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  • Author or Editor: Jonna A. K. Mazet x
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Objective—To determine the effects of petroleum exposure on hematologic and clinical biochemical results of mink and to identify variables that may be useful for making management decisions involving sea otters (Enhydra lutris) that have been exposed to oil in their environment.

Animals—122 American mink (Mustela vison).

Procedures—Mink were exposed once to a slick of oil (Alaskan North Slope crude oil or bunker C fuel oil) on seawater or via low-level contamination of their daily rations.

Results—In the acute phase of exposure, petroleum directly affected RBC, WBC, neutrophil, and lymphocyte counts, fibrinogen, sodium, calcium, creatinine, total protein, and cholesterol concentrations, and alanine transaminase, creatine kinase, alkaline phosphatase, and γ−glutamyltransferase activities. Aspartate transaminase, alkaline phosphatase, γ− glutamyltransferase, and lactate dehydrogenase activities and cholesterol concentration also varied as a result of chronic low-level contamination of feed.

Conclusions and Clinical Relevance—Our results are in agreement with reports that attribute increased alanine transaminase and alkaline phosphatase activities and decreased total protein concentration to petroleum exposure in sea otters during an oil spill. Sodium, calcium, creatinine, cholesterol, and lactate dehydrogenase may be valuable variables to assess for guidance during initial treatment of sea otters exposed to oil spills as well as for predicting which petroleum-exposed sea otters will reproduce following an oil spill. Measurement of these variables should aid wildlife professionals in making decisions regarding treatment of sea otters after oil spills. (Am J Vet Res 2000;61: 1197–1203)

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in American Journal of Veterinary Research


Objective—To validate a luciferase bioassay, which is based on a recombinant mouse hepatoma cell line, for the detection of exposure to petroleum in mustelid species.

Animals—122 American mink (Mustela vison) and 15 sea otters (Enhydra lutris).

Procedures—Mink were exposed to Bunker C fuel oil or Alaska North Slope crude oil externally as a single exposure or internally via low dose concentrations in their ration for 6 months. Serum samples were analyzed for cytochrome P450 1A1 induction by quantification of luciferase activity in the bioassay. Mink liver specimens were also evaluated for cytochrome P450 1A1 induction by quantification of ethoxyresorufin-o-deethylase activity. Serum collected from exposed and unexposed sea otters was also analyzed using the luciferase bioassay.

Results—Serum samples from mink externally exposed to petroleum had significantly increased luciferase activities at 1 week after exposure. Serum samples taken at later time points or from mink exposed to either product in the ration did not cause significant luciferase induction. Samples from otters exposed to petroleum had significantly higher luciferase induction as compared with samples from otters not exposed to petroleum at 2 and 8 years after the spill. Cytochrome P450 1A1 activity in liver specimens collected from mink that were internally exposed through diet was significantly increased at the conclusion of our study.

Conclusion and Clinical Relevance—The luciferase bioassay is a sensitive and specific method for determining recent exposure to petroleum in mink. The lack of luciferase activity in serum samples collected from mink greater than 1 week after experimental exposure was likely attributable to lower overall petroleum exposure in our trial, compared with natural exposures. (Am J Vet Res 2002;63:963–968)

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in American Journal of Veterinary Research


Objective—To describe cardiac lesions and identify risk factors associated with myocarditis and dilated cardiomyopathy (DCM) in beach-cast southern sea otters.

Animals—Free-ranging southern sea otters.

Procedure—Sea otters were necropsied at the Marine Wildlife Veterinary Care and Research Center from 1998 through 2001. Microscopic and gross necropsy findings were used to classify sea otters as myocarditis or DCM case otters or control otters. Univariate, multivariate, and spatial analytical techniques were used to evaluate associations among myocarditis; DCM; common sea otter pathogens; and potential infectious, toxic, and nutritional causes.

Results—Clusters of sea otters with myocarditis and DCM were identified in the southern aspect of the sea otter range from May to November 2000. Risk factors for myocarditis included age, good body condition, and exposure to domoic acid and Sarcocystis neurona. Myocarditis associated with domoic acid occurred predominantly in the southern part of the range, whereas myocarditis associated with S neurona occurred in the northern part of the range. Age and suspected previous exposure to domoic acid were identified as major risk factors for DCM. A sample of otters with DCM had significantly lower concentrations of myocardial L-carnitine than control and myocarditis case otters.

Conclusions and Clinical Relevance—Cardiac disease is an important cause of death in southern sea otters. Domoic acid toxicosis and infection with S neurona are likely to be 2 important causes of myocarditis in sea otters. Domoic acid–induced myocarditis appears to progress to DCM, and depletion of myocardial L-carnitine may play a key role in this pathogenesis. (Am J Vet Res 2005;66:289–299)

Full access
in American Journal of Veterinary Research
in Journal of the American Veterinary Medical Association