Sterility in an Atlantic Bottlenose Dolphin (Tursiops truncatus) with a Hypertrophic Pituitary and Hypogonadism
IAAAM 1998
Elsa M. Haubold; Daniel F. Cowan
Department of Pathology, University of Texas Medical Branch, Galveston, TX, USA and Texas Marine Mammal Stranding Network

Abstract

A 250 cm female bottlenose dolphin, Tursiops truncatus, stranded in Dec. 1997 in Galveston, Texas. External examination revealed a single ulcerating lesion on the tip of the upper rostrum. The animal appeared emaciated. Numerous Xenobalanus were attached to the flukes and flippers. Tooth aging (by J.P. Turner, Texas A&M University, Galveston, TX) revealed 27 annual growth layer groups.

All organs were systematically examined, weighed and sampled for histology. The ovaries were small, smooth and shiny with no grossly apparent scars or corpora. Despite her age, both ovaries fell within observed limits for immature dolphins examined by our laboratory, weighing just half (2.8 and 2.4 left and right, respectively) of the minimum observed weight for mature dolphin ovaries (6.0 and 4.8 gms, respectively). The pituitary was removed and immediately placed in formalin. Once fixed, extraneous connective tissue was trimmed and the pituitary was determined to weigh 3.33 gm. In our previous observations of 35 T. truncatus, weights ranged from 1.6-2.6 gm. All other organ weights were within limits normally observed by our laboratory for Texas stranded dolphins.

Histologically, the ovaries showed no evidence of follicles in any stage of development, and no corpora to indicate she had ever been reproductively active. The pituitary contained nodules and colloid cysts frequently seen in other animals but was otherwise not remarkable. Immunohistochemistry was performed on the pituitary with antibodies for luteinizing hormone (LH) and follicle stimulating hormone (FSH) (DAKO Corporation, Carpinteria, CA). Abnormally abundant cells showing positive staining for both LH and FSH were identified, in comparison to animals previously examined. This animal seems to fit the pattern of premature ovarian failure with secondary hyperplasia.

Acknowledgments

Elsa M. Haubold is supported by the James W. McLaughlin Fellowship Fund.

Speaker Information
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Daniel F. Cowan, MD, CM
Department of Pathology, University of Texas Medical Branch
Galveston, TX, USA
Texas Marine Mammal Stranding Network

Elsa M. Haubold, BS, MS
Department of Pathology, University of Texas Medical Branch
Galveston, TX, USA
Texas Marine Mammal Stranding Network


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