Background: Salmonella enterica is a facultative intracellular pathogen of worldwide importance. Over 2,500 serovars exist and infections in humans and animals may produce a spectrum of symptoms from enteritis to typhoid depending on serovar-and host-specific factors. S. Enteritidis is the most prevalent non-typhoidal serovar isolated from humans with acute diarrhoeal illness in many countries. Human infections are frequently associated with direct or indirect contact with contaminated poultry meat or eggs owing to the ability of the organism to persist in the avian intestinal and reproductive tract. The molecular mechanisms underlying colonisation of poultry by S. Enteritidis are ill-defined. Targeted and genome-wide mutagenesis of S. Typhimurium has revealed conserved and host-specific roles for selected fimbriae in intestinal colonisation of different hosts. Here we report the first systematic analysis of each chromosomally-encoded major fimbrial subunit of S. Enteritidis in intestinal colonisation of chickens.

Enterohaemorrhagic Escherichia coli (EHEC) comprise a group of animal and zoonotic pathogens of worldwide importance. Our previous research established that intestinal colonization of calves by EHEC serotypes O5 : H-and O111 : H-requires EHEC factor for adherence (Efa-1), also known as lymphostatin (LifA). Towards an understanding of the mode of action of Efa-1/LifA, chromosomal in-frame deletions of predicted glycosyltransferase (DXD) and cysteine protease (CHD) motifs were created in a Dstx1 derivative of EHEC O26 : H-. The magnitude and duration of faecal excretion of EHEC O26 : H-were significantly reduced by null mutation of efa-1/lifA, but were not impaired by DDXD or DCHD mutations, in contrast to observations made with truncated Efa-1/LifA mutants of Citrobacter rodentium in mice. Although C. rodentium Efa-1/LifA influences the induction of colonic hyperplasia in mice, EHEC O26 : H-Efa-1/LifA was not required for fluid accumulation or neutrophil recruitment in bovine ileal loops. In contrast to observations with EHEC O5 : H-or O111 : H-mutants, inactivation of efa-1/lifA in EHEC O26 : H-did not significantly affect adherence or secretion of type III secreted proteins that play pivotal roles in calf colonization. Lymphostatin activity could not be reliably demonstrated in lysates of EHEC O26 : H-; however, deletion of the glycosyltransferase and cysteine protease motifs in Efa-1/LifA from enteropathogenic E. coli O127 : H6 abolished lymphostatin activity. Our data uncouple the role of Efa-1/LifA in calf colonization from effects on type III secretion and reinforce the potential for pathotype-and serotype-specific phenotypes.

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