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
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
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:
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.
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.
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)