The normal blood supply to the canine mandible and mandibular teeth was determined by microangiography and correlated histology. Branches of the inferior alveolar artery supplied the cortical bone of the mandibular body. Vessels from the periosteal and endosteal surfaces supplied symphyseal cortical bone. Direct vascular anastomoses were not found to cross the fibrous mandibular symphysis. Blood supply to the mandibular teeth was via dental arteries derived from the inferior alveolar artery, with interdental and interradicular arteries supplying the alveolar bone and periodontal ligament.

In addition to the 3-striped blister beetles (Epicauta temexa and E occidentalis), other sources of equine cantharidin toxicosis were identified at the Texas Veterinary Medical Diagnostic Laboratory and included E albida and E attrivittata and the previously incriminated E pardalis and E pennsylvanica. Improved methods for diagnosing cantharidin or blister beetle toxicosis involve partial purification of urine and gastric content extracts, using silica cartridges, followed by analysis, using capillary gas chromatography/mass spectrometry. During a 26-month period, 53 episodes of cantharidin toxicosis in horses were confirmed at our diagnostic laboratory. Concentrations of cantharidin in urine and gastric contents ranged from 0.0003 to 3.50 microgram/g. Peak incidences were observed in late summer and early fall.

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.

Serum vitamin E and blood glutathione peroxidase values were determined in 40 horses with a histologically confirmed diagnosis of degenerative myeloencephalopathy and in 49 age-matched control horses with normal neurologic function. Significant differences were not detected in serum vitamin E or blood glutathione peroxidase values between horses affected with degenerative myeloencephalopathy and control horses. These findings fail to support a reported role of vitamin E deficiency as a cause of equine degenerative myeloencephalopathy.

Twelve male cats were fed 2 diets that differed in the source of P. In diet 1 (1.4% P), 62.7% of P originated from poultry, meat, and fish meal, and the remainder from other organic ingredients of food. In diet 2 (1.6% P), 63.5% of P was derived from neutral monobasic/dibasic salts, and the remainder from other organic ingredients of the food. The P intake was nearly the same with both diets, but there was a significant (P less than 0.05) difference between diets in the percentage of ingested P that was excreted in the urine (14.7 +/- 5.3% for diet 1; 34.9 +/- 8.4% for diet 2), and in 6-day urinary P excretion (774 +/- 290 mg for diet 1; 2,004 +/- 556 mg for diet 2). The P concentrations in urine samples obtained by cystocentesis after cats ate were significantly (P less than 0.05) higher when cats were fed diet 2 than when those same cats were fed diet 1. Plasma P concentrations increased after ingestion of diet 2, but were unchanged after ingestion of diet 1. Seemingly, urinary excretion of P was markedly influenced by dietary composition. Diets with the same P content have potential for different biologic effects because of differences in availability of P.

Serum trypsinogen concentration was studied in 6 adult mixed-breed dogs randomly fed diets containing 6.8, 31.4, or 39.7% protein (dry weight) for 3 weeks each. Blood was collected on days 20, 21, and 22 of each feeding period, and serum trypsinogen concentrations were determined by radioimmunoassay of trypsin-like immunoreactivity (TLI). Mean serum TLI concentrations for each dog fed each diet were compared. A significant (P < 0.05) positive linear relationship (P < 0.02) was determined between serum TLI concentrations and the percentage of dietary protein. Mean serum TLI concentrations for each dog fed all diets ranged from 5.7 to 20.2 microgram/L.

Ten Holstein heifers were fed a selenium-deficient (SeD) diet (0.04 mg of Se/kg on a total ration dry-matter basis) 3 months before calving and throughout their first lactation. A selenium-supplemented (SeS) diet (2 mg of Se/head/d) was fed to a group of 10 heifers. In about the 14th week of lactation, the cows were challenge-exposed to Escherichia coli by administering 15 to 40 colony-forming units (CFU) into 1 mammary gland. Selenium concentration microgram/ml) in blood around the time of challenge exposure was 0.033 +/-0.002 (mean +/- SEM) in SeD and 0.132 /-0.006 in SeS cows. Infections were established in all challenge-exposed quarters. The frequency of quarter atrophy and agalactia, and reduction in whole-udder milk yield in the first 4 days after challenge exposure, were greater (P < 0.05) in the SeD cows. Log10 peak bacterial concentrations in milk were higher (P < 0.05) in SeD (7.63 +/- 0.34 CFU/ml) than in SeS cows (5.57 0.66 CFU/ml). Mean log bacterial concentration was significantly higher (P < 0.05) from 12 to 20 hours after challenge exposure in SeD than in SeS cows. Duration of infection was significantly greater (P < 0.05) in SeD (162.0 +/- 12.0) than in SeS cows (114.4 +/- 18.0 hours). Milk somatic cell counts increased significantly more slowly (P < 0.05) in SeD than in SeS cows from 8 to 16 hours after challenge exposure. Ratios of milk somatic cells to bacteria in milk were significantly lower (P < 0.05) in SeD than in SeS cows at l2 and 16 hours after challenge exposure.

Phagocytic and oxidative metabolic activities of bovine blood neutrophils were determined in the presence of glycolytic (NaF) and cytoskeletal (colchicine, cytochalasin B, and prostaglandin E1) inhibitors. Phagocytosis and postphagocytic oxidative metabolic activity, measured by nitroblue tetrazolium reduction, were determined using zymosan, Escherichia coli, Staphylococcus aureus, or Streptococcus agalactiae. Sodium fluoride (1.25 micromolar to 1.25 mM concentrations) did not significantly (P greater than 0.05) inhibit phagocytosis of S aureus and Str agalactiae, whereas phagocytosis of zymosan and E coli was significantly (P less than 0.05) inhibited only at 1.25 mM concentration. Colchicine at 1.25 nM to 1.25 micromolar conce ntrations significantly inhibited phagocytosis of zymosan and E coli, but not of S aureus and Str agalactiae. Cytochalasin B at 1.25 nM to 1.25 micromolar concentrations significantly inhibited phagocytosis of zymosan and all 3 bacteria, whereas prostaglandin E1 was noninhibitory at similar concentrations. Nitroblue tetrazolium reduction, in general, was not significantly affected by NaF and cytoskeletal inhibitors.

Twenty-one mixed-breed pony foals, reared and maintained under parasite-free conditions, were used to test the efficacy of ivermectin in oral drench and paste formulations (200 microgram/kg) against 11-day-old migrating larvae of Parascaris equorum. Three replicates of 4 foals and 3 replicates of 3 foals were formed on the basis of age. Foals in replicates of 4 were randomly allocated to be indicators, or to receive vehicle (control) or ivermectin paste or ivermectin liquid. Foals in replicates of 3 were randomly allocated to receive vehicle or ivermectin paste or ivermectin liquid. The recovery of larvae from the lungs, liver, and small intestines of the indicator foals showed that 99.9% of the larvae were in the lungs 11 days after inoculation (day 0 of treatment). The recoveries of larvae from lungs and small intestines of controls at 25 days after inoculation indicated that all larvae had migrated to the small intestine by this time. The mean length of larvae recovered from the lungs (11 days after inoculation) was 0.87 mm; the mean length of those recovered from the small intestine (25 days after inoculation) was 3.65 mm. Using larvae recovered from small intestinal contents for calculations, ivermectin in both formulations was 100% effective against 11-day P equorum (P less than 0.01, compared with control group geometric mean of 1498.4).

The uptake of colostral IgG and IgM, their serum half-lives, and the rates of endogenous synthesis of IgG and IgM were evaluated in 6 newborn foals fed bovine colostrum (principals) and 6 foals allowed to suckle their dams (controls). The principal foals were fed 400 ml of bovine colostrum (IgG, 10,000 mg/dl and IgM, 200 mg/dl) at 2-hour intervals, from 2 to 20 hours after foaling (total dose, 4 L). Serum IgG and IgM concentrations were determined by single radial immunodiffusion from birth to 98 days of age. At foaling, principal foals had no detectable serum equine IgG, but 1 control foal had serum equine IgG of 185 mg/dl. AFter ingestion of colostrum, there was no significant difference in the maximal serum bovine IgG concentration (range, 1,350 to 3,300 mg/dl) in the principal foals, and maximal serum equine IgG concentration (range, 500 to 6,000 mg/dl). The calculated biological bovine and equine IgG half-life in the principal and control groups was 9.4 and 26 days, respectively. Endogenous IgG synthesis was first detected in 1 principal foal at 3 days of age, but was detected first between 28 and 42 days in the other principal foals. Starting on day 56 there was no significant difference in serum equine IgG concentration between groups. At foaling, foals in both groups had low equine IgM concentrations. In the control foals, there was marked individual variation in the increases in equine IgM concentration (range, 5 to 73 mg/dl) after ingestion of colostrum. With the exception of day 49 after foaling, there was no statistical difference between groups for serum IgM concentration after day 3, and both groups had parallel rates of IgM synthesis. Bovine IgM was undetectable at foaling and maximal serum concentration ranged from 200 to 350 mg/dl following ingestion of colostrum. The calculated bovine and equine IgM half-lives were 8 and 5 days, respectively. The coefficients of absorption of bovine IgG and IgM were 30.9 and 84, respectively, in the principal foals. In the control foals, the coefficient of absorption of equine IgG and IgM was 35 and 30, respectively. One principal foal was excluded from the study because it died of aspiration pneumonia at 2 days of age.