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In this study, Salmonella enterica serovar Typhimurium challenge models were tested to identify the best conditions under which to perform the experimental infection of 3-wk-old broilers. Such a model would be useful to study the efficiency of therapeutic treatments that could take place at the end of the grow-out period. Salmonella-free chicks were obtained from a breeder flock vaccinated with Salmonella. Intestinal maternal immunity was monitored by ELISA analyses at 2, 9, and 16 d of age. Data indicated that protection of maternal origin was not maintained over time and was drastically reduced at 9 d of age (P < 0.01). At 21 d of age, chickens were orally inoculated with Salmonella Typhimurium. The effects of the oral challenge dose (0, 3 × 10(3), 3 × 10(6), and 3 × 10(9) cfu/bird) and vancomycin pretreatment (no administration or 25 mg/bird) on intestinal immune responses, growth performance, and Salmonella colonization of chickens were investigated. After infection, the mucosal immune response was rapid, with increased (P < 0.01) anti-Salmonella Typhimurium IgA titers measured at 8 d postinfection in intestinal contents. A linear relationship (P < 0.05) existed between specific IgA levels in intestinal and cecal contents and the challenge dose inoculated. None of the challenge protocols caused mortality or clinical symptoms after infection. Nevertheless, the experimental infection induced a significant deterioration of growth performance. The pretreatment with 25 mg of vancomycin at 3 h before Salmonella inoculation was able to establish stable infection rates among the population of 3-wk-old infected chickens. Nevertheless, Salmonella shedding was not stable over the rearing period, and the bacteria seemed to be naturally eliminated from most birds at 22 d postinfection. This natural clearance of the gut, which was related, at least in part, to the intestinal immune response, should limit the usability of the created mature challenge model within 1 to 2 wk after inoculation.

Enterohemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC) organisms are groups of pathogenic strains whose infections are characterized by a typical lesion of enterocyte attachment and effacement. They are involved in enteric diseases both in humans and in animals, and EHEC strains can be responsible for hemolytic uremic syndrome in humans. Previously, it was shown that the 2F3 monoclonal antibody (MAb) is specific for the O26 EHEC and EPEC strains (P. Enterohemorrhagic Escherichia coli (EHEC) strains are an important class of pathogens for humans and animals. The term EHEC denotes E. coli strains that cause attaching and effacing lesions on epithelial cells, express Shiga toxin-encoding genes, possess a 60-MDa virulence plasmid, and produce hemorrhagic colitis and/or hemolytic uremic syndrome (17,18).KerrBesides those of the O157:H7 and O157:H Ϫ serotypes, EHEC strains of serogroup O26 are the most common strains found in human infections (4, 17). In addition, O26 EHEC strains are an important cause of enteritis in calves (12). One of the most important steps in the pathogenic mechanism of enteric bacteria is the initial adhesion of the bacteria to the intestinal wall. Several stages of colonization have been recognized in attaching and effacing E. coli pathogenesis, some of which await characterization. Some level of host specificity is shown by EHEC strains, but the role in host specificity of the recognized virulence factors, such as Shiga toxin 1 (Stx1) and/or Stx2 and the intimin protein (a protein that is encoded by the eae gene and necessary for the production of the attaching and effacing lesion), is unknown (8, 19). The bovine host specificity shown by O26 EHEC and enteropathogenic E. coli (EPEC) strains could be based on the production of a colonization factor, such as an adhesin, that is specific for cattle; such a colonization factor has been demonstrated to be the basis of the host specificity of classical human EPEC strains. Such an adhesin is likely to be a specific immunogen exposed at the bacterial cell surface (3,13,15,17,23,24).A monoclonal antibody (MAb), 2F3, was derived against a surface antigen extracted from the bovine O26 EHEC strain 4276; it tested positive in an enzyme-linked immunosorbent assay (ELISA) with all of the O26 and half of the O111 bovine and human EHEC and EPEC strains (9). Recent reexamination of six of the O111 EHEC and EPEC strains that tested positive revealed a contamination by O26 EHEC or EPEC strains. Purification of the strains in the mixed culture demonstrated that the O111 strains were 2F3 negative and the O26 strains were 2F3 positive (J. McCappin and H. Ball, unpublished data).Since the 2F3 MAb is specific for the O26 EHEC and EPEC strains, it may not only represent a diagnostic tool of these confirmed pathogens but also recognize a factor involved in the production of the attaching and effacing lesion. In view of these results, this study was initiated (i) to characterize the antigen recognized by the 2F3 MAb and its genetic determinant an...