A study was undertaken to estimate the role of the liver in digoxin metabolism and excretion in dogs with experimental cholestasis. Eighteen dogs were divided into 3 groups: a control group (C) of sham operation, a group (L) ligation of the common bile duct, and a group (P) of ligation of the common bile performed 2 weeks after phenobarbital treatment. They were injected intravenously of with a single dose of digoxin. Plasma digoxin (PD) concentrations were measured by radioimmunoassay. Pharmacokinetic parameters were calculated by least square regression analysis. The PD concentration time curve for individual subjects and for mean data was best described by the sum 2 exponents. The mean correlation coefficients between the measured and calculated digoxin value were 0.997 or more, indicating an excellent fit, in each group. In group C, the mean biological half-life of PD (T1/2β) was about 20 hours. The distribution volume estimated by extrapolation was 6.6 l/kg. Calculated by the area under the PD concentration curve, the volume was 9.4 l/kg. There was on significant difference among the 3 groups in the PD concentration at any time. Plasma elimination rate of digoxin, however, tended to be delayed in group L. Phenobarbital pretreatment increased the activity of hepatic microsomal enzymes, shortened the T1/2β, and decreased the distribution volume. In no pharmacokinetic parameters was there a significant difference between groups C and P. These results suggest that the liver may affect digoxin pharmacokinetics in the dog. The liver may be affected less than the kidney. In clinical situations, precaution should be taken when digoxin is administered to dogs with cholestasis or other hepatic disorders.
A total of 29 cows that were +++ by the California Mastitis Test Hokurikushijo method (CMT) were subjected to the bromophenol blue filter paper methods. Of them, 10 were found acute mastitis and 19 latent or chronic mastitis. The former were treated with antibiotics. The latter were not treated but milked by an improved methos. Two month later of the former and 6 of the latter were mitigated. It was considered that this methods was effective to diagnose mastitis, especially during the milking period.
A long-term survey was carried out to detect bovine rotavirus and K99+Escherichia coliin diarrheic calves on a closed beef cow-calf farm during two calving seasons. Rotavirus was detected in the feces of 18 of 25 (72.0%) calves in March and April, 1983 and in 15 of 51 (29.4%) in the same months of 1984. K99+Escherichia coliwas detected in the feces of 24 of 51 (47.1%) calves under 2 days old examined in February to April, 1984. All, the isolated bacteria were ST-and LT-and their Oserotype was 20A. Therefore, on the farm, calf diarrhea associated with the viral and bacterial infections was related to time and age, respectively.
For dissolution. of an unusual absorbance appearing in enzyme-linked immunosorbent assay (ELISA) for the diagnosis of Aujeszky's sidease in swine, kaolin and acetone treatment were compared in the microplate method. As a result, the optical density of microplate _kaolin treatment was around zero in serum neutralization test (SNT) negative sera. The microplate kaolin treatment was found to be useful to remove false positive reactions in ELISA.
Seventy-six puppies 2-4 months old were examined for parasitic helminths in Kanagawa Prefecture over a period from November, 1984 to March, 1985. All of them were killed to recover parasitic helminths after their EPG and EPD were calculated. Of them, fifty-eight (76.3%) were positive for the following species of helminths, incidence rates being in parentheses: Spirometra erinacei (1.3%), Dipylidium caninum (17.1%), Taenia pisiformis (1.3%), Trichuris vulpis (10.5%), Toxocara canis (68.4%), andAncylostoma caninum (1.3%). The number ofT. canisorganisms obtained from one dog ranged from 1 to 28 with an average of 8.5., while those ofD. caninumandT. vulpisorganisms exceeded one hundred in some puppies. The number ofT. caniseggs excreted into the feces was much larger than that ofA. caninumorT. vulpiseggs.
The in vitro sensitivity test to 16 drugs was conducted on 112 strains of Mycoplasma gallisepticum (MG) and 23 strains of Mycoplasma synoviae (MS). These strains had been isolated from the respiratory organs and joints of 53 broiler chickens (on 26 farms) and of 82 layer chickens (on 48 farms) over a period of 1979 through 1985. As a result, the MG strains were highly sensitive to tetracycline antibiotics (DOXY, TC, OTC) and DFZ, followed by CTC, CP and SPCM. Of them, 7 strains (15.2%) from 46 broiler chickens and 38 strains (59.1 %) from 66 layer chickens were resistant to macrolide antibiotics (EM, OL, SPM, TS) and LCM. The isolation rate of macrolide-resistant strains increased in layer chickens as they got older. The MS strains were highly sensitive to tetracycline antiviotics (DOXY, TC, OTC), TS and DFZ, followed by CTC, LCM, SPM, SPCM and CP. They were poorly sensitive to any other drugs.
In October, 1985, 2 piglets approximately 50 days old showed high fever, swelling of the leg joints and listlessnes on a farm in the Matsumoto area. At autopsy, one of them exhibited a large quantity of yellowish fibrinous exudate in the thoracic and abdominal organs and abundant synovial fluid in the Ieg joints. Purulent fibrinous polyserositis was observed.Haemophilus parasuiswas purely isolated from main organs, exudate and synovial fluid. The isolate was determined as setroype 5 by the gel diffusion method and as PAGE type II by SDS-polyacrylamide gel electrophoresis. In conclusion, the present case was diagnosed as Glasser's disease.
A 30-day-old calf died suddenly on a farm in July, 1982. At necropsy, it revealed severe hemorrhage in the small intestine. Histologically, the mucous membrane of the small intestine presented necrotic enteritis, growth of rods and a large number of coccidial gametes. Toxin from the jejunal contents was proved by inoculation to mice. Toxigenic Clostridium perfringens Type A (108 CFU/g) was isolated. The disease was diagnosed as enterotoxemia caused by C. perfringens Type A. It may have been induced by coccidial infection.