Non-neoplastic Enlargement of the Thyroid Gland

Non-neoplastic Enlargement of the Thyroid Gland
(Goiter)

Congenital Hypothyroidism and Dysmaturity Syndrome of Foals

Non-neoplastic and noninflammatory enlargements of the thyroid gland develop in all domestic mammals as well as birds. The major causes of goiter include iodine deficiency, goitrogenic substances, dietary iodine excess, and inherited enzyme defects in the biosynthesis of thyroid hormones. Many animals with goiter appear to remain euthyroid, but clinical signs of hypothyroidism may develop in some, especially in newborns.

Iodine Deficiency:

Thyroid hyperplasia due to iodine deficiency was common in many goitrogenic areas throughout the world before the widespread supplementation of iodized salt to animal diets. Although outbreaks of iodine-deficient goiter are now sporadic and fewer animals are affected, iodine deficiency is still responsible for most goiters seen in large domestic animals.

Insufficient iodine reduces the ability of the thyroid to make thyroid hormone. With reduced circulating thyroid hormone levels, the pituitary secretes more TSH, which acts as a stimulus for hyperplasia of the thyroid gland and goiter. The hyperplastic gland may, and usually does, compensate for the reduced availability of iodine; therefore, goiter is in no way synonymous with hypothyroidism. However, animals born to females on iodine-deficient diets are more likely to develop severe thyroid enlargement and have clinical signs of hypothyroidism.

Enlarged thyroid, foal

Goiter caused by iodine deficiency is most common in newborn pigs, lambs, calves, and foals in iodine-deficient areas. The thyroid lobes of the young animal usually are at least twice normal size, soft, and dark red. In severe cases, there is an accompanying 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 mildly affected animals, treatment with iodized salt (containing >0.007% iodine) may resolve the goiter and associated clinical signs, but many die before or soon after birth. Prophylaxis is more effective than treatment. The use of stabilized iodized salt is recommended in all areas known or suspected to be iodine deficient.

Iodine Toxicity:

Foals of dams fed excess iodine may develop extreme thyroid enlargement and die before birth or shortly thereafter. Clinical signs include general weakness, long hair, and marked limb abnormalities.

Goitrogenic Substances:

Certain plants may produce goiter when ingested in sufficient amounts, especially in the absence of adequate iodine intake. Soybeans are most notable, but cabbage, rape, kale, and turnips all contain less potent goitrogens. Cooking or heating (and the usual processing of soybean meal) destroys the goitrogenic substance in these plants. All of the goitrogenic substances act by interfering with production of thyroid hormone. As with iodine deficiency, the pituitary responds to the reduced circulating thyroid hormone levels by increasing its secretion of TSH, which results in thyroid gland enlargement. In adult animals the disease is usually not significant, but severe thyroid enlargement and hypothyroidism may develop in newborns.

Congenital Hypothyroidism and Dysmaturity Syndrome of Foals:

This syndrome of neonatal foals first recognized in the early 1980s is characterized by hyperplasia of the thyroid gland and multiple congenital musculoskeletal anomalies. It is most common in western Canada. Foals with this syndrome are born weak or dead with hyperplasia of the thyroid gland, flexural deformities of the forelimbs, ruptured tendons of the common digital extensor muscles, mandibular prognathia, and immature carpal and tarsal bones. The underlying etiology is unknown but may be the result of diets that contain high levels of nitrate (eg, greenfeed).

Familial Dyshormonogenetic Goiter:

This has been reported in sheep, cattle, goats, and pigs, and appears to be inherited as an autosomal recessive trait. Essentially, it is a genetic enzyme defect in the biosynthesis of thyroid hormones. As with iodine deficiency, reduced thyroid hormone production leads to secretion of increased levels of TSH and subsequent goiter. Clinical signs may include subnormal growth rate, absence of normal wool development or a sparse coat, myxedematous swelling of subcutaneous tissues, and weakness. Many affected animals die shortly after birth or are very sensitive to adverse environmental conditions.