**5. Clinical findings**

**Figure 1.** Enlarged thyroid gland/congenital goiter in a kid presented to the University clinics (Courtesy of Dr. R.K.Bhardwaj).

Among different breeds of goats, Boer goat of South Africa seems to be more susceptible to develop iodine deficiency due to rapid growth. Indigenous breeds of Himalayan region are more resistant to iodine deficiency than Barbari and Alpine goats. The Angora goat is also

Inadequate iodine in the thyroid gland results in the synthesis of uniodinated inactive prehormone instead of the thyroxine, which stimulates the pituitary gland to secrete thyroidstimulating hormone (TSH). This commonly results in hyperplasia of the thyroid tissue and

considerable enlargement of the gland, that is, goiter (**Figures 1** and **2**).

reported to be very susceptible to iodine deficiency [3].

**4. Pathogenesis**

78 Goat Science

Iodine deficiency occurs in many species of animals and develops different signs in different animals. Goiter is a cardinal sign of iodine deficiency manifested mostly in young ones, that is, kids. The normal thyroid gland is 0.20% of body weight, but it is markedly enlarged up to the size of an orange in iodine-deficient goats [3]. The thyroid gland of goats/kids may be graded as palpable and plum size (+), easily palpable and lemon size (++), and duck egg size, hanging and visible from the distance (+++) (**Figure 3c**). Kids who survive the initial danger period after birth may recover except for partial persistence of goiter (**Figure 1**). The gland may pulsate with the normal arterial pulse and may extend down a greater part of the neck and cause some local edema. Auscultation and palpation of the jugular furrow may reveal the presence of a murmur and thrill (the thyroid thrill) due to the increased arterial blood supply of the glands [12, 13].

Affected kids are born with enlarged thyroid gland or goiter, and enlargement of pituitary gland is also reported [14]. There may be birth of premature kids which are very weak and die within few hours of birth due to severe dyspnea caused by compression of the trachea by enlarged thyroid glands. Majority of new born kids may be hairless/bald (**Figure 3a**) or covered with very fine hair due hypoplasia of hair follicles [15]. Kids may appear dumb or unwilling to suckle the dam [3]. Growth rate of kids is stunted. Fertility of does is affected. Iodine supplementation in goats is found to increase conception, succeed in the first insemination, and reduce abortion rate and dystocia due to goiter [16, 17].

The rate of excretion of iodine in milk and urine can provide useful diagnostic criteria in simple iodine deficiency since iodine intake is positively correlated with urinary iodine excretion. The milk iodine level of sheep is 80 μg/l and in the deficiency level is below 8 μg/l. Similarly,

Iodine Deficiency in Goats

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http://dx.doi.org/10.5772/intechopen.72728

Normal thyroid gland contains acini lined by low cuboidal epithelium filled with colloid, whereas in goiter, it is replaced by tall columnar epithelium, papillary in foldings, and reduced colloid. A hyperplasic goiter is characterized by enlarged gland with much colloid also known as colloid goiter when dietary supplementation of iodine is made to goats. Iodine content of the thyroid gland is reduced (**Figure 4a**–**c**). Subclinical iodine deficiency can be diagnosed histopathologically by hyperplasia of the thyroid epithelium with grossly normal

**Figure 4.** (a) Histopathology of enlarged thyroid gland at 10×, (b) 40×, and (c) 100× showing various sizes of thyroid

follicle with colloid and hyperplasia of the epithelium of thyroid follicles (Courtesy of Dr. R.K. Bhardwaj).

lower normal limit of iodine in urine is 50 μg/l.

size of the thyroid gland [3].

**Figure 3.** (a) Premature kids aborted with goiter and baldness. (b) Dead kid with goiter. (c) Exposed enlarged thyroid gland (Courtesy of Dr. R.K. Bhardwaj).

## **6. Diagnosis**

Diagnosis of iodine deficiency is based on the history of supplementation of mineral mixture and iodine in the diet of animal and clinical signs like stillbirth, abortion, birth of weak kids, or dead kids with congenital goiter. It is easy to diagnose clinical iodine deficiency. The subclinical deficiency is of more importance as it is difficult to diagnose and goes unnoticed. Subclinical iodine-deficient animals show few or no clinical signs, but production, growth rate, and fertility are affected.

Thyroid hormone (triiodothyronine and thyroxine) assay is used to confirm iodine deficiency or hypothyroidism in goats. Normal range of thyroxine is 3.3–7.0 μg/dl and is decreased in iodine deficiency [3]. Triiodothyronine is an active form of thyroid hormone at the cellular level which needs to be converted from thyroxine to triiodothyronine by selenium-containing enzyme deiodinase. Deficiency of selenium may result in increase in the level of thyroxine and decrease in triiodothyronine and elevated plasma cholesterol.

Estimation of protein-bound (organic) iodine in blood is highly sensitive for diagnosis of iodine deficiency. Low protein-bound (organic) iodine below 8.1 μg/dl is suggestive of iodine deficiency [3].

The rate of excretion of iodine in milk and urine can provide useful diagnostic criteria in simple iodine deficiency since iodine intake is positively correlated with urinary iodine excretion. The milk iodine level of sheep is 80 μg/l and in the deficiency level is below 8 μg/l. Similarly, lower normal limit of iodine in urine is 50 μg/l.

Normal thyroid gland contains acini lined by low cuboidal epithelium filled with colloid, whereas in goiter, it is replaced by tall columnar epithelium, papillary in foldings, and reduced colloid. A hyperplasic goiter is characterized by enlarged gland with much colloid also known as colloid goiter when dietary supplementation of iodine is made to goats. Iodine content of the thyroid gland is reduced (**Figure 4a**–**c**). Subclinical iodine deficiency can be diagnosed histopathologically by hyperplasia of the thyroid epithelium with grossly normal size of the thyroid gland [3].

**6. Diagnosis**

80 Goat Science

(Courtesy of Dr. R.K. Bhardwaj).

deficiency [3].

Diagnosis of iodine deficiency is based on the history of supplementation of mineral mixture and iodine in the diet of animal and clinical signs like stillbirth, abortion, birth of weak kids, or dead kids with congenital goiter. It is easy to diagnose clinical iodine deficiency. The subclinical deficiency is of more importance as it is difficult to diagnose and goes unnoticed. Subclinical iodine-deficient animals show few or no clinical signs, but production, growth rate, and fertility are affected.

**Figure 3.** (a) Premature kids aborted with goiter and baldness. (b) Dead kid with goiter. (c) Exposed enlarged thyroid gland

Thyroid hormone (triiodothyronine and thyroxine) assay is used to confirm iodine deficiency or hypothyroidism in goats. Normal range of thyroxine is 3.3–7.0 μg/dl and is decreased in iodine deficiency [3]. Triiodothyronine is an active form of thyroid hormone at the cellular level which needs to be converted from thyroxine to triiodothyronine by selenium-containing enzyme deiodinase. Deficiency of selenium may result in increase in the level of thyroxine

Estimation of protein-bound (organic) iodine in blood is highly sensitive for diagnosis of iodine deficiency. Low protein-bound (organic) iodine below 8.1 μg/dl is suggestive of iodine

and decrease in triiodothyronine and elevated plasma cholesterol.

**Figure 4.** (a) Histopathology of enlarged thyroid gland at 10×, (b) 40×, and (c) 100× showing various sizes of thyroid follicle with colloid and hyperplasia of the epithelium of thyroid follicles (Courtesy of Dr. R.K. Bhardwaj).
