Goiter in Animals

Thyroid hyperplasia due to iodine deficiency was common throughout the world in areas with iodine-deficient soil before the widespread supplementation of iodized salt in animal diets. Although outbreaks of iodine-deficient goiter are now sporadic and fewer animals are affected, iodine deficiency is still responsible for most non-neoplastic goiters in large domestic animals in which a definitive cause is determined.

Iodine atoms are part of the thyroid hormones thyroxine and triiodothyronine; thus, insufficiency of iodine impairs the ability of the thyroid to make these hormones.

With lower concentrations of circulating thyroid hormones, the pituitary secretes more thyroid-stimulating hormone (TSH), which stimulates hyperplasia of the thyroid gland and subsequent development of a goiter. The hyperplastic gland can, and usually does, compensate for the decreased availability of iodine; therefore, goiter is in no way synonymous with hypothyroidism.

Compared to those of adults, fetal thyroid glands are more susceptible to the effects of high or low iodine intake. Animals born to females on iodine-deficient diets are more likely to develop severe thyroid enlargement and show clinical signs of hypothyroidism (see foal and adult horse goiter images).

Goiter, foal

Image

Courtesy of Dr. Janice Kritchevsky.

Goiter, adult horse

Image

Courtesy of Dr. Janice Kritchevsky.

Goiter that is due to iodine deficiency is most common in neonatal pigs, lambs, and calves in areas with iodine-deficient soil. The thyroid lobes of the young animal usually are at least twice their normal size, soft, and dark red. Severe cases are accompanied by a lack of hair (especially in pigs) or wool (lambs). The neck is usually grossly enlarged, and the skin and other tissue may be thickened, flabby, and edematous.

In mild cases of goiter, treatment with iodized salt (containing > 0.007% iodine) may resolve the goiter and its associated clinical signs. However, because thyroid hormone is critical to normal fetal development, iodine deficiency during gestation may result in death in utero or soon after birth.

To combat goiter, prophylaxis is more effective than treatment. Feeding stabilized iodized salt or ensuring that the ration is balanced for iodine content is recommended in all areas known or suspected to have iodine-deficient soil.

Another important measure to prevent goiter is to bar access to goitrogenic plants. For example, members of the family Brassicaceae (cruciferous vegetables) can contain goitrogens that interfere with iodine metabolism.

Goiter and hypothyroidism can occur in foals of dams fed excess iodine during gestation. TSH levels initially increase in response to excess iodine, which results in hypertrophy of the gland. Ultimately, however, the organification of iodine within the thyroid gland ceases beyond a critical iodine concentration, and hormone production fails as a result. Mares supplemented with iodine at ≥ 35 mg, PO, every 24 hours may produce affected foals. Mineral supplements derived from kelp are a common source of excess iodine in the diet.

Foals receive excess iodine both in utero and via the milk, because mares on high-iodine diets secrete higher-than-normal amounts of iodine in their milk.

Clinical signs of iodine toxicosis vary and can include the following:

• goiter

• weakness

• musculoskeletal abnormalities

Mares show no clinical signs of iodine toxicosis. Foals may improve after the excess iodine is removed.

Certain plants (notably soybeans) may produce goiter when ingested in sufficient amounts, especially in the absence of adequate iodine intake. Cabbage, rape, kale, and turnips are also goitrogenic; however, the goitrogens they contain are less potent than those in soybeans. Cooking or heating (and the usual processing of soybean meal) destroys the goitrogenic substance in these plants.

In addition to the goitrogenic substances found in some plants, organochlorines (such as DDT) and related compounds, as well as lithium, can cause goiter.

All goitrogenic substances interfere with the production of thyroid hormones. As in cases of iodine deficiency, the pituitary gland responds to lower concentrations of circulating thyroid hormones by increasing its secretion of TSH, leading to thyroid gland enlargement.

In adult animals exposed to goitrogenic substances, disease is usually not clinically important. In neonates, however, severe thyroid enlargement and hypothyroidism may develop.

Congenital hypothyroidism and dysmaturity (CHD) syndrome of neonatal foals was first recognized in the early 1980s. CHD syndrome is characterized by hyperplasia of the thyroid gland (goiter) and multiple congenital musculoskeletal anomalies. It is most common in western Canada but has been reported in the Pacific Northwest and sporadically in other areas of the US and Europe.

There is no sex or breed predilection for CHD syndrome. Foals with the syndrome are born after a prolonged gestation (340–400 days); however, they appear dysmature, with pliable ears, muscle weakness, and incomplete skeletal development. Common musculoskeletal defects include flexural deformities of the forelimbs, ruptured tendons of the common digital extensor muscles, mandibular prognathism, and immature carpal and tarsal bones.

Multiple cases of CHD syndrome may appear on a farm, with no recurrence in subsequent years.

The underlying etiology of CHD syndrome is unknown; however, it may result from diets that contain high concentrations of nitrate (eg, immature plants ["greenfeed" forage]) combined with low iodine intake or ingestion of an unidentified goitrogen. Most affected foals either die or are euthanized within the first week of life (1).

Familial dyshormonogenetic goiter has been reported in sheep, cattle, goats, and pigs. It appears to be inherited as an autosomal recessive trait. The cause is a genetic enzyme defect in the biosynthesis of thyroid hormones. As with iodine deficiency, in this condition decreased production of thyroid hormones leads to increased concentrations of TSH and subsequent goiter.

Clinical signs of familial dyshormonogenetic goiter may include the following:

• subnormal growth rate

• absence of normal wool development or a sparse coat

• myxedematous swelling of subcutaneous tissues

• weakness

Many animals with familial dyshormonogenetic goiter die shortly after birth or are very susceptible to adverse environmental conditions.

• Ferlazzo A, Cravana C, Fazio E, Medica P. The contribution of total and free iodothyronines to welfare maintenance and management stress coping in ruminants and equines: physiological ranges and reference values. Res Vet Sci. 2018;118:134-143.

• Hart K. Equine endocrine and metabolic diseases. In: Smith B, Van Metre DC, Pusterla N, eds. Large Animal Internal Medicine. 6th ed. Elsevier; 2020:1352-1420.

• Kritchevsky J. Hypothyroidism in other species. In: Rand J, ed. Clinical Endocrinology of Companion Animals. Wiley-Blackwell; 2013:278-290.

1. Allen AL, Townsend HG, Doige CE, Fretz PB. A case-control study of the congenital hypothyroidism and dysmaturity syndrome of foals. Can Vet J. 1996;37(6):349-351,354-358.