Day-old Ducklings Research Articles

Immunization Field Trials in Susceptible White Pekin Ducklings against Duck Virus Hepatitis with Modified-Live-Virus Vaccines

SUMMARY When day-old ducklings susceptible to duck virus hepatitis (DVH) were inoculated with a DVH classic modified-live-virus (DVH-C-MLV) vaccine (1960 isolate) on a Long Island duck farm in 5 subsequent hatches and then exposed almost simultaneously to pathogenic field virus, average mortality was 33%, while the range of hatch mortality was 11 to 76%. Ducks started to die 4 days after hatching. Peak mortality was on the 6th day in 1 hatch and on the 8th day in the 4 other hatches. From the 9th to 12th day there was a limited mortality, with no losses thereafter in any hatch. Groups of 3 hatches of ducklings of the Duck Research Laboratory (DRL), susceptible to DVH, were inoculated with the monovalent DVH-C-MLV vaccine, a monovalent DVH-variant-MLV (DVH-V-MLV) vaccine (1970 isolate), or a bivalent DVH-CVMLV vaccine. The inoculated groups and their unvaccinated hatchmates were exposed to field virus on the above-mentioned farm 5, 6, and 8 days after vaccination. Average mortalities of the 3 hatches were: unvaccinated controls, 65% (range 34 to 81%o); DVH-V-MLV inoculated groups, 57% (44 to 66%); DVH-CV-MLV inoculated groups, 29% (18 to 46%); and the DVH-C-MLV-inoculated ducks, 24% (10 to 46%). Eight days were not enough to develop a complete protection in ducklings inoculated by any of the tested vaccines. Although the

A Study of Aflatoxicosis in Laying Hens

INTRODUCTIONTHE lethal potential of aflatoxins was recognized when aflatoxins were discovered and found to be the etiological agent responsible for the losses of turkey poults (Blount, 1961), ducklings and chickens (Asplin and Carnaghan, 1961), swine (Loosmore and Harding, 1961), and calves (Loosmore and Markson, 1961) in Great Britain. Carcinogenic properties were attributed to aflatoxins (Lancaster et al., 1961) soon after their discovery.Some attention has focused on the potential public health hazard of foods derived from animals fed aflatoxin-contaminated feeds. Allcroft and Carnaghan (1963) reported that milk from cows fed aflatoxin-contaminated feed was toxic to day-old ducklings. De Iongh et al. (1964) and Van Der Linde et al. (1965) have also reported on the toxicity to ducklings of milk from cows receiving aflatoxin-contaminated feeds. Brown and Abrams (1965) reported neither aflatoxins nor their fluorescing toxic metabolites were present in the milk of cows fed on highly toxic rations, and…

Metabolism of aflatoxin in susceptible and resistant animal species

Dietary aflatoxin B 1 was excreted in the urine of rats, goats and guinea-pigs as aflatoxin M 1, while some unchanged B 1 was excreted in the faeces. M 1 was not confirmed in the excreta of ducklings given B 1 orally but was found in the tissues of ducklings shortly after an intraperitoneal dose of B 1. Comparative studies in nine avian and mammalian species showed that there was no correlation between the known susceptibility of the different species to aflatoxin B 1 and the basal levels of hepatic microsomal enzymes (NADPH oxidase and aniline hydroxylase) or the rates of in vitro metabolism of the toxin by liver homogenates. Although liver preparations of several species metabolized aflatoxin B 1 almost completely, only minute amounts of M 1 were formed. However, an unidentified non-fluorescent metabolite (designated metabolite X) was also detected. The optimal formation of this metabolite depended on the presence of both liver microsomes and 105,000 g supernatant as well as NADPH as cofactor. The ability of liver preparations obtained from susceptible species to transform aflatoxin B 1 into products not toxic to day-old ducklings suggested that aflatoxin B 1 may exert its acute toxicity through the agency of a highly toxic and unstable metabolite.

Experimental Bile Duct Hyperplasia in Ducklings

INTRODUCTIONTHE biological effects of aflatoxins, the toxic factors isolated from groundnuts contaminated with some strains of Aspergillus flavus, have been described extensively (Wogan, 1965).Asplin and Carnaghan (1961) showed that day-old ducklings are highly susceptible to aflatoxins; they found that these animals are eminently suitable for screening suspected samples of groundnut meal and for other experimental work connected with this type of toxin: aflatoxins caused extensive bile duct proliferation in ducklings, even within a few days. Newberne et al. (1964b) stated that aflatoxin B1, the major toxic metabolite, administered in 5 daily doses of 0.4 μg., initiated clearly defined bile duct hyperplasia. The extent of this hyperplasia appeared to be related to the dose of aflatoxin (Chang et al., 1963).Various investigators have demonstrated that aflatoxin-containing diets led to the development of liver tumours in rats (Lancaster et al., 1961; Le Breton et al., 1962; Newberne et al., 1964a), .