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    <title>Price, L.J.</title>
    <link>http://repub.eur.nl/res/aut/11080/</link>
    <description>List of Publications</description>
    <language>en</language>
    <image>
      <url>http://repub.eur.nl/static-eur/img/logo.png</url>
      <title>RePub, Erasmus University Rotterdam</title>
      <link>http://repub.eur.nl</link>
    </image>
    <item>
      <title>Risk factors associated with Campylobacter jejuni infections in Curacao, Netherlands Antilles (Article)</title>
      <link>http://repub.eur.nl/res/pub/10271/</link>
      <pubDate>2003-01-01T00:00:00Z</pubDate>
      <description>A steady increase in the incidence of Guillain-Barre syndrome (GBS) with a
      seasonal preponderance, almost exclusively related to Campylobacter
      jejuni, and a rise in the incidence of laboratory-confirmed Campylobacter
      enteritis have been reported from Curacao, Netherlands Antilles. We
      therefore investigated possible risk factors associated with diarrhea due
      to epidemic C. jejuni. Typing by pulsed-field gel electrophoresis
      identified four epidemic clones which accounted for almost 60% of the
      infections. One hundred six cases were included in a case-control study.
      Infections with epidemic clones were more frequently observed in specific
      districts in Willemstad, the capital of Curacao. One of these clones
      caused infections during the rainy season only and was associated with the
      presence of a deep well around the house. Two out of three GBS-related C.
      jejuni isolates belonged to an epidemic clone. The observations presented
      point toward water as a possible source of Campylobacter infections.</description>
    </item> <item>
      <title>Molecular characterization of Campylobacter jejuni from patients with Guillain-Barré and Miller Fisher syndromes (Article)</title>
      <link>http://repub.eur.nl/res/pub/9376/</link>
      <pubDate>2000-01-01T00:00:00Z</pubDate>
      <description>Campylobacter jejuni has been identified as the predominant cause of
          antecedent infection in Guillain-Barre syndrome (GBS) and Miller Fisher
          syndrome (MFS). The risk of developing GBS or MFS may be higher after
          infection with specific C. jejuni types. To investigate the putative
          clonality, 18 GBS- or MFS-related C. jejuni strains from The Netherlands
          and Belgium and 17 control strains were analyzed by serotyping (Penner and
          Lior), restriction fragment length polymorphism analysis of PCR products
          of the flaA gene, amplified fragment length polymorphism analysis,
          pulsed-field gel electrophoresis, and randomly amplified polymorphic DNA
          analysis. Serotyping revealed 10 different O serotypes and 7 different
          Lior serotypes, thereby indicating a lack of serotype clustering. Two new
          O serotypes, O:35 and O:13/65, not previously associated with GBS or MFS
          were found. Serotype O:19 was encountered in 2 of 18 strains, and none was
          of serotype O:41. The results of all genotypic methods also demonstrated
          substantial heterogeneity. No clustering of GBS- or MFS-related strains
          occurred and no molecular marker capable of separating pathogenic GBS or
          MFS from non-GBS- or non-MFS-related enteritis strains could be identified
          in this study. Sialic-acid-containing lipopolysaccharides (LPS) are
          thought to be involved in the triggering of GBS or MFS through molecular
          mimicry with gangliosides in human peripheral nerves. Therefore, further
          characterization of GBS- or MFS-related C. jejuni should target the genes
          involved in the synthesis of LPS and the incorporation of sialic acid.</description>
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