Increase of invasive meningococcal serogroup W disease in Europe, 2013 to 2017.

Publications

Krone M, Gray S, Abad R, Skoczyńska A, Stefanelli P, van der Ende A, Tzanakaki G, Mölling P, João Simões M, Křížová P, Emonet S, Caugant DA, Toropainen M, Vazquez J, Waśko I, Knol MJ, Jacobsson S, Rodrigues Bettencourt C, Musilek M, Born R, Vogel U, Borrow R

Euro Surveill. 24 (14) - [2019-04-00; online 2019-04-11]

BackgroundThe total incidence of invasive meningococcal disease (IMD) in Europe has been declining in recent years; however, a rising incidence due to serogroup W (MenW), predominantly sequence type 11 (ST-11), clonal complex 11 (cc11), was reported in some European countries.AimThe aim of this study was to compile the most recent laboratory surveillance data on MenW IMD from several European countries to assess recent trends in Europe.MethodsIn this observational, retrospective study, IMD surveillance data collected from 2013-17 by national reference laboratories and surveillance units from 13 European countries were analysed using descriptive statistics.ResultsThe overall incidence of IMD has been stable during the study period. Incidence of MenW IMD per 100,000 population (2013: 0.03; 2014: 0.05; 2015: 0.08; 2016: 0.11; 2017: 0.11) and the proportion of this serogroup among all invasive cases (2013: 5% (116/2,216); 2014: 9% (161/1,761); 2015: 13% (271/2,074); 2016: 17% (388/2,222); 2017: 19% (393/2,112)) continuously increased. The most affected countries were England, the Netherlands, Switzerland and Sweden. MenW was more frequent in older age groups (≥ 45 years), while the proportion in children (< 15 years) was lower than in other age groups. Of the culture-confirmed MenW IMD cases, 80% (615/767) were caused by hypervirulent cc11.ConclusionDuring the years 2013-17, an increase in MenW IMD, mainly caused by MenW cc11, was observed in the majority of European countries. Given the unpredictable nature of meningococcal spread and the epidemiological potential of cc11, European countries may consider preventive strategies adapted to their contexts.

Clinical Genomics Örebro [Collaborative]

PubMed 30968827

DOI 10.2807/1560-7917.ES.2019.24.14.1800245

Crossref 10.2807/1560-7917.ES.2019.24.14.1800245