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Chapter 2 : Genotypic Changes in Enterohemorrhagic During Human Infection

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Genotypic Changes in Enterohemorrhagic During Human Infection, Page 1 of 2

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Abstract:

The chapter begins with an overview of epidemiology and clinical pathogenesis of Enterohemorrhagic (EHEC). EHEC causes diarrhea, bloody diarrhea, and hemolytic-uremic syndrome (HUS). The major virulence factor of EHEC responsible for the microvascular endothelial injury is Shiga toxin (Stx). In additon to Stx, several other potential virulence determinants have been identified in EHEC. Next, the chapter focuses on genomes of EHEC. The lability of horizontally acquired genomic elements, such as pathogenicity islands, and especially of bacteriophages, increases the possibility of genomic alterations during human infections. Most EHEC strains possess one or more large plasmids. To investigate genetic changes of EHEC in patients with HUS, consecutive stool samples from such patients was analyzed by detecting and genes and by using a cytotoxicity assay to detect free Stx. Further, the chapter talks about interserotype differences in conversion of EHEC to EHEC-LST, and consequences of in vivo genetic changes in EHEC. To identify both EHEC and EHEC-LST in stool samples, detection of must be complemented by detection of -independent target(s) which are common to both pathotypes. Genetic changes in EHEC during infection might influence clinical outcome and have impacts on diagnosis, epidemiology, and evolution. For clinicians, awareness of a potential conversion of the pathotype of the infecting EHEC during infection is essential in making decisions about correct management of the patients and appropriate therapies.

Citation: Mellmann A, Bielaszewska M, Karch H. 2012. Genotypic Changes in Enterohemorrhagic During Human Infection, p 16-26. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch2

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FIGURE 1

Minimum spanning tree based on the allelic profiles of an MLST analysis of 42 / EHEC strains (red), representing all currently known serotypes and MLST sequence types (ST) of HUS-associated EHEC, and 17 / strains (EHEC-LST; green) from corresponding serogroups O26, O103, O121, O145, and O157. Each ST is represented by a circle labeled with its ST. The numbers on the connecting lines represent the number of differing alleles from the seven housekeeping genes of the MLST scheme. Clonal complexes (CC) are, if applicable, shaded in grey and named in accordance with the MLST website (http://mlst.ucc.ie/mlst/dbs/Ecoli)

Citation: Mellmann A, Bielaszewska M, Karch H. 2012. Genotypic Changes in Enterohemorrhagic During Human Infection, p 16-26. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch2
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Image of FIGURE 2
FIGURE 2

Schematic presentation of loss and gain during the development of new EHEC clones by phage induction, release, and transduction of phages. Q, transcription activator, S, cell lysis protein.

Citation: Mellmann A, Bielaszewska M, Karch H. 2012. Genotypic Changes in Enterohemorrhagic During Human Infection, p 16-26. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch2
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