M.D. Copland1; D.J. Needham2,1
Introduction
Dolphins are obligate swimmers and for this reason their transport presents particular difficulty in comparison with other mammals.
The movement of 6 captive dolphins by air within Australia from Adelaide, South Australia to South Port, Queensland presented us with the opportunity to observe changes in clinical pathology tests before and after transport.
In this paper we report hematology and chemistry results obtained immediately before and immediately after transport of captive dolphins.
Materials and Methods
The subjects were 2 female and 4 male dolphins: 1 dolphin was 6 months of age, another was 4 years of age and the remainder were aged 1 0 or more years.
The dolphins were last fed at 8 am on the day preceding transport (excluding fish containing medication).
The sequence of events on the day of transport was: 5 am adult dolphins fed 3mg/kg diazepam, 8 am caught and placed in crates, 9 am trucked to airport where the first blood samples were taken, 1 0 am departed on a three hour flight, loaded on a truck within 10 minutes of landing for a 47 minute journey to their final destination where the second blood samples were taken before they were released. The first samples were taken 4.76 ± .1 3 h after the diazepam was administered, 1.68 ± .49 h after capture and 6.53 ± .84 h before the second samples.
Blood was placed into dipotassium ethylene-diamine tetra-acetate (EDTA) tubes for hematological analysis and in lithium heparin and plain tubes for biochemical analysis.
Red and white blood cells were counted on a Coufter Counter model ZF1, hemogibin concentration was measured by the cyanmethemoglobin method using a Coufter Hemoglobinometer, packed cell volume (PCV) was determined using a microhematocrit centrifuge and blood smears were stained with Jonner-Giemsa's stain (Dacie and Lewis, 1968).
1Coulter Electronics Pty. Ltd., Brookvale, New South Wales 2100, Australia
Chemical analyses were performed using a Cobas Mira2 random access analyzer. Sodium, potassium and chloride concentrations were measured using ion selective electrodes. Other serum constituents were assayed at 37C using commercially available kits. Globulin was calculated as the difference between total protein and albumin.
Plasma cortisol was measured by radioimmunoassay.3
Differences between means were compared using paired samples T-test.
The following abbreviations are used for chemical terms: ALP Alkaline Phosphatase, AST Aspartate Amino Transferase, ALT Alanine Amino Transferase, GGT Gamma Glutamyl Transferase, LD Lactic Dehydrogenase and CK Creatine kinase.
2Roche Products Pty Ltd, Doe Why, New South Wales, Australia 2111, 3Amerlex Cortisol RIA Kit code IM.2021, Amersham Pty. Ltd., North Ryde, New South Wales 2113, Australia.
Results
Serum cortisol increased during transport from 90±17 nmoI/L to 126 ± 26 nmoI/L (P < .05).
Table 1 compares hematological results of blood taken before and after transport. There were fewer lymphocytes (p < .01) and possibly fewer eosinophils (p = .08) after transport.
Table 1. | Hematology results expressed as mean values and the probability of difference between means indicated as P. |
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Table 2 compares the results of clinical chemistry tests. Creatinine, phosphate, albumin, ALP and GGT were increased and glucose and chloride were decreased (P < .05).
Table 2. | Chemistry results expressed as mean values and the probability of difference between means indicated as P. |
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Discussion
In some species excitement will result in splenic contraction with the release of fresh red blood cells from the spleen into the general circulation and this is reflected in a hemogram when there is a sudden increase in PCV, hemoglobin and red blood cell values (Jain, 1986). Dolphins have particularly small spleens (Geraci, 1986a) and these animals have been frequently handled so ft is not surprising that there was no evidence of splenic contraction.
The elevation in cortisol suggests that the dolphins found the travel experience stressful. Increased amounts of circulating cortisol can induce hematologic and chemical changes. Typical hematologic changes are neutrophilia, lymphopenia, eosinopenia and in some animals monocytosis (Duncan and Prasse, 1986). In dolphins cortisone administration can produce eosinopenia and possibly lymphopenia (Medway et al, 1968) and eosinopenia has been associated with stress (Geraci, 1986b). It is likely that the lymphopenia and apparent eosinopenia observed in these dolphins is the result of stress. The most common chemical change induced by cortisol is induction of ALP and this may explain the elevated ALP observed in these dolphins. Hyperglycemia commonly recorded in stressed animals was not observed here.
A number of changes where observed in the clinical chemistry tests and while they might do not suggest pathologic changes they may indicate physiologic change associated with management or transportation.
Caution is necessary when interpreting these data because of the low number of animals involved, the influence of medication and the possibility of artifactual change. However, there does seem to be some consistency in the results. The most likely interpretation for the small increase in albumin is a reduction in blood volume which may also have the effect of decreasing renal circulation and marginally reducing the excretion of creatinine and phosphate.
Fluid intake in dolphins is largely associated with feed intake (Geraci, 1986a; Geraci, 1986c) which provides both free water and metabolic water from the oxidation of fats. It is possible that the changes observed here are more related to starvation than to the effects transport or are a combination of both. Starvation may also be responsible for the low glucose and increased GGT in these dolphins.
When considered collectively the LD, AST and CK results could indicate minor muscle damage prior to transport.
Acknowledgments
We would like to acknowledge the excellent technical assistance of Kevin Mattschoss and Peter Zviedrans.
References
1. Dacie JV, and Lewis SM (1 968) Practical Haematology. J and A Churchill Ltd., London. Duncan JR and Prasse KW (1 986) Leukocytes In Veterinary Laboratory Medicine. Iowa State University Press p44.
2. Geraci JR (1986a) Introduction and identification In Fowler ME (ed): Zoo and Wild Animal Medicine. WB Saunders and Co.
3. Geraci JR (1986b) Clinical Pathology of Marine Mammals In Fowler ME (ed): Zoo and Wild Animal Medicine. WB Saunders and Co.
4. Geraci JR (1986c) Nutrition and Nutritional Disorders In Fowler ME (ed): Zoo and Wild Animal Medicine. WB Saunders and Co.
5. Jain NC (1986) In Schalm's Veterinary Hematology. Lea and Febiger, Philadelphia, Pennsylvania, pl 89.
6. Malvin RL and Rayner M (1968) Renal function and blood chemistry in Cotacea. Am J Physiol 214: 187-191.
7. Medway W, Geraci JR, Kein LV (1970) Hematologic Response to Administration of a Corticosteroid in the Bottle-Nosed Dolphin (Tursiops trunctaus) J Am Vet Med Assoc 157:563.