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Euro Surveill. Genetic characterisation of the emerging invasive Neisseria meningitidis serogroup Y in Sweden, 2000 to 2010

Giuseppe

Emeritus
[Source: Eurosurveillance, full text: (LINK). Abstract, edited.]


Eurosurveillance, Volume 16, Issue 23, 09 June 2011
Surveillance and outbreak reports
Genetic characterisation of the emerging invasive Neisseria meningitidis serogroup Y in Sweden, 2000 to 2010



S Thulin Hedberg<SUP>1</SUP>, B T?r?s<SUP>1</SUP>, H Fredlund<SUP>1</SUP>, P Olc?n<SUP>1</SUP>, P M?lling ()<SUP>1</SUP>
  1. National Reference Laboratory for Pathogenic Neisseria, Department of Laboratory Medicine, Clinical Microbiology, ?rebro University Hospital, ?rebro, Sweden
<HR>
Citation style for this article: Thulin Hedberg S, T?r?s B, Fredlund H, Olc?n P, M?lling P. Genetic characterisation of the emerging invasive Neisseria meningitidis serogroup Y in Sweden, 2000 to 2010. Euro Surveill. 2011;16(23):pii=19885. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19885
Date of submission: 11 March 2011
<HR>Neisseria meningitidis serogroups B and C have been responsible for the majority of invasive meningococcal disease in Europe. Recently, an increase of N. meningitidis disease due to serogroup Y has been noted in Sweden (in 2010, the proportion was 39%, with an incidence of 0.23 per 100,000 population), as well as in other northern European countries. We aimed to investigate the clonal pattern of the emerging serogroup Y in Sweden during 2000 to 2010. The serogroup Y isolates identified during this time (n=85) were characterised by multilocus sequence typing and sequencing of the fetA, fHbp, penA, porA and porB genes. The most frequent clone (comprising 28 isolates) with identical allele combinations of the investigated genes, was partly responsible for the observed increased number of N. meningitidis serogroup Y isolates. It was sulfadiazine resistant, with genosubtype P1.5-2,10-1,36-2, sequence type 23, clonal complex 23, porB allele 3-36, fetA allele F4-1, fHbp allele 25 and penA allele 22. The first case with disease due to this clone was identified in 2002: there was a further case in 2004, six during 2006 to 2007, eight during 2008 to 2009, with a peak of 12 cases in 2010. An unusual increase of invasive disease in young adults (aged 20?29 years) caused by this clone was shown, but no increase in mortality rate was observed.

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