Hostname: page-component-848d4c4894-m9kch Total loading time: 0 Render date: 2024-05-16T12:04:32.368Z Has data issue: false hasContentIssue false

High case-fatality rates of meningococcal disease in Western Norway caused by serogroup C strains belonging to both sequence type (ST)-32 and ST-11 complexes, 1985–2002

Published online by Cambridge University Press:  02 May 2006

I. SMITH
Affiliation:
Institute of Medicine, University of Bergen, Bergen, Norway
D. A. CAUGANT
Affiliation:
Department of Airborne Infections, Division of Infectious Disease Control, Norwegian Institute of Public Health, Oslo, Norway Department of Oral Biology, University of Oslo, Oslo, Norway
E. A. HØIBY
Affiliation:
Department of Airborne Infections, Division of Infectious Disease Control, Norwegian Institute of Public Health, Oslo, Norway
T. WENTZEL-LARSEN
Affiliation:
Centre for Clinical Research, Haukeland University Hospital, Bergen, Norway
A. HALSTENSEN
Affiliation:
Institute of Medicine, University of Bergen, Bergen, Norway Department of Medicine, Haukeland University Hospital, Bergen, Norway
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

A total of 293 meningococcal disease (McD) patients from Western Norway hospitalized during 1985–2002 were examined for risk factors related to death. The case-fatality rate (CFR) increased from 4% during 1985–1993 to 17% during 1994–2002. We analysed the phenotypic and genotypic characteristics of the meningococcal patient isolates, with the aim of identifying whether highly virulent meningococcal strains contributed to the increased CFR. The Norwegian epidemic strain B:15:P1.7,16/ST-32 complex was overall the most common phenotype/genotype (n=75) and caused most deaths (n=9; CFR 12·0%). However, fatality was significantly associated with disease caused by serogroup C meningococcal strains; C:15:P1.7,16/ST-32 and C:2a/ST-11 complex strains, which had the highest CFRs of 21·1% and 18·2% respectively. Serogroup B strains of the ST-32 complex differing by serotype and/or serosubtype from the epidemic strain had a CFR of 5·1%, while the CFR of disease caused by other strains (all phenotypes and genotypes pooled) was 2·2%. The distribution of phenotypes/clonal complexes varied significantly between 1985–1993 and 1994–2002 (P<0·001); B:15/ST-32 complex strains decreased whereas both C:15:P1.7,16/ST-32 complex strains and strains with other phenotypes/clonal complexes increased. Our results indicate that C:15:P1.7,16/ST-32 and C:2a/ST-11 complex strains were highly virulent strains and contributed to the high CFR of McD in patients from Western Norway. To reduce fatality, rapid identification of such virulent strains is necessary. In addition, early and specific measures should include public information, vaccination of populations at risk of disease and carriage eradication, when clustering of patients occurs.

Type
Research Article
Copyright
2006 Cambridge University Press