Virulence properties of Campylobacter jejuni isolates of poultry and human origin.

Campylobacter jejuni is one of the leading causes of food-borne gastroenteritis. Because of the high prevalence of C. jejuni in poultry, poultry meat is considered a major source of C. jejuni infections for humans. However, it is not known whether all poultry-associated C. jejuni strains are capable of causing disease in humans. Four different virulence properties of C. jejuni strains were compared between 20 poultry isolates and 24 human isolates. Strains were chosen based on their PFGE pattern to represent a heterogeneous population. The isolates were compared for their ability to invade and induce interleukin-8 (IL-8) production in T84 cells, their production of functional cytolethal distending toxin (CDT) using HEp-2 cells, and their sodium deoxycholate resistance. All four virulence factors were present among strains of human and poultry origin, with strong differences observed among strains. For invasion and IL-8 induction, no difference was observed between the two populations. However, on average, human isolates arrested more HEp-2 cells in their cell cycle than did the poultry isolates (P=0.041), suggesting higher CDT production by the former. The ability to survive 16 000 mug sodium deoxycholate ml(-1) was significantly more pronounced (P=0.006) among human isolates than poultry isolates, although all strains possessed the cmeABC operon. These data suggest that all four virulence properties are widespread among C. jejuni isolates, but that a higher degree of bile-salt resistance and more pronounced CDT production are associated with strains causing enteritis in humans.

Effect of a single in ovo injection of 2,3,7,8-tetrachlorodibenzo-p-dioxin on protein expression in liver and ovary of the one-day-old chick analyzed by fluorescent two-dimensional difference gel electrophoresis and mass spectrometry.

The polyhalogenated aromatic hydrocarbon 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an ubiquitously distributed environmental pollutant which can induce a broad spectrum of toxic responses in animals, including birds. In this study, we investigated the impact of 0 or 20 ng TCDD injections into the yolk of chicken eggs before start of development, on liver and ovarian protein expression in hatchlings using fluorescent two-dimensional difference gel electrophoresis (2-D-DIGE) under a pH range of 4-7, combined with MS. Despite considerable interindividual variability, exposure to TCDD prior to the start of embryonic development resulted in significant changes in expression of a small set of proteins. Expression of fibrinogen gamma chain precursor in the liver and 60 kDa heat shock protein in the ovary were significantly higher as a result of the very early exposure to TCDD. NADH ubiquinone oxidoreductase (42 kDa subunit) and regucalcin expression was decreased by early TCDD treatment in the liver and ovary, respectively. These proteins could not be directly linked with drug metabolism per se but are involved in blood clotting, oxidative stress, electron transport, and calcium regulation. It remains to be elucidated how these changes in the hatchling might be linked to the observed long-term consequences during posthatch life of the chicken.

Effects of early prenatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on postnatal reproduction in the laying hen (Gallus gallus).

This study demonstrates the long-term effects of very early embryonic exposure to a single dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (0, 10 and 20 ng/egg), administered before the beginning of embryonic development, on growth and reproductive performance in laying hens. Hatchability and body weight gain from 11 weeks onwards were significantly depressed in 20 ng treated hens. All hens started laying egg at around the same age and the laying performance of TCDD-treated hens was normal. No disturbances in the age-related pattern and concentrations of oestradiol, LH or FSH in plasma could be found but mean progesterone concentrations were significantly lower in 20 ng treated hens. Moreover, follicular distribution was changed with less small white follicles and smaller yellow follicles, which probably resulted in the lower egg weight of the 20 ng treated hens. At 43 weeks of age, hens treated in ovo with TCDD showed a retained right oviduct, mostly filled with clear fluid. From these results, it seems that in ovo exposure to TCDD interferes in the right oviduct regression during embryonic development and induces some changes in follicular distribution but without impairment of reproductive performance in the adult laying hen.