Search Results

Abstract

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)

Abstract

Case Description—A 10-year-old Lipizzaner stallion was evaluated over the course of 1.5 years because of intermittent, recurrent colic.

Clinical Findings—The horse was initially treated medically for gastric ulcers; dietary changes were made, and a deworming protocol was instituted, without resolution of colic episodes. Subsequently, the horse underwent exploratory celiotomy and a large colon volvulus was identified with diffuse colonic wall thickening. A pelvic flexure biopsy sample was submitted for histologic examination, which revealed lymphocytic (CD3-positive T cells) myenteric ganglionitis (MG). The horse developed a cecal impaction after surgery, which did not resolve, despite aggressive medical management; subsequently a complete cecal bypass was performed. Cecal and colonic wall biopsy samples were evaluated histologically and confirmed the diagnosis of MG. After surgery, the horse developed a large colon impaction, which initially responded to aggressive medical treatment, and the horse was discharged.

Treatment and Outcome—Despite rigorous feed restrictions and prokinetic and corticosteroid treatment, the horse continued to have signs of colic and was euthanized 3 weeks after discharge from the hospital because of a recurrent large colon impaction. Intestinal biopsy samples obtained at the time of death revealed chronic changes in intramural ganglia consistent with generalized MG.

Clinical Relevance—MG is a rare disease in horses, causing gastrointestinal motility dysfunction and signs of colic, which is challenging to diagnose and treat successfully. Further studies are needed to identify the etiology of this disease and to explore treatment options.

Abstract

Objective—To determine the effects of meloxicam on values of hematologic and plasma biochemical analysis variables and results of histologic examination of tissue specimens of Japanese quail (Coturnix japonica).

Animals—30 adult Japanese quail.

Procedures—15 quail underwent laparoscopic examination of the left kidneys, and 15 quail underwent laparoscopic examination and biopsy of the left kidneys. Quail in each of these groups received meloxicam (2.0 mg/kg, IM, q 12 h; n = 10) or a saline (0.9% NaCl) solution (0.05 mL, IM, q 12 h; control birds; 5) for 14 days. A CBC and plasma biochemical analyses were performed at the start of the study and within 3 hours after the last treatment. Birds were euthanized and necropsies were performed.

Results—No adverse effects of treatments were observed, and no significant changes in values of hematologic variables were detected during the study. Plasma uric acid concentrations and creatine kinase or aspartate aminotransferase activities were significantly different before versus after treatment for some groups of birds. Gross lesions identified during necropsy included lesions at renal biopsy sites and adjacent air sacs (attributed to the biopsy procedure) and pectoral muscle hemorrhage and discoloration (at sites of injection). Substantial histopathologic lesions were limited to pectoral muscle necrosis, and severity was greater for meloxicam-treated versus control birds.

Conclusions and Clinical Relevance—Meloxicam (2.0 mg/kg, IM, q 12 h for 14 days) did not cause substantial alterations in function of or histopathologic findings for the kidneys of Japanese quail but did induce muscle necrosis; repeated IM administration of meloxicam to quail may be contraindicated.

Abstract

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)