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Diseases

Contagious equine metritis - (CEM)

Contagious equine metritis (CEM) is an acute, highly contagious venereal disease of horses (and experimentally of donkeys) characterized by a profuse, mucopurulent vaginal discharge and early return to estrus in most affected mares. Infected stallions and chronically infected mares show no clinical signs.

The disease is seen primarily in Europe, but technical challenges in propagation of the causative organism prevent accurate determination of the precise distribution of the disease.

Dourine - (DOUR)

Dourine is a chronic or acute contagious disease of breeding equids that is transmitted directly from animal to animal during coitus. The causal organism is Trypanosoma (Trypanozoon) equiperdum (Doflein, 1901). Dourine is the only trypanosomosis that is not transmitted by an invertebrate vector.

Trypanosoma equiperdum differs from other trypanosomes in that it is primarily a tissue parasite that is rarely detected in the blood. There is no known natural reservoir of the parasite other than infected equids. It is present in the genital secretions of both infected males and females. The incubation period, severity, and duration of the disease vary considerably; it is often fatal, however it was claimed that spontaneous recoveries do occur and latent carriers do exist as well. Subclinical infections can occur.

Donkeys and mules are more resistant than horses and may remain unapparent carriers. Infection is not always transmitted by an infected animal at every copulation. Although adaptation to other hosts is not always possible, laboratory rodents, such as rabbits, rats and mice, can be infected experimentally and can be used to maintain strains of the parasite indefinitely. Trypanosoma equiperdum strains are best stored in liquid nitrogen.

The clinical signs are marked by periodic exacerbation and relapse, ending in death, sometimes after paraplegia or, possibly, recovery. Moderate fever, local oedema of the genitalia and mammary glands, cutaneous eruptions, incoordination, facial and lip paralysis, ocular lesions, anaemia, and emaciation may all be observed. Oedematous cutaneous plaques, 5-8 cm in diameter and 1 cm thick, are still considered as pathognomonic, although they were also found in equids infected with T. evansi occasionally.

Equine malignant hyperthermia - (EMH)

Equine malignant hyperthermia (EMH) is a dominant disease (one copy of the mutation is sufficient to produce disease) identified in Quarter Horses and American Paint Horses that can cause severe typing up and even death when horses are subjected to anesthesia. It has been shown that a gene mutation in the calcium release channel causes a dysfunction in skeletal muscles resulting in excessive release of calcium inside the muscle cell. This triggers a series of events resulting in a hyper-metabolic state and/or death.

Symptoms include fever, excessive sweating, elevated heart rate, abnormal heart rhythm, shallow breathing, muscle rigidity, and death with acute rigor mortis.

Equine viral arteritis - (EVA)

Equine viral arteritis (EVA) is an acute, contagious, viral disease of equids caused by equine arteritis virus (EAV). Typical cases are characterized by fever, depression, anorexia, leukopenia, dependent edema (especially of the lower hind extremities, scrotum, and prepuce in the stallion), conjunctivitis, supra- or periorbital edema, nasal discharge, respiratory distress, skin rash, temporary subfertility in affected stallions, abortion, and infrequently, illness and death in young foals. A variable percentage of postpubertal colts and stallions become carriers and semen shedders after infection with EAV

Glycogen-branching enzyme disorder - (GBED)

Glycogen-branching enzyme disorder (GBED) has likely been a cause of neonatal mortality in Quarter Horses for decades, according to Stephanie Valberg, DVM, PhD, who gave an update on her research on the disorder at the recent conference of the American Quarter Horse Association, held March 11-14 in St. Louis, Mo. Additionally, she reported that all the known affected foals and carriers of GBED are descendants of the Quarter Horse sire Zantanon and his son King, and about 8% of King descendants are carriers of GBED.

This fatal disease is seen in Quarter Horses and related breeds. The foals lack the enzyme necessary to store glycogen (sugars) in its branched form and therefore cannot store sugar molecules. This disease is fatal as the heart muscle, brain and skeletal muscles are unable to function. Valberg and Jim Mickelson, PhD, associate professor veterinary pathobiology at the University of Minnesota College of Veterinary Medicine, identified GBED and described it to the public in 2004.

The disease causes a wide variety of clinical signs, so it might be confused with other conditions. It can cause abortion or stillbirth. Alternatively, foals can be weak at birth and need assistance to suck and stand. If helped through the first few days, foals might survive for up to two months. All foals diagnosed with GBED have died or had to be euthanatized because of muscular weakness by 18 weeks of age.

Hereditary equine regional dermal asthenia - (HERDA)

Hereditary equine regional dermal asthenia (HERDA) is a genetic skin disease predominantly found in the American Quarter Horse. Within the breed, the disease is prevalent in particular lines of cutting horses. HERDA is characterized by hyperextensible skin, scarring, and severe lesions along the back of affected horses. Affected foals rarely show symptoms at birth. The condition typically occurs by the age of two, most notably when the horse is first being broke to saddle.

There is no cure, and the majority of diagnosed horses are euthanized because they are unable to be ridden and are inappropriate for future breeding. HERDA has an autosomal recessive mode of inheritance and affects stallions and mares in equal proportions. Research carried out in Dr. Danika Bannasch's laboratory at the University of California, Davis, has identified the gene and mutation associated with HERDA. The diagnostic DNA test for HERDA that has been developed allows identification of horses that are affected or that carry the specific mutation.

Other skin conditions can mimic the symptoms of HERDA. The DNA test will assist veterinarians to make the correct diagnosis. For horse breeders, identification of carriers is critical for the selection of mating pairs. Breedings of carrier horses have a 25% chance of producing an affected foal. Breedings between normal and carrier horses will not produce a HERDA foal although 50% of the foals are expected to be carriers.

Hyperkalemic periodic paralysis - (HYPP)

Hyperkalemic periodic paralysis (HYPP) is an inherited disease of the muscle which is caused by a genetic defect. In the muscle of affected horses, a point mutation exists in the sodium channel gene and is passed on to offspring. Sodium channels are "pores" in the muscle cell membrane which control contraction of the muscle fibers. When the defective sodium channel gene is present, the channel becomes "leaky" and makes the muscle overly excitable and contract involuntarily. The channel becomes "leaky" when potassium levels fluctuate in the blood. This may occur with fasting followed by consumption of a high potassium feed such as alfalfa.

Hyperkalemia, which is an excessive amount of potassium in the blood, causes the muscles in the horse to contract more readily than normal. This makes the horse susceptible to sporadic episodes of muscle tremors or paralysis. This genetic defect has been identified in descendents of the American Quarter Horse sire, Impressive. The original genetic defect causing HYPP was a natural mutation that occurred as part of the evolutionary process.

The majority of such mutations, which are constantly occurring, are not compatible with survival. However, the genetic mutation causing HYPP produced a functional, yet altered, sodium ion channel. This gene mutation is not a product of inbreeding. The gene mutation causing HYPP inadvertently became widespread when breeders sought to produce horses with heavy musculature. To date, confirmed cases of HYPP have been restricted to descendants of this horse.

Overo lethal white syndrome - (OLWS)

The overo coat pattern features white markings that do not cross the back of the horse between its withers and its tail. An overo may be either predominantly dark or white. OLWS is a recessive disorder (two copies of the mutation are necessary to produce disease) that appears to have been selected for in horses where white spotting is a desirable trait. The defective gene has been found in American Paint Horses, American Miniature Horses, Half-Arabians, Thoroughbreds, and crop-out (horses with excessive white markings) Quarter Horses.

OLWS foals are homozygous for the mutation and are born alive with blue eyes and a white coat. Small black markings on the head, mane and tail can occur in OLWS foals. These foals initially appear normal except for their unusual coloring. After a varying period of time, signs of colic emerge due to the foal's inability to pass feces. The OLWS foal has an underdeveloped, defective intestine caused by a failure of the embryonic cells that form nerves in the gastrointestinal system. Oddly enough, these cells also play a role in determining skin color.

Testing for the OLWS gene is performed at the Veterinary Genetics Laboratory at the University of California, Davis. This test is recommended for all frame overos and their descendants. Mares or stallions that have previously produced an OLWS foal are in all likelihood heterozygous for the mutation. Carriers should not be bred to each other to avoid the birth of OLWS foals. The horses at greatest risk of carrying the defective allele are overos

Polysaccharide storage myopathy - (PSSM)

Polysaccharide storage myopathy (PSSM) is characterized by the abnormal accumulation of the normal form of sugar stored in muscle (glycogen) as well as an abnormal form of sugar (polysaccharide) in muscle tissue. Thousands of horses have been identified with tying-up associated with polysaccharide accumulation in muscles.

There are two forms Type 1 and Type 2 PSSM. We know that both are the result of the accumulation of muscle glycogen which is the storage form of glucose in muscles.
  • Type 1 PSSM is caused by a mutation in the GYS1 gene. The mutation causing PSSM is a point mutation on the GYS1 gene which codes for the skeletal muscle form of the glycogen synthase enzyme.
  • The cause of Type 2 PSSM has yet to be identified.
Both types have an abnormal type of glycogen staining in muscle biopsies, and the types can be distinguished by genetic testing. Horses with Type 2 PSSM lack the mutation that is specific for Type 1 PSSM. At present there is not a specific genetic test for type 2 PSSM and we do not have conclusive evidence that it is inherited. Carbohydrates that are high in starch, such as sweet feed, corn, wheat, oats, barley, and molasses, appear to exacerbate type 1 and type 2 PSSM. That is why they should be avoided and extra calories can be provided in the form of fat. An important part of the management of PSSM horses is daily exercise.

This enhances glucose utilization, and improves energy metabolism in skeletal muscle. If only the diet is changed, we found that approximately 50% of horses improve. If both diet and exercise are altered, then 90% of horses have had no or few episodes of tying-up. An old theory about tying-up is that it is due to too much lactic acid in the muscle. Many exercise studies have proven that this is absolutely not the case with PSSM. PSSM is actually a glycogen storage disease and there are several diseases in other species and in human beings that also result in the storage of too much glycogen in skeletal muscle. In these other diseases, glycogen accumulates because the muscle lacks an enzyme (protein) necessary to burn glycogen as an energy source. These similarities led us to test PSSM horses for the disorders in glycogen metabolism identified in human beings.

We found that PSSM is a unique glycogen storage disease because the PSSM horses have all the necessary enzymes to burn glycogen as a fuel in their muscles. With exercise, PSSM horses show the expected decrease in muscle glycogen as it is burned as fuel. The unique feature of PSSM is that the muscle cells in PSSM horses remove sugar from the blood stream and transported into their muscle at a faster rate, and make more glycogen than normal horses. Our recent research shows that the reason for this is that PSSM muscles are very sensitive to insulin beginning as early as 6 months of age. Insulin is a hormone released by the pancreas into the bloodstream in response to a carbohydrate meal. It stimulates the muscle to take up sugar from the bloodstream. Once inside the cell the muscles of PSSM horses make much more glycogen than a normal horse due to an overactive enzyme called glycogen synthase in the case of type 1 PSSM.

Defects

Cryptorchid

Cryptorchid, ridgling, and even rig are terms used to describe a stallion with at least one undescended testis. The retained testis fails to produce viable sperm, so fertility rates are affected. However, the testis is still capable of producing testosterone, so the animal will show stallion-like behavior. The cost of castrating a cryptorchid is significantly higher than standard castration, and retained testes are at a higher risk of developing malignant (cancerous) tumors.

Parrot Mouth

Overlapping of the upper jaw, resulting in overgrown front teeth, malnutrition
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