Extraintestinal pathogenic Escherichia coli (ExPEC) strains of human and avian origin show similarities that suggest that the avian strains potentially have zoonotic properties. However, the phylogenetic relationships between avian and human ExPEC strains are poorly documented, so this possibility is difficult to assess. We used PCR-based phylotyping and multilocus sequence typing (MLST) to determine the phylogenetic relationships between 39 avian pathogenic E. coli (APEC) strains of serogroups O1, O2, O18, and O78 and 51 human ExPEC strains. We also compared the virulence genotype and pathogenicity for chickens of APEC strains and human ExPEC strains. Twenty-eight of the 30 APEC strains of serogroups O1, O2, and O18 were classified by MLST into the same subcluster (B2-1) of phylogenetic group B2, whereas the 9 APEC strains of serogroup O78 were in phylogenetic groups D (3 strains) and B1 (6 strains). Human ExPEC strains were closely related to APEC strains in each of these three subclusters. The 28 avian and 25 human strains belonging to phylogenetic subcluster B2-1 all expressed the K1 antigen and presented no significant differences concerning the presence of other virulence factors. Moreover, human strains of this phylogenetic subcluster were highly virulent for chicks, so no host specificity was identified. Thus, APEC strains of serotypes O1:K1, O2:K1, and O18:K1 belong to the same highly pathogenic clonal group as human E. coli strains of the same serotypes isolated from cases of neonatal meningitis, urinary tract infections, and septicemia. These APEC strains constitute a potential zoonotic risk.

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Selection in broiler chickens has increased muscle mass without similar development of the cardiovascular and respiratory systems, resulting in limited ability to sustain high ambient temperatures. The aim of this study was to determine the long-lasting effects of heat manipulation of the embryo on the physiology, body temperature (Tb), growth rate and meat processing quality of broiler chickens reared in floor pens. Broiler chicken eggs were incubated in control conditions (37.8°C, 56% relative humidity; RH) or exposed to thermal manipulation (TM; 12 h/d, 39.5°C, 65% RH) from d 7 to 16 of embryogenesis. This study was planned in a pedigree design to identify possible heritable characters for further selection of broiler chickens to improve thermotolerance. Thermal manipulation did not affect hatchability but resulted in lower Tb at hatching and until d 28 post-hatch, with associated changes in plasma thyroid hormone concentrations. At d 34, chickens were exposed to a moderate heat challenge (5 h, 32°C). Greater O2 saturation and reduced CO2 partial pressure were observed (P < 0.05) in the venous blood of TM than in that of control chickens, suggesting long-term respiratory adaptation. At slaughter age, TM chickens were 1.4% lighter and exhibited 8% less relative abdominal fat pad than controls. Breast muscle yield was enhanced by TM, especially in females, but without significant change in breast meat characteristics (pH, color, drip loss). Plasma glucose/insulin balance was affected (P < 0.05) by thermal treatments. The heat challenge increased the heterophil/lymphocyte ratio in controls (P < 0.05) but not in TM birds, possibly reflecting a lower stress status in TM chickens. Interestingly, broiler chickens had moderate heritability estimates for the plasma triiodothyronine/thyroxine concentration ratio at d 28 and comb temperature during the heat challenge on d 34 (h(2) > 0.17). In conclusion, TM of the embryo modified the physiology of broilers in the long term as a possible adaptation for heat tolerance, without affecting breast meat quality. This study highlights the value of 2 new heritable characters involved in thermoregulation for further broiler selection.

1. Individual growth curves of 7143 chickens selected for the form of the growth curve were fitted using the Laird form of the Gompertz function, BW4=BW0xe(L/K)(1-e-Kt) where BWt is the body weight at age t, BW0 the estimated hatching weight, L the initial specific growth rate and K the maturation rate. 2. Line and sex effects were significant for each parameter of the growth curve. In males, L, BW0, age and body weight at inflection (T(I)and BWI) were higher whereas K was lower than in females. Lines selected for high adult body weight had higher BW0 and BW(I) whereas lines selected for high juvenile body weight had larger estimates of L and lower estimates of T(I). 3. Data from 38,474 animals were included in order to estimate the genetic parameters of growth curve parameters in males and females, considering them as sex-limited traits. Genetic parameters were estimated with REML (REstricted Maximum Likelihood) and an animal model. Maternal genetic effects were also included. 4. Heritabilities of the growth curve parameters were moderate to high and ranged between 0.31 and 0.54, L, BW0 in both sexes and BW(I) in males exhibited significant maternal heritability. Heritabilities differed between males and females for BWI and T(I). Genetic correlations between sexes differed significantly from one for all parameters. L, K and T(I) were highly correlated but correlations involving BW0 and BW(I) were low to moderate. 5. Sexual dimorphism of body weight at 8 and 36 weeks and of L, K and T(I) was moderately heritable. Selection on growth curve parameters could modify the difference between sexes in precocity and thus in body weight at a given age.

The short-term effects of delayed feeding (DF) for 2 d posthatching were measured in neonate chicks and compared to early feeding (EF). Chicks from 10 independent families were used in this study to determine whether genetic background control of growth may be influenced by EF and DF. Early feeding maintained significant interfamily body weight variations from hatch to 4 d of age, whereas there were no significant differences from 1 d of age when feeding was delayed to 48 h posthatching. These results suggest that posthatching feeding delay may distort genetic selection by masking the expression of genetic potential and disturbing the estimation of chick breeder value. In DF chicks, overall body growth was delayed until the beginning of feeding and body weight at 6 d of age was 25% lower than EF chicks. Availability of feed after the fasting period was not sufficient to compensate for the retardation of weight gain in either body weight or in intestine and breast muscle weight. However, initiation of intestine growth in DF chicks occurred from 1 d of age despite the lack of feeding, whereas feed intake was essential to enhance muscle growth. The potential for protein synthesis was lower in DF than in EF chicks during the first 2 d posthatching (P < 0.001) and then reached similar values after feed intake. These results confirm that initiation of growth in neonate chicks is improved by earlier feeding after hatching. Awareness of changes in overall body weight caused by posthatching food deprivation, especially in the intestine and muscle might help in the development of new diets which could minimize retardation of body weight gain in chicks.