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dc.contributor.authorToma, Claudia-
dc.contributor.authorMartínez Espinosa, Estela-
dc.contributor.authorSong, Tianyan-
dc.contributor.authorMiliwebsky, Elizabeth-
dc.contributor.authorChinen, Isabel-
dc.contributor.authorIyoda, Sunao-
dc.contributor.authorIwanaga, Masaaki-
dc.contributor.authorRivas, Marta-
dc.date.accessioned2012-10-25T04:36:03Z-
dc.date.available2012-10-25T04:36:03Z-
dc.date.issued2004-
dc.identifier.issn1098-660X-
dc.identifier.urihttp://sgc.anlis.gob.ar/handle/123456789/274-
dc.identifier.urihttp://jcm.asm.org/content/42/11/4937.full.pdf+html-
dc.descriptionThe distribution of eight putative adhesins that are not encoded in the locus for enterocyte effacement (LEE) in 139 Shiga toxin-producing Escherichia coli (STEC) of different serotypes was investigated by PCR. Five of the adhesins (Iha, Efa1, LPFO157/OI-141, LPFO157/OI-154, and LPFO113) are encoded in regions corresponding to genomic O islands of E. coli EDL933, while the other three adhesins have been reported to be encoded in the STEC megaplasmid of various serotypes (ToxB [O157:H7], Saa [O113:H21], and Sfp [O157:NM]). STEC strains were isolated from humans (n 54), animals (n 52), and food (n 33). They were classified into five seropathotypes (A through E) based on the reported occurrence of STEC serotypes in human disease, in outbreaks, and in the hemolytic-uremic syndrome (M. A. Karmali, M. Mascarenhas, S. Shen, K. Ziebell, S. Johnson, R. Reid-Smith, J. Isaac-Renton, C. Clark, K. Rahn, and J. B. Kaper, J. Clin. Microbiol. 41:4930-4940, 2003). The most prevalent adhesin was that encoded by the iha gene (91%; 127 of 139 strains), which was distributed in all seropathotypes. toxB and efa1 were present mainly in strains of seropathotypes A and B, which were LEE positive. saa was present only in strains of seropathotypes C, D, and E, which were LEE negative. Two fimbrial genes, lpfAO157/OI-141 and lpfAO157/OI-154, were strongly associated with seropathotype A. The fimbrial gene lpfAO113 was present in all seropathotypes except for seropathotype A, while sfpA was not present in any of the strains studied. The distribution of STEC adhesins depends mainly on serotypes and not on the source of isolation. Seropathotype A, which is associated with severe disease and frequently is involved in outbreaks, possesses a unique adhesin profile which is not present in the other seropathotypes. The wide distribution of iha in STEC strains suggested that it could be a candidate for vaccine development.ES
dc.descriptionFil: Toma, Claudia. University of the Ryukyus. Division of Bacterial Pathogenesis; Japón.ES
dc.descriptionFil: Martínez Espinosa, Estela. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Fisiopatogenia; Argentina.ES
dc.descriptionFil: Song, Tianyan. University of the Ryukyus. Division of Bacterial Pathogenesis; Japón.ES
dc.descriptionFil: Miliwebsky, Elizabeth. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Fisiopatogenia; Argentina.ES
dc.descriptionFil: Chinen, Isabel. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Fisiopatogenia; Argentina.ES
dc.descriptionFil: Iyoda, Sunao. National Institute of Infectious Diseases. Department of Bacteriology; Japón.ES
dc.descriptionFil: Iwanaga, Masaaki. University of the Ryukyus. Division of Bacterial Pathogenesis; Japón.ES
dc.descriptionFil: Rivas, Marta. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Servicio de Fisiopatogenia; Argentina.ES
dc.formatapplication/pdfES
dc.language.isoengen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.sourceJournal of Clinical Microbiology, 2004, 42(11), 4937–4946.en_US
dc.subjectEscherichia coli O157en_US
dc.subjectAdhesinas de Escherichia colien_US
dc.subjectInfecciones por Escherichia colien_US
dc.subjectMicrobiología de Alimentosen_US
dc.subjectToxinas Shigaen_US
dc.subjectSerotipificaciónen_US
dc.subjectHumanosen_US
dc.subjectAnimalesen_US
dc.titleDistribution of putative adhesins in different seropathotypes of Shiga toxin-producing Escherichia colien_US
dc.typeArtículoes
anlis.essnrd1es
item.grantfulltextopen-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.openairetypeArtículo-
item.fulltextWith Fulltext-
crisitem.author.deptAdministración Nacional de Laboratorios e Institutos de Salud “Dr. Carlos G. Malbrán” (ANLIS)-
crisitem.author.deptInstituto Nacional de Enfermedades Infecciosas (INEI)-
crisitem.author.deptDepartamento de Bacteriología-
crisitem.author.deptServicio de Fisiopatogenia-
crisitem.author.deptAdministración Nacional de Laboratorios e Institutos de Salud “Dr. Carlos G. Malbrán” (ANLIS)-
crisitem.author.deptInstituto Nacional de Enfermedades Infecciosas (INEI)-
crisitem.author.deptDepartamento de Bacteriología-
crisitem.author.deptServicio de Fisiopatogenia-
crisitem.author.deptAdministración Nacional de Laboratorios e Institutos de Salud “Dr. Carlos G. Malbrán” (ANLIS)-
crisitem.author.deptInstituto Nacional de Enfermedades Infecciosas (INEI)-
crisitem.author.deptDepartamento de Bacteriología-
crisitem.author.deptServicio de Fisiopatogenia-
crisitem.author.parentorgAdministración Nacional de Laboratorios e Institutos de Salud “Dr. Carlos G. Malbrán” (ANLIS)-
crisitem.author.parentorgInstituto Nacional de Enfermedades Infecciosas (INEI)-
crisitem.author.parentorgDepartamento de Bacteriología-
crisitem.author.parentorgAdministración Nacional de Laboratorios e Institutos de Salud “Dr. Carlos G. Malbrán” (ANLIS)-
crisitem.author.parentorgInstituto Nacional de Enfermedades Infecciosas (INEI)-
crisitem.author.parentorgDepartamento de Bacteriología-
crisitem.author.parentorgAdministración Nacional de Laboratorios e Institutos de Salud “Dr. Carlos G. Malbrán” (ANLIS)-
crisitem.author.parentorgInstituto Nacional de Enfermedades Infecciosas (INEI)-
crisitem.author.parentorgDepartamento de Bacteriología-
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