Vaccination of calves with yeast- and bacterial-expressed paramyosin from the bovine lungworm Dictyocaulus viviparus.

Previously, vaccination of cattle with Escherichia coli-expressed bovine lungworm paramyosin (EcPMY) adjuvanted with Quil A resulted in considerable reduction in worm burden and larvae shedding (Strube et al., 2015). To further evaluate the protective potential of PMY, cattle vaccination trials were performed using either E. coli- (EcPMY) or Pichia pastoris-expressed PMY (PpPMY) with different adjuvants (Matrix-Q(™) or Quil A). Combinations EcPMY+Matrix-Q(™) (trial 1), PpPMY+Matrix-Q(™) (trial 2) and PpPMY+Quil A (trial 3) were tested against challenge infections with 2000 Dictyocaulus viviparus larvae. Even though GM worm burden and larvae shedding was lower in almost all vaccinated groups, there were high variations between individuals hampering significant differences. However, in all vaccinated groups, lungworms were significantly shorter compared with those in controls. In vitro stimulation of peripheral blood mononuclear cells (PBMC) with recombinant (r)PMY revealed no significant proliferation following vaccinations or challenge infection. All vaccinated cattle showed a significant rise in specific antibodies, particularly IgG and its subclass IgG1, and detected the native lungworm PMY in immunoblots starting 2 weeks after the first vaccination. The use of a different rPMY-adjuvant combination or combined vaccination with additional recombinant antigens might be a promising future approach towards a new vaccine against lungworms in cattle.

Interaction of mu-opioid antagonistic drugs with antiepileptics.

Interactions of the mu-opioid receptor antagonists, naloxone (0.3 and 1 mg/kg), cyprodime and clocinnamox (3 and 10 mg/kg for both drugs) with phenytoin (7 mg/kg), phenobarbital (7 mg/kg), carbamazepine (10 mg/kg) and valproic acid (130 mg/kg) were investigated using the electroconvulsive threshold in mice as a model in order to elucidate a possible role of mu-receptor mediated reactions in the mechanism of action of antiepileptic drugs. All 3 mu-antagonists are devoid of an effect on the electroconvulsive threshold. Pretreatment with the mu-antagonists resulted partly in an increase of anticonvulsant action, partly in a decrease, and partly the pretreatment had no effect on the electroconvulsive threshold. The anticonvulsant effect of phenytoin was antagonized dose-dependently by naloxone, that of phenobarbital by the dose of 10 mg/kg of clocinnamox. A common denominator of the mu-antagonistic interactions with anticonvulsants cannot be found and the effects observed are therefore considered as "unspecific".

Pharmacokinetics of oxcarbazepine in the dog.

Oxcarbazepine has been proven to be a promising new antiepileptic drug for the treatment of human epilepsy. Unlike carbamazepine, it is not oxidatively metabolized in humans, and therefore causes almost no induction of hepatic enzymes at clinically effective dosages. Though showing similar efficacy to carbamazepine, it has been reported to cause significantly fewer side-effects. It was the purpose of the present study to determine whether oxcarbazepine might be suitable for the treatment of canine epilepsy. In single-dose experiments, 40 mg/kg oxcarbazepine as a suspension was administered to seven dogs via gastric tube. Plasma concentrations reached peak concentrations of 2.4-8.8 micrograms/mliter at about 1.5 h and declined with an elimination half-life of approximately 4 h. The corresponding concentrations of its metabolite, 10,11-dihydro-10-hydroxycarbamazepine, did not exceed 1 micrograms/mliter. During continued treatment for 8 days, doses of 30 and 50 mg/kg were administered orally in capsules to two dogs three times a day. Plasma concentrations showed a pronounced decline from day 3, and the terminal half-life decreased to 2 h and 1 h. This is considered to be the result of oxcarbazepine inducing its own metabolism. The data reveal that oxcarbazepine, compared with former results with carbamazepine, offers no advantage for the treatment of epileptic dogs.