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PubMed2025

4CMenB vaccine coverage of invasive serogroup B meningococci collected in Belgium between 2016 and 2022.

Neisseria meningitidis infections can cause life-threatening meningitis and septicemia. In Europe, serogroup B (MenB) is the leading cause of invasive meningococcal disease (IMD), particularly in young children. Genomic surveillance of circulating MenB strains through whole genome sequencing (WGS) provides a powerful tool to assess the potential impact of vaccination strategies, including the 4CMenB vaccine, which is available for infants from 2 months of age. Here, we present a retrospective WGS-based analysis of clinical MenB IMD cases (n = 311) recovered in Belgium from 2016 to 2022 by the Belgian National Reference Center. High-quality WGS data were obtained for 281 of these strains, demonstrating high genetic diversity of the antigen targets included in the 4-component meningococcal serogroup B vaccine 4CMenB (fHbp, PorA, NHBA and NadA) and at the 4CMenB Antigen Sequence Types (BAST) level. Novel antigen combinations, not yet assigned a BAST ID, were detected in 23.5% of isolates. Vaccine coverage was predicted using the Genetic Meningococcal Antigen Typing System (gMATS) and the Meningococcal Deduced Vaccine Antigen Reactivity (MenDeVAR) index. Of the 281 strains, 79.5% (lower limit-upper limit: 68.0-91.5%) were predicted to be covered by the vaccine by gMATS, and 80.7% (lower limit-upper limit: 66.5-95.4%) by MenDeVAR. No evidence of variation in vaccine coverage was found throughout the study period nor between different age groups, demonstrating the broad applicability of 4CMenB. This study highlights the benefits of a pathogen surveillance program and the need for experimental characterization of continuously evolving antigenic subvariants of Neisseria meningitidis.

Humans↗
PubMed1975

Pili on meningococci from primary cultures of nasopharyngeal carriers and cerebrospinal fluid of patients with acute disease.

The nasopharynx of known meningococcal carriers without signs of acute meningococcal disease as well as cerebrospinal fluid from patients with acute meningococcal disease were cultured on Thayer-Martin agar. Pili were observed in negatively stained preparations of over 80% cells from all primary cultures of both nasopharnyx and cerebrospinal fluids. Although pili were abundant on cells from all primary cultures, all pili were lost on serial subculture in the laboratory. This loss of pili from the cell surface on laboratory subculture was not accompanied by a concomitant loss of cell wall blebs.

Acute Disease↗
PubMed1986

A human monoclonal macroglobulin with specificity for alpha(2----8)-linked poly-N-acetyl neuraminic acid, the capsular polysaccharide of group B meningococci and Escherichia coli K1, which crossreacts with polynucleotides and with denatured DNA.

We have described an IgM antibody from a patient with macroglobulinemia specifically reacting with poly-alpha(2----8)N-acetyl neuraminic acid (NeuNAc) the capsular polysaccharide of two important human pathogens, group B meningococcus and E. coli K1. This antibody has a narrowly defined specificity in its interactions with polysaccharides, being unable to bind poly-alpha(2----9)NeuNAc or alternating poly-alpha(2----8)alpha(2----9)NeuNAc. However, it shows interesting crossreactivity with seemingly unrelated polynucleotides and denatured DNA, supporting the hypothesis that charged groups with a given spacing may determine the specificity of antigen-antibody interactions on otherwise dissimilar molecular structures. Despite the crossreactivity with denatured DNA and polynucleotides, the antibody does not appear to have adverse effects in the patient. The antibody protects newborn rats against E. coli K1 infection, as well as the standard horse antiserum H46, and one would expect it to prove useful in humans as an adjunct to antibiotic therapy in infections with group B meningococcus and E. coli K1. We have attempted to clone the antibody-producing cells from peripheral blood, and have shown that the relevant cells are present and can be cultured.

Aged↗
PubMed2005

A chromosomally integrated bacteriophage in invasive meningococci.

Cerebrospinal meningitis is a feared disease that can cause the death of a previously healthy individual within hours. Paradoxically, the causative agent, Neisseria meningitidis, is a common inhabitant of the human nasopharynx, and as such, may be considered a normal, commensal organism. Only in a small proportion of colonized people do the bacteria invade the bloodstream, from where they can cross the blood-brain barrier to cause meningitis. Furthermore, most meningococcal disease is caused by bacteria belonging to only a few of the phylogenetic groups among the large number that constitute the population structure of this genetically variable organism. However, the genetic basis for the differences in pathogenic potential remains elusive. By performing whole genome comparisons of a large collection of meningococcal isolates of defined pathogenic potential we brought to light a meningococcal prophage present in disease-causing bacteria. The phage, of the filamentous family, excises from the chromosome and is secreted from the bacteria via the type IV pilin secretin. Therefore, this element, by spreading among the population, may promote the development of new epidemic clones of N. meningitidis that are capable of breaking the normal commensal relationship with humans and causing invasive disease.

Base Sequence↗
PubMed2006

Antiidiotypic DNA vaccination induces serum bactericidal activity and protection against group B meningococci.

No vaccine is available for preventing infections by serogroup B Neisseria meningitidis (MenB), which accounts for a major portion of meningococcal cases in developed countries, because of the poor immunogenicity of the capsular polysaccharide (CP) even after protein conjugation. We have previously induced anticapsular antibodies by immunization with a single chain variable fragment (scFv), which mimics a protective CP epitope. This surrogate antigen, however, was ineffective at inducing serum bactericidal activity, an accepted marker of protection in humans. Serum bactericidal activity was consistently achieved by immunizing mice with the scFv-encoding gene. Immunization with vectors without a secretory signal sequence before the scFv resulted in markedly higher bactericidal activity relative to those with such a sequence. The induced antibodies were capsule specific, as shown by complete inhibition of bactericidal activity by purified MenB CP and by resistance to killing of MenA or MenC. Moreover, these antibodies were predominantly of the IgG2a isotype, reflecting a T helper type 1 response. Administration of sera from scFv gene-vaccinated animals protected infant rats against MenB bacteremia. These data illustrate the potential of vaccination with genes encoding capsular mimics in providing protection against MenB and other encapsulated bacteria.

Animals↗
PubMed1953

Transformation of type specificity of meningococci; change in heritable type induced by type-specific extracts containing desoxyribonucleic acid.

Heritable type-specific traits have been induced in meningococcus populations by exposure to desoxyribonucleic acid (DNA)-containing extracts derived from meningococcus cells of the type desired. The DNA has been shown to be an essential component of the transforming extract. As in the H. influenzae system, the reaction between the susceptible cell and the DNA responsible for the heritable change requires less than 15 minutes. Only a minute proportion of the total cells exposed to the DNA extracts for a short time are susceptible to the change; but in the growth and reproduction of bacteria susceptible cells appear with fairly predictable frequency. Type I specific traits have been induced in populations of RIIa and SIIa cells. Type IIa specificity has been induced in RIIa cells.

DNA↗
PubMed2001

Rifampicin-resistant meningococci causing invasive disease: detection of point mutations in the rpoB gene and molecular characterization of the strains.

Mutations in the rpoB gene affecting two amino acids were found in eight rifampicin-resistant Neisseria meningitidis group B and C strains isolated in Italy. The Asp542-->Val substitution, documented for the first time in N. meningitidis, was found in four of the isolates; the His552-->Tyr or Asn substitution in the other four resistant strains. Mutations in the mtr gene did not seem to be involved in the resistance since the same mutations occurred in both resistant and susceptible strains. Two different clusters were identified among these resistant strains, without any correlation with the specific mutations detected in the rpoB gene.

Antibiotics, Antitubercular↗