Tags

Type your tag names separated by a space and hit enter

Enterohaemorrhagic Escherichia coli O26:H11/H-: a human pathogen in emergence.
Berl Munch Tierarztl Wochenschr. 2007 Jul-Aug; 120(7-8):279-87.BM

Abstract

Enterohaemorrhagic Escherichia coli (EHEC) O26:H11 have emerged as the most important non-O157:H7 EHEC, with respect to their ability to cause diarrhoea and the haemolytic uraemic syndrome (HUS). HUS is a leading cause of acute renal failure in children, and is mainly caused by EHEC expressing Shiga toxins (Stx) 1 and/or 2. Since 1996, EHEC O26, which produce Stx2 only and appear to have enhanced virulence, have been increasingly isolated from HUS patients in Germany. In contrast, EHEC O26 found in cattle predominantly produce Stx1 as the sole Stx. Additional potential virulence factors of EHEC O26 include cytolysins (EHEC hemolysin), serine proteases (EspP), lymphotoxins (Efal) and adhesins (intimin). The genes encoding the virulence factors are located within pathogenicity islands (eae, efa1), bacteriophages (stx) or plasmids (EHEC-hlyA, espP). In addition, EHEC O26 possess, in contrast to other EHEC, the "high pathogenicity island" (HPI), which is also present in pathogenic Yersiniae. This island contains genes involved in the biosynthesis, regulation and transport of the siderophore yersiniabactin. Comparative genomic analyses between EHEC O26 and non-pathogenic E. coli, as well as investigations of mechanisms involved in the transfer of virulence genes, provide a deeper insight into the evolution of EHEC O26. These studies demonstrate how horizontal transfer of virulence genes, even from distantly related organisms, can lead in brief intervals to the rise of a highly virulent clone within a particular E. coli serotype.The classical bacteriological methods are no longer sufficient to determine the risk posed by EHEC O26. However, knowledge of the complete virulence profiles of these pathogens and understanding their stepwise evolution form a foundation for developing new strategies to prevent human infections and new methods for their laboratory diagnosis.

Authors+Show Affiliations

Institut für Hygiene, und Nationales Konsiliarlaboratorium für Hämolytisch-Urämisches Syndrom, Universität Münster, Robert Koch Str. 41, 48149 Münster, Germany. mbiela@uni-muenster.deNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

17715820

Citation

Bielaszewska, Martina, et al. "Enterohaemorrhagic Escherichia Coli O26:H11/H-: a Human Pathogen in Emergence." Berliner Und Munchener Tierarztliche Wochenschrift, vol. 120, no. 7-8, 2007, pp. 279-87.
Bielaszewska M, Zhang W, Mellmann A, et al. Enterohaemorrhagic Escherichia coli O26:H11/H-: a human pathogen in emergence. Berl Munch Tierarztl Wochenschr. 2007;120(7-8):279-87.
Bielaszewska, M., Zhang, W., Mellmann, A., & Karch, H. (2007). Enterohaemorrhagic Escherichia coli O26:H11/H-: a human pathogen in emergence. Berliner Und Munchener Tierarztliche Wochenschrift, 120(7-8), 279-87.
Bielaszewska M, et al. Enterohaemorrhagic Escherichia Coli O26:H11/H-: a Human Pathogen in Emergence. Berl Munch Tierarztl Wochenschr. 2007 Jul-Aug;120(7-8):279-87. PubMed PMID: 17715820.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Enterohaemorrhagic Escherichia coli O26:H11/H-: a human pathogen in emergence. AU - Bielaszewska,Martina, AU - Zhang,Wenlan, AU - Mellmann,Alexander, AU - Karch,Helge, PY - 2007/8/25/pubmed PY - 2007/9/20/medline PY - 2007/8/25/entrez SP - 279 EP - 87 JF - Berliner und Munchener tierarztliche Wochenschrift JO - Berl Munch Tierarztl Wochenschr VL - 120 IS - 7-8 N2 - Enterohaemorrhagic Escherichia coli (EHEC) O26:H11 have emerged as the most important non-O157:H7 EHEC, with respect to their ability to cause diarrhoea and the haemolytic uraemic syndrome (HUS). HUS is a leading cause of acute renal failure in children, and is mainly caused by EHEC expressing Shiga toxins (Stx) 1 and/or 2. Since 1996, EHEC O26, which produce Stx2 only and appear to have enhanced virulence, have been increasingly isolated from HUS patients in Germany. In contrast, EHEC O26 found in cattle predominantly produce Stx1 as the sole Stx. Additional potential virulence factors of EHEC O26 include cytolysins (EHEC hemolysin), serine proteases (EspP), lymphotoxins (Efal) and adhesins (intimin). The genes encoding the virulence factors are located within pathogenicity islands (eae, efa1), bacteriophages (stx) or plasmids (EHEC-hlyA, espP). In addition, EHEC O26 possess, in contrast to other EHEC, the "high pathogenicity island" (HPI), which is also present in pathogenic Yersiniae. This island contains genes involved in the biosynthesis, regulation and transport of the siderophore yersiniabactin. Comparative genomic analyses between EHEC O26 and non-pathogenic E. coli, as well as investigations of mechanisms involved in the transfer of virulence genes, provide a deeper insight into the evolution of EHEC O26. These studies demonstrate how horizontal transfer of virulence genes, even from distantly related organisms, can lead in brief intervals to the rise of a highly virulent clone within a particular E. coli serotype.The classical bacteriological methods are no longer sufficient to determine the risk posed by EHEC O26. However, knowledge of the complete virulence profiles of these pathogens and understanding their stepwise evolution form a foundation for developing new strategies to prevent human infections and new methods for their laboratory diagnosis. SN - 0005-9366 UR - https://www.unboundmedicine.com/medline/citation/17715820/Enterohaemorrhagic_Escherichia_coli_O26:H11/H_:_a_human_pathogen_in_emergence_ L2 - https://medlineplus.gov/ecoliinfections.html DB - PRIME DP - Unbound Medicine ER -