The Histopathology and Etiology of Goiter in Captive Elasmobranchs

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The Histopathology and Etiology of Goiter in Captive Elasmobranchs

 

By Paul Tomlinson

 

The endocrine system consists of several glands located throughout an elasmobranch’s body. This system uses hormones, so-called chemical messengers, to communicate with other cells. That is, the endocrine glands secrete their hormones into the bloodstream, and in direct correlation with the nervous system, help control and regulate many kinds of bodily functions (homeostasis).

In elasmobranchs, the thyroid gland is an encapsulated organ located in the loose connective tissues in the middle of the lower jaw muscles. The thyroid tissue is made up of follicles having a highly vascular capillary system. Each follicle is surrounded by a fluid-filled lumen. This lumen contains a colloidal suspension of an iodine-rich protein, called thyroglobulan. Therefore, the thyroid gland and the hormones produced are dependent on the uptake of environmental iodine.

The Histopathology and Etiology of Goiter in Captive Elasmobranchs

A healthy Elasmobranch.
The thyroid is located in the lower jaw muscles.

The two main hormones produced by the thyroid gland are triiodothyronine (T3) and thyroxine (T4). These hormones are vital to all cells of the body for the regulation of cellular metabolism and physiology. Depending on the uptake of available iodine, the thyroid gland may produce an excess or a reduction of these hormones. When an excess of T3 and/or T4 is produced and secreted, the condition is termed hyperthyroidism. On the other hand, the opposite condition is termed hypothyroidism. These conditions may lead to an enlargement of the thyroid gland called goiter. This swelling of the gland, which may progress to three hundred times its normal size, can cause death in elasmobranchs, if untreated and rectified, due to the fact that the swelling can block the esophagus.

There are several ways the thyroid gland can result in goiter. In hyperthyroidism, there is an elevated production and secretion of the thyroid hormones. As for hypothyroidism, there is a low concentration of the circulating thyroid hormones. Another condition, called thyroiditis, causes the thyroid gland to enlarge due to infectious processes. Other conditions that may affect thyroid hormone concentrations are congenital anomalies and tumors.

According to Crow et al., 2001, the enlargement of the thyroid gland in captive elasmobranchs is the result of both hypertrophy (size increase) and hyperplasia (increase in cell number) of the follicles. The shape and amount of colloid present in the follicles vary. Examination of goiters in captive elasmobranchs has been documented as having three morphological forms:

  1. Diffuse Hyperplastic: thyroid gland consists of small to medium-sized follicles having little to no colloid; follicular cells tend to be columnar in shape; results from a reduction of circulating thyroid hormones with an elevation of thyrotropin (a pituitary hormone that stimulates the thyroid gland to produce T3 and T4); caused by an iodine deficiency or from a goitrogenic agent that restricts the uptake of iodine.
  2. Diffuse Colloid: thyroid gland consists of large rounded follicles having colloid; follicular cells vary from cuboidal to columnar in shape; results from diffuse hyperplastic thyroid glands that begin receiving enough iodine so as to produce normal concentrations of the thyroid hormones; may also be a slow growing goiter from an intermittent iodine deficiency.
  3. Multinodular Colloid: thyroid gland consists of small and large follicles having mostly colloid; follucular cells vary from flattened, to cuboidal, to columnar in shape; thyroid gland divided into nodules by fibrous bands; results from a thyroid enlargement that has been iodine deficient for some course of time.

The Histopathology and Etiology of Goiter in Captive Elasmobranchs

In captive environments elasmobranch susceptibility to goiter formation has been documented numerous times. However, the etiology of this disease is not fully understood. It is know that goiter is caused by a lack of iodine or from a biochemical interaction with a goitrogenic compound. A goitrogen is any compound that interferes with the function of the thyroid, inhibiting normal iodine uptake.

Iodine is an essential element for cellular activities and for the prevention of goiter. Seawater conatins two forms of dissolved iodine, iodine and iodate. Elasmobranchs uptake iodine in the form of iodine, which is the form of iodine believed to be the most biologically active. This uptake of iodine occurs across the gills and stomach.

There is no formulation for iodine supplementation in captive elasmobranchs, due to water chemistry in closed systems and the bio-diversity of elasmobranchs. Moreover, iodine levels in closed systems are continuously lowered or depleted by filtration and biological processes. So based on natural seawater, having a concentration of iodine of 0.006 mg 10-1, a closed system should test for that level. Too much iodine is toxic, and too little may cause goiter.

The Histopathology and Etiology of Goiter in Captive Elasmobranchs

Ozonation in captive environments also reduces environmental iodine causing development of goiter because it converts aquatic iodine to iodate. This form of iodine is biologically unusable in thyroid hormone synthesis. Elasmocranchs absorb iodine primarily from the environment and secondarily from their diet. Therefore, because ozonation reduces the bio-availability of iodine, elasmobranchs in a closed system with an ozonizer in use, are subject to an iodine deficient environment.

Nitrate is another factor in the etiology of goiter in closed systems because of its goitrogenic properties. As water ages in the captive environments, nitrate, the end product of the nitrogen cycle, accumulates because the biological processes that break it down to free nitrogen are complex and slow. Elasmobranchs produce large amounts of ammonia. Ammonia is broken down to nitrite and then to nitrate by aerobic bacteria. These two processes are quite quick in comparison to the anaerobic break-down of nitrate. The accumulation of nitrate inhibits the ability of the thyroid gland to uptake environmental iodine, which results in a reduction of the thyroid hormone synthesis and possibly causing the development of goiter.

In conclusion, enlargement of the thyroid gland takes months to form and two to three times longer to rectify. Captive elasmobranchs should not be exposed to iodine deficient environments, which may be prevented through open re-circulating aquaria or by frequent water changes where iodine must be monitored.  


References:

 

Crow, Gerald L., William H. Luer, and John C. Harshbarger. “Histological Assessment of Goiters in Elasmobranch Fishes.” Journal of Aquatic Animal Health 13.1 (2001): 1-7. Web.

Smith, Mark. The Elasmobranch Husbandry Manual: Captive Care of Sharks, Rays and Their Relatives. Columbus, OH: Ohio Biological Survey, 2004. Print.

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