Dietary rapeseed meal and the incidence of tainted eggs

1. Incorporating 0, 3, 6 or 9% rapeseed meal in the diet of brown‐egg laying birds for 28 d resulted in the production of 0, 1.2, 19.3 and 20.9% tainted eggs respectively, the first tainted eggs being laid on the fifth day.

2. During the second and third weeks the incidence of tainted eggs exceeded 20% but fell to 11.4% during the final week.

3. Omission of the rapeseed meal from the diets halted the production of tainted eggs.

4. Neither egg production nor the health of the birds was adversely affected by the treatments.

5. The taint was described as “ fishy ” or “ crabby ” and was distinctive, but the source was not identified.     

Rapeseed Meal and egg taint

1. Certain rapeseed meals in the diet of hens laying brown eggs result in the production, from some birds, of eggs which have a “ fishy ” or “ crabby ” odour because of the presence of trimethylamine.

2. Such susceptible birds have been used to demonstrate that the activity can be extracted from rapeseed meal with appropriate solvents.     

THE USE OF FLUFF COUNTS IN A STUDY OF HYGIENE IN QUEENSLAND HATCHERIES

During 1972, 333 fluff samples were tested from 13 Queensland hatcheries and assessed according to the English standards for total count, coliforms and fungi. They were also assessed as being "standard" or "substandard", using a combination of the criteria of the English system. All hatcheries had at least 2 substandard samples and all the samples from 2 hatcheries were substandard.     

Q fever (Coxiella burnetii) investigations in dairy cattle: persistence of antibodies after vaccination.

The immune response and persistence of antibodies were investigated in dairy cattle vaccinated with formalin-inactivated phase (ph) I Coxiella burnetii vaccine agglutinating antibody geometric mean titer (GMT) of 193.2 at 1 month after vaccination compared to a GMT of 2.0 for nonvaccinated calves. The agglutinating antibodies gradually decreased in vaccinated cattle, but the GMT remained approximately 4 times higher than that for the nonvaccinated group for at least 20 months. Results of serotests at 2 months after revaccination indicated a rapid increase in the GMT to 177.0 with agglutinating titers between 1:64 and 1:512.     

Elimination of sulfamethazine from edible tissues, blood, urine, and feces of turkey poults.

Sulfamethazine was administered to 8- to 10-week-old turkey poults intravenously (IV) at the dose level of 71.5 mg/kg of body weight, orally at the dose level of 143 mg/kg of body weight, or in the drinking water at the concentration of 0.1% over a 6-day period. The concentrations of free sulfamethazine in blood, muscle, skin, kidney, and liver were determined and semilogarithmic plots of concentration vs time for the various tissues indicated that the curve had a linear portion within the first 72-hour period of drug withdrawal. The rates of disappearance of sulfamethazine from the various tissues were proportional to the concentration in the tissues. After 72 hours of withdrawal and for as long as 14 days, sulfamethazine concentrations in kidney, liver, and skin of turkeys given the drug in the drinking water fluctuated between 0.1 and 0.4 ppm. Only 8.6% of the oral dose (143 mg/kg) and 16.5 to 17% of the IV dose (71.5 mg/kg) were recovered in urine and feces as the parent compound during the initial 72-hour period.     

Antifungal mode of action of triforine

Rapidly growing mycelia of Aspergillus fumigatus treated with 10 μg/ml triforine (N,N′-bis-(1-formamido-2,2,2-trichloroethyl)-piperazine) showed little or no inhibition in dry weight increase prior to 2 h. By 2.5–3 h, triforine inhibited dry weight increase by 85%. The effects of triforine on protein, DNA, and RNA syntheses corresponded to the effect on dry weight increase both in time of onset and magnitude. Neither glucose nor acetate oxidation were inhibited by triforine.Ergosterol synthesis was almost completely inhibited by triforine even in the first hour after treatment. Inhibition of ergosterol synthesis was accompanied by an accumulation of the ergosterol precursors 24-methylenedihydrolanosterol, obtusifoliol, and 14α-methyl-Δ^{8, 24 (28)}-ergostadienol. Mycelia treated with 5 μg/ml of triarimol (α-(2,4-dichlorophenyl)-α-phenyl-5-pyrimidinemethanol) also accumulated the same sterols as well as a fourth sterol believed to be Δ^{5, 7}-ergostadienol.Identification of 4,4-dimethyl-Δ^{8, 24 (28)}-ergostadienol in untreated mycelia indicates that the C-14 methyl group is the first methyl group removed in the biosynthesis of ergosterol by A. fumigatus. The lack of detectable quantities of 4,4-dimethyl-Δ^{8, 24 (28)}-ergostadienol in triforine or triarimol-treated mycelia and the accumulation of C-14 methylated sterols in treated mycelia suggests that both fungicides inhibit sterol C-14 demethylation. The accumulation of Δ^{5, 7}-ergostadienol in triarimol-treated mycelia further implies that triarimol also inhibits the introduction of the sterol C-22(23) double bond.Two strains of Cladosporium cucumerinum tolerant to triforine and triarimol were also tolerant to the fungicide S-1358 (N-3-pyridyl-S-n-butyl-S′-p-t-butylbenzyl imidodithiocarbonate).