Fasting and postprandial gastroesophageal sphincter pressure (GESP) and plasma gastrin immunoreactivity were measured in 6 dogs from 9 through 60 months after treatment for and recovery from gastric dilatation-volvulus (GDV). The GESP was not significantly increased in these dogs, compared with that in clinically normal dogs in either the fasting or postprandial state. Corresponding plasma gastrin immunoreactivity was not significantly increased in dogs of the GDV-recovered group, compared with that in clinically normal dogs (fasting or postprandial). An exaggerated increase in GESP in response to food-induced gastrin release was not observed in dogs of the GDV-recovered group. Exogenously administered pentagastrin (3-micrograms/kg bolus, IV) increased fasting GESP in clinically normal dogs over a 4-minute test period (P = 0.01). Gastric distention in response to oral administration of isosmolar saline solution (500 ml) did not significantly increase GESP or plasma gastrin immunoreactivity in clinically normal dogs. In anesthetized clinically normal dogs, gastric distention in response to use of balloons filled to exert intragastric pressure of 30 mm of Hg also did not cause significant increase in plasma gastrin immunoreactivity. Increased GESP, secondary to hypergastrinemia or gastric distention, is an unlikely cause of eructation failure in dogs with GDV.

Ruminal microorganisms in cattle at a Florida agriculture research station did not have the ability to detoxify leucaena by degradation of 3-hydroxy-4(lH)-pyridone (3,4,-DHP), but a DHP isomer (2,3-DHP) was degraded in some cattle. Cattle with microorganisms that degraded 2,3-DHP were mostly Senepol cattle imported from St. Croix, US Virgin Islands, where leucaena is an indigenous species. Hereford cattle at the research station in Florida generally did not degrade 3,4-DHP or 2,3-DHP. An experiment was conducted in which a pure culture of 3,4-DHP-degrading bacteria was inoculated into Hereford cattle (with ruminal fistula) grazing leucaena. The bacteria successfully colonized the rumen of recipient cattle and persisted through the following winter when there was no leucaena in the diet.

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.

Sixteen primiparous sows were bred and fed either a control ration (n = 8) or a diet containing purified zearalenone (n = 8; 1 mg/kg of body weight) from days 7 to 10 after breeding. On day 7 after breeding, the jugular vein of each sow was cannulated and blood was collected at 20-minute intervals for 4 hours before feeding and 4 hour after feeding. On day 10 after breeding, blood samples were collected from 4 control sows and 4 zearalenonefed sows at 20-minute intervals for 4 hours before collection of blastocysts. A similar blood sampling schedule was followed for the remaining 4 control and 4 zearalenone sows on day 14 after breeding. On day 10 after breeding, spherical blastocysts were recovered from all control sows and from 3 of 4 zearalenone-treated sows. Average diameter of blastocysts from zearalenone-treated sows were similar to that of control sows. On day 14 after breeding, blastocysts were recovered from all control sows and 3 of 4 zearalenone-treated sows. Blastocysts from the control sows were filamentous, whereas blastocysts from zearalenone-treated sows were fragmented and contained foci of necrosis. Incidence of luteinizing hormone (LH) secretory spikes per sow was less (P less than 0.01) in zearalenone-treated sows (0.25 +/- 0.25/4 h) than control sows (1.75 +/- 0.25/4 h) on day 10 after breeding. Incidence of follicle-stimulating hormone (FSH) secretory spikes was simillar (P = 0.45) among treatments on days 7, 10, and 14 after breeding. Mean serum concentrations of LH were less on day 10 (P = 0.07) and day 14 (P less than 0.01) in zearalenone-treated sows than in control sows (3.3 +/- 0.2 ng/ml vs 6.2 +/- 1.3). These data indicate that administration of zearalenone on days 7 to 10 after breeding altered secretory patterns of serum LH during days 10 and 14 after breeding, which may have contributed to the death of blastocysts by day 14 after breeding.

Keratinocytes from explants of the oral mucosa of dogs were grown in culture for five passages. The ultrastructure of primary cultures and fully developed subcultures passaged 1, 3, and 5 times was examined. At every stage, the cells had the morphologic characteristics of epithelial cells and formed a multilayered squamous epithelium. The basal cells had the characteristics of metabolically active cells, whereas the suprabasal cells and the cells at the media interface expressed many, but not all, of the organelles and cell surface characteristics associated with keratinocyte differentiation. Keratohyalin granules were located in the suprabasal and superficial cells. Cell size and shape and the relationship between cells in the layers also reflected the morphologic characteristics of the parent tissue. Cells maintained this typical structure through all passages and the cultures changed minimally for up to a week after development.

A study was performed to determine the effect of proadifen hydrochloride on prostacyclin (prostaglandin I2 [PGI2]) and thromboxane A2 (TxA2) synthesis by equine peritoneal macrophages and the effect of proadifen on endotoxin-induced synthesis of PGI2 and TxA2 by equine macrophages. Peritoneal macrophages (2.5 X 10(6)/ml) were incubated for 6 hours in tissue culture media containing 1) nothing (nontreated control), 2) proadifen hydrochloride (20, 100, 250, and 500 micromol/L, 3) endotoxin (5 ng/ml), or 4) the calcium ionophore A23187 (0.95 micromol/L). In a second series of experiments, peritoneal macrophages were incubated with endotoxin (5 ng/ml) and proadifen (250 micromol/L), for 6 hours. Concentrations of 6-keto-prostaglandin F 1alpha (6-keto-PGF 1alpha) and thromboxane B2, the stable metabolites of PGI2 and TxA2, were determined in the incubation media by radioimmunoassay. Proadifen caused increased synthesis of PGI2 by equine macrophages, without affecting TxA2 production. The increased PGI2 production was similar to that induced by endotoxin and calcium ionophore; however, the latter 2 agents significantly stimulated TxA2 production as well (P less than 0.05). There were no significant differences among mean concentrations of 6-keto-PGF 1alpha in media from macrophages treated with 100, 250, or 500 micromol/L proadifen, but there was a significant curvilinear regression between their concentrations. The ratio of thromboxane B2 to 6-keto-PGF 1alpha was significantly lower than baseline in incubation media from macrophages exposed to proadifen, endotoxin, and calcium ionophore. Proadifen hydrochloride did not significantly change equine peritoneal macrophage production of PGI2 or TxA2 in response to endotoxin.

We evaluated the efficacy of buparvaquone in eliminating Babesia equi of European origin in carrier horses and in experimentally infected splenectomized ponies. When administered at the rate of 2.5 mg/kg of body weight, IM, 4 times at 96-hour intervals, buparvaquone was effective in eliminating B equi carrier infection in 1 horse. Such results could not be repeated at the same dosage or at 3.5 or 5 mg/kg, IM. Buparvaquone given at the rate of 4 to 6 mg/kg IV and/or IM was therapeutically effective in 4 of 5 acute B equi infections in splenectomized ponies. The treated ponies became carriers.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing barrows and was evaluated for its potential to ameliorate the clinical signs of aflatoxicosis. The experimental design consisted of 6 treatments of 5 barrows each at concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control), 5 g of HSCA/kg of feed (0.5%), 20 g of HSCAS/kg of feed (2.0%), 3 mg of AF/kg of feed, 5 g of HSCAS (0.5%) plus 3 mg of AF/kg of feed, or 20 g of HSCAS (2.0%) plus 3 mg of AF/kg of feed. Barrows were maintained in indoor concrete-floored pens, with feed and water available ad libitum for 28 days (from the age of 7 to 11 weeks). Barrows were observed twice daily and were weighed weekly, and blood samples were obtained weekly for hematologic and serum biochemical measurements. At the termination of the study, barrows were euthanatized and necropsied. Body weight gains were diminished significantly (P less than 0.05) by consumption of 3 mg of AF/kg of feed, whereas body weight gain in barrows consuming diets containing HSCAS or HSCAS plus AF did not differ from that in control barrows. Serum enzymatic activities of alkaline phosphatase and gamma-glutamyl transferase and prothrombin time were increased in barrows consuming 3 mg of AF/kg of feed, but not in those consuming HSCAS or HSCAS plus AF. Aflatoxin alone induced decreased serum concentrations of urea nitrogen, albumin, total protein, calcium, phosphorus, cholesterol, and glucose, as well as serum total iron-binding capacity, whereas HSCAS or HSCAS plus AF did not induce such effects. Liver weight was increased in barrows of the AF-alone treatment group, compared with control barrows. Hepatic lesions in barrows of the AF-alone treatment group were charaterized as peripheral lobular lipidosis accompanied by periportal and interlobular fibrosis and bile duct hyperplasia. Hepatic lesions were not observed in barrows of the 0.5% HSCAS plus AF or 2.0% HSCAS plus AF treatment groups. These findings suggested that HSCAS can modulate the toxicity of AF in growing barrows (perhaps via sequestration and reduced bioavailability in vivo) and may offer a novel approach to the preventive management of aflatoxicosis in animals.

Premature calving, typified by early expulsion (17 to 43 days) of weak or dead calves and accompanied by retained placentas, was induced in 8 of 9 pregnant cows fed a mixture of Ponderosa pine needles and alfalfa hay. Five control cows of comparable gestation age fed only alfalfa hay maintained normal pregnancies until they were euthanatized at the time the pine needle-treated cows were producing premature calves. Serum specimens from all cows were assayed for progesterone concentration and ovaries and placentomes were examined for histopathologic changes. There were no bacterial, fungal, chlamydial, or viral agents determined to be associated with the premature births. Serum progesterone concentration in the treated cows decreased progressively and were 0.4 to 1.5 ng/ml at the time of premature calving. Histopathologic changes were evident in the placenta and corpora lutea of treated cows only. The number of binucleate trophoblastic giant cells in placentomes was less than normal and the number of necrotic luteal cells in corpora lutea was greater than normal.