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Veterinary drugs and feed additives (especially some coccidiostats) can be absorbed by the digestive tract of laying hens and transferred to the egg. Physicochemical characteristics of these compounds determine their pharmacokinetic behavior and distribution to and within the egg. Traditionally the quite lipid soluble drugs and additives are expected to yield residues only in the fat-rich yolk. However, the quite lipid soluble drug doxycycline--as well as many other drugs--showed during long-term administration higher residues in white than in yolk. In a model study with 11 sulfonamides differing in pK(a) value and lipid solubility, their distribution in vivo between yolk and white was determined. Neither differences in pK(a) values nor those in lipid solubility could explain the distributions found. Binding to egg white macromolecules in vivo as an explanatory factor was tested with five sulfonamides, and no correlation between binding and the distribution of sulfonamides between white and yolk was found. Literature data on the distribution of drugs between egg white and yolk showed a reasonable consistency within drugs and a large variability among drugs (as could be expected). This larger database also did not provide a clue as to what factor determines the distribution of a drug between egg white and yolk when given to laying hens.

Induction of quinolone resistance in campylobacters by a quinolone treatment of Campylobacter‐colonized broilers was studied. Six groups of 15 broiler chicks each were administered a quinolone‐sensitive Campylobacter jejuni strain at 19 d of age. At the age of 26 d, two dosages (15 or 50 ppm) of flumequine or enrofloxacin were given via the drinking water for 4 d. One group was treated with enrofloxa‐cin during the first 4 d of life. Quinolone treatment did not eradicate Campylobacter colonization in the broilers. On days 29, 33 and 43 (at slaughter) of life, chicks in both enrofloxacin‐treated groups harboured nalidixic acid‐, flumequine‐ and enrofloxacin resistant‐campylobacters. Campylobacter isolates from all other groups remained sensitive to these quinolones. Two Campylobacter‐free control groups were not colonized by campylobacters during the whole experiment.

Laying hens were fed with compound feed containing six different levels of dioxins, dioxin-like PCBs and indicator PCBs for a period of 56 days. This was followed by a period of 56 days on clean feed. Dioxin levels in feed varied from background levels to three times the current EU tolerance limit of 0.75 ng TEQ/kg. At all dose levels a rapid increase was observed in the dioxin levels in eggs. There was a clear linear dose-response relationship between the dioxin levels in eggs and feed. The feed containing 0.4 ng TEQ dioxins per kg resulted in egg levels just above the EU limit of 3 pg TEQ/g fat. Dioxin-like and indicator PCB residues followed a pattern very similar to that of dioxins. Exposure to the highest indicator PCB level of 32 mg/kg resulted in egg levels around 300 ng/g fat. Exposure to dioxins through contaminated soil, mixed at 10% into the feed, resulted in a similar carry-over as from feed. Mycotoxin binders, mixed at 0.5% into the feed, had little effect on the carry-over of dioxins from the feed to the egg. It can be concluded that consumption of feed or soil with even moderate levels of dioxins and dioxin-like PCBs rapidly results in increased levels in eggs. The current EU dioxin limit for feed cannot guarantee egg dioxin levels below the EU-limit.

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