15 Popular Horse Breeds Vets Wish Buyers Knew More About

Read all the way to the end. The last breed's problem only appears once it leaves home.

1. 1

   Muscles and skin

   1. American Quarter Horse

   

   Have you owned one?

   America's most popular breed carries the best-documented set of genetic diseases in the horse world. Hyperkalemic periodic paralysis, or HYPP, causes muscle tremors, weakness and collapse, and traces to the halter stallion Impressive. It is dominant, so one copy is enough. Hereditary equine regional dermal asthenia, or HERDA, is recessive and common in cutting-horse lines. The skin along the back stretches, tears and scars, and it usually shows at about two years old when the horse is first saddled.

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   Polysaccharide storage myopathy type 1, or PSSM1, is dominant and causes stiffness, sweating and tying-up after light work. Glycogen branching enzyme deficiency kills foals before or soon after birth, and malignant hyperthermia can cause a fatal reaction under anesthesia.

   One faulty gene in one famous stallion can reach an entire breed within a few generations.

   Before you buyAsk for the five-panel genetic test, which most laboratories have now extended to six with a muscle disease called MYHM. Reputable sellers have it on file, and the registry requires it for breeding stallions.
2. 2

   Foals

   2. Arabian

   

   Have you owned one?

   The Arabian is one of the oldest and soundest breeds, but it carries three recessive conditions that matter to anyone who breeds. Severe combined immunodeficiency, or SCID, leaves a foal with no working immune system. The foal looks normal at birth, protected by antibodies in the mare's first milk, then succumbs to infections before it is five months old. No treatment saves it.

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   Cerebellar abiotrophy destroys cells in the part of the brain that controls balance. Signs appear between about six weeks and four months of age: a head tremor, a wide-legged stance and a startled, exaggerated gait. Lavender foal syndrome produces a foal with a pale, silvery coat that has seizures and cannot stand.

   Carriers of all three are perfectly healthy and can compete, work and live long lives. The danger arises only when two carriers are mated, which gives a one in four chance of an affected foal each time.

   A carrier is a perfectly healthy horse. The risk begins only when two carriers meet.

   Before you buyAsk for SCID, cerebellar abiotrophy and lavender foal test results on the horse, or on both parents. It matters most if you plan to breed, and it applies to part-Arabians too.
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3. 3

   Legs and lungs

   3. Thoroughbred

   

   Have you owned one?

   The Thoroughbred was bred for one thing, speed over a distance, and its weak points follow from that. There is no single gene to test for. The problems are structural. Many Thoroughbreds have thin hoof walls and flat, thin soles that bruise easily and hold shoes poorly. Fine bone and long tendons carry a large body at high speed, so bowed tendons, bone chips in the knees and ankles, and arthritis are common in horses that raced.

   Exercise-induced pulmonary hemorrhage, or EIPH, means bleeding from the small vessels of the lungs during hard effort. Most racehorses bleed to some degree. You rarely see blood at the nostrils. A vet finds it by passing an endoscope down the windpipe after work. Stomach ulcers are also very common in horses coming off the track, and show as poor appetite, a dull coat and a sour attitude when the girth is tightened.

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   Before you buyHave a vet X-ray the feet, ankles and knees of any ex-racehorse before you commit, and look up its race record. A horse that ran sound for many seasons has proven its legs.
4. 4

   Heart and gut

   4. Friesian

   

   Have you owned one?

   The Friesian nearly died out more than once, and every horse alive today descends from a very small group of ancestors. That narrow gene pool shows. Two recessive conditions have genetic tests. Dwarfism produces a foal with a normal-sized head and body on short legs, with lax tendons that let the fetlocks sink. Hydrocephalus, or fluid on the brain, causes a domed skull and usually a stillborn foal and a dangerous delivery for the mare.

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   Other problems have no test yet. Friesians are prone to rupture of the aorta, the main artery leaving the heart, typically in young adult horses and often without warning. Megaesophagus, a slack and widened gullet, causes repeated choke, with feed and saliva running from the nostrils. Mares also retain the placenta after foaling far more often than other breeds, which is an emergency.

   Before you buyAsk for the dwarfism and hydrocephalus results on both parents, and buy from breeders who work within the studbook, which tracks carrier status in its approved stallions.
5. 5

   Eyes

   5. Appaloosa

   

   Have you owned one?

   The spotted coat comes from a gene called leopard complex, and that same gene affects the eyes. Appaloosas are several times more likely than other breeds to develop equine recurrent uveitis, once called moon blindness. It is an inflammation inside the eye that flares, settles and returns, doing more damage each time. Owners see squinting, tearing, a cloudy or bluish cornea and a small, tight pupil. In Appaloosas it is often the quiet, insidious form that causes little obvious pain, so it is found late. It is the leading cause of blindness in horses.

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   Horses with two copies of the leopard complex gene, usually the few-spot and snowcap patterns, are born with congenital stationary night blindness. They see normally by day and cannot see in the dark. It does not get worse, and many owners never realize it.

   Before you buyA hair test shows whether a horse has one or two copies of the leopard complex gene. Have a vet examine both eyes with the pupils dilated, and ask directly whether the horse has ever had an eye treated.
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6. 6

   Foals

   6. American Paint Horse

   

   Have you owned one?

   Lethal white overo syndrome is one of the simplest and saddest genetic conditions in horses. It is tied to the frame overo pattern, the one with jagged white patches on the sides that seem framed by color. A horse with one copy of the gene has the pattern and is healthy. A foal that inherits two copies is born entirely or almost entirely white with blue eyes, and without the nerve cells that make the intestine move. It cannot pass manure. Colic begins within 12 to 24 hours, and the only humane course is euthanasia.

   When two carriers are bred, each foal has a one in four chance of being affected. The trap is that some carriers show so little white that they are registered as solid. You cannot judge by looking. Because Paints share bloodlines with Quarter Horses, they also carry HYPP, HERDA and PSSM1.

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   You cannot tell a frame overo carrier by looking at it. Only the test knows.

   Before you buyAsk for the lethal white overo test on any Paint you might breed, however little white it has, along with the Quarter Horse panel. Two carriers should never be bred together.
7. 7

   Teeth and size

   7. Miniature Horse

   

   Have you owned one?

   A Miniature Horse has a full set of horse-sized teeth in a skull a fraction of the size. Crowding, retained baby teeth, overbites and underbites are routine, and a mouth that cannot chew properly leads to weight loss, choke and sinus infections. Minis also carry several recessive dwarfism mutations in a gene called ACAN. Affected foals have short, bowed legs, a bulging forehead, a potbelly and often breathing trouble, and many live in pain. A hair test identifies carriers.

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   The third problem is weight. Minis stay fat on very little, and an overweight Mini is at risk of laminitis, the painful inflammation inside the hoof. When a fat Mini stops eating for any reason, it can develop hyperlipemia, in which fat floods the bloodstream and overwhelms the liver. That is a true emergency.

   Before you buyAsk for the dwarfism panel on both parents and look inside the mouth before you buy. Budget for a dental check twice a year, and plan on a dry lot or a grazing muzzle.
8. 8

   Muscles and legs

   8. Belgian Draft

   

   Have you owned one?

   Polysaccharide storage myopathy type 1 is more common in Belgians than in almost any other breed. It is the same dominant mutation found in Quarter Horses, and a large share of the breed carries it. The muscles store sugar abnormally, so the horse becomes stiff, reluctant to move, sweaty and sore across the hindquarters, sometimes with dark, coffee-colored urine after work. Some affected Belgians show nothing more than weakness and trouble backing up or lifting a hind foot for the farrier.

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   Belgians also carry junctional epidermolysis bullosa, a recessive condition in which a newborn foal's skin and hooves slough off within days. It is always fatal, and a test identifies carriers. Chronic progressive lymphedema, the lower-leg swelling of heavy feathered breeds, affects Belgians as well.

   Before you buyAsk for the PSSM1 and junctional epidermolysis bullosa results, and ask what the horse is fed. Affected drafts do far better on a low-starch, higher-fat diet with daily turnout and regular work.
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9. 9

   Legs

   9. Clydesdale and Shire

   

   Have you owned one?

   Under the long silky feather that makes these breeds so handsome, many horses have chronic progressive lymphedema. The lymph vessels of the lower legs fail, fluid builds up, and the skin thickens into folds and hard nodules. It starts early, often before the horse is three, and advances for life. Early on, you feel only a slight thickening and scurf around the pastern. Later the folds crack, ooze and smell, and infections and feather mites move in and make everything worse. Horses stamp and rub their legs from the itching.

   There is no cure and no genetic test, although it clearly runs in families. Management slows it: clipping the feather so the skin can be treated, controlling mites, keeping the legs clean and dry, and daily exercise to move the fluid.

   Feather hides a great deal. Your fingers will tell you what your eyes cannot.

   Before you buyPart the feather on all four legs and feel the skin from fetlock to heel. It should be smooth and supple, with no ridges, lumps or folds. Ask to see the legs of the sire and dam.
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10. 10

    Weight

    10. Morgan

    

    Have you owned one?

    Morgans are the classic easy keepers. They hold their weight on sparse feed, a great advantage on a nineteenth-century New England farm and a liability on modern pasture. The breed is strongly predisposed to equine metabolic syndrome, in which the body stops responding properly to insulin. An affected horse develops a thick, hard, cresty neck and pads of fat behind the shoulders, over the ribs and around the tail head.

    The danger is laminitis. High insulin damages the tissue that holds the hoof wall to the bone inside, and the first sign is often a short, pottery stride on hard ground or a horse rocking its weight back onto its heels. Rings on the hoof wall that are wider at the heel than the toe show it has happened before. There is no genetic test, but a blood test measures insulin directly.

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    Before you buyAsk your vet to run an insulin test as part of the pre-purchase exam, and look for hoof rings and a cresty neck. Plan on a grazing muzzle in spring and fall.
11. 11

    Back

    11. American Saddlebred

    

    Have you owned one?

    Saddlebreds have a much higher rate of lordosis, or swayback, than other breeds, and in this breed it is inherited and appears young. The back begins to dip between the withers and the croup in the first year or two of life, well before the horse carries a rider. Researchers have linked it to a region on one chromosome and it behaves as a recessive trait, but no commercial test is offered yet.

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    Affected horses are usually not in pain, and many show and work for years. The practical problem is saddle fit, since a normal saddle bridges the dip and presses hard at the front and back. The breed also carries junctional epidermolysis bullosa, the recessive skin disease that is fatal to newborn foals, and that one does have a test.

    Before you buyLook at the horse standing square from the side, without a saddle, and press along the spine for soreness. Ask for the junctional epidermolysis bullosa result if you intend to breed.
12. 12

    Foals and joints

    12. Warmbloods

    

    Have you owned one?

    Hanoverians, Dutch Warmbloods, Oldenburgs and the other European sport horse registries share bloodlines, so they share problems. Warmblood fragile foal syndrome is a recessive defect in the way the body builds collagen. An affected foal is born with thin skin that tears at a touch, open wounds and joints that bend far past their normal range. It cannot survive. Many affected pregnancies are lost before term. Roughly one warmblood in ten is a healthy carrier, and a hair test finds them.

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    The second issue is osteochondrosis, often called OCD. In large, fast-growing youngsters, joint cartilage fails to turn into bone properly, and flaps or loose fragments form in the hock, stifle or fetlock. You see a puffy joint in a yearling or two-year-old, sometimes with lameness. Genetics, rapid growth and rich feeding all contribute, and many cases are fixed with keyhole surgery.

    Before you buyAsk for the fragile foal result on any horse you might breed, and have the hocks, stifles and fetlocks of a young horse X-rayed before purchase.
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13. 13

    Feet

    13. Ponies

    

    Have you owned one?

    Shetlands, Welsh ponies, Dartmoors and their cousins evolved on moor and mountain, where survival meant extracting every calorie from poor grass. On fertilized pasture that thrift turns against them. Ponies are the group most prone to equine metabolic syndrome and to the laminitis that follows. An attack shows as reluctance to walk, a stance with the front feet stretched forward, hooves that are warm to the touch and a pounding pulse at the back of the fetlock. Severe cases leave the bone inside the hoof rotated or sunk, and the pony is never fully sound again.

    Older ponies add a second risk. Pituitary pars intermedia dysfunction, also called Cushing's disease, is common after age 15 and brings a long, curly coat that does not shed, muscle loss and more laminitis. Both conditions are confirmed with blood tests.

    A pony was built to thrive on a hillside that would starve a horse.

    Before you buyAsk whether the pony has ever had laminitis and check the hooves for rings and a stretched white line. Treat spring and fall grass like candy.
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14. 14

    Eyes

    14. Rocky Mountain Horse

    

    Have you owned one?

    The chocolate coat and flaxen mane that define this Kentucky breed come from the silver dapple gene, and that gene also shapes the eye. The condition is called multiple congenital ocular anomalies. Horses with one copy of the silver gene usually have fluid-filled cysts toward the back of the eye, on the side nearest the ear, which seldom affect vision. Horses with two copies have the full syndrome: a bulging, rounded cornea, a malformed iris, pupils that do not widen properly in the dark, and sometimes cataracts or a displaced lens.

    The condition is present from birth and does not progress, so a horse that sees adequately at three will see the same at twenty. The same gene causes the same problem in Kentucky Mountain Saddle Horses, some Miniature Horses and other silver-colored breeds.

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    Before you buyA hair test for the silver gene shows whether a horse has one copy or two. Request an eye exam by a veterinary ophthalmologist, and avoid breeding two silver horses together.
15. 15

    Skin

    15. Icelandic Horse

    

    Have you owned one?

    Iceland has no biting midges, the tiny gnats of the genus Culicoides. Horses born there never meet them as foals, so their immune systems never learn to tolerate the bite. When an adult Icelandic is exported, a large proportion develop insect bite hypersensitivity, also called sweet itch or summer eczema, usually within their first few summers abroad. It is an allergy to proteins in midge saliva.

    The itching is intense. Horses rub out the mane and the top of the tail and scrape the belly, withers and rump until the skin is bald, thickened and raw. It returns every warm season and eases in winter. There is no genetic test, since many genes are involved. Control means a full-body fly sheet, stabling at dawn and dusk when midges feed, and strong fans in the stall. Iceland allows no horses in, so one that leaves can never return.

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    Before you buyAsk where the horse was born. Icelandics foaled in North America are far less affected than imports, and a seller should tell you plainly how the horse came through last summer.