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The role of the Escherichia coli iron-regulated gene homologue adhesin (Iha) in the pathogenesis of urinary tract infections (UTIs) is unknown. We performed a series of complementary analyses to confirm or refute the hypothesis that Iha is a virulence factor in uropathogenic E. coli. Fecal E. coli isolates exhibited significantly lower prevalences of iha (range, 14 to 22%) than did clinical isolates from cases of pediatric cystitis or pyelonephritis, adult pyelonephritis or urosepsis, or bacteremia (range, 38 to 74%). Recombinant Iha from E. coli pyelonephritis isolate CFT073 conferred upon nonadherent E. coli ORN172 the ability to adhere to cultured T-24 human uroepithelial cells. In a well-established mouse model of ascending UTI, CFT073 and its derivative UPEC76 (a pap [P fimbriae] mutant version of strain CFT073) each significantly outcompeted their respective iha deletion mutants in CBA/J mice 48 h after bladder challenge (P < 0.03 for urine, both kidneys, and bladders of both constructs, except for bladders of mice challenged with UPEC76 and its deletion mutant, where P = 0.11). These data suggest that Iha(CFT073) is a virulence factor and might be a target for anti-UTI interventions.

The diseases and virulence genes associated with Shiga toxin-producing Escherichia coli (STEC) are characterized incompletely. We analyzed, by polymerase chain reaction, 82 STEC isolates collected prospectively in Montana and profiled associated illnesses by patient chart review. All E. coli O157:H7 contained stx2-group genes, as well as eae, iha, espA, and ehxA; 84% contained stx1. Non-O157:H7 STEC less frequently contained stx1 (P=.046), stx2 (P<.001), iha (P<.001), eae, and espA (P=.039 for both), were isolated less often from patients treated in emergency departments (P=.022), and tended to be associated less frequently with bloody diarrhea (P=.061). There were no significant associations between stx genotype and bloody diarrhea, but isolates containing stx2c or stx(2d-activatable) were recovered more often from patients who underwent diagnostic or therapeutic procedures (P=.033). Non-O157:H7 STEC are more heterogeneous and cause bloody diarrhea less frequently than do E. coli O157:H7. Bloody diarrhea cannot be attributed simply to the stx genotype of the infecting organism.

Frequent unintended secondary mutations occurred in extraintestinal pathogenic Escherichia coli strains CP9, CFT073, and RS218 during suicide plasmid-mediated, putatively specific deletions of hlyA, papG allele III, and iha. Pulsed-field gel electrophoresis and PCR analyses demonstrated genomic alterations and/or unintended loss of defined virulence genes (papG, the F7-2 papA allele, iutA, sat, hlyD, and cnf). Caution is warranted when attributing the observed phenotypic changes to the intended mutation.

Increased thrombin generation and impaired fibrinolysis during Escherichia coli O157:H7-associated hemolytic uremic syndrome (HUS) plausibly diminish myocardial blood flow, but the frequency of cardiac ischemia during HUS is unknown. We identified a 9-year-old boy with HUS in whom myocardial diastolic dysfunction was demonstrated by echocardiography, who also had elevated serum troponin-I and creatine kinase MB mass. However, eight additional patients with HUS did not have elevated markers of cardiac injury. When present, elevated troponin-I should be considered to represent myocardial injury, and not attributed simply to renal insufficiency. It is possible that myocardial ischemia and secondary arrhythmias account for some sudden deaths that occur during acute HUS. [ABSTRACT FROM AUTHOR]

The role of platelet-activating factor (PAF), a phospholipid inflammatory mediator, in Escherichia coli O157:H7-associated hemolytic uremic syndrome (HUS) is unknown. PAF is synthesized by diverse cells and is degraded by PAF-acetylhydrolase (PAF-AH). Deficient PAF-AH activity results from a G→T transversion at position 994 of exon 9. We examined children infected with E. coli O157:H7 to determine if PAF levels or the PAF-AH (G994T) mutation reflects the risk of developing HUS. Plasma PAF concentrations were determined using chloroform/methanol extraction, thin layer chromatography purification, and scintillation proximity assay in 10 patients with uncomplicated infection (UI), 10 infected patients who subsequently developed HUS (pre-HUS), 5 HUS patients, and 8 healthy controls. The PAF-AH (G994T) allele frequency was determined in 52 UI children, 15 with HUS, and 11 controls. Wilcoxon rank sum tests were performed to test differences in location (median) of pairs of groups. PAF levels were higher in the UI (P=0.04) and pre-HUS (P=0.01) groups than in healthy controls. No subject had the PAF-AH (G994T) allele. Thus, elevated plasma PAF levels occur in E. coli O157:H7-infected children, even without HUS, but diminish when HUS develops. The PAF-AH (G994T) allele does not contribute to the risk of developing HUS. [ABSTRACT FROM AUTHOR]

Reports on the characterization of gnd alleles in Escherichia coli with specific lipopolysaccharide antigens in a variety of lineages. Relationship between Escherichia coli O55 and O157 gnd alleles; Nucleotide divergence between gnd sequences at synonymous and nonsynonymous sites; Evidence for intragenic recombination of alleles A and C.