Clonal analysis of the serogroup B meningococci causing New Zealand's epidemic

• Published in: Epidemiology and infection Vol. 134; no. 2; pp. 377 - 383
• Main Authors: DYET, K. H., MARTIN, D. R.
• Format: Journal Article
• Language: English
• Published: Cambridge, UK Cambridge University Press 01.04.2006
• Subjects: Alleles; Bacteriology; Biological and medical sciences; Clone Cells; Disease Outbreaks; DNA; DNA, Bacterial - analysis; Environmental science; Epidemics; Epidemiology; Fundamental and applied biological sciences. Psychology; Genetic loci; Genetic Variation; Glycerol; Humans; Laboratories; Meningitis, Meningococcal - epidemiology; Microbiology; Miscellaneous; Molecular Epidemiology; Neisseria meningitidis; Neisseria meningitidis, Serogroup B - genetics; Neisseria meningitidis, Serogroup B - pathogenicity; New Zealand - epidemiology; Nucleotides; Polymerase Chain Reaction; Polymorphism, Restriction Fragment Length; RNA, Ribosomal, 16S; rRNA genes; Sequencing; New Zealand; Oceania; United States > US; Germany; Epidemic; Human; Microbiology; Neisseriaceae; Bacteria; Micrococcales; Neisseria meningitidis; Epidemiology
• ISSN: 0950-2688; 1469-4409
• DOI: 10.1017/S0950268805004954

An epidemic of meningococcal disease caused by serogroup B meningococci expressing the P1.7-2,4 PorA protein began in New Zealand in 1991. The PorA type has remained stable. Different porB have been found in association with the P1.7-2,4 PorA, although type 4 has been most common. The clonal origins of B:P1.7-2,4 meningococci isolated from cases during 1990 to the end of 2003 were analysed. In 1990, the year immediately preceding the recognized increase in disease rates, all three subclones (ST-41, ST-42, and ST-154) of the ST-41/44 clonal complex occurred among the five isolates of B:P1.7-2,4. The two sequence types, ST-42 and ST-154, continued to cause most disease throughout New Zealand. Isolates belonging to subclone ST-41 were mostly identified early in the epidemic and in the South Island. 16S rRNA typing indicated that isolates belonging to the subclones ST-41 and ST-154 share a common ancestor, with those typing as ST-42 more distantly related with some genetically ambiguous. It is possible that ST-41 and ST-154 may have evolved one from the other but evolution to ST-42 is more difficult to explain. It is possible that one or more of the ST types could have been introduced into New Zealand prior to the first detection of clinical cases in 1990. Genetic diversity may have occurred during carriage in the community.