Investigation of a combination of amiodarone and itraconazole for treatment of American trypanosomiasis (Chagas disease) in dogs.

OBJECTIVE: To evaluate clinical, serologic, parasitological, and histologic outcomes of dogs with naturally occurring Trypanosoma cruzi infection treated for 12 months with amiodarone and itraconazole. ANIMALS: 121 dogs from southern Texas and southern Louisiana. PROCEDURES: Treatment group dogs (n = 105) received a combination of amiodarone hydrochloride (approx 7.5 mg/kg [3.4 mg/lb], PO, q 24 h, with or without a loading dosage protocol) and itraconazole (approx 10 mg/kg [4.5 mg/lb], PO, q 24 h, adjusted to maintain a plasma concentration of 1 to 2 µg/mL) for 12 months. Control group dogs (n = 16) received no antitrypanosomal medications. Serologic assays for anti-T cruzi antibodies, PCR assays for T cruzi DNA in blood, and physical evaluations were performed 1, 6, 9, 12, and 24 months after study initiation. Adverse events were recorded. Outcomes of interest were recorded and compared between groups. RESULTS: 86 of 105 treatment group dogs and 8 of 16 control group dogs survived and completed the study (5/19 and 6/7 deaths of treatment and control group dogs, respectively, were attributed to T cruzi infection). Mean survival time until death attributed to T cruzi was longer (23.19 vs 15.64 months) for the treatment group. Results of PCR assays were negative for all (n = 92) tested treatment group dogs (except for 1 dog at 1 time point) from 6 to 24 months after study initiation. Clinical improvement in ≥ 1 clinical sign was observed in 53 of 54 and 0 of 10 treatment and control group dogs, respectively; adverse drug events were minor and reversible. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested efficacy of this trypanocidal drug combination for the treatment of T cruzi infection in dogs.

Platelet activation in a population of critically ill dogs as measured with whole blood flow cytometry and thromboelastography.

OBJECTIVE: To determine whether critically ill dogs had increased platelet activation and whether the proportion of activated platelets correlated with severity of illness. ANIMALS: 82 dogs in the intensive care unit of a veterinary teaching hospital and 24 healthy control dogs. PROCEDURES: Flow cytometry with monoclonal mouse anti-human CD61 and CD62 antibodies in resting and ADP-treated samples and kaolin-activated thromboelastography were used to compare platelet activation in blood samples of critically ill and control dogs. Serum antithrombin, von Willebrand factor, fibrinogen, and activated protein C concentrations; prothrombin time (PT); and activated partial thromboplastin time (aPTT) were measured. Revised survival prediction index, acute patient physiology and laboratory evaluation, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome scores were used to estimate severity of illness. Severity of illness scores and platelet activation measurements were compared with survival time and duration and cost of hospitalization. RESULTS: Critically ill and control dogs had no differences in platelet activation for non-ADP-treated samples measured. Critically ill dogs had significantly increased platelet activation in response to 2, 6, and 10 µM ADP. Critically ill dogs had significantly increased maximum amplitude, α angle, and global clot strength and significantly decreased clot formation time. Critically ill dogs had significantly increased fibrinogen concentration, PT, and aPTT and significantly decreased antithrombin concentration. Survivors and nonsurvivors had similar flow cytometry and thromboelastography values. Three dogs developed macrothrombosis. CONCLUSIONS AND CLINICAL RELEVANCE: In this study, critically ill dogs had hyperreactive platelets, which may have contributed to a high incidence of hypercoagulability in this patient population.

Septic pericarditis in a cat with pyometra.

OBJECTIVE: To describe a unique cause of septic pericarditis in a cat and detail the successful case management strategy. CASE SUMMARY: A 6-year-old sexually intact female Ragdoll cat was evaluated for a 7-day history of progressive lethargy, anorexia, and vaginal discharge. Thoracic radiographs revealed a markedly globoid cardiac silhouette and pleural effusion while the initial echocardiogram showed moderate volume pericardial effusion. Following pericardiocentesis, cytologic evaluation of the pericardial effusion revealed septic suppurative inflammation with intra- and extracellular Gram-negative rod-shaped bacteria. Abdominal ultrasound demonstrated a moderate amount of echogenic uterine fluid accumulation with a right-sided uterine horn mass. After stabilization with pericardiocentesis, IV fluid therapy and IV antimicrobials, the cat underwent ovariohysterectomy and partial pericardiectomy. Histopathology confirmed a diagnosis of pyometra and septic pericarditis. Uterine and pericardial fluid bacterial culture yielded Escherichia coli with identical antimicrobial sensitivity spectrums. NEW OR UNIQUE INFORMATION PROVIDED: Septic pericarditis is a rare cause of pericardial effusion in the cat. Previous reported cases have either suggested the cause to be secondary to transient bacteremia resulting from a local infection seeding the pericardium or for the cause to remain unknown. To the authors' knowledge, this is the first veterinary report of septic pericarditis resulting from hematogeneously spread bacteria originating from a urogenital infection. It is also the first report of successful surgical management of septic pericarditis in the cat.