ArticleEpidemiology and infection2006
Clonal analysis of the serogroup B meningococci causing New Zealand's epidemic.
Article in Epidemiology and infection, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- The elusive meningococcal meningitis serogroup: a systematic review of serogroup B epidemiology.BMC infectious diseases · 2010Pooled it
- Functional and specific antibody responses in adult volunteers in new zealand who were given one of two different meningococcal serogroup B outer membrane vesicle vaccines.Clinical and vaccine immunology : CVI · 2007Trial
- Pangenome graphs in infectious disease: a comprehensive genetic variation analysis ofFrontiers in genetics · 2023Article
- Genomic Surveillance of a Globally Circulating Distinct Group W Clonal Complex 11 Meningococcal Variant, New Zealand, 2013-2018.Emerging infectious diseases · 2021Article
- Diversity of meningococci associated with invasive meningococcal disease in the Republic of Ireland over a 19 year period, 1996-2015.PloS one · 2020Article
- Impact of meningococcal vaccination on carriage and disease transmission: A review of the literature.Human vaccines & immunotherapeutics · 2018Review
- Vaccination strategies for the prevention of meningococcal disease.Human vaccines & immunotherapeutics · 2018Review
- Meningococcal Carriage in Military Recruits and University Students during the Pre MenB Vaccination Era in Greece (2014-2015).PloS one · 2016Article
- An expanded age range for meningococcal meningitis: molecular diagnostic evidence from population-based surveillance in Asia.BMC infectious diseases · 2012Article
- Clonal analysis of Neisseria meningitidis serogroup B strains in South Africa, 2002 to 2006: emergence of new clone ST-4240/6688.Journal of clinical microbiology · 2012Article
- Population structure and capsular switching of invasive Neisseria meningitidis isolates in the pre-meningococcal conjugate vaccine era--United States, 2000-2005.The Journal of infectious diseases · 2010Article
- Clonal distribution of disease-associated and healthy carrier isolates of Neisseria meningitidis between 1983 and 2005 in Cuba.Journal of clinical microbiology · 2010Article
- Ex vivo model of meningococcal bacteremia using human blood for measuring vaccine-induced serum passive protective activity.Clinical and vaccine immunology : CVI · 2009Article
- Bactericidal antibody responses induced by meningococcal recombinant chimeric factor H-binding protein vaccines.Infection and immunity · 2008Article
- Vaccine-induced opsonophagocytic immunity to Neisseria meningitidis group B.Clinical and vaccine immunology : CVI · 2008Article
- The VR2 epitope on the PorA P1.7-2,4 protein is the major target for the immune response elicited by the strain-specific group B meningococcal vaccine MeNZB.Clinical and vaccine immunology : CVI · 2006Article
- Article
- Characterization of invasive Neisseria meningitidis from Atlantic Canada, 2009 to 2013: With special reference to the nonpolysaccharide vaccine targets (PorA, factor H binding protein, Neisseria heparin-binding antigen and Neisseria adhesin A).The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicaleArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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