The prevalence and intensity of Cryptosporidium infection were examined in 445 Holstein calves at 10 dairy farms in western Washington, near Seattle. Fifty-one percent (176) of calves in the 7- to 21-day-old age group (n = 342) were positive for oocysts in the feces by carbolfuchsin staining. Prevalence and intensity of infection were highest in calves 8 to 14 days old; prevalence was 60% in this group, and 48% of the Cryptosporidium-positive calves had oocyst shedding at a 4+ level. A seasonal pattern in prevalence was not evident.

Fifty-five dogs, naturally infected with Taenia sp or Dipylidium caninum or both, were assigned to the following treatment groups for dose titration studies with epsiprantel: nonmedicated control dogs (n = 14), medicated dogs given a dosage of 2.75 mg/kg of body weight (n = 15), medicated dogs given a dosage of 5.5 mg/kg (n = 16), and medicated dogs given a dosage of 8.25 mg/kg (n = 10). Medication was given orally in a tablet formulation. Feces were examined for cestodes passed and the gastrointestinal tract was examined at necropsy for retained cestodes. Efficacy of epsiprantel was 92.9% against Taenia and 44.8% against Dipylidium for a dosage of 2.75 mg/kg, 100% against Taenia and 99.8% against Dipylidium for a dosage of 5.5 mg/kg, and 94.6% against Taenia and 100% against Dipylidium for a dosage of 8.25 mg/kg. For dose confirmation, 36 dogs naturally infected with Taenia sp or D caninum or both were allotted to 2 treatment groups: nomedicated control dogs (n = 16) and dogs medicated with epsiprantel at a dosage of 5.5 mg/kg (n = 20). Efficacy was 100% for both Taenia sp and D caninum.

Eighteen female Holstein calves, raised as natural herd additions under conditions typical of a well-managed midwestern United States dairy farm, were used in a natural-exposure study to determine the anticoccidial efficacies of lasalocid and decoquinate. Calves were allotted to 6 treatment blocks of 3 calves each as they were weaned. Within each block, calves were randomly assigned to be given either lasalocid or decoquinate or to remain as a nonmedicated control. Calves were given medication for 90 days and remained separated from other calves for 120 days. Adjusted weight gains were consistently greater in calves that were given medication; however, differences were not statistically significant. Fecal specimens were obtained from calves at weekly intervals during the study. Overall, oocyst shedding was low. During the medication period, quantitative mean fecal shedding of oocysts was reduced eightfold in calves given decoquinate and fourfold in calves given lasalocid, as compared with nonmedicated control calves. During the period following the medication period, calves that had been controls shed fewer oocysts than did calves that had previously been given medication. A pairwise comparison of the proportion of specimens that were oocyst-positive was made to assess qualitative oocyst shedding among treatment groups. During the medication period, qualitative oocyst shedding (all species, Eimeria bovis, E zuernii, species other than E bovis and E zuernii) was greater in controls than in either lasalocid-or decoquinate-treated groups. Likewise, lasalocid-medicated calves shed oocysts more frequently than did the decoquinate-medicated group. After medication, qualitative findings were reversed. Little diarrhea was noticed in treatment or control calves during the study. However, calves given either lasalocid or decoquinate had glossier coats and a healthier appearance by the end of the medication period than did nonmedicated controls. It was concluded that, under the exposure conditions of the study, trends in weight gain and oocyst shedding patterns approximated those resulting from previous studies that used experimental inoculation of oocysts.

The minimal inhibitory concentrations (MIC) of sulfonamides were determined against Bordetella bronchiseptica (n = 10), Pasteurella multocida (n = 10), Haemophilus pleuropneumoniae (n = 20), and Streptococcus suis (n = 10) strains isolated from pigs with atrophic rhinitis, pneumonia, or meningitis. Sulfonamides tested in an agar dilution method were sulfachloropyridazine, sulfadiazine, sulfadimethoxine, sulfamethazine, sulfadoxine, sulfisoxazole, sulfamerazine, sulfamethoxazole, sulfamethoxypyridazine, sulfanilamide, sulfatroxazole, and sulfisomidine. Results indicated that monotherapy of S suis infections with sulfonamides should not be encouraged because the MIC50 of all sulfonamides investigated was greater than 32 microgram/ml. The MIC50 of the sulfonamides against B bronchiseptica ranged from 0.5 to 8 migrogram/ml, against P multocida from 2 to 32 microgram/ml, and against H pleuropneumoniae from 8 to 64 microgram/ml. The MIC50 of sulfachloropyridazine, sulfadiazine, sulfadimethoxine, sulfamerazine, and sulfamethoxazole for the gram-negative bacteria did not exceed 16 microgram/ml. Among these compounds, sulfamethoxazole had the highest activity. The frequently prescribed sulfamethazine had an overall low antimicrobial activity.

The effects of single IV administered doses of dexamethasone on response to the adrenocorticotropic hormone (ACTH) stimulation test (baseline plasma ACTH, pre-ACTH cortisol, and post-ACTH cortisol concentrations) performed 1, 2, and 3 days (experiment 1) or 3, 7, 10, and 14 days (experiment 2) after dexamethasone treatment were evaluated in healthy Beagels. In experiment 1, ACTH stimulation tests were carried out after administration of 0, 0.01, 0.1, 1, and 5 mg of dexamethasone/kg of body weight. Dosage greater than or equal to 0.1 mg of dexamethasone/kg decreased pre-ACTH plasma cortisol concentration on subsequent days whereas dosages greater than or equal to 1 mg/kg also decreased plasma ACTH concentration. Treatment with 1 or 5 mg of dexamethasone/kg suppressed (P less than 0.05) post-ACTH plasma cortisol concentration (on day 3 after 1 mg of dexamethasone/kg; on days 1, 2, and 3 after 5 mg of dexamethasone/kg). In experiment 2, IV administration of 1 mg of dexamethasone/kg was associated only with low (P less than 0.05) post-ACTH plasma cortisol concentration in dogs on day 3. In experiment 2, pre-ACTH plasma cortisol and ACTH concentrations in dogs on days 3, 7, 10, and 14 and post-ACTH plasma cortisol concentration on days 7, 10, and 14 were not affected by dexamethasone administration. The results suggest that, in dogs a single IV administration. The results suggest that, in dogs, a single IV administered dosage of greater than or equal to 0.1 mg of dexamethasone/kg can alter the results of the ACTH stimulation test for at least 3 days. The suppressive effect of dexamethasone is dose dependent and is not apparent 7 days after treatment with 1 mg of dexamethasone/kg. The magnitude of the decrease in post-ACTH plasma cortisol concentration did not exceed 35% (compared with control values), regardless of the dose of dexamethasone used.

Urinary protein loss was determined in 12 healthy cats. Voided urine was collected and protein quantitated by the Coomassie blue method. Mean protein loss for all cats was 12.65 mg/kg24 h (5.45 SD). Protein loss for male cats (n=6) was 16.62 mg/kg24 h (3.3 SD), which was significantly different (P less than 0.01) from 8.69 mg/kg/24 h (4.09 SD) for females (n = 6). A single urine protein-creatinine ratio correlated well with the total urinary protein loss in mg/kg/24 h. The correlation coefficient for the protein-creatinine ratio in voided urine (UPCV) vs 24-hour urinary protein (UP-24) loss was 0.968, and that for the protein-creatinine ratio in urine obtained by cystocentesis (UPCC) vs UP-24 was 0.945. The regression equations were UPCV = 0.02145 + 0.02338 x UP-24 (mg/kg), and UPCC = 0.02667 + 0.02133 x UP-24 (mg/kg). Using the mean value plus 3 SD of urinary protein loss from the healthy cats in this study, a healthy cat would be expected to have a urinary protein loss of less than 29 mg/kg/24 h. A protein-creatinine ratio from a single urine sample provides an accurate estimate of urinary protein loss in healthy cats.

We evaluated the hemodynamic effects of IV and intraaortic (aortic root) administation of 7.5% NaCl solution on hemodynamic in anesthetized cats with severe hypovolemia. Hypovolemic shock was induced by exsanguinating cats to a mean arterial blood pressure of 50 mm of Hg, which was maintained for 30 minutes prior to treatment. Shed blood volume was 38.4 +/- 2.1 ml/kg of body weight. The cats were treated with a small volume (4 ml/kg) of 0.9% NaCl solution IV, 7.5% NaCl solution IV, or 7.5% NaCl solution administered into the aortic root. The IV administration of 0.9% NaCl aolution did not improve hemodynamics. The IV administration of 7.5% NaCl solution induced rapid restoration of arterial blood pressure, aortic blood flow, and cardiac contractility. Total peripheral vascular resistance decreased. The administration of 7.5% NaCl solution into the aortic root induced a further deterioration in hemodynamics resulting in death in 3 cats and a marked improvement in hemodynamics similar to that observed after IV administration of 7.5% NaCl solution in 2 cats. The duration of the beneficial hemodynamic effects after IV or intra-aortic administration of 7.5% NaCl solution did not exceed 60 minutes. Results of these studies suggested that either the IV or intra-aortic administration of 7.5% NaCl solution in cats can induce beneficial hemodynamic effects that may be of value in the field resuscitation of hypovolemic patients.

Six adult specific-pathogen-free cats were inoculated intraperitoneally with a cell culture-adapted strain of feline infectious peritonitis virus. Plasma samples were evaluated for antithrombin-III (AT-III) activities at post-inoculation days (PID) 0,4, and 11 and at termination on PID 16 (1 cat) or 21 (5 cats). Other hemostatic values evaluated were activated partial thromboplastin times, pro-thrombin times, thrombin times, fibrinogen, platelet counts, and fibrin/fibrinogen degradation products. Antithrombin-III activity remained within normal or above normal range (89 to 246%) in all cats, with the exception of one cat on Pid 4, 11, and 16 or 21 was 98, 162, and 130%, respectively. On PID 4 and 16 or 21, results of coagulation screening tests indicated that all cats had disseminated intravascular coagulation. Histologically, cats also had severe fibrinonecrotizing thrombovasculitis.

Nucleic acid hybridization, bacteriologic culture, and a fluorescent antibody test were compared for detection of Leptospira interrogans serovar hardjo type hardjo-bovis in bovine urine. Seventy-five urine samples were collected from pregnant cows challenge exposed with type hardjo-bovis. Twenty samples were collected from steers not exposed to hardjo-bovis. Sediments from each sample were examined, using fluorescent antibodies and a repetitive sequence element nucleic acid probe, to detect the presence of leptospires. Urine samples were processed for bacteriologic culture, using standard techniques. Under laboratory conditions typically used for these techniques, leptospires were detected in 60 of 75 urine samples from challenge exposed cows by nucleic acid hybridization, in 24 samples by fluorescent antibody test, and in 13 samples by bacteriologic culture. Leptospires were not detected in the urine of steers not exposed to hardjo-bovis.

The arrhythmogenic dose of epinephrine (ADE) was determined in heartworm-infected and noninfected (control) dogs during thiamylal-induced and halothane-maintained anesthesia to assess the myocardial sensitization. The ADE in heartworm-infected dogs (2.42 +/- 0.26 micrograms/kg of body weight) was significantly lower than that for the controls (3.36 +/- 0.29 micrograms/kg). After 2 weeks, ADE was determined again in these dogs after atropine treatment. Atropine treatment lowered the ADE to 1.76 +/- 0.33 micrograms/kg and 1.77 +/- 0.19 micrograma/kg in heartworm-positive and negative dogs, respectively. After 2 weeks more the ADE was determined after administration of prazosin, an alpha 1-antagonist. Only 2 of 6 controls and 3 of 6 heartworm-positive dogs had arrhythmias after a threefold increase of ADE. The mean ADE in the dogs that responded to treatment were 7.4 micrograms/kg and 7.2 micrograms/kg for heart worm-positive and negative dogs, respectively. The findings of this study indicated that ADE in heartworm-infected dogs were lower than those in the control dogs, which makes the heartworm-infected dogs more vulnerable to arrhythmia during anesthesia. Atropine did not protect the dogs of either group. However, prazosin protected the dogs of both groups by significantly increasing the threshold of the ADE. On the basis of our findings, to reduce the risk of arrhythmia, we suggest that routine screening of dogs for heartworm infection be done before anesthetics are used.