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- Author or Editor: Allen R. Dillon x
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Abstract
Objective
To evaluate effect of alternate-day oral administration of prednisolone on endogenous plasma ACTH concentration and adrenocortical response to exogenous ACTH in dogs.
Animals
12 Beagles.
Procedure
Dogs were allotted to 2 groups (group 1, 8 dogs treated with 1 mg of prednisolone/kg of body weight; group 2, 4 dogs given excipient only). During a 30-day period, blood samples were collected for determination of plasma ACTH and Cortisol concentrations before, during, and after treatment with prednisolone. From day 7 to 23, prednisolone or excipient was given on alternate days. Sample collection (48-hour period with 6-hour intervals) was performed on days 1, 7, 15, 21, and 28; on other days, sample collection was performed at 24-hour intervals. Pre-and post-ACTH plasma Cortisol concentrations were determined on days 3, 9, 17, 23, and 30.
Results
A significant difference was detected between treatment and time for group 1. Plasma ACTH concentrations significantly decreased for 18 to 24 hours after prednisolone treatment in group-1 dogs. At 24 to 48 hours, ACTH concentrations were numerically higher but not significantly different in group-1 dogs. Post-ACTH plasma Cortisol concentration significantly decreased after 1 dose of prednisolone and became more profound during the treatment period. However, post-ACTH Cortisol concentration returned to the reference range 1 week after prednisolone administration was discontinued.
Conclusions and Clinical Relevance
Single oral administration of 1 mg of prednisolone/kg significantly suppressed plasma ACTH concentration in dogs for 18 to 24 hours after treatment. Alternate-day treatment did not prevent suppression, as documented by the response to ACTH. (Am J Vet Res 1999;60:698–702)
SUMMARY
To determine the drug dose required to inhibit platelet reactivity by at least 50%, 2 drug regimens were evaluated in heartworm-negative, heartworm-infected, and heartworm-infected dogs embolized with dead heart-worms. Aspirin, or a combination of aspirin and dipyridamole, were administered to 2 groups of Beagles (n = 5 each) for 5 to 9 days; a third group of 5 Beagles served as nontreated controls. For heartworm-negative dogs, mean (± sd) aspirin dosage that inhibited collagen-induced platelet reactivity by at least 50% was 6 (± 2) mg/kg of body weight given once daily. The aspirin/dipyridamole combination dosage was 1 mg of each drug/kg given every 12 hours. All dogs (n = 15) were implanted with 7 adult heartworms each and remedicated (or not treated) beginning at 21 days after heartworm implantation. In heartworm-infected dogs, mean aspirin dosage required to inhibit collagen-induced platelet reactivity ≥ 50% was 10 ( ± 6) mg/kg. Mean dosage of aspirin/dipyridamole combination was 1.6 ± (0.5) mg of each drug/kg given every 12 hours.
When platelet reactivity in response to collagen was determined to be inhibited by at least 50% in all medicated dogs, each dog (n = 15) was embolized with 7 dead adult heartworms to mimic heartworm adulticidal treatment. Platelet reactivity was monitored for 21 days after treatment, and drug dose was adjusted to maintain platelet inhibition by at least 50%. In embolized dogs, mean aspirin dosage was 17 (± 14) mg/kg given once daily. Mean dosage of the aspirin/dipyridamole combination was 2.8 (± 1.3) mg of each drug/kg given every 12 hours.
All dogs (n = 15) were euthanatized 21 days after heartworm embolization. Each lung lobe was evaluated for severity of lesions and presence of organized or fibrinous thrombi. Lesion severity in the aspirin- and aspirin/dipyridamole-treated dogs was not significantly different from that in control dogs.
SUMMARY
Ticlopidine hydrochloride was evaluated for its effectiveness in inhibiting platelet aggregation and serotonin release in 5 laboratory Beagles before and after heart-worm implantation with 7 adult Dirofilaria immitis, and after embolization with 7 dead heartworms to mimic what happens after heartworm adulticide treatment. Five other laboratory Beagles, similarly implanted and embolized with heartworms, were used as nonmedicated controls. During the heartworm-negative stage, the dosage of ticlopidine that inhibited adenosine diphosphate (adp)-induced platelet aggregation in 5 dogs by at least 50% after 5 days of treatment was 62 mg/kg of body weight once a day. In the same dogs implanted with 7 adult heartworms 21 days previously, mean (± sd) ticlopidine dosage required to obtain similar results was 71 (± 13) mg/kg given once daily. During the 21 days after dead heartworms were implanted in heartworm-infected dogs, mean ticlopidine dosage was 108 (± 35) mg/kg (range, 62 to 150 mg/kg). Ticlopidine treatment was associated with increased platelet numbers in all 5 dogs during the heartworm-negative stage and in 4 of 5 dogs during the heartworm implantation and heartworm embolization stages. Mean platelet volume tended to decrease as platelet numbers increased. At necropsy, gross and histologic pulmonary lesions were less severe in ticlopidine-treated dogs than in nonmedicated control dogs.
Objective—
To document hepatozoonosis in dogs from Alabama and Georgia and to report associated clinical signs, method of diagnosis, response to treatment, and course of disease.
Design—
Retrospective case series.
Animals—
22 dogs in which Hepatozoon canis was identified by microscopic examination of skeletal muscle.
Procedure—
We reviewed medical records of all dogs with a definitive diagnosis of hepatozoonosis that were referred to the Auburn University Small Animal Clinic between 1989 and 1994.
Results—
Diagnoses were confirmed by microscopic identification of H canis schizont or merozoite stages in skeletal muscle. The gametocyte stage was not detected in smears of blood obtained from a peripheral vein, buffy-coat smears, or bone marrow evaluation. Common clinical signs included fever, cachexia, ocular discharge, pain, stiffness, and paresis. Laboratory abnormalities included marked leukocytosis, hypoglycemia, hypoalbuminemia, mild anemia, hyperphosphatemia, and high alkaline phosphatase activity. Periosteal bone proliferation was evident radiographically in 18 of 22 dogs. Renal lesions included amyloidosis (1 dog), interstitial nephritis (3), and mesangioproliferative glomerulonephritis (4). Treatment with the anticoccidial drug toltrazuril, despite an initial favorable response, failed to prevent relapse in all but 3 of 21 treated dogs. Mean survival time was 12.6 ± 2.2 months, with a mean time of remission before recurrence of clinical signs of 6 months.
Clinical Implications—
H canis infection in dogs can be associated with a distinct clinical syndrome that involves chronic myositis, debilitation, and death. The dogs of this report represent the first substantial number of domestic dogs naturally infected with H canis in the United States outside of the Texas Gulf Coast. Hepatozoon canis appears to be a serious pathogen in the United States that is becoming more widespread geographically. (J Am Vet Med Assoc 1997;210:916–922)
Abstract
Objective—To determine clinical and pathologic findings before and after short-term (group 1) and longterm (group 2) treatment in dogs with Hepatozoon americanuminfection.
Design—Retrospective study.
Animals—53 dogs with H americanuminfection.
Procedure—Medical records of dogs that were treated for hepatozoonosis diagnosed on the basis of meront or merozoite stages in skeletal muscle were reviewed.
Results—Circulating gametocytes of H americanum were identified in 12 of 53 dogs. Dogs were treated with various drugs, including toltrazuril, trimethoprimsulfadiazine, clindamycin, pyrimethamine, and decoquinate. Mean WBC counts prior to treatment were 85,700 and 75,200 cells/µl in groups 1 and 2, respectively, and 1 month after initiation of treatment were 12,600 and 14,600 cells/µl, respectively. Initial response to treatment was excellent in all dogs. Twenty-three of 26 dogs in group 1 relapsed at least once and died within 2 years; mean (± SD) survival time was 12.6 ± 2.2 months. Twenty-two of 27 group-2 dogs survived; 11 dogs had no clinical signs and were still receiving decoquinate (mean duration of treatment, 21 months), 11 dogs had no clinical signs after treatment for 14 months (range, 3 to 33 months; mean survival time, 39 months [range, 26 to 53 months]), 2 dogs were lost to follow-up, and 3 dogs were euthanatized because of severe disease.
Conclusions and Clinical Relevance—Although no treatment effectively eliminated the tissue stages of H americanum, treatment with trimethoprim-sulfadiazine, clindamycin, and pyrimethamine followed by long-term administration of decoquinate resulted in extended survival times and excellent quality of life. ( J Am Vet Med Assoc 2001;218:77–82)
