Population genetics and molecular epidemiology of Neisseria meningitidis

WHO Collaborating Centre for Reference and Research on Meningococci, Department of Bacteriology, National Institute of Public Health, Oslo, Norway.
Apmis (Impact Factor: 2.04). 06/1998; 106(5):505-25. DOI: 10.1111/j.1699-0463.1998.tb01379.x
Source: PubMed


Under non-epidemic conditions, Neisseria meningitidis causes disease primarily in children under the age of 5 and the cases are sporadic without any evident relationship between them. Occasionally, localized outbreaks of meningococcal disease occur, and sometimes epidemic waves of disease may spread to several countries or even continents and constitute a pandemic. In the past 10 years or so, population genetic analyses have provided insights into the biology of the bacterium and the epidemiology of meningococcal disease, improving our understanding of the cause of epidemics. Through the application of molecular methods, and especially multilocus enzyme electrophoresis, to N. meningitidis strains of worldwide origin, it has been possible to identify virulent clones and provide a surveillance system to warn of meningococcal epidemics. The characteristics of the predominant clones which are nowadays causing meningococcal disease in the world are summarized here and the importance of population genetics in interpreting the epidemiological data is illustrated.

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    • "Despite low carriage rates, ST-11 meningococci continue to be associated with sporadic outbreaks worldwide [4]. These hyper-invasive strains require massive public health investigations and interventions due to the high mortality among cases [19-21]. "
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    ABSTRACT: To assess changes in the pattern of Invasive Meningococcal Disease (IMD) in Italy after the introduction of conjugate menC vaccine in the National Vaccine Plan 2005-2007 and to provide information for developing timely and appropriate public health interventions, analyses of microbiological features of isolates and clinical characteristics of patients have been carried out. In Italy, the number of serogroup C meningococci fell progressively following the introduction of the MenC conjugate vaccine, recommended by the Italian Ministry of Health but implemented according to different regional strategies. IMD cases from January 2005 through July 2008 reported to the National Meningococcal Surveillance System were considered for this study. Serogrouping and sero/subtyping were performed on 179 serogroup C strains received at the National Reference Laboratory of the Istituto Superiore di Sanità. Antibiotic susceptibility testing was possible for 157 isolates. MLST (Multilocus sequence typing), porA VRs (Variable Region) typing, PFGE (Pulsed Field Gel Electrophoresis), VNTR (Variable Number Tandem Repeats) analyses were performed on all C:2a and C:2b meningococci (n = 147), following standard procedures. In 2005 and 2008, IMD showed an incidence of 0.5 and 0.3 per 100,000 inhabitants, respectively. While the incidence due to serogroup B remained stable, IMD incidence due to serogroup C has decreased since 2006. In particular, the decrease was significant among infants. C:2a and C:2b were the main serotypes, all C:2a strains belonged to ST-11 clonal complex and all C:2b to ST-8/A4. Clinical manifestations and outcome of infections underlined more severe disease caused by C:2a isolates. Two clusters due to C:2a/ST-11 meningococci were reported in the North of Italy in December 2007 and July 2008, respectively, with a high rate of septicaemia and fatal outcome. Public health surveillance of serogroup C invasive meningococcal disease and microbiological/molecular characterization of the isolates requires particular attention, since the hyper-invasive ST-11 predominantly affected adolescents and young adults for whom meningococcal vaccination was not recommended in the 2005-2007 National Vaccine Plan.
    BMC Infectious Diseases 09/2009; 9(1):135. DOI:10.1186/1471-2334-9-135 · 2.61 Impact Factor
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    • "Despite their high diversity, meningococcal populations are structured into lineages that are identified as clonal complexes (cc) by multilocus sequence typing (MLST) (Maiden et al., 1998). Only a minority of these, the socalled hyperinvasive lineages, are regularly associated with human disease (Caugant, 2001; Maiden et al., 1998; Yazdankhah et al., 2004). The prevalence of these lineages varies geographically and temporally but each complex tends to be associated with a particular repertoire of surface antigens (Urwin et al., 2004). "
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    ABSTRACT: A comprehensive meningococcal vaccine is yet to be developed. In the absence of a vaccine that immunizes against the serogroup B capsular polysaccharide, this can only be achieved by targeting subcapsular antigens, and a number of outer-membrane proteins (OMPs) are under consideration as candidates. A major obstacle to the development of such a vaccine is the antigenic diversity of these OMPs, and obtaining population data that accurately identify and catalogue these variants is an important component of vaccine design. The recently proposed meningococcal molecular strain-typing scheme indexes the diversity of two OMPs, PorA and FetA, that are vaccine candidates, as well as the capsule and multilocus sequence type. This scheme was employed to survey 323 meningococci isolated from invasive disease in England and Wales from 1975 to 1995, before the introduction of meningococcal conjugated serogroup C polysaccharide vaccines in 1999. The eight-locus typing scheme provided high typeability (99.4 %) and discrimination (Simpson's diversity index 0.94-0.99). The data showed cycling of meningococcal genotypes and antigenic types in the absence of planned interventions. Notwithstanding high genetic and antigenic diversity, most of the isolates belonged to one of seven clonal complexes, with 11 predominant strain types. Combinations of PorA and FetA, chosen on the basis of their prevalence over time, generated vaccine recipes that included protein variants found in 80 % or more of the disease isolates for this time period. If adequate immune responses can be generated, these results suggest that control of meningococcal disease with relatively simple protein component vaccines may be possible.
    Microbiology 05/2008; 154(Pt 4):1170-7. DOI:10.1099/mic.0.2007/014761-0 · 2.56 Impact Factor
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    • "Neisseria meningitidis is a common cause of disease worldwide, responsible for significant morbidity and mortality in infants and young children (Bilukha and Rosenstein, 2005). Without appropriate antimicrobial treatment, most cases of meningococcal meningitis are fatal (Flexner, 1913), and even with prompt intervention the case fatality rate (CFR) reaches 10% (Caugant, 1998). Among those who survive, permanent sequelae, including deafness, cognitive impairment and paralysis, are common (Edwards and Baker, 1981;Kirsch et al., 1996). "
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    ABSTRACT: This study aimed to describe the clinical, epidemiological and microbiological features of meningococcal meningitis in Salvador, Brazil. Between February 1996 and January 2001, a hospital-based surveillance prospectively identified cases of culture-positive meningococcal meningitis. Demographic and clinical data were collected through interview and medical chart review. Antisera and monoclonal antibodies were used to determine the serogroup and serotype:serosubtype of the isolates, respectively. Surveillance identified a total of 408 cases of meningococcal meningitis, with a case fatality rate of 8% (32/397). The mean annual incidence for the 304 culture-positive cases residing in metropolitan Salvador was 1.71 cases per 100,000 population. Infants <1 year old presented the highest incidence (14.7 cases per 100,000 population). Of the 377 serogrouped isolates, 82%, 16%, 2% and 0.3% were serogroups B, C, W135 and Y, respectively. A single serotype:serosubtype (4,7:P1.19,15) accounted for 64% of all cases. Continued surveillance is necessary to characterise strains and to define future prevention and control strategies.
    Transactions of the Royal Society of Tropical Medicine and Hygiene 11/2007; 101(11):1147-53. DOI:10.1016/j.trstmh.2007.06.012 · 1.84 Impact Factor
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