Neonatal gut colonization by Staphylococcus aureus strains with certain adhesins and superantigens is negatively associated with subsequent development of atopic eczema.

BACKGROUND: Insufficient early immune stimulation may predispose to atopic disease. Staphylococcus aureus, a skin and gut colonizer, produces the B-cell mitogen protein A and T-cell-activating superantigens. Early gut colonization by S. aureus strains that possess the superantigens encoded by the enterotoxin gene (egc) cluster and elastin-binding protein is negatively associated with development of atopic eczema. OBJECTIVES: To investigate (i) whether these findings could be replicated in a second birth cohort, FARMFLORA, and (ii) whether nasal colonization by S. aureus also relates to subsequent atopic eczema development. METHODS: Faecal samples and nasal swabs from infants in the FARMFLORA birth cohort (n = 65) were cultured for S. aureus. Individual strains were distinguished by random amplified polymorphic DNA and assessed for adhesin and superantigen gene carriage by polymerase chain reaction. Atopic eczema at 18 months of age was related to nasal and gut S. aureus colonization patterns during the first 2 months of life (well before onset of eczema). RESULTS: Staphylococcus aureus colonization per se was unrelated to subsequent eczema development. However, gut S. aureus strains from the infants who subsequently developed atopic eczema less frequently carried the ebp gene, encoding elastin-binding protein, and superantigen genes encoded by egc, compared with strains from children who remained healthy. Nasal colonization by S. aureus was less clearly related to subsequent eczema development. CONCLUSIONS: The results precisely replicate our previous observations and may suggest that mucosal colonization by certain S. aureus strains provides immune stimulation that strengthens the epithelial barrier and counteracts the development of atopic eczema.

Superantigens and adhesins of infant gut commensal Staphylococcus aureus strains and association with subsequent development of atopic eczema.

BACKGROUND: According to the hygiene hypothesis, insufficient immune activation by microbes increases the risk of allergy development. Staphylococcus aureus, which is part of the skin and gut microbiota of infants in Western countries, produces a variety of T-cell-activating enterotoxins, called superantigens. OBJECTIVES: To investigate whether early (0-2 months of age) gut colonization by S. aureus strains that carry specific superantigens and adhesins was related to subsequent development of atopic eczema in a Swedish birth cohort. METHODS: Staphylococcus aureus was isolated from rectal swabs and cultured quantitatively from faecal samples, with individual strains being tested for carriage of genes for superantigens and adhesins. Atopic eczema was diagnosed at onset of symptoms and at 18 months of age. RESULTS: Although the frequency of early gut colonization by S. aureus was not related to subsequent eczema development, the S. aureus strains that were found to colonize those infants who developed atopic eczema were less likely to carry the gene encoding the superantigen SElM (P = 0·008) and the gene for elastin-binding protein (P = 0·03), compared with strains that were isolated from infants who had not developed atopic eczema by 18 months of age. CONCLUSIONS: Gut colonization by S. aureus strains carrying a certain combination of superantigen and adhesin genes was negatively associated with subsequent development of atopic eczema. Such strains may provide stimulation and promote maturation of the infant immune system.

Impacts of enterotoxin gene cluster-encoded superantigens on local and systemic experimental Staphylococcus aureus infections.

Staphylococcus aureus is both a component of the normal skin flora and an important pathogen. It expresses a range of recognized and putative virulence factors, such as enterotoxins with superantigenic properties. Several superantigen genes, i.e., seg, sei, selm, seln, and selo, are encoded by the enterotoxin gene cluster (egc), which is found in the majority of S. aureus isolates. Carriage of egc is associated with fitness of S. aureus in the gut microbiota, but it is not known if it contributes to pathogenicity. We constructed egc+ (functional for the seg, selm, and selo genes) and isogenic egc- S. aureus mutants, and investigated their virulence profiles in murine infection models. No effect of egc was seen in a local skin and soft tissue infection model, but in an invasive infection model, increased weight loss was observed after infection with the egc+ as compared to the egc- mutant. Mortality and arthritis were not affected by egc status. Our data suggest that egc has limited effects on the virulence of S. aureus. It may primarily function as a colonization factor increasing commensal fitness, although it might have some aggravating effects on the infection when the bacteria reach the blood.

Phylogenetic group B2 Escherichia coli strains from the bowel microbiota of Pakistani infants carry few virulence genes and lack the capacity for long-term persistence.

Escherichia coli strains of phylogenetic group B2 obtained from Western human hosts are enriched in virulence-associated genes and have a superior capacity to persist in the colonic microbiota. Here, E . coli strains from 22 infants born in Pakistan whose rectal flora was sampled regularly over the first 6 months of life were examined. B2 strains did not carry the virulence-associated genes sfaD/E, papC, neuB or hlyA more often than strains of other phylogenetic groups. B2 origin was not associated with persistence in the bowel microbiota. As compared with B2 strains from Swedish infants, Pakistani B2 strains carried significantly less often the virulence genes fimH (p 0.04), papC (p 0.02), papG class III (p 0.01), sfaD/E (p < or =0.0001), neuB (p < or =0.0001), and hlyA (p 0.005), and also the high-pathogenicity island (p < or =0.0001). A minority of Pakistani B2 strains belonged to recognized uropathogenic O-groups, which are common among 'Western' B2 strains. Thus, extra-intestinal pathogenicity may be the foremost characteristic of B2 strains colonizing Western populations.

Fluoroquinolone-resistant uropathogenic Escherichia coli in Norway: evidence of clonal spread.

Prevalence, resistance profiles, virulence gene complements, and phylogenetic and clonal affinities of fluoroquinolone-resistant Escherichia coli from urinary tract infections (UTIs) in Norway were investigated. Of 7302 E. coli UTI isolates from 2003, 1.2% were fluoroquinolone-resistant; 35 of these fluoroquinolone-resistant isolates were included in the present study. The isolates were predominantly multiresistant, carried few virulence factors, and tended to belong to the less-virulent phylogroups A and B1. Although the isolates were genetically heterogeneous, there was evidence of a limited degree of clonal dissemination.

A comparison of phylogenetic group, virulence factors and antibiotic resistance in Russian and Norwegian isolates of Escherichia coli from urinary tract infection.

Isolates of Escherichia coli from 31 Norwegian and 31 Russian females with significant bacteruria who presented with clinical signs of urinary tract infection (UTI) were tested for antimicrobial sensitivity, the presence of virulence genes, phylogroup distribution and clonal affinity. Twenty isolates, representing the full clonal diversity of a collection of 138 intestinal isolates of E. coli from healthy Norwegian females, served as a reference group. Russian UTI isolates belonged more often to phylogroup A and possessed fewer virulence genes than did Norwegian isolates. UTI isolates of E. coli were genetically heterogeneous and had a high degree of antimicrobial sensitivity.

Effect of human milk on type 1 and P-fimbrial mRNA expression in intestinal Escherichia coli strains.

AIMS: Escherichia coli from breastfed infants express more type 1 fimbriae and less P fimbriae than E. coli from bottle-fed infants. In this study we investigated the effect of human milk on production of mRNA for fimA (type 1 fimbriae) and papC (P fimbriae) in E. coli. METHODS AND RESULTS: Production of adhesin gene mRNA was estimated using a reverse transcriptase polymerase chain reaction in E. coli strains under different culture conditions. More type 1 fimbrial mRNA was produced after culture in human milk (P=0.001) or Luria broth (P=0.014) than after culture on agar, whereas P-fimbrial mRNA production was similar under all tested growth conditions. When cultured on agar, E. coli strains carrying both the fim and pap operons produced less type 1 and P-fimbrial mRNA than strains that had only the fim or pap operons, respectively (P=0.03 and 0.056). SIGNIFICANCE AND IMPACT OF THE STUDY: Environmental regulation of adhesin expression may be influenced by cross-talk between fimbrial operons.