The variant rpoS allele of S. enteritidis strain 27655R does not affect virulence in a chick model nor constitutive curliation but does generate a cold-sensitive phenotype

Abstract

Adherence of pathogenic Escherichia coli and Salmonella spp. to host cells is in part mediated by curli fimbriae which, along with other virulence determinants, are positively regulated by RpoS. Interested in the role and regulation of curli (SEF17) fimbriae of Salmonella enteritidis in poultry infection, we tested the virulence of naturally occurring S. enteritidis PT4 strains 27655R and 27655S which displayed constitutive and null expression of curli (SEF17) fimbriae, respectively, in a chick invasion assay and analysed their rpoS alleles. Both strains were shown to be equally invasive and as invasive as a wild-type phage type 4 strain and an isogenic derivative defective for the elaboration of curli. We showed that the rpoS allele of 27655S was intact even though this strain was non-curliated and we confirmed that a S. enteritidis rpoS: :str r null mutant was unable to express curli, as anticipated. Strain 27655R, constitutively curliated, possessed a frameshift mutation at position 697 of the rpoS coding sequence which resulted in a truncated product and remained curliated even when transduced to rpoS: :str r . Additionally, rpoS mutants are known to be cold-sensitive, a phenotype confirmed for strain 27655R. Collectively, these data indicated that curliation was not a significant factor for pathogenesis of S. enteritidis in this model and that curliation of strains 27655R and 27655S was independent of RpoS. Significantly, strain 27655R possessed a defective rpoS allele and remained virulent. Here was evidence that supported the concept that different naturally occurring rpoS alleles may generate varying virulence phenotypic traits. z

Complex Regulatory Network Controls Initial Adhesion and Biofilm Formation in Escherichia coli via Regulation of the csgD Gene

“…The observation that, unlike the situation in other E. coli strains and in S. enterica serovar Typhimurium (2,44), the rpoS gene is no longer necessary for csgD transcription in the ompR234 strain (Fig. 6) might suggest that the L43R substitution results in a better interaction of OmpR with 70 RNA polymerase.…”

The chicken, the egg andSalmonella enteritidis

“…However, single nucleotide polymorphisms (SNPs) have been linked to LPS O‐chain microheterogeneity and to the source of the isolate (Parker et al ., 2001a). S. enteritidis produces other types of mutants that are recoverable from the environment of hens (Allen‐Vercoe et al ., 1998; Humphrey et al ., 1998; Guard‐Petter et al ., 1999). As undirected genetic mutation arises in Salmonella in response to environmental stressors (Kolter et al ., 1993; Massey et al ., 1999), it is reasonable that some of these genetic events enhance survival and fitness of the pathogen, whereas others are of no consequence or are even deleterious.…”

Variation in Resistance to High Hydrostatic Pressure and rpoS Heterogeneity in Natural Isolates of Escherichia coli O157:H7

“…Some alleles that do not result in a null rpoS phenotype nevertheless cause distinct phenotypic changes in stress resistance and in other properties (1,26,27). Recent evidence suggests that O157:H7 strains also show polymorphisms in the downstream mutS-rpoS region compared to K-12 serotypes (9).…”