Many carried meningococci lack the genes required for capsule synthesis and transport
               The GenBank accession number for the sequence of the cnl-1 allele is AJ308327.

Claus, Heike; Maiden, Martin C. J.; Maag, R.; Frosch, Matthias; Vogel, Ulrich

doi:10.1099/00221287-148-6-1813

Cited by 158 publications

(141 citation statements)

References 39 publications

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“…Interestingly, seven samples were ctrA PCR-negative. All ctrA PCR-negative samples were non-groupable, so this could be explained by meningococci not possessing the genes necessary for capsule expression, as reported by Claus et al (2002). Of the seven ctrA PCR-negative samples, three were porA PCR-positive and four were nested porA PCR-positive; although potential false-positives have been reported when using IS1106 as a target (Borrow et al, 1998b), this was clearly not the case in this study.…”

Section: Discussioncontrasting

confidence: 42%

Detection and genotyping of meningococci using a nested PCR approach

Diggle

Clarke

2003

Journal of Medical Microbiology

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An effective vaccine against Neisseria meningitidis serogroup B is required. Outer-membrane protein vaccines have been developed, which may provide protection against common circulating serotypes and serosubtypes in some countries. However, limited genosubtyping data are available because most laboratories use mAbs directed against a limited number of specific serotypes and serosubtypes and laboratories do not genosubtype directly from body fluids due to the lack of a sensitive PCR method. A nested PCR was therefore developed that enables the amplification of the porA gene directly from clinical samples and has the required sensitivity for nucleotide sequencing of the three main variable regions, VR1, VR2 and VR3. Data were compared with those from culturebased nucleotide sequencing, and the use of this method increased the availability of genosubtype information by 45 %, thereby indicating the impact that this methodology has on the data provided and the implications for vaccine design. INTRODUCTIONMeningococcal disease remains a significant public health problem, and a vaccine against Neisseria meningitidis serogroup B is urgently needed (Rosenstein et al., 2001). However, the use of a capsule-based vaccine is unlikely because the meningococcal polysaccharide is identical to a human carbohydrate [AE (2 ! 8) N-acetyl neuraminic acid or polysialic acid] (Finne et al., 1987;Hayrinen et al., 1995). Vaccines based on other antigens therefore require development and the outer-membrane proteins (OMPs) of the meningococcus have been investigated (Rosenstein et al., 2001;Al'Aldeen & Cartwright, 1996). Although OMP-based vaccines are not the solution for combating serogroup B meningococcal infection, they may be useful in some circumstances (Al'Aldeen & Cartwright, 1996;Rappuoli, 2001). However, such proteins are highly antigenically variable, and an OMP vaccine cannot protect against all serotypes and serosubtypes of N. meningitidis. Therefore, selected OMPs must be used, based on the prevalent serotypes and serosubtypes in a given population. However, to develop such vaccines, high-quality data must be gained to determine such prevalence. To date, the characterization of meningococci has relied on serogrouping, serotyping and serosubtyping using serological methods, thereby limiting the designation of serotypes and serosubtypes because a panel of mAbs is used. Newer nucleotide sequence methods, based on the detection and sequencing of the porB and porA genes for serotype (class 2/3 OMP) and serosubtype (class 1 OMP), respectively, have led to a better understanding of the variability of these proteins (Urwin et al., 1998a, b, c;Clarke et al., 2001a;Jelfs et al., 2000;Molling et al., 2000;Feavers et al., 1996;Saunders et al., 1993;Smith et al., 1995). However, most of these methods are only useful when N. meningitidis has been isolated from blood or cerebrospinal fluid (CSF) and they therefore rely on the availability of a culture (Jelfs et al., 2000;Feavers et al., 1996). Other methods rely on sufficient numbers of me...

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Section: Discussioncontrasting

confidence: 42%

Detection and genotyping of meningococci using a nested PCR approach

Diggle

Clarke

2003

Journal of Medical Microbiology

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“…These hyperinvasive lineages are known to be persistent, having spread worldwide over many decades (22). Our model also accommodates the phenomenon of unencapsulated meningococci occurring commonly in carriage (30). The hyperinvasive phenotype of meningococci is polygenic with the possession of a capsule a necessary but not sufficient factor; thus, within our framework it may be treated as an element of excess virulence and the lack of it may be simply explained by the frequencies of avirulent forms of all cocirculating STs.…”

Section: Discussionmentioning

confidence: 96%

Role of selection in the emergence of lineages and the evolution of virulence in Neisseria meningitidis

Buckee

Jolley

Recker

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Neisseria meningitis is a human commensal bacterium that occasionally causes life-threatening disease. As with a number of other bacterial pathogens, meningococcal populations comprise distinct lineages, which persist over many decades and during global spread in the face of high rates of recombination. In addition, the propensity to cause invasive disease is associated with particular ''hyperinvasive'' lineages that coexist with less invasive lineages despite the fact that disease does not contribute to host-to-host transmission. Here, by combining a modeling approach with molecular epidemiological data from 1,108 meningococci isolated in the Czech Republic over 27 years, we show that interstrain competition, mediated by immune selection, can explain both the persistence of multiple discrete meningococcal lineages and the association of a subset of these with invasive disease. The model indicates that the combinations of allelic variants of housekeeping genes that define these lineages are associated with very small differences in transmission efficiency among hosts. These findings have general implications for the emergence of lineage structure and virulence in recombining bacterial populations.bacteria ͉ meningococcus ͉ population structure ͉ strain ͉ mathematical model A spectrum of population structures has been identified among bacterial pathogens by multilocus studies of genetic variation in housekeeping genes (1, 2). It ranges from the extremely low diversity observed in Yersinia pestis (3) and Salmonella enterica var Typhi (4) to the very high levels of unstructured diversity found in Helicobacter pylori (5). The majority of pathogenic bacteria investigated to date, however, occupy an intermediate position within this spectrum, being composed of distinct cocirculating lineages that constitute a small subset of the possible allele combinations (6). These intermediate population structures exhibit apparently conflicting signals of both clonal descent and genetic exchange, and the mechanisms whereby they arise and are maintained remain incompletely understood (7).Neisseria meningitidis, the meningococcus, was one of the first bacteria where such an intermediate population structure was described (8-10). Populations of this highly recombining bacterium (11), which has an essentially commensal relationship with the human host, also present the intriguing feature that only certain lineages, the so-called hyperinvasive lineages, are associated with disease (12). These observations present two conceptual challenges: first, how does lineage structure arise in the face of the observed high rates of recombination; and, second, why are some lineages especially virulent, when invasive disease confers no benefit in terms of host-to-host spread (13)?Here, we address these questions by means of a survey of 1,108 meningococci isolated from asymptomatic carriage and disease in the Czech Republic over a 27-year period. The isolates were characterized at seven housekeeping loci by multilocus sequence typing (MLST) (14) and...

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“…Isolates that are rplF negative are characterised by sequencing a fragment of the 16S (small subunit) rRNA gene to confirm genus or lack of bacterial DNA suitable for PCR amplification. All samples are also tested with an assay that sequences the capsule null (cnl) region of the meningococcal chromosome (Claus et al 2002). This region is present in genetically characterised meningococci without a capsule and in all Neisseria species other than meningococci.…”

Section: Molecular Characterisation Of Neisseriamentioning

confidence: 99%