Objective—To determine effects of long-distance racing exercise on iron status in endurance racing sled dogs, with or without anemia.
Design—Prospective cohort study.
Animals—114 dogs that participated in the 2007 Iditarod Trail Sled Dog Race (59 and 55 dogs that did or did not complete the race, respectively).
Procedures—Stored serum samples obtained from 85 endurance-racing sled dogs that were expected to participate in the race were used to establish study reference intervals and prerace group values for iron-related variables. Blood samples collected from 114 study dogs before (ie, baseline) and after participation in the race were used to determine PCV and serum total protein concentrations before and after racing and assess iron-related variables after racing.
Results—Mean values for PCV and serum total protein concentration were decreased after racing, compared with baseline values in the same dogs. Mean serum iron concentration was low, and mean serum ceruloplasmin and C-reactive protein (CRP) concentrations were high in dogs after racing, compared with prerace group values. Mean serum ferritin concentration was high in dogs that did not complete the race, compared with the prerace group value and that of dogs that finished the race; 4 of 113 (3.5%) study dogs had low ferritin concentrations (< 73 ng/mL) after racing, suggestive of possible iron deficiency.
Conclusions and Clinical Relevance—Decreased PCV and serum total protein concentrations were consistently detected, whereas iron deficiency appeared to be uncommon, in study dogs after race participation. High serum concentrations of ceruloplasmin and CRP after racing suggested that changes indicative of iron deficiency may be masked by inflammation. Alternatively, changes in serum iron and CRP concentrations may reflect a physiologic response.
Objective—To describe the character and frequency of causes of death and associated lesions in long-distance racing sled dogs.
Design—Retrospective case series.
Procedures—Medical records of dogs that died during or soon after competition in the Iditarod Trail sled dog races (1994 through 2006) were examined for findings of gross necropsy and histologic evaluation of tissue samples. From the data, descriptive and comparative statistics were obtained.
Results—Recognized causes of death included aspiration of gastric contents (n = 4), aspiration pneumonia (4), acute blood loss secondary to gastric ulceration (3), and sled dog myopathy (2). A cause of death was not established for 7 dogs. Prevalent lesions among the study population included rhabdomyolysis (n = 15), enteritis (10), gastritis (10), aspiration pneumonia (8), and gastric ulceration (8). All dogs with aspiration pneumonia had concurrent gastric mucosal lesions. Subjective biventricular cardiac hypertrophy was evident in most dogs; other lesions detected frequently included centrilobular hepatic fibrosis, gastric dilatation, and mild cardiac myodegeneration and necrosis.
Conclusions and Clinical Relevance—Unexpected death is a rare event among conditioned sled dogs during competition in endurance races. Potentially life-threatening conditions of dogs that are associated with periods of long-distance physical exertion include aspiration pneumonia, gastric mucosal lesions, and severe rhabdomyolysis. Dogs that develop clinical signs suggestive of these conditions should be excluded from strenuous activities. Epidemiologic investigations are required to clarify the risk for death associated with these lesions in dogs competing in endurance races.
Objective—To determine whether administration of
Crandell-Rees feline kidney (CRFK) cell lysates or vaccines
against feline viral rhinotracheitis, calicivirus,
and panleukopenia (FVRCP vaccines) that likely contain
CRFK cell proteins induces antibodies against
CRFK cell or feline renal cell (FRC) lysates in cats.
Animals—14 eight-week-old cats.
Procedure—Before and after the study, renal biopsy
specimens were obtained from each cat for histologic
evaluation. Each of 4 FVRCP vaccines was administered
to 2 cats at weeks 0, 3, 6, and 50. Between
weeks 0 and 50, another 3 pairs of cats received 11
CRFK cell lysate inoculations SC (10, 50, or 50 µg
mixed with alum). Clinicopathologic evaluations and
ELISAs to detect serum antibodies against CRFK cell
or FRC lysates were performed at intervals.
Results—Cats had no antibodies against CRFK cell
or FRC lysates initially. All cats administered CRFK
cell lysate had detectable antibodies against CRFK
cell or FRC lysates on multiple occasions. Of 6 cats
vaccinated parenterally, 5 had detectable antibodies
against CRFK cell lysate at least once, but all 6 had
detectable antibodies against FRC lysate on multiple
occasions. Cats administered an intranasal-intraocular
vaccine did not develop detectable antibodies
against either lysate. Important clinicopathologic or
histologic abnormalities were not detected during
Conclusions and Clinical Relevance—Parenteral
administration of vaccines containing viruses likely
grown on CRFK cells induced antibodies against
CRFK cell and FRC lysates in cats. Hypersensitization
with CRFK cell proteins did not result in renal disease
in cats during the 56-week study. (Am J Vet Res 2005;66:506–511)
Objective—To determine hepatotoxicity of stanozolol
in cats and to identify clinicopathologic and
histopathologic abnormalities in cats with stanozololinduced
Design—Clinical trial and case series.
Animals—12 healthy cats, 6 cats with chronic renal
failure, and 3 cats with gingivitis and stomatitis.
Procedures—Healthy cats and cats with renal failure
were treated with stanozolol (25 mg, IM, on the first
day, then 2 mg, PO, q 12 h) for 4 weeks. Cats with
gingivitis were treated with stanozolol at a dosage of
1 mg, PO, every 24 hours.
Results—Most healthy cats and cats with renal failure
developed marked inappetence, groomed less,
and were less active within 7 to 10 days after initiation
of stanozolol administration. Serum alanine transaminase
(ALT) activity was significantly increased in 14 of
18 cats after stanozolol administration, but serum
alkaline phosphatase activity was mildly increased in
only 3. Four cats with serum ALT activity > 1,000 U/L
after only 2 weeks of stanozolol administration had
coagulopathies; administration of vitamin K resolved
the coagulopathy in 3 of the 4 within 48 hours. All 18
cats survived, and hepatic enzyme activities were
normal in all cats tested more than 4 weeks after
stanozolol administration was discontinued. Two of
the 3 cats with gingivitis developed evidence of
severe hepatic failure 2 to 3 months after initiation of
stanozolol treatment; both cats developed coagulopathies.
Histologic evaluation of hepatic biopsy
specimens from 5 cats revealed diffuse hepatic lipidosis
and cholestasis without evidence of hepatocellular
Conclusions and Clinical Relevance—Results suggest
that stanozolol is hepatotoxic in cats. (J Am Vet
Med Assoc 2000;217:681–684)