Abstract

Seven perinatal dolphin mortalities associated with a histologic diagnosis of diffuse hyperplastic goiter were obtained from three separate zoologic or aquarium facilities (Table 1). Dolphins 1 and 2 were from the Edmonton Mall Aquarium, Alberta, Canada. Dolphin 3 was from the Minnesota Zoo, and dolphins 4–7 were from the Indianapolis Zoo, United States. Five dolphins were males and two were females. Dolphin 2 was 6–8 weeks premature, dolphins 1, 3–5 lived less than 1 day, and dolphins 6 and 7 were stillborn. All dams were wild caught. Dolphins 1 and 2 had the same dam, and Dolphins 4 and 6 had the same dam. Dams were different for dolphins 3, 5 and 7. Duration in captivity for the dams at the time calf births averaged 11.5 years, with range of 6–23 years. Thyroid morphology was compared with the histologically normal thyroids of two stranded wild bottlenose dolphins, a neonate and a 2-month-old calf, that died of unrelated causes. Compared to the stranded dolphin calves and the published literature,³ histologic changes consistent with diffuse follicular goiter were seen in the thyroid glands of all captive-born dolphins. Changes included reduced follicular luminal diameter, markedly reduced or absent luminal colloid, and hypertrophy of follicular epithelium. Additional histologic findings included lymphoid depletion in dolphin 2, sepsis in dolphin 3, and atrophy of fat in dolphin 7. Cause of death could not be determined for these animals but was presumed to be due to metabolic derangements associated with the thyroid lesion, drowning, or dystocia.

Table 1. Neonatal dolphin mortalities associated with congenital goiter

^aClosed system, salt water synthesized from road salt obtained from salt bed. Water filtered through carbon and diatomaceous earth mechanical filters, chlorinated.
^bClosed system, salt water synthesized by addition of salt, eight sand and gravel filters, ozonated.
^cClosed system, salt water synthesized by addition of salt, 12 sand and gravel filters, ozonated and chlorinated.

Congenital goiters can be acquired or heritable, and are almost always diffuse follicular goiters, rather than nodular or colloid goiters.¹ Acquired diffuse follicular goiter is due to high or low levels of maternal dietary iodine, the latter sometimes exacerbated by concurrent goitrogenic dietary substances.^1,4,6 Diffuse acquired follicular goiter is well documented in humans, horses, and domestic ruminants.^1,2,4,6 Heritable diffuse follicular goiter is documented in humans and several breeds of cattle.¹ Because the dams to the dolphins of our study were wild caught, and there is a wide demographic spread in incidence of this condition, it seems unlikely that this represents a heritable disorder. The water used in the dolphin exhibits is treated through filters that can potentially remove microminerals. Ozone treatment of artificial seawater may alter the relative concentrations of iodine species in a closed tank system.⁵ Additionally, a number of potentially goiterogenic compounds may be present in the aquatic environment, including chlorine, chlorine compounds, ammonia, nitrates, nitrites, and urea.⁵ We believe that the congenital goiter in these dolphin calves is an acquired disorder associated with derangements in thyroid and/or iodine metabolism; maternal and fetal thyroid and iodine values may be affected by inappropriate levels of iodine in the diet or in the aquatic environment. It is interesting to note that the dam to dolphin 2 subsequently died and had hyperplastic changes in the thyroid gland.

Additional studies at facilities with this problem should include: 1) evaluation of iodine levels in exhibit water and comparison with known values for natural seawater, 2) evaluation of thyroid values for affected neonatal and adult dolphins and comparison with known values for normal captive and wild dolphins; and 3) evaluation of thyroid to body weight ratios for affected juvenile and adult dolphins, and comparisons with known values for normal dolphins.

Acknowledgments

For slide preparation, we gratefully acknowledge the excellent technical support of Roy Brown, Histology Consulting Service, Oak Harbor, Washington. We thank B.E. Beck, DVM, Veterinary Pathology Laboratory, Edmonton, Alberta; Dr. Detlef Onderka, Animal Health Laboratories, Agriculture, Food and Rural Development, Alberta; and Dr. David Gribble, Central Veterinary Laboratory, Vancouver, BC, for providing slides and original diagnoses on Cases 1 and 2. We also thank the Animal Disease diagnostic Laboratory, Purdue University, West Lafayette, IN, for providing slides and original diagnoses on cases 5–7.

Literature Cited

1.  Capen, C.C. 1993. The endocrine glands. In: Pathology of Domestic Animals. 4th ed, Jubb KVF, Kennedy PC and Palmer N., eds. Academic Press, Inc.; San Diego, CA: 306–319.

2.  Drew B, Barber WP, Williams DG. 1975. The effect of excess dietary iodine on pregnant mares and foals. Vet Rec. 97:93–95.

3.  Harrison R.J. and B.A. Young. 1970. The thyroid gland of the common (Pacific) dolphin, Delphinus delphis bairdi. J. Anat. 106:243–254.

4.  Osame, S. and S. Ichijo. 1994. Clinicopathological observations on thoroughbred foals with enlarged thyroid gland. J Vet Med Sci. 56:771–772.

5.  Sherrill, J., B. Whitaker, and G.T.F. Wong. 2000. Ozonation effects on the speciation of dissolved iodine in artificial seawater at the National Aquarium in Baltimore. In: Proceedings: Joint conference of American Association of Zoo Veterinarians/International Association for Aquatic Animal Medicine. New Orleans, LA: 181–183.

6.  Silva, C.A., H. Merkt, P.N. Bergamo, S.S. Barros, C.S. Barros, M.N. Santos, H.O. Hoppen, P. Heidemann, and H. Meyer. 1987. Consequence of excess iodine supply in a Thoroughbred stud in southern Brazil. J Reprod Fertil Suppl. 35:529–533.