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Barb Wire
photo credit: Montana “Barb Wire” a beautiful Damele mare

DNA Tests for Genetic Diseases in Horses

Infectious diseases are illnesses caused by something in the environment, a toxin or pathogen etc. Genetic diseases are hereditary; conditions brought on by a defective gene; from a mutation in the animal's DNA, that is passed down and inherited from one or both of its parents. Genetic mutations start out originally in one individual animal. Over time, if the animal produces a lot of foals, that defective gene is spread out through that bloodline, and can eventually become breed-associated. Depending on how many years the mutation has been around, determines how long and how far a mutation gets passed around, and spreads across breeds over time. Inbreeding does not cause mutations, but will certainly expose them if they exist. Probably all living animals (including us) carry at least one lethal recessive mutation in one of their genes; perhaps several. Mutations are a natural source of diversity in animal populations. We only know about a very few of them, due to breeding related animals (bloodlines or breeds).


Should I DNA Test My Curly Horse?

Usually, yes, if you are going to breed it...

Is it DNA PV tested (parentage verified)? ... If so, then, are its parents DNA tested clear of all genetic conditions known to the breeds that are in its pedigree? If both parents are tested negative the horse in question is obligate free, as long as it is DNA parentage verified as offspring of those 2 parents.

If the horse in question is not parentage verified, or if one or neither parent is tested, you have DNA testing to do. Analyze the pedigree of the horse you want to breed, and determine which breeds and/or bloodlines exist in its pedigree. Test for all of those genetic mutations.

Recessive conditions: If your horse is a carrer (tests positive for any recessive mutation), only breed it to a horse proven not to be a carrier.

Dominant & Semi-Dominant conditions: If your horse tests positive for any of these, it should not be bred. If a stallion tests positive for a dominant condition, geld him. If a mare tests positive for a dominant condition, keep her away from any stallions to prevent unintentional breeding, including un-weaned colts. Spaying is an option, but the expense and the genuine risk of major surgery is a serious consideration.

So when you need to test your Curly Horse, what should you test for? This report was compiled to help you determine which DNA tests would be indicated for what breeds that might exist in the pedigree of a Curly Horse. See table below, and compare to your Curly Horse's pedigree and bloodlines. Compare to any tests that have already been run on its parents (and whether your horse is actually parentage verified). Then, you will know if you should test your horse before breeding it, what to test for, and what to check for when selecting a mate to breed it to.


What's in Your Curly Horse's Pedigree?

Disease or Disorder

breeds associated
bloodlines associated
Androgen Insensitivity Syndrome
R Stockhorses Quarter Horses
Glycogen Branching Enzyme Deficiency
R Stockhorses King, Zantanon
Hereditary Equine Regional Dermal Asthenia
R Stockhorses
Poco Bueno
Hyperkalemic Periodic Paralysis Disease
S/D Stockhorses
Malignant Hyperthermia
S/D Stockhorses
2 undisclosed bloodlines
Myosin-Heavy Chain Myopathy
S/D Stockhorses
reining, reined cow horse, halter bloodlines
Polysaccharide Storage Myopathy Type 1
S/D over 20 breeds
Congenital Stationary Night Blindness
R Appaloosa, Spanish
all Lp gene horses
(LWS), (OLWS), (WFS)
Overo Lethal White Foal Syndrome
R Stockhorses, others frame overo bloodlines
Equine Metabolic Syndrome (obesity, founder)
S/D many breeds
Glanzmann Thrombasthenia
R many breeds
widespread; 2 mutations
Cerebellar Abiotrophy
R Arabians Arab-derived
Lavender Foal Syndrome
R Arabians Arab-derived
Severe Combined Immunodeficiency
R Arabians Arab-derived
(DIS) Distichiasis (2020) ingrown eyelashes R Friesians Friesian-derived
(DWF) Dwarfism in Friesian Horses R Friesians Friesian-derived
(DIS) Hydrocephalus R Friesians Friesian-derived
Junctional Epidermolysis Bullosa Type 1
R Belgian
Junctional Epidermolysis Bullosa Type 2
R American Saddlebred
Myotonia Myotonia R New Forest ponies New Forest-derived


*This table of genetic conditions listed by breed(s) is not complete. There may be other mutations that exist in other breeds, that cause the same conditions (like dwarfism as one example). It is imperative that you read up on known genetic conditions in breeds that are in your horse's pedigree. This is one good reason to register your horses; it provides you with the known genetic variables you may be dealing with, according to its breed profile.


More About the Genetic Diseases



Androgen Insensitivity Syndrome (AIS), is a simple recessive genetic mutation that alters sexual development of the fetus, resulting in a female horse with XY chromosomes. She will usually have female external genitalia, with undescended testes and studdish behavior.


Glycogen Branching Enzyme Deficiency (GBED) is a simple recessive lethal condition that disrupts glycogen metabolism. It is caused by the body's inability to properly store sugar. The affected foal is not able to store enough energy to fuel important organs, such as the heart, skeletal muscles and brain. Foals born affected by GBED suffer from a range of symptoms associated with this lack of fuel, such as low energy, weakness, difficulty rising, low body temperature, contracted muscles, seizures, and sudden death. Unfortunately, GBED is always fatal; most affected foals die before the age of 8 weeks. GBED often causes abortions; as many as 3% of aborted Quarter Horse foals were found to be homozygous for the GBED mutation. A DNA test will determine the GBED status of a horse – either affected, or a carrier of the disease. The GBED mutation may be present in 8 to10% of all Quarter Horses and related breeds. It is very possible that this disease has existed in Quarter Horse bloodlines for many years, but went undetected.

GBED is an autosomal recessive trait, meaning a foal will only by affected if it inherits the disease from both parents. Horses that are carriers of the GBED have 1 copy of the mutation, but do not have any symptoms associated with the disorder. This makes DNA testing important to screen for carriers and prevent this fatal condition. (Animal Genetics Inc)


Hereditary Equine Regional Dermal Asthenia (HERDA) also known as Hyperelastosis Cutis (HC), is a rare genetic skin disease found predominately in the Quarter Horse. This disorder is recessive, which means that a horse must be homozygous positive or have two copies of the defective gene for the disease to manifest. Foals appear normal at birth, but develop skin lesions in response to mild abrasions. Areas under saddle seem to be most prone to these lesions often leaving permanent scars, soon preventing the horse from being ridden. HERDA causes 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. Researchers at Mississippi State University and Cornell University believe that the origin of this genetic disorder may be the Poco Bueno's sire line. Scientists at the University of California mapped and identified the genetic mutation responsible for this disease. (UKY and Animal Genetics Inc)


Hyperkalemic Periodic Paralysis Disease (HYPP) is caused by a dominant gene and a single copy of the gene can cause the disease. Horses with 2 copies of the gene may be more severely affected. Symptoms of HYPP may include muscle twitching, unpredictable paralysis attacks which can lead to sudden death, and respiratory noise. The severity of attacks can vary from unnoticeable to collapse to sudden death. The cause of death is usually respiratory failure and/or cardiac arrest. The gene encodes a potassium channel for cells. Cells with the mutation are unable to regulate the amount of potassium and the muscles undergo involuntary contractions. These contractions constitute exercise and the muscles become large and prominent. Bulky muscling is selected for by Quarter Horse halter horse breeders, and this disease made its appearance in a heavily used successful sire named Impressive. It is also known as the Impressive disease (or syndrome). I could not find a figure for what percent Impressive horses carry HYPP. All I know is, if your horse goes back to Impressive, test it, unless both its parents were already tested N/N. Quarter Horse foals born after 1998 that are offspring of an affected parent have a statement recommending DNA testing for HYPP on the Certificate of Registration. Scientists from the University of California and Pittsburgh identified this gene defect based on the occurrence of a similar defect in people. (KY Equine Research Nutrition Conference report,


Malignant hyperthermia (MH) is a genetic disorder that may occur in conjunction with type 1 PSSM. MH occurs in Quarter Horse bloodlines (with a high frequency in two specific lines), and horses are generally mature before exhibiting clinical signs. (

Malignant hyperthermia (MH) was initially recognized as a fatal syndrome in humans. It is most prevalent in swine but this syndrome has also been reported in dogs (especially Greyhounds), cats and horses. Its occurrence in swine is known as porcine stress syndrome. In horses MH is thought to be confined to Quarter Horses and members of related breeds such as Appaloosas and Paints. Less than 1% of Quarter Horses are affected, and those that are seem to trace to two specific bloodlines. The genetic disorder is apparently an autosomal dominant trait. MH is a potentially fatal disease that can be triggered by factors like exercise, stress, breeding, illnesses, anesthesia and concurrent myopathies. An additional genetic mutation in RYR1 gene (MH) influences PSSM and can increase the severity of the symptoms of PSSM in Quarter Horses and related breeds. (Animal Genetics Inc)

While researching and identifying the gene mutation responsible for PSSM1, there were 2 Quarter Horse sires consistently present in all the early findings. The 2 bloodlines were not publicly disclosed, which put researchers at odds with breeders. When simple genetic testing became available for PSSM1 in 2008, researchers discovered that PSSM1 was probably at least 1200 years old, and was widespread throughout 20 or more breeds, not just the sire lines of those 2 Quarter Horses. As I understand it, the same thing exists in the MH studies right now. The announcement of whether and which certain bloodlines carry MH is still pending more conclusive research.


Myosin-Heavy Chain Myopathy (MYHM) is a muscle disease in Quarter Horses and related breeds that results in two distinct clinical disease presentations. The first presentation is called immune-mediated myositis or IMM and it is characterized by episodes of severe muscle atrophy following an autoimmune event. The second is severe muscle pain and damage termed non-exertional rhabdomyolysis or “tying-up” that is not associated with exercise and may or may not have muscle atrophy. The specific genetic mutation associated with risk for MYHM is in the MYH1 gene and was first identified in horses with immune-mediated myositis or IMM and is why the DNA test for this mutation was initially named IMM. Then it was learned that are two distinct clinical forms associated with the same mutation, and the name of the DNA test was changed to Myosin-heavy chain myopathy (MYHM) to better reflect both of its resulting clinical syndromes.

With the IMM form of myosin-heavy chain myopathy, horses initially experience stiffness, weakness, and a decreased appetite followed by the rapid loss of 40% of muscle mass within 72 hours. Inflammatory cells, particularly lymphocytes, are present in muscle fibers and surrounding blood vessels, with preferential targeting over the top of the horse's body; the gluteal (hindquarter) and back muscles.

With the non-exertional rhabdomyolysis form of myosin-heavy chain myopathy, horses initially show stiffness, a short stride, firm muscles and may quickly lie down and be unable to get back up. These horses can have dark coffee-colored urine and blood samples show very high levels of muscle enzymes. There is often no evidence of lymphocytes in the muscle of horses with non-exertional rhabdomyolysis.

Triggers for expression of this disease in horses that have this mutation include respiratory infections, especially strangles, pigeon fever, intramuscular vaccinations, immune stimulants and other forms of muscle damage.


Polysaccharide Storage Myopathy Type 1 (PSSM1). Two forms of PSSM exist in horses, Type 1 and Type 2. Type 1 PSSM is the one we include in this report, because it is the one that is easily identified by a genetic test. It is a dominant autosomal hereditary condition - a genetically caused form of tying-up with muscle damage and inability to move. PSSM (Type1) is characterized by abnormal and excessive storage of sugar (polysaccharide) in muscle cells. At least 20 breeds have been identified with Type 1 PSSM, including stockhorse breeds, Belgians, Percherons, Morgans, Mustangs, Tennessee Walking Horses, and some Warmblood breeds. The prevalence of this mutation is as high as 35-50% in Percherons and Belgians. It is rare in Clydesdales and Shires. It is present in about 8% of the Quarter Horse-related breeds and is most common in halter horse bloodlines. Several other mutations have also been identified as possibly being associated with some form of PSSM.

Symptoms usually begin by 2 to 3 years of age. Some horses that test positive for the mutations will exhibit only minor problems and some are subclinical – they may never exhibit any noticeable problems at all. Clinical signs can include skin twitching, stiffness, firm painful muscles, sweating, weakness, and reluctance to move with light exercise. Occasionally gait abnormalities, mild colic and muscle wasting may also occur. In blood tests, serum CK and AST activity is elevated (except in draft horses). An additional genetic mutation in RYR1 gene (MH) increases the severity of the symptoms of PSSM in Quarter Horses and related breeds. Not all cases of tying up are caused by the PSSM mutation.

Type 2 PSSM (PSSM2): Breeds affected: Quarter Horse-related breeds, a few Arabians and possibly other light breeds. Like PSSM Type 1, signs usually begin by 2 to 3 years of age but may occur in weanlings. Clinical signs are typically Rhabdomyolysis with or without exercise. (Rhabdomyolysis is the breakdown of muscle tissue that causes kidney damage. When muscle is damaged, a protein called myoglobin is released into the bloodstream which is filtered out of the body by the kidneys. Myoglobin breaks down into substances that can damage kidney cells.) Testing is not a simple DNA genetic test: A muscle biopsy is required to diagnose type 2 PSSM. Dr. Stephanie Valberg collaborates with Kentucky Equine Research, and accepts muscle biopsies there. (MSU, Univ of MN, AG Inc and


Glanzmann Thrombasthenia (GT) is a blood clotting disorder in horses. This is caused by a dysfunction of the blood platelets (thrombocytes). Affected horses often suffer from recurrent nosebleeds and frequent excessive bleeding, and show a lack of clotting. This condition may also result in improper wound closure or healing, and may cause serious problems with large wounds. Unfortunately, there is no effective treatment. Two mutations in the gene encoding platelet glycoprotein IIb, Integrin Alpha-2B ( ITGA2B ), have been implicated in the GT condition. Although GT has been associated with a recessive mode of inheritance, heterozygous combinations from both variants have been implicated in GT cases.

Affected Breeds: Thoroughbred, Standardbred, Oldenburg, Peruvian Paso, American Paint Horse, Appaloosa and American Quarter Horse


Appaloosa Coat Pattern / Leopard Print Pattern (Lp) / Congenital Stationary Night Blindness (CSNB). According to Animal Genetics, Inc., it has long been understood that Appaloosas are affected by both Equine Recurrent Uveitis and Congenital Stationary Night Blindness (CSNB) a condition making it difficult or even impossible to see in relatively low light. Research has now shown that CSNB is a recessive disorder that is directly linked to the leopard complex (spotted coat pattern) in Appaloosa horses. The DNA test for the LP mutation is used to confirm that an animal is a true Appaloosa horse, and to identify those animals that are homozygous (LP/LP) and will be affected by CSNB.

In 2003 researchers linked the positional candidate gene for leopard complex (LP) to the TRPM1 gene on chromosome 1. Further investigations headed by Dr. Rebecca Bellone and The Appaloosa Project (a team of researchers from Canada and the US) identified several SNPs in TRPM1 showing complete association. Soon after that, the causal mutation was also discovered. Both the SNP's and the causal mutation can be used to develop a genetic test to identify horses with leopard complex." Animal Genetics, Inc. (

Conclusion: Horse who are few spot & near few spot; horses that are homozygous for Lp have night blindness. Congenital Stationary Night Blindness (CSNB) which is the inability to see in low to no-light conditions. Knowing if horses are homozygous for leopard complex spotting can help to inform management decisions. Homozygous LP horses do NOT always appear as few spots and can have very minimal LP appearance.

Lp gene & thin hair: Thin mane and tail hair is common in horses that carry the Lp gene, especially in black based horses. This lack of hair is caused by the Lp pattern gene mutation, and is not caused by the breed. In KRT25 Curly Horses, extremes (homozygous KRT25/KRT25) will also have a thin-haired mane and tail, but the genetics is not the same as the Lp cause. Breeding Lp horses to Curly Horses will increase the chance of thin hair in the offspring, if the offspring inherits Lp. As for color & pattern, the Lp gene has the greatest effect after the horse is over one year of age, and change can continue for many years after.


Lethal white syndrome (LWS). Also called Overo Lethal White Syndrome (OLW/OLWS) or, less often, White Foal Syndrome (WFS) is linked to a recessive gene associated with the frame overo pattern. Horses that are heterozygous carriers of the gene do not develop the condition and are physically healthy. However, when a foal is born that is homozygous O/O for the LWS gene, it should be humanely euthanized shortly after birth, or else will die within 36 hours from complications involving an underdeveloped intestinal tract. A DNA test is available for LWS so that horses who are carriers of this gene are not bred to one another. Horses can carry the LWS gene and not visibly exhibit overo coloring; cases have appeared in the offspring of both tobiano and solid-colored parents, though all cases to date are horses that had overo ancestors. LWS can occur in any equine breed where the frame overo coat pattern is found. Scientists at the University of Minnesota, University of California, and from Australia discovered the mutation based on its similarity to a human disease (Hirschsprungs Disease). (UKY and Wiki-pedia)


Cerebellar Abiotrophy (CA) is a neurological disease which occurs in Arabian and Arabian cross horses. The mutation causing this disease is recessive, and is fairly common. Foals affected with CA do not usually develop symptoms until six weeks to 4 months of age. "The disease causes the death of neurons in the cerebellum of affected foals, leading to head tremor (intention tremor) and a lack of balance equilibrium (ataxia). Affected horses may show exaggerated action of the forelegs, a wide-based stance, and be unable to rise from a reclining position. They tend to startle easily and often fall due to ataxia. The neurological problems may not be apparent to owners and are frequently thought to be a consequence of a fall rather than the cause of it. CA symptoms vary in severity. Some foals show very severe symptoms, including the exaggerated gaits and a dramatic lack of balance. Others have little more than the head tremor, which may only manifest itself during goal-directed movement. Regardless of the severity of the symptoms, CA foals are often euthanized or restricted to life as pasture pets, as they are never coordinated enough to be ridden safely. They are also a danger to themselves because the condition predisposes them to accidents and injury." (UC Davis) The mutation linked definitively to this disease was identified by the University of California at Davis.


Lavender Foal Syndrome (LFS) is an inherited lethal neurologic disorder known to affect Arabian foals and is named for its characteristic expression of a dilute coat color. LFS is a recessive genetic disorder causing newborn foals to have problems standing, often after a difficult birth. Clinical signs include seizure-like limb rigidity, hyperextension of the head, neck and spine (opisthotonus) and involuntary movement of the eyeballs (nystagmus). All affected foals are usually euthanized within days after birth. The DNA test for detecting LFS was developed by Cornell University.


Severe Combined Immunodeficiency (SCID) is a fairly common recessive gene defect in Arabian and Arabian cross breeds. The carrier frequency is at about 28% which means that one out of every three to four adult Arabian horses carries the gene for this deadly disease. Similar to the "bubble boy" condition in humans, the disease is always fatal in affected foals, which are born with no immune system, are unable to fight infections, and die within a few months. The discovery of the genetic cause of SCID in Arabian horses was made by Dr. Lance Perryman and Dr. Katherine Meek at North Carolina State University and the University of Texas in Dallas. (VetGen LLC)


Junctional epidermolysis bullosa (JEB1, JEB2) is an inherited disease also known as Red Foot Disease or Hairless Foal Syndrome. Two separate genetic mutations have been identified: JEB1 occurs in Belgian draft horses and related draft breeds and JEB2 which occurs in American Saddlebred horses.

This inherited disorder is caused by a mutation that inhibits the body's ability to produce certain proteins responsible for holding the skin onto the body. Affected horses are typically born alive with little symptoms, however, after 4 to 5 days of age the foal begins to develop lesions at the pressure points. These lesions quickly grow larger, creating patches all over the foal's body. Because the same protein responsible for skin adhesion is also involved in the hoof attachment, the foal also begins to slough the hoof wall, and the hoof may detach. Oral ulcers are also seen with JEB, as well as foals being born with front teeth. Foals that do not die from infections are almost always euthanized by 8 days of age for humane reasons.

JEB is inherited as a recessive trait. Horses that carry two copies of the mutated gene (homozygous recessive) will develop the disease. Animals that carry one copy of the mutated gene and one copy of the normal gene (heterozygous) are carriers of JEB. Carriers do not develop the disease and have normal epithelia. French scientists isolated the gene mutation responsible for this and developed the test for it. (UC Davis, UKY and Animal Genetics Inc)


Myotonia is another inherited neuromuscular disorder that was identified in New Forest ponies by the University of Kentucky and a Swiss researcher. It is another autosomal recessive mutation, which means a carrier is not affected, but if 2 carriers are bred together, there is 25% chance of producing an infected foal, which will be weak and exhibit gait abnormalities. (UKY)


Modes of Inheritance

A Basic Understanding of Genetics: ( There are two general types of genetic characteristics to be considered:
A qualitative trait is a trait that is either present or not. Using cattle for example, a beef animal is either polled or horned. So the horned/ polled gene is called a qualitative trait. Similarly, hide color in Angus cattle is a qualitative trait. A Red Angus beef animal carries two copies of the recessive red gene whereas a Black Angus, the black-hided beef animal, carries at most one copy of the red gene. In general, management and environment do not affect qualitative genetic traits. ...
Other characteristics include quantitative traits. They vary in a continuum from one animal to another. Traits such as marbling, tenderness, mature weight, and fat cover are quantitative traits in cattle, and are affected by a combination of genetics, management and environment. These traits are typically influenced by numerous genes. This is where gene testing comes in. Here are some examples of modes of inheritance, and of qualitative and quantitative genetics:

Simple Mendelian Genetics: This is the simplest genetic pattern of inheritance; when a dominant allele masks the existence of a recessive allele.
Autosomal inheritance: The gene causing this trait is located on a non-sex chromosome.
The trickier genes are those with several other types of intermediate inheritance patterns...

Co-dominance: When the combination of 2 different alleles both influence the phenotype (both alleles are expressed, or dominant).
Incomplete Dominance: When one dominant allele mutatation expresses partially (heterozygous), and two mutated alleles express fully (homozygous).
Epistasis: When the effect of a gene mutation is determined or affected by the presence or absence of other independently inherited genes. Refers to any relationship of nonadditive interaction between two or more genes in their combined effects on a phenotype. Epistasis is only defined in the context of genetic variation at multiple loci.
Polygenic traits: Traits that are influenced by several pairs of alleles.
Multiple Alleles: When more than 2 alleles exist for one loci.
Compound Heterozygote traits: When 2 different recessive mutations (that each cause a similar condition) occur on same allele, cause the same effect as if both were the exact same mutation
Multifactorial inheritance: When the expression of a gene is influenced by environmental conditions (heredity + environment = trait).

RECESSIVE genes that cause disease occur when both parents carry the mutation, and a foal inherits a copy of the mutation from both of them. Recessive mutations are almost always harmless when inherited singly (the foal inherits only one copy, or one mutated allele of the gene). Recessive mutations are often lethal when inherited doubly (the foal inherits two copies, one from each parent of the mutation on the gene). Takeaway: Any horse tested positive as a carrier, can safely (and guilt-freely) be bred to another horse, as long as the other horse is tested free for the same genetic disease, and proven not a carrier.

DOMINANT genes that cause disease would typically only be passed down from a parent to a foal, if the disease does not show, or if it is a disease that presents late in life. Obviously, a diseased horse would not be bred to intentionally pass it on. Mutations in dominant genes, therefore, that cause disease, are going to be found in incomplete or variable penetrance or semi-dominant genes. This means, the gene is not a simple dominant. There is more to the story; there are conditions that trigger the disease, or there are other genes that play a part in whether the disease presents or remains hidden. Takeaway: All breeding horses should be tested for all known dominant genetic diseases that exist in its bloodline or its breed. No horse found to carry a disease-causing mutation on a dominant gene, should ever be bred.


Additional Information

Large scale sequencing of the complete equine genome in 2008 (Wade et al., 2009) opened up a new frontier to researchers. That has led to more and more simple hereditary diseases being isolated every year that can be identified with a simple genetic DNA-based test.

Most DNA tests can be ordered by filling out a form, and sending in a hair sample (30 to 50 mane or tail hairs including roots) to a lab that is licensed to test for that condition, for a modest fee. It is recommended to stash about 20 hairs and establish your own genetic bank for testing later on. DNA test panels are offered for some types and breeds. Different labs attain various licenses to test for different mutations or diseases. Some labs don't accept or recognize tests from other labs (such as parentage verification) and some tests are replaced with more modern techniques that make older tests un-comparable. Tests may be owned by a lab, a registry, or the animal's owner.



use a graph like this to shop & compare labs for test availability and prices
labs buy license to run different tests from the original trademarked source lab;
so availability and prices are subject to change

  1. Animal Genetics Inc, Tallahassee, Florida
  2. Etalon Diagnostics, California
  3. University of California, Davis, UC Davis, CA
  4. Veterinary Genetic Services, VetGen, Ann Arbor, Michigan
  5. University of Minnesota Equine Center, PSSM1, Neuromuscular Diagnostic Lab, St Paul MN
  6. University of Kentucky Gluck Equine Research Center, Genetic Testing Lab, Lexington KY

  7. Weatherbys Scientific, UK
GBED (stockhorse)              
HERDA (stockhorse)              
HYPP (stockhorse)              
MH (stockhorse)              
MYHM (stockhorse)              
5+ panel (stockhorses)              
GT (widespread)              
PSSM1 (widespread)              
CSNB (Lp horses)              
OLWS (frame overo line)              
CA (Arabian)              
LFS (Arabian)              
SCID (Arabian)              
3 panel (Arabian)              
3 panel (Friesian)              
JEB1 (Belgian)         *registry only?              
JEB2 (Saddlebred)    *registry only?              
Myotonia (New Forest)              

   * Registry only: some tests may have restricted access, available only through a breed registry. You should research DNA test result ownership for any testing you do on your horses. Do not give up control of the information on your horses, that you paid for. What this amounts to is, if you do not own your DNA test results, you do not have access to the results of those DNA tests. The information is owned by a registry or a private registrar.

I do not have all DNA testable conditions included in this report. And more are being discovered & isolated each year. If there are any additional testable conditions you believe should be included in this report, let me know.


Other Diseases?

This report may not include every simple DNA genetic testable equine disease, but it includes a lot of the basics that that we need to be aware of. The advances made in equine genetic disease diagnosis are fast-paced, and responsible breeders will need to stay informed about recent developments. This report deals only with those disorders that can be diagnosed with simple equine genetic tests done from hair samples. There are other genetic equine diseases and disorders that are not as easily diagnosed as with these inexpensive and simple genetic DNA tests. These include such diseases as PSSM Type 2, DSLD, and more, that may be common enough to be or become a threat to the Curly Horse. As breeders we need to stay informed about any breed-related or genetically heritable disorders. Constant vigilance by staying informed of the latest research will be the key to helping keep the Curly Horse as free from inheritable disease as possible.


In Conclusion

This report has a few basic takeaway points for all Curly Horse breeders to consider:

Updated 2023: I have tried to credit all sources I used in the area where I applied their information, and will try to keep this report updated as additional information comes to light. I welcome any participation to keep this information as current and accurate as possible. Please send any updates / corrections to Reprints of this article are not allowed without written permission dated after last update. Individuals are welcome to share or reprint this report as long as it is not done for profit or any compensation, and proper credit with links are included.

Related Reading:

Reading Equine Blood Tests (by David Ramey,
Inherited Diseases of Cattle; a report much like the equine DNA report above, except it compiles known genetic mutations in cattle. Some are found in most cattle, and some are breed specific. Most are testable, and include production traits, cosmetic traits, genetic conditions & diseases.
Genetic Mutations: DNA Facts; 12 things a genetics lab may not tell you


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This report was researched and compiled by Donna Grace Vickery.
report initially published: Spring 2014
most recent update: Spring 2023