ABO and P1 Blood Group Antigen Expression and<i>stx</i>Genotype and Outcome of Childhood<i>Escherichia coli</i>O157:H7 Infections

Jelačić, Srdjan; Wobbe, Cheryl L.; Boster, Daniel R.; Ciol, Márcia A.; Watkins, Sandra L.; Tarr, Phillip I.; Stapleton, Ann E.

doi:10.1086/338480

Cited by 33 publications

(16 citation statements)

References 30 publications

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“…A similar hypothesis has been proposed for P blood types in human patients (32). However, a recent study refuted this possibility by showing that the P1 blood group was equally represented in healthy controls and E. coli O157:H7-infected children regardless of whether patients had uncomplicated illness or HUS (13), confirming the findings of previous studies that failed to associate P1 expression with diminished risk for the development of HUS after infection with E. coli O157:H7 (2,21,24,27).…”

Section: Discussionsupporting

confidence: 73%

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Binding of Shiga Toxin 2e to Porcine Erythrocytes In Vivo and In Vitro

et al. 2003

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Section: Discussionsupporting

confidence: 73%

“…Stx bind to human RBCs, monocytes, and neutrophils in vitro without causing morphological changes in these cells (4,26,34 (32). However, epidemiological data suggest that the P1 phenotype does not protect STEC-infected patients from HUS (2,13,21,24,27).…”

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confidence: 99%

Binding of Shiga Toxin 2e to Porcine Erythrocytes In Vivo and In Vitro

et al. 2003

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“…The bacteriophage that encodes Stx2 is integrated into wrbA (32,40), which encodes a novel multimeric flavodoxin-like protein (13), and is flanked by duplications of GACATATTGAAAC. Almost all E. coli O157:H7 strains possess stx 2 , and approximately three-quarters contain, in addition, stx 1 (strains lacking stx 1 are referred to hereafter as stx 1 -negative strains) (23,38,45). Most human non-O157:H7 Stx-producing E. coli (STEC) strains possess stx 1 but lack stx 2 (5,6,28,51).…”

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confidence: 99%

Escherichia coli O157:H7 Shiga Toxin-Encoding Bacteriophages: Integrations, Excisions, Truncations, and Evolutionary Implications

2003

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As it descended from Escherichia coli O55:H7, Shiga toxin (Stx)-producing E. coli (STEC) O157:H7 is believed to have acquired, in sequence, a bacteriophage encoding Stx2 and another encoding Stx1. Between these events, sorbitol-fermenting E. coli O157:H ؊ presumably diverged from this clade. We employed PCR and sequence analyses to investigate sites of bacteriophage integration into the chromosome, using evolutionarily informative STEC to trace the sequence of acquisition of elements encoding Stx. Contrary to expectations from the two currently sequenced strains, truncated bacteriophages occupy yehV in almost all E. coli O157:H7 strains that lack stx 1 (stx 1 -negative strains). Two truncated variants were determined to contain either GTT or TGACTGTT sequence, in lieu of 20,214 or 18,895 bp, respectively, of the bacteriophage central region. A single-nucleotide polymorphism in the latter variant suggests that recombination in that element extended beyond the inserted octamer. An stx 2 bacteriophage usually occupies wrbA in stx 1 ؉ /stx 2 ؉ E. coli O157:H7, but wrbA is unexpectedly unoccupied in most stx 1 -negative/stx 2 ؉ E. coli O157:H7 strains, the presumed progenitors of stx 1 ؉ /stx 2 ؉ E. coli O157:H7. Trimethoprim-sulfamethoxazole promotes the excision of all, and ciprofloxacin and fosfomycin significantly promote the excision of a subset of complete and truncated stx bacteriophages from the E. coli O157:H7 strains tested; bile salts usually attenuate excision. These data demonstrate the unexpected diversity of the chromosomal architecture of E. coli O157:H7 (with novel truncated bacteriophages and multiple stx 2 bacteriophage insertion sites), suggest that stx 1 acquisition might be a multistep process, and compel the consideration of multiple exogenous factors, including antibiotics and bile, when chromosome stability is examined.Shiga toxins 1 and 2 (Stx1 and Stx2) are cardinal virulence factors of Escherichia coli O157:H7. Stx1 is nearly identical to Stx, the principal extracellular cytotoxin of Shigella dysenteriae serotype 1 (8). Stx2 has 56% identity to Stx1 (36). The stx 1 and stx 2 A and B subunit genes exist as tandem open reading frames (ORFs) in the central portion of lambdoid bacteriophages in E. coli O157:H7 (19). In Sakai and EDL933, the two E. coli O157:H7 strains that have been completely sequenced, the bacteriophage that encodes Stx1 is integrated into yehV (57), which encodes a protein that positively regulates curli expression (7), and is flanked by duplications of CCCTGT CACGTTACGCGCGTG. The bacteriophage that encodes Stx2 is integrated into wrbA (32, 40), which encodes a novel multimeric flavodoxin-like protein (13), and is flanked by duplications of GACATATTGAAAC. Almost all E. coli O157:H7 strains possess stx 2 , and approximately three-quarters contain, in addition, stx 1 (strains lacking stx 1 are referred to hereafter as stx 1 -negative strains) (23,38,45). Most human non-O157:H7 Stx-producing E. coli (STEC) strains possess stx 1 but lack stx 2 (5, 6, 28, 51). Except for an Stx2...

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“…For example, reliance on an abnormal urinalysis to define HUS, especially if the serum creatinine is normal, risks consideration of incorrect diagnoses such as urinary tract infections, especially as the possibility of contamination with fecal material is high in the setting of diarrhea. Moreover, these widely available blood tests enable physicians to relate their patient's course to those described in many other studies during the past 3 decades from multiple countries (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31).…”

Section: Definitionsmentioning

confidence: 99%

Shiga Toxin/Verocytotoxin-Producing Escherichia coli Infections: Practical Clinical Perspectives

2014

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Escherichia coli strains that produce Shiga toxins/verotoxins are rare, but important, causes of human disease. They are responsible for a spectrum of illnesses that range from the asymptomatic to the life-threatening hemolyticuremic syndrome; diseases caused by E. coli belonging to serotype O157:H7 are exceptionally severe. Each illness has a fairly predictable trajectory, and good clinical practice at one phase can be inappropriate at other phases. Early recognition, rapid and definitive microbiology, and strategic selection of tests increase the likelihood of good outcomes. The best management of these infections consists of avoiding antibiotics, antimotility agents, and narcotics and implementing aggressive intravenous volume expansion, especially in the early phases of illness.

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ABO and P1 Blood Group Antigen Expression andstxGenotype and Outcome of ChildhoodEscherichia coliO157:H7 Infections

Cited by 33 publications

References 30 publications

Binding of Shiga Toxin 2e to Porcine Erythrocytes In Vivo and In Vitro

Binding of Shiga Toxin 2e to Porcine Erythrocytes In Vivo and In Vitro

Escherichia coli O157:H7 Shiga Toxin-Encoding Bacteriophages: Integrations, Excisions, Truncations, and Evolutionary Implications

Shiga Toxin/Verocytotoxin-Producing Escherichia coli Infections: Practical Clinical Perspectives

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