Non-neoplastic Enlargement of the Thyroid Gland
An enlarged thyroid gland is, by definition, a goiter. 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, ingestion of 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.
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 non-neoplastic goiters seen in large domestic animals.
Iodine atoms are a part of the thyroid hormones thyroxine and triiodothyronine; thus, insufficient iodine reduces the ability of the thyroid to make these hormones. With reduced circulating thyroid hormone levels, the pituitary secretes more thyroid-stimulating hormone (TSH), which acts as a stimulus for hyperplasia of the thyroid gland and subsequent development of a goiter. The hyperplastic gland may, and usually does, compensate for the reduced availability of iodine; therefore, goiter is in no way synonymous with hypothyroidism. 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 have clinical signs of hypothyroidism.
Goiter caused by iodine deficiency is most common in newborn pigs, lambs, and calves 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. Using stabilized iodized salt or ensuring that the ration is balanced for iodine content is recommended in all areas known or suspected to be iodine deficient.
Goiter and hypothyroidism occur in foals of dams fed excess iodine during gestation. Mares supplemented with iodine at ≥35 mg/day may produce affected foals. Foals receive the 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 vary and may include goiter, weakness, and musculoskeletal abnormalities. Mares are invariably asymptomatic. Foals may improve or recover once the excess iodine is removed.
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 neonatal foals was first recognized in the early 1980s and is characterized by hyperplasia of the thyroid gland, goiter, and multiple congenital musculoskeletal anomalies. It is most common in western Canada but has been seen in the Pacific Northwest and sporadically in other areas of the USA. There is no sex or breed predilection. Foals with this syndrome are born after a prolonged gestation (340–400 days) but 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 prognathia, and immature carpal and tarsal bones. Multiple cases may appear on a farm, with no recurrence in subsequent years. The underlying etiology is unknown but may be the result of diets that contain high levels of nitrate (eg, greenfeed) 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.
Familial dyshormonogenetic goiter 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.