Annales de recherches veterinaires. Annals of veterinary research最新文献

Young rainbow trout (Oncorhynchus mykiss) were immunized with killed Aeromonas salmonicida, bled 5 wk later, and tested for the presence of serum agglutinins. The positive antisera were pooled and fractionated in a Ultrogel AcA 34 column. Seven fractions were collected and concentrated. The higher agglutinin titres were found in the 2nd fraction, which also contained IgM revealed by immunoelectrophoresis. The 7 fractions were heated for 30 min at 45 degrees C to inactivate the complement system, and used to opsonize non-virulent cells of A salmonicida, which were subsequently put in contact with trout adherent cell cultures. Controls were carried out with non-heated immune and heated or non-heated normal sera. Non-opsonized bacteria and bacteria opsonized with heated normal trout serum or with fractions 4-7 were not phagocytized. Non-heated sera allowed observation of approximately 33% of phagocytic cells. A noticeable opsonizing activity (approximately 28% of phagocytic cells) was observed only in fraction 2, which contained the highest titres of specific antibodies. It appears that in the absence of complement opsonizing properties clearly persist in the fraction which contains specific antibodies.

Newcastle disease virus (NDV) envelope glycoproteins that are expressed at the surface of fixed NDV (Ploufragan strain)-infected chick fibroblasts induce interferon (IFN) in mouse spleen cells. HN protein appears to be involved, since an anti-HN monoclonal antibody (Mab 3115) reduces the IFN production to 6% at most. However, the precise site of the molecule responsible for IFN induction is probably not exactly superimposed on the Mab 3115-epitope, since the NDV (83309 strain)-HN protein, which exhibits a modified Mab 3115-epitope, is also able to induce IFN. These preliminary results require further investigation in order to characterize the IFN herein demonstrated, to establish whether this induction mechanism exists in chicken lymphoid cells and to more accurately define the part of the HN molecule involved.

The enterotoxins are macro-proteins, produced by enterotoxic bacterial strains acting in the human or animal intestine during digestive infections. In most cases, they induce diarrhoea (associated or not with tissue damage). These molecules differ in their structure and mechanism of action. Some of them (cholera toxin, Escherichia coli LT) activate a cyclase system (adenylate or guanylate cyclase), inducing water and electrolyte flux in the gut. Conversely, others (toxins A and B, Clostridium difficile; Clostridium perfringens enterotoxin; verotoxin), provoke diarrhoea, intestinal damage associated with inflammatory response acting on cellular functions (protein synthesis, permeability to small molecules). Most enterotoxins act via membrane receptors which they specifically recognize on the surface of the enterocyte.

The synthetic anabolic steroid trenbolone acetate (TBA) was evaluated by the Joint FAO-WHO Expert Committee on Food Additives (JECFA) in 1981, 1982, 1987 and 1989. Effects on reproductive function in rats were observed, with no-effect level of 0.5 mg TBA/kg diet. No evidence was found for a teratogenic potential of TBA in rats. From the results of in vitro as well as in vivo mutagenicity assays it was concluded that TBA was probably not genotoxic and that the increased tumour incidence observed in long-term studies in mice and rats arose as a consequence of the hormonal activity of TBA. The concentration of sex hormones in the circulation was significantly reduced and histopathological abnormalities (particularly in testes, ovaries and uteri) were observed in male and female pigs fed with high doses of TBA. The marginal no-effect level for these effects was 0.1 mg/kg diet, equal to approximately 2 micrograms/kg bw. The 34th JECFA meeting established an acceptable daily intake of 0-0.02 micrograms/kg bw of TBA.

Thirteen crossbred wethers were given intravenously tritiated d-alpha-tocopherol (2 microCi/kg of bw) dissolved in emulsion or ethanol. Kinetic evaluation of the plasma specific activity versus time data was performed using either the 2- or 3-compartment model. The disappearance of the radiolabelled alpha-tocopherol from the plasma pool was affected by the nature of the vehicle administered. Radiotocopherol was cleared from plasma much faster when it was dissolved in ethanol than in emulsion; when radiotocopherol was injected as an emulsion concentration time curves were best described as a 2-compartment open model and in ethanol the kinetic data fitted a sum of three exponentials. The data showed higher bioavailability of the intravenously injected vitamin E in emulsion over ethanol.

Pharmacokinetic characteristics of an extemporaneous form of colistin sulfate in young calves were studied for a dosage of 25,000 IU.kg-1. The intravenous route (IV) is characterized by a 3-compartment model whose main parameters are: volume of distribution (1.02 l.kg), body clearance (0.15 l.h-1 kg-1) and mean residence time (3.87 h). By intramuscular route (IM), a mean serum peak of 37 IU.ml-1 was reached at a mean time of 0.5 h. The mean half-time of terminal phase (6.47 h) does not differ significantly from that of the intramuscular route (4.52 h). Absolute bioavailability calculated based on 4 calves was 109 +/- 28%. Repeated IM administrations seem to be adapted to maintain a bactericidal activity and to reduce risks of toxicity and neurological disorders (25,000 IU.kg-1) every 12 h over 3d.

The frequency of shedding of rotavirus in faeces of diarrhoeic piglets was studied in 2 farms. In farm I, where 82% of the litters had diarrhoea, group A rotavirus was detected in 52/117 (44%) faeces of pigs with diarrhoea while atypical groups B to E rotaviruses were detected in 2/117 (2%) faeces of diarrhoeic piglets that came from litters where group A rotavirus had also been found. In farm II where the morbidity due to diarrhoeas was lower (57% of the litters had diarrhoea), 8/141 (6%) faeces of piglets with diarrhoea had group A rotavirus and 4/141 (3%) had groups B to E atypical rotaviruses. It was concluded that group A and groups B to E rotaviruses can coexist in the same farm but group A rotavirus seems to induce more diarrhoeas in piglets.

In a preliminary study, 3 different chloramphenicol doses were tested by intramuscular (im) route, the highest one (90 mg/kg) being selected, based upon the duration of therapeutic serum levels (41.7 h). Following intravenous (iv) administration at this dose rate, the main pharmacokinetic parameters were: half-life of 6.0 h; body clearance, 0.101 l.kg-1.h-1; steady-state volume of distribution, 0.864 l.kg-1. Following a single im administration at the same dose, a mean maximum serum concentration of 22.9 microgram.ml-1 (Cmax) was reached in a mean time of 8.9 h (Tmax), therapeutic serum levels were achieved in an average period of 41.3 h. The mean half-life of the terminal phase was 10.3 h. Absolute bioavailability calculated based on 3 calves was 70.9 +/- 23.3% by im route. Pharmacokinetics of the long-acting formulation were confirmed in a repeated-dose study using the dosage schedule selected (2 injections im of 90 mg/kg at a 48 h interval).

Retroviruses from small ruminants are spread between susceptible animals by mononuclear phagocytes which are also virus targets. Young seronegative goats were inoculated with in vitro infected monocytes producing caprine arthritis encephalitis virus (10(5) cells/animal) by intravenous route corresponding to 10(5) syncytia forming units. After 3 months the same goats received dexamethasone treatment (5 mg/animal each 2 days over a 10-day period). The observed immune response differed if the animal was infected with its own cells or with homologous cells. Before dexamethasone treatment, antibody production evaluated by gel precipitation, ELISA or western blot was delayed in autologous by comparison with homologous conditions. After dexamethasone treatment, the appearance of infectious monocytes in blood and subsequent arthritis were observed in all animals in homologous conditions and only in 1 animal out of 3 in autologous conditions. Host reaction to the infected cells determines virus expression at the time of contamination.

After oral administration of 40 mg/kg of thiophanate to dairy cows, the active metabolite, ethyl-1H-benzimidazol-2-yl carbamate (EBC) reached a maximal concentration of 0.44 microgram/ml during the first milking and was eliminated by the mammary gland after 60 h. BCE is teratogenic in rats at doses of over 6.8 mg/kg while thiophanate at doses of up to 148 mg/kg is not. These results indicate that thiophanate treatment for dairy cattle may be questionable.