A controlled test was performed to titrate the anthelmintic dosage of dienbendazole in 24 mixed-breed ponies naturally infected with Strongylus vulgaris, S edentatus, and small strongyle species, as determined by parasitic egg and larval counts in feces. Comparison of results of treatment was made among 3 dienbendazole dosages--2.5, 5, and 10 mg/kg of body weight-and a gum (excipient) mixture given by nasogastric intubation. All ponies were euthanatized and necropsied at 7 or 8 days after treatment. Trichostrongylus axei, Habronema muscae, S vulgaris, S edentatus, small strongyles, and Oxyuris equi were efficaciously eliminated in response to all doses of dienbendazole; Gasterophilus spp were not affected by any dose. There were not sufficient numbers of Draschia megastoma, Anoplocephala spp, or Parascaris equorum in the ponies to evaluate drug effect. Changes in the appearance of the intestinal lining were dose-dependent; in the ponies treated with 5 and 10 mg of dienbendazole/kg, the mucosa appeared clean and smooth, though in ponies given 2.5 mg/kg, it appeared clean, but was nodular and moderately reactive to embedded immature small strongyles. In the gum mixture-treated ponies, the large intestinal mucosa was inflamed, with edematous areas, in response to infections caused by large and small strongyles. A limited clinical titration was done in 12 ponies that were fecal culture negative for S vulgaris larvae, although other strongyles were detected. Two ponies in each of 6 groups were given the following dosages: 0 (gum mixture only), 0.5, 1, 2.5, and 5 mg of dienbendazole/kg. One group of 2 ponies was given 5 mg of fenbendazole/kg as a standard treatment control. On the basis of pre- and posttreatment fecal examinations (for egg and larval counts), dienbendazole at dosages that ranged from 1 to 5 mg/kg was highly effective and as effective as fenbendazole given at a dosage of 5 mg/kg. Small strongyles were most responsive to fenbendazole and dienbendazole at all dosages. Egg production by S edentatus was eliminated by administration of fenbendazole and dienbendazole (at dosages of 2.5 and 5 mg/kg). Administration of dienbendazole at a dosage of 1 mg/kg resulted in partial elimination of S edentatus egg production. Trichostrongylus axei egg production was eliminated by administration of dienbendazole at dosages of 2.5 and 5 mg/kg, but not by the administration of 1 mg/kg. Parascaris equorum egg production was eliminated from the single infected pony given dienbendazole at a dosage of 5 mg/kg.

Data from slaughter plants (n = 3) and feedlots (n = 18) in eastern Washington were analyzed to characterize occurrence patterns of cysticercosis in Washington during 1984. Three concurrent peaks in cysticercosis rates (0.6/1,000 to 5/1,000 slaughtered cattle) were detected at 3 slaughter plants. Peaks were observed at 8 feedlots from December 1983 to March 1984, at 6 feedlots from April to July 1984, at 2 feedlots from August to October 1984, and at 3 feedlots from November 1984 to February 1985. Affected feedlots were not closely associated geographically and were feeding cattle from many, predominantely northwestern, origins. For 3 feedlots for which time in the feedlot was available for each slaughter shipment, an increase in cysticercosis rate with increasing time in the feedlot was noticed. Within these 3 feedlots, cases of cysticercosis were widely scattered spatially. The pattern of cysticercosis indicated human fecal contamination of a regionally available feed source. Of feedstuffs in use, potato waste, a byproduct of the processed potato industry, appeared to be the most likely source of Taenia saginata ova.

Oxidative respiratory burst activity was examined in lavage-procured bovine pulmonary alveolar macrophages. Nonstimulated alveolar macrophages released a minimal quantity of superoxide anion and had small amounts of glucose flux through the pathways of energy metabolism. Nonstimulated cells metabolized substantial amounts of glucose through the hexose monophosphate shunt. Stimulation with opsonized zymosan particles induced a tonfold increase in the release of superoxide anion and a twofold increase in the flux of glucose through the hexose monophosphate shunt and the pathways of energy metabolism. Preliminary observations also indicated that the magnitude of the burst varied between sets of bronchoalveolar cells obtained from the same calf over time.

When sheets of mucosa from the cecum of clinically normal horses were incubated in vitro with radiolabeled L-alanine, they could accumulate this amino acid against an apparent concentration gradient after 60 to 150 minutes of incubation. The active transport system for L-alanine was on the serosal surface of the mucosal sheet only. L-Alanine accumulation at 60 minutes was partly inhibited by 20 mM glycine (P < 0.01), 0.5 mM ouabain (P < 0.05), and Na deprivation (P < 0.02). Anoxia for 60 minutes increased L-alanine accumulation, but had adverse effects on cell structure and intracellular cation distributions. Transmucosal fluxes induced a small, but significant (P < 0.05), net secretion of L-alanine, and the mean (+/- SEM) transmucosal potential difference was 7.3 +/- 0.7 mV over the period of flux measurement. It was concluded that L-alanine was accumulated by the serosal surface of the cecal mucosa, possibly to provide substrate for tissue metabolism. There was no evidence that the cecal mucosa could actively transport this amino acid from the luminal bathing medium.

Changes in renal function, determined by pharmacokinetics of phenolsulfonphthalein (PSP), and renal morphologic features were examined in adult pony mares given 20 mg of gentamicin sulfate/kg of body weight, IV, q 8 h (group A) n = 7 or isotonic saline solution, IV, q 8 h, n = 5 (group B) for 14 days. Susceptibility of ponies to gentamicin-induced nephrotoxicosis was varied. Two group-A ponies developed acute renal failure and were euthanatized before treatment day 14, whereas 5 group-A ponies did not develop physical or behavioral abnormalities after 14 days of gentamicin administration. All group-A ponies but none of group-B ponies developed ultrastructural abnormalities of the proximal tubular epithelium, consistent with gentamicin-induced nephrotoxicosis. Significant (P less than 0.05) differences were not detected in pharmacokinetic values of either group. Clearance of PSP was reduced in 4 group-A ponies that developed the most severe gentamicin-induced nephrotoxicosis. Changes in clearance of PSP were significantly (P less than 0.05) correlated with changes in the serum creatinine concentration.

The abdominal portion of the aorta was catherized in 27 cows. Local analgesia was achieved by infiltration of anesthetic agents. A 10-cm skin incision was made caudal and parallel to the 13th rib at the lateral border of the epaxial muscles. The dorsal costoabdominal artery was exposed at its first lateral cutaneous branch by careful dissection through fascial layers. A sterile polyvinyl catheter (1.52 mm OD) was inserted into the artery and was advanced 35 to 40 cm to the abdominal portion of the aorta. Catheter patency was maintained for up to 5 weeks. Concentrations of plasma progesterone and estradiol-17 beta in samples obtained from the abdominal portion of the aorta were similar to simultaneously obtained concentration in samples from the jugular vein before and after parturition.

To evaluate the effects of intra-articular injection of dimethylsulfoxide (DMSO) on normal equine articular structures, 7 adult horses with clinically normal carpi were allotted to 2 treatment groups (group A, n = 4; group B, n = 3). In each horse after collection of synovial fluid samples, the right antebrachial carpal and middle carpal joints were aseptically injected with 2 ml of a 40% solution of 90% medical grade DMSO in lactated Ringer solution, and the corresponding joints of the left forelimb (controls) were injected with 2 ml of lactated Ringer solution. In group-A horses, 2 ml of synovial fluid was obtained prior to injections of 40% DMSO at 24 hours and 72 hours, for a total of 3 injections. At necropsy, synovial fluid, synovial membrane, and articular cartilage specimens were obtained. Group-B horses were injected with 40% DMSO in the same sequence; however, the series was repeated following a 1-week interval. Clinical evaluation of these horses revealed no evidence of carpal inflammation associated with any injection in any group. Synovial fluid analysis of DMSO-injected and control joints revealed insignificant differences in leukocyte counts and total protein content. There was no evidence of cartilage degradation on gross, histologic, or histochemical evaluation of any of the joints. Intercellular matrix staining of the articular cartilage failed to reveal any observable difference in glycosaminoglycan content between injection with DMSO or lactated Ringer solution.

The effects of dietary aflatoxin and ochratoxin, fed singly and in combination, were evaluated in growing crossbred pigs. Five barrows (7 weeks old at beginning of study) per group were fed either control feed, 2.0 mg of aflatoxin (AF)/kg of feed, 2.0 mg of ochratoxin (OA)/kg of feed, or 2.0 mg of AF and 2.0 mg of OA/kg of feed for 28 days. Production performance, serum biochemical, hematologic, and pathologic evaluations were made. Body weights were reduced by the combination treatment, whereas body weight gain was decreased by all toxin treatments. The effect of AF and OA in combination on body weight gain was additive. Liver weights were increased by the combination treatment, whereas kidney weights were increased only in the OA group. Aflatoxin caused decreases in serum calcium, sodium, phosphorus, urea nitrogen, cholesterol, and glucose concentrations, whereas OA alone caused decreases in serum phosphorus, cholesterol, and hematologic values. The AF-OA treatment induced decreases in mean corpuscular volume, packed cell volume, and in serum concentrations of phosphorus, cholesterol, and urea nitrogen. The AF-OA treatment increased serum alkaline phosphatase activities and triglycerides. It was concluded that AF and OA, singly or in combination, can affect clinical preformance, serum biochemical and hematologic values, and organ weights of barrows. Although values of some measurements were affected more by the combination than by either toxin alone and suggested synergism or antagonism, the toxic interactions could best be described as additive.

An ELISA has been developed for measurement of milk and serum IgG concentrations directed against Salmonella dublin. Four groups of cows were studied: group A-7 experimentally challenge-exposed cows (infected, recovered group); group B-6 normal uninfected randomly selected control cows; group C-7 naturally occurring S dublin carrier cows; and group D-6 normal uninfected S dublin negative cows from the same herd as group C. Group-A cows were inoculated orally, or inoculated orally and then IV, but none became a S dublin carrier. As expected, all 7 group-A cows responded with a marked increase in ELISA titer after oral exposure to virulent S dublin, starting with a mean serum titer of 17.7% and reaching a peak mean serum titer of 79.3% approximately 76 days after initial exposure. As determined by necropsy and organ culturing of the remaining cows, none of the group-A cows became carriers. The mean serum ELISA titer for group-B uninfected control cows was 14.1% (SD +/- 12.8%). The mean milk ELISA titer was -1.0% (SD +/- 5.5%). Colostrum and then milk gave false-positive results for up to 2 weeks after onset of lactation. Group-B cows were culture negative for S dublin in feces and milk during lactation, and when tissues were cultured after euthanasia. Milk and serum samples for ELISA, and milk and fecal samples for culturing were taken from all group-A and -B cows twice a week for 6 months. Statistical correlation (P less than 0.05) was found between serum and milk ELISA titers. A highly significant (P less than 0.001) difference in serum ELISA titers was demonstrated between control (group B) and infected cows (group A). Milk and feces from group-C carrier cows were cultured for S dublin 5 days a week for 11 to 13 months. Six of the 7 cows calved during this period. Fecal shedding was sporadic in 7 cows. Milk shedding was frequent in certain quarters of 4 of the cows and was sporadic or absent in other quarters of these cows and it was sporadic in 2 cows, and 1 cow had culture-positive milk only twice. The overall milk-shedding rate was 46% (792 positives/1,733 samples), whereas the overall fecal-shedding rate was 4% (65 positives/1,733 samples). Shedding in the 4 weeks after parturition was 28% in milk and 5% in feces. Six group-C cows had strongly positive ELISA titers in serum and milk, whereas 1 cow (the cow that had only 2 positive milk cultures) had relatively low ELISA titers. Group-C cows had a mean serum titer of 85.2% (SD +/- 19%) and mean milk titer of 70.6% (SD +/- 35.5%). These results indicate that IgG ELISA may be useful in detection of S dublin milk shedding (mammary gland infection) carrier cows. Milk shedding in the 4 persistent shedders ranged from 10(1) to 10(5) organisms/ml, and was associated with evidence of chronic active mastitis. Group-D cows, culture-negative herd mates of group-C carrier cows, were monitored in a manner identical to that used for group-C cows. All cows remained culture-negative for S dublin in feces and milk and results of organ culturing were negative for S dublin after euthanasia. The ELISA titers remained negative, with a mean group-D titer of 8 +/- 7.7% on serum, and 0.6 +/- 5.5% on milk. A highly significant difference in serum (P less than 0.0001) and milk (P less than 0.0001) ELISA titers was demonstrated between group-C carrier cows and group-D uninfected herd mates.

Protein kinase (PK) C activity in the liver of cattle with fatty liver syndrome was evaluated and compared with that in liver of healthy cattle. The PKC activities in cytosolic and particulate fractions were reduced in fatty livers, compared with those in livers from healthy cattle. The decrease of PKC activity was more distinct in cytosolic (P = 0.0016) than particulate (P = 0.069) fractions. Protein kinase activities other than PKC were not substantially changed. Seemingly, PKC was involved in the pathogenesis of fatty liver syndrome in cattle.