Abstract

Administration of medication to anorectic cetaceans is problematic. Intramuscular injections may produce abscessation or cellulitis, and force-feeding is rarely successful. Frequent handling may be harmful to the animal and the personnel, as well as having a negative impact on the goal of reestablishing an appetite. Because glucocorticoids can be effective oral appetite stimulants, they are frequently used to manipulate appetite.⁵

Besides having an effect on appetite, glucocorticoids induce a number of clinical laboratory value changes.^1,2,4 Many glucocorticoid-induced changes in marine mammals parallel those in terrestrial mammals and may include lymphopenia, eosinopenia, hyperglycemia, and elevated levels of triglycerides and liver enzymes.^2,3

Two Atlantic bottlenose dolphins (Tursiops truncatus) were given 0.11mg/kg dexamethasone p.o. CBC/serum chemistry analyses along with insulin, thyroxine, adrenocorticotrophic hormone and cortisol level determinations were at 0 hr, 24 hr, 36 hr, 48 hr, 7 days, 17 days, and 154 days. Within 24 hr of administration, significant changes included neutrophilia, eosinopenia, lymphopenia, elevated insulin, and depressed ACTH and cortisol levels. These effects were rapid and values returned to normal within 48 hr, with no untoward long-term effects.

At no time during the monitoring period did either dolphin become ill. Their appetites increased as evidenced by intense solicitation for food within 24 hr of medication, and then tapered to normal by 48 hr. For the clinician who is treating a sick bottlenose dolphin, these data may aid in differentiating biochemical values caused by glucocorticoids used to stimulate appetite from those produced by a disease process.

References

1.  Byrne CJ, DF Saxton, PK Pelikan, PM Nugent (eds.). 1986. Laboratory Tests. Chemistry: Routine Studies. Addison-Wesley Publishing Co., Menlo Park, California. Pp. 189-193.

2.  Drent M, NA Cobben, RF Henderson, EF Wouters, M van Dieijen-Visser. 1996. The usefulness of lactate dehydrogenase and its isoenzymes as indicators of lung damage or inflammation. Eur. Respir. J. 9:1736-1742.

3.  Levinson SS, GA Hobbs. 1994. Usefulness of various lactate dehydrogenase isoenzyme 1 profiles after myocardial infarction. Ann. Clin. Lab. Sci. 24:364-370.

4.  Lossos IS, R Breuer, O Intrator, M Sonenblick. 1997. Differential diagnosis of pleural effusion by lactate dehydrogenase isoenzyme analysis. Chest 111: 648-651.

5.  Patel PS, SG Adhvaryu, DB Balar. 1994. Serum lactate dehydrogenase and its isoenzymes in leukemia patients: Possible role in the diagnosis and treatment monitoring. Neoplasm 41:55-59.

6.  Sanchez Navarro MR, C Oliver Almendros, M Pena Caballero, JA Hurtado, M Samaniego Munoz. 1996. Lactate dehydrogenase isoenzymes in the serum and bronchial aspirate of newborn infants with respiratory difficulty of different etiologies. An. Esp. Pediatr. 45:62-66.

7.  Tilkian SM, MV Conover, AG Tilkian. 1983. Clinical Implication of Laboratory Tests, 3rd ed. C.V. Mosby Co, St. Louis, Missouri. Pp. 107-131.

8.  van Krugten M, NA Cobben, RJ Lamers, MP van Dieijen-Visser, SS Wagenaar, EF Wouters, M Drent. 1996. Serum LDH: A marker of disease activity and its response to therapy in idiopathic pulmonary fibrosis. Neth. J. Med. 48:220-223.

9.  Widmann FK. 1983. Clinical interpretation of laboratory tests. 9th ed. F.A. Davis Co., Philadelphia, Pennsylvania. Pp. 216-220.