Veterinarians in western Canada report that 2004 has been a disappointing year for many breeders because of an increase in cases of fatal congenital hypothyroidism in foals. Newborns with the disease can exhibit clinical signs such as contracted tendons, protruding lower jaws, and an inability to stand. While researchers haven't been able to pinpoint the definite cause of congenital hypothyroidism, they suspect it might be linked to high levels of nitrate in feedstuffs or water consumed by broodmares, which interferes with iodine metabolism in the mares. It has been suggested that the source of these high levels of nitrate are feedstuffs derived from stressed or immature plants.

The report, which ran in the fall issue of the Western College of Veterinary Medicine's (WCVM) Horse Health Lines, provided viewpoints from breeders who had been affected by the disease this year. In some cases, breeders had 100% of their foals show clinical signs of the disease, with up to 75% of the foals dying or requiring euthanasia within the first several days of their lives.

Congenital hypothyroidism was first described by researchers at the WCVM in Saskatoon, Saskatchewan, in 1981, and it has been known to cause foal deaths in Western Canada and parts of the United States, mainly the Northwest. The disease is caused by decreased thyroid function in foals developing in their dams' wombs.

Andy Allen, DVM, MVetSc, PhD, a veterinary pathologist at WCVM said, "This is one of the busiest foaling seasons I've had since I started researching this disease in 1990." Allen said he received calls about cases as far east as Brandon, Manitoba, and as far West as the British Columbia interior. Some veterinarians have reported twice the amount of cases that they see in a typical year--some see three to four per year but are now seeing seven to eight affected foals. It is suspected there are more cases that horse owners do not report to veterinarians.

What's unsettling to many breeders is their mares that gave birth to affected foals looked healthy and as if pregnancies are progressing normally. Signs don't appear until parturition. According to Allen, "Mares giving birth to congenitally hypothyroid foals appear to be about 30 times more likely to have difficult deliveries than mares giving birth to healthy foals. Of those mares, a small portion experience injuries that are fatal or jeopardize their reproductive future."

Allen described what he and horse owners have observed in cases of the disease: "Generally speaking, these foals are born full term or have very long gestations. The average would be about a year instead of 330 days, and some gestations have been as long as 400 days." Often the mares will lactate prematurely and will appear to get ready to foal at the time the owners would expect. However, in time, the signs of imminent foaling wane, and eventually the owner is surprised by the birth.

"Despite the normal-to-long gestation, the foals are dysmature (immature) in many ways," explained Allen. "They have soft, silky haircoats, and they look like preemies, but obviously aren't. They have soft, pliable ears, and if you stand them up, they have very lax tendons and joints. Their joints can bend in all directions and their toes can point up into the air."

Additionally, Allen said the foals often have umbilical hernias, contracted front legs, occasionally contracted hind legs, which is considered a flexural deformity, their lower jaw sticks out beyond their upper, and they are poorly muscled. "The foals that have enough energy to try and stand thrash about and tend to rupture the common digital extensor tendon (swelling of the knees is reported in many of these foals cases, and the tendon rupture is what causes this)," Allen reported. "Many of the bones of the knees and of the hocks are mildly to markedly underdeveloped, or not properly ossified." (Click here to view images of the anomalies.)

The combination of signs listed above are not easily confused with other diseases, according to Allen. If there is any doubt what has caused the clinical signs, the clincher is when the thyroid function of live foals is tested, or the thyroid gland of dead foals is examined. "When they are brought in for a necropsy, if we look at the thyroid glands microscopically, they are terribly abnormal," he said.

So what's happening at a cellular level in these foals? "A normal thyroid gland is made up of follicles," explained Allen. "They are a little ball that on the outside is lined by cells and in the middle contains colloid. This colloid is the storage form of thyroid hormone, and when the animal needs more of that hormone, colloid is released." The outside layer of cells is usually one layer thick, kind of like a balloon, with a thin outer layer and a large center. In the hypothyroid foals, the follicles have very little or no colloid, and instead of having one layer of cells in the follicles' outer layer, it is several layers thick and irregular.

Allen explained that the disease is technically a hyperplastic (characterized by an abnormal multiplication or increase in number of normal cells) goiter. "Historically, to most people, goiter describes someone with a noticeable swelling in their neck, but in foals, they don't have a markedly enlarged thyroid," he said. "Only when you look at it under a microscope do you realize it's abnormal."

Thyroid hormones are critical for growth and development of the fetus during gestation. Therefore, the inappropriate development of the thyroid gland and abnormally low levels of circulating thyroid hormones during gestation accounts for the retarded growth in these foals.

Deciphering a Cause
Allen and his colleagues have determined that the main risk factors for the disease's occurrence are the presence of nitrate in the feed or water supply of pregnant mares, and a less-than-adequate supply of vitamins and minerals in the pregnant mares' diets. "I suspect that the nitrate somehow interferes or competes with the iodine supply in mares," said Allen, and if the mares are receiving "lower or minimal doses of iodine, the presence of nitrate in the water or feed could make things worse."  But presence of the disease doesn't infer poor management. Some of Western Canada's best-managed breeding farms have experienced the disease in the past 20 years, and if the nitrate theory pans out, one could target and alter a number of environmental conditions and management practices that might prevent development of the disease.

Allen first suspected nitrate because horse owners who were feeding green feed (a cereal crop that is harvested or gets a killing frost before it has a chance to mature) seemed to have more of the disease in their horses. Green feed typically has higher nitrate levels, said Allen.

Allen's current theory is nitrate and iodine are in competition; in a sense, nitrate could be interfering with iodine utilization by the thyroid gland. The good news is that even if a broodmare is ingesting high nitrates levels, if she has a complete balanced ration including enough iodine, it could counteract the effects of nitrate.

Additionally, surface water and shallow wells might be affected by runoff from agricultural activities that could drive up nitrate levels. Allen explained that in certain areas of the world where there are higher levels of nitrate in surface water, there has been noticeable increase in cases of goiter. "Nitrate that gets into the water is certainly just as likely to cause this disease as in the feed, and as with most things is probably more bioavailable in water than in food."

Allen has emphasized that good-looking, high-quality hay can still contain high amounts of nitrate. If there is a nitrate link to congenital hypothyroidism, Allen is concerned about next year's foal crop, because there have been early, harsh frosts in parts of Western Canada. He encourages broodmare owners to get their hay and water tested with a local extension office or nearby university.

"Anecdotal evidence would suggest that fetal exposure (to the disease-causing agent) even as early as in the first month or two after breeding might be sufficient to lead to this disease," said Allen. He suggests getting the hay tested at each harvest before feeding it to the horses.
Tools for Study
Last year, Allen and Genevieve D'Amours, DVM, MVetSc (a former graduate student at WCVM) demonstrated that they could use guinea pigs (a species that shares many similarities with the horse) as a study model for congenital hypothyroidsm. Allen says that it is difficult to get funding for congenital hypothyroidism research, but that the use of guinea pigs makes the research much less expensive and more efficient, since guinea pigs are easier to manage in a research environment and their gestation is a mere 65 days.

Allen plans to continue looking into dietary causes of congenital hypothyroidism and for ways to prevent the disease. If the current theories on nitrate and iodine are ruled out, they can use the guinea pigs to test other theories.

To learn more about Allen's research on CH, please visit WCVM's Fall 2004 Horse Health Lines.

About the Author

Stephanie L. Church, Editor-in-Chief

Stephanie L. Church, Editor-in-Chief, received a B.A. in Journalism and Equestrian Studies from Averett College in Danville, Virginia. A Pony Club and 4-H graduate, her background is in eventing, and she is schooling her recently retired Thoroughbred racehorse, Happy, toward a career in that discipline. She also enjoys traveling, photography, cycling, and cooking in her free time.

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