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Background: Streptococcus pneumoniae serotype 1 has a high likelihood of causing invasive disease. Serotype 1 isolates belonging to CC228 are associated with low mortality, while CC217 isolates exhibit high mortality in patients.Methods: Clinical pneumococcal isolates and mutants were evaluated in wild-type C57BL/6 mice, macrophage-depleted mice, neutrophil-depleted mice, and SIGN-R1 knockout mice. In vitro models included binding and phagocytosis by THP-1 cells, capsule measurements, hydrogen peroxide production, and viability assays.Results: During early systemic infection in mice with serotype 1, large-colony variants appeared in blood. Similar large colonies were found in blood specimens from patients with invasive disease. Large morphotypes contained higher numbers of viable bacteria, grew faster, produced no or little hydrogen peroxide, and contained mutations in the spxB gene. spxB mutants were considerably more virulent in wild-type mice, less susceptible to early host clearance than wild-type strains after intravenous infection, but impaired in colonization. spxB mutants were less efficiently phagocytosed by macrophages than wild-type bacteria, which, in contrast to spxB mutants, caused more-severe disease when macrophages or SIGN-R1 were depleted.Conclusions: Hypervirulent spxB mutants are selected in both mice and patients and are resistant to early macrophage-mediated clearance. [ABSTRACT FROM AUTHOR]

Background. Pneumococcal serotypes are represented by a varying number of clonal lineages with different genetic contents, potentially affecting invasiveness. However, genetic variation within the same genetic lineage may be larger than anticipated.Methods. A total of 715 invasive and carriage isolates from children in the same region and during the same period were compared using pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing. Bacterial genome sequencing, functional assays, and in vivo virulence mice studies were performed.Results. Clonal types of the same serotype but also intraclonal variants within clonal complexes (CCs) showed differences in invasive-disease potential. CC138, a common CC, was divided into several PFGE patterns, partly explained by number, location, and type of temperate bacteriophages. Whole-genome sequencing of 4 CC138 isolates representing PFGE clones with different invasive-disease potentials revealed intraclonal sequence variations of the virulence-associated proteins pneumococcal surface protein A (PspA) and pneumococcal choline-binding protein C (PspC). A carrier isolate lacking PcpA exhibited decreased virulence in mice, and there was a differential binding of human factor H, depending on invasiveness.Conclusions. Pneumococcal clonal types but also intraclonal variants exhibited different invasive-disease potentials in children. Intraclonal variants, reflecting different prophage contents, showed differences in major surface antigens. This suggests ongoing immune selection, such as that due to PspC-mediated complement resistance through varied human factor H binding, that may affect invasiveness in children. [ABSTRACT FROM PUBLISHER]

Reports that vaccination with FimH adhesin protects cynomolgus monkeys from colonization and infection by uropathogenic Esherichia coli. Bladder infections with type 1-piliated Escherichia coli; Antibody response to FimCH immunization; Effect of adhesin vaccine on normal gut flora.

Studies expression of and cytokine activation by Escherichia coli curli fibers in human sepsis. Nature and biological role of curli, a novel class of bacterial surface structures, in Escherichia coli and Salmonella infection; Different expressing levels of curli fibers among sepsis Escherichia coli isolates; Dose-dependent induction of tumor necrosis factor-alpha by curli-expressing Escherichia coli.

Type I Helicobacter pylori strains frequently recognize the Lewisb (Leb) blood group antigen. This binding property and expression of the Leb oligosaccharide were required for adherence to fixed normal or pathologic gastric tissue. In contrast, both type I and type II strains adhered to cultured cells in the absence of the Leb epitope. For the gastric cell line AGS, adherence was significantly higher when viable type I strains were allowed to interact with viable AGS cells compared with fixed cells. The observation that chloramphenicol and cycloheximide, inhibitors of bacterial and eukaryotic protein synthesis, respectively, significantly reduced adherence of type I but not type II isolates suggests that in type I strains, adherence depends on the up-regulation of one or more host cell receptors triggered by the bacterium. [ABSTRACT FROM PUBLISHER]

Helicobacter pylori isolates from 32 children and adolescents were characterized with respect to putative virulence and colonization-associated properties. Only 3 of the subjects had duodenal ulcer. All but 2 of the remaining 29 had various degrees of chronic gastric inflammation. No significant correlation between degree of inflammation and presence of the cag-pathogenicity island, cytotoxin production, vacA alleles associated with cytotoxin expression, and binding ability to the Lewisb (Leb) oligosaccharide was found. Only 4 isolates expressed the Leb-specific adhesin, of which 3 were also cag region-positive. This is in contrast to adults with gastritis or peptic ulcer disease (or both), in whom most of the H. pylori isolates bind Leb. In an in situ binding assay H. pylori were less able to adhere to gastric surface mucous cells in biopsies taken from children compared with adults, suggesting a lower expression of the Leb oligosaccharide in the children. [ABSTRACT FROM PUBLISHER]