempting to nurse, known as intention tremor), apparent lack of awareness of where the feet are (sometimes standing or trying to walk with a foot knuckled over), poor depth perception, and a general inability to determine space and distance. There is a marked tendency to rear up and occasionally fall over backwards when a handler reaches for the halter or pulls abruptly on a lead shank. Clinical signs of CA may become exacerbated when the horse is excited.
Signs may worsen from the time of onset for six to 12 months, but if not severe enough to mandate euthanasia, they gradually stabilize over a period of one or two years. Most affected animals have normal intelligence and mildly affected animals can, in theory, live out a normal lifespan. However, they are quite accident-prone. Horses may experience difficulty stepping up and over objects, run into fences, fall easily, and even if allowed to mature to full growth, are generally considered unsafe to ride. Thus, many horses that develop CA are euthanized for humane reasons. There is anecdotal evidence that affected animals partially compensate for the condition by cognitively learning alternative methods for moving or to determine distance. Thus, they appear to improve because they become less accident-prone and may learn to control levels of activity when anxious.
Glycogen Branching Enzyme Deficiency (GBED)
Glycogen branching enzyme deficiency (GBED) is a disorder first recognized by clinicians at the University of Minnesota that causes muscle weakness in Quarter Horse and related breeds. The clinical presentation of this disease is variable. Late term abortion or stillbirth is described for GBED. Recent research suggests that at least 3% of abortions in Quarter horses are due to GBED. Some foals are born alive but are often weak and require warming and assistance to nurse after birth. These foals may appear healthy for a time but eventually the may develop seizures, become too weak to stand, or in some cases, they die suddenly. Owners may note that GBED foals are less active than other foals. In spite of aggressive treatment, all known cases of GBED have been euthanized or died by 18 weeks of age.
Until recently, GBED was not recognized in horses because the wide variety of clinical signs resembles many other foal diseases. The signs can be:
* Abortion or still birth of a foal.
* Weakness and low body temperature at birth. Treatment with a bottle, tubing the foal with milk, and assistance to stand and suckle regularly helps the foal become stronger.
* Sudden death on pasture of foals from the heart stopping or from seizures (due to low blood sugar).
* High respiratory rate and weakness of the muscles used to breathe in foals.
* Contracted tendons found in all four legs of a foal.
* Overall weakness and the inability of the foal to get up from lying on its side.
Research done at the University of Minnesota suggests that this mutation may be present in about 10% of all Quarter Horses and related bloodlines. This means breeding carriers would result in a 25% chance of getting a foal affected with GBED. All GBED foals verified to date have been Quarter Horses and American Paint horses.
DISEASES AFFECTING PRIMARILY QUARTER HORSES AND PAINTS
DISEASES AFFECTING PRIMARILY ARABIANS
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Genetic Diseases in Horses
