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PubMed1987

Opsonisation and phagocytosis of group B meningococci by polymorphonuclear leucocytes: comparison of sulphonamide sensitive and resistant strains.

A large proportion of disease caused by sulphonamide resistant strains of group B type 15 meningococci affects patients 10-24 years. In contrast, disease caused by sulphonamide sensitive strains conforms to the usual pattern, and most infection occurs in early childhood. In an attempt to explain this phenomenon possible differences in susceptibility of resistant and sensitive strains to phagocytosis by polymorphonuclear leucocytes were investigated, using radioactively labelled bacteria. In initial experiments a group B resistant strain required higher concentrations of normal human serum and longer opsonisation times for phagocytosis than an ungroupable non-pathogenic meningococcus. Comparison of sulphonamide resistant and sensitive group B meningococci showed that with either heat inactivated serum or agammaglobulinaemic serum, phagocytosis did not occur with any of the strains, whereas if these two sera were used together, phagocytosis was restored to the level seen with normal human serum. Thus both antibody and complement are required for phagocytosis. Furthermore, opsonisation depended on an intact classical pathway of complement for each group B strain. In all the experiments there was no significant difference between the phagocytosis of sulphonamide sensitive and resistant group B strains neither with regard to the efficiency of opsonisation by normal human serum nor the exact requirements for antibody and complement.

Adolescent↗

PubMed2003

Effectiveness of a mass immunization campaign against serogroup C meningococci in children in the federal state of Santa Catarina, Brazil.

In addition to vaccine efficacy studies, there is a pressing need to evaluate vaccine effectiveness in a way that takes into account the limitations of health care systems in certain settings. An attempt to reach this objective was exemplified by a vaccination campaign against serogroup C meningococci in the federal state of Santa Catarina, in Brazil. A polysaccharide vaccine against serogroup C meningococci was administered to all individuals between 6 months and 14 years of age in March, 1996, in the municipalities that had the highest incidence of meningococcal disease in the previous year. All cases of the disease due to this serogroup observed in Santa Catarina during a 1-year period before and after the vaccination were included in the analysis. The cumulative incidence rate ratio was calculated for the unvaccinated compared to the vaccinated area. As a second step, the ratio of this quantity for the period before and after the vaccination, i.e. the ratio of the rate ratios (RRR), was calculated. One minus RRR was used to estimate the vaccine effectiveness. In the general population, the vaccine effectiveness was 74.3% (95% confidence intervals 52.7% to 99.6%). In children 6 months to 14 years, vaccine effectiveness was 93.1% (85.2% to 100%). Vaccine effectiveness could not be confirmed within more specific age bands, probably due to the lack of statistical power. It is concluded that group C meningococcal vaccine is effective in reducing the occurrence of meningococcal disease in children 6 months to 14 years of age, and that the ratio of rate ratios (RRR) in a useful method to evaluate vaccine effectiveness.

Adolescent↗

PubMed1987

Endotoxin release from invasive meningococci related to sulfonamide resistance, serogroup and serotype.

The relationship between endotoxin liberation, sulfonamide resistance, serogroups and serotypes was studied in 28 Neisseria meningitidis strains isolated from patients with meningococcal disease. Sulfonamide resistance was present in 15/28 strains. 22 strains belonged to serogroup B, and 5 to group C; 1 strain was non-groupable. Free endotoxin activity in growing cultures of meningococci with endotoxin titre of greater than or equal to 10(2) was found in 27/28 strains. A high endotoxin activity was present in both sulfonamide-sensitive and -resistant invasive meningococci. A high endotoxin release with titre greater than or equal to 10(3) seemed to be more associated with serogroup C than B, and more to the serotypes 2 and 15/16 than to the non-typable strains.

Drug Resistance, Microbial↗

PubMed2004

Protective immunization against group B meningococci using anti-idiotypic mimics of the capsular polysaccharide.

Use of the serogroup B meningococcal capsular polysaccharide (MenB CP) as a vaccine is hampered by the presence of epitopes that cross-react with human polysialic acid. As non-cross-reactive, protective capsular epitopes have also been described, we set out to develop protein mimics of one of such epitopes using as a template a highly protective mAb (mAb Seam 3) raised against a chemically modified form of the MenB CP (N-Pr MenB CP). Using phage display, anti-idiotypic single-chain Ab fragments (scFvs) were obtained from spleen cells of mice immunized with the Seam 3 mAb. Two Seam 3-specific scFvs competed with N-Pr MenB CP for binding to either mAb Seam 3 or rabbit Abs present in typing sera. Moreover, in mice and rabbits the scFvs elicited the production of Abs reacting with both N-Pr MenB CP and whole meningococci, but not with human polysialic acid. These scFv-induced Ab responses were boostable and of the Th1 type, as shown by a predominance of IgG2a. In addition, passive immunization with sera from scFv-immunized animals partially protected neonatal mice from experimental infection with group B meningococci. In conclusion, we have produced anti-idiotypic scFvs that mimic a protective MenB CP epitope and may be useful in the development of an alternative group B meningococcal vaccine.

Animals↗

PubMed2002

[Molecular epidemiology of meningococci].

By using the techniques of molecular biology, such as multilocus enzyme electrophoresis and multilocus sequence typing, it has been possible to identify the clones of meningococci that have been responsible for major epidemics in the world and to elucidate the routes of spread of these bacteria. Although meningococci can rearrange very rapidly their genome through the process of transformation, some clones or some groups of closely related clones have been stable and have been associated with increases of incidence of disease during decades. A clone with an epidemic potential can be disseminated globally within a few years, but the reasons for the development of an epidemic in a particular population are still not fully understood.

Bacterial Typing Techniques↗

PubMed2005

[Meningococci infection by a bacteriophage with a virulence factor].

Meningococci are bacteria dreaded for their ability to kill young people. However, meningococci and humans usually live together peacefully. In a minority of cases, the co-existence results in disease. Recently, whole genome comparisons between hyperinvasive clones and clones not associated with disease revealed that a chromosomally integrated bacteriophage was related to invasiveness. Many examples of bacteriophage-encoded virulence factors are known--as such, this finding is not remarkable. However, the way this virulence factor was found is a nice example of unravelling the pathogenesis of infectious diseases in the genomic era.

Bacteriophages↗

PubMed1976

[Group Y meningococci as respiratory pathogens (author's transl)].

Serogroup Y meningococci are more frequently respiratory pathogens than one might suppose from their prevalence in meningitis and septicemia. A case of a peracute fatal septicemia caused by group Y meningococci is reported here in which post mortem hemorrhagic lesions of the pharyngeal, laryngeal and tracheal mucosae as well as a beginning pneumonia and pleurisy have been found. The association of meningococcal and respiratory viral infections is discussed.

Adenoviridae Infections↗

PubMed1990

[Immunochemical properties of a protective cross-reacting antigen of meningococci].

The study of protective cross-reacting antigenic preparations isolated from meningococci of groups A and C in the blot immunoassay has shown the presence of a group of proteins with a molecular weight ranging from 23 to 31 KD and common for 8 tested serological groups of meningococci, gonococci and 4 nonpathogenic Neisseria species. The possible role of these structures as common Neisseria antigen in the formation of natural resistance to meningococcal infection is discussed.

Antigens, Bacterial↗

PubMed1987

An IgG monoclonal antibody to group B meningococci cross-reacts with developmentally regulated polysialic acid units of glycoproteins in neural and extraneural tissues.

The structurally similar polysialic acid capsules of group B meningococci and Escherichia coli K1 are poor immunogens, and attempts are currently being made to improve their immunogenicity by chemical modifications. An IgG monoclonal antibody to these polysialic acid capsules was used for the study of the presence of structurally similar components in tissue glycoproteins to investigate the reasons for the poor immunogenicity and to evaluate potential dangers in active or passive immunization. By immunoblotting polysialic acid was detected outside the brain in newborn rat kidney, heart, and muscle. It appeared in immunoblots as one component and with similar mobility to the neural cell adhesion molecule N-CAM. Specificity studies of the antibody and endosialidase treatment showed that the polysialic acid glycans detected were composed of chains as long as eight sialic acid residues or more. The polysialic acid was not detected in the corresponding tissues of the adult animal. These results indicate that polysialic acid units are developmentally regulated components of both neural and extraneural tissues, and are bound to components with properties similar to a known cell-adhesion molecule. This together with the presence of low amounts of polysialic acid even in the adult brain, suggests potential hazards in vaccination trials and suggested immunotherapy of meningitis caused by group B meningococci or E. coli K1, which should be carefully assessed.

Animals↗

PubMed1981

[Use of ristomycin diffused into the culture medium for separation of meningococci from nasopharyngeal mucus].

The method for enhancing the growth of meningococci after the inoculation of the specimens of nasopharyngeal mucus is proposed. The method is based on the diffusion of ristomycin into agar from ristomycin-impregnated filter paper strips. During the study of 694 specimens of nasopharyngeal mucus the above-mentioned method allowed isolation of 108 meningococcal cultures, while in serum agar only 21 cultures were isolated. The effectiveness coefficient of this method was found to be 80.6%, its effectiveness index being 5.1. The method facilitated the isolation of meningococci and in some cases reduced the time of analysis by 1 day.

Culture Media↗

PubMed1984

[Serotypes of meningococci isolated in the USSR and the Republic of Cuba].

The results of serotyping of 101 meningococcal strains isolated in the Soviet Union and 23 strains isolated in the Republic of Cuba are presented. Typing within groups was carried out by Frasch's method in the double diffusion test in gel. For this purpose serotype antigens were prepared from each strain. These antigens were used in the test only after their purification by ultracentrifugation. In all cases the prevalence of serotype 2 was revealed. A great number of Cuban strains contained a wide spectrum of type antigens of both protein and lipopolysaccharide nature. Serotype antigen 15 occurred in meningococci isolated both in the USSR and in Cuba. In most cases type 15 occurred in combination with types 2 and 8. The comparison of the results obtained in the serotyping of meningococci isolated in situations, nonepidemic (USSR) and epidemic (Cuba) for serogroup B, gives no grounds for considering type 2 as the "marker of virulence". Probably, this problem will be solved by the differentiation of subtypes within type 2. Attention should be paid to the serotype antigens of the lipopolysaccharide nature with a view to their epidemiological evaluation.

Antigens, Bacterial↗

PubMed1980

[Intragroup serotyping of meningococci].

The method for obtaining antisera to meningococci of different serotypes are described and the scheme for the preparation of serotyping is presented, as well as the method for the preparation of the determinate fraction of serotype 2. Antisera to typing antigens 1, 2, 2-7, 2-10, 4, 5, 6, 8 (1) have been obtained, their specificity tested in parallel experiments with American and French typing sera. When typing meningococci, the use of antisera to purified protein antigen 2 is recommended.

Animals↗

PubMed1981

[Experimental allergic encephalomyelitis in guinea pigs caused by meningococci].

The sensitization of guinea-pigs with the mixture of meningococci and heterologous-cerebral tissue commonly induces the development of the typical clinical and pathomorphological picture of allergic encephalomyelitis. Unlike Mycobacterium tuberculosis and other acid-resistant bacterial and much like Bordetella pertussis, meningococci are capable of inducing allergic encephalomyelitis when introduced in mixture with oil without cerebral tissue. The vaccinal strain induces allergic encephalomyelitis with a more moderate course of the disease.

Animals↗

PubMed1978

[Bactericidal antibody micro-assay for detection of antibodies against meningococci (author's transl)].

The best way to detect protective antibodies against meningococci in human serum seems to prove its bactericidal activity. For this a bactericidal antibody assay was described by WHO. For this test, however, a high amount of baby rabbit-serum is required. Therefore a modification was introduced by reducing the test volumes, performing the test in microtiterplates and using TTC (triphenyl tetracolium chloride), as a growth indicator that changes from colourless to purple red in the presence of growing meningococci. The end point of serum titration is the last well containing colourless medium.

Antibodies, Bacterial↗

PubMed1997

Phenotypic variants of meningococci and their potential in phagocytic interactions: the influence of opacity proteins, pili, PilC and surface sialic acids.

In previous studies we have examined the roles of meningococcal surface structures (capsule, lipopolysaccharides, pili and opacity proteins: Opa and Opc) in bacterial interactions with human epithelial, endothelial and mononuclear phagocytic cells. In the current investigations, using defined derivatives of a serogroup A strain C751 and a serogroup B strain MC58, we studied the roles of these structures with human polymorphonuclear phagocytes (PMN). In addition, we examined the potential influence of the pilus-associated protein, PilC, previously known to affect epithelial cell interactions. The data show, that, as with monocytes, opacity proteins affect bacterial interactions with PMN and require surface sialic acids (on capsule and LPS) to be down-modulated in order to function. Also, in contrast to their role in human epithelial and endothelial adherence, neither pili nor PilC expression had any effect on phagocytic cell interactions with respect to induction of chemiluminescence as well as phagocytic killing. Examination of the relative influence of Opa and Opc indicated that Opa proteins are more effective than Opc in PMN interactions whereas the reverse was the case with monocytes. These results suggest that Opa and Opc mediate interactions with phagocytic cells via distinct mechanisms. Observations presented here and reported previously collectively show that the structural requirements of meningococci for interacting with phagocytes, in the absence of opsonins, are present in the phenotype which is often isolated from the nasopharynx (asialylated, piliated, Opa/Opc+) whereas the phenotype prevalent in the blood (sialyted, piliated, Opa/Opc+) retains the ability to adhere to endothelial cells (via pili) but appears to be refractory to interactions with phagocytic cells.

Antigens, Surface↗

PubMed1996

Assessment of the effect of candidate anti-inflammatory treatments on the interaction between meningococci and inflammatory cells in vitro in a whole blood model.

A wide range of immunomodulating agents are now available which may be of benefit in reducing inflammatory cell activation in meningococcal sepsis. In order to facilitate selection of candidate anti-inflammatory agents for clinical trials, we have used an in vitro whole blood model to evaluate the effects on meningococcal induced neutrophil and monocyte activation, of dexamethasone, prostacyclin, pentoxifylline and a human IgM anti-lipid A monoclonal antibody (HA-1A). Known concentrations of heat and penicillin killed meningococci were added to whole blood and the time course of cellular activation was determined. Using elastase alpha 1-antitrypsin (elastase-alpha 1-AT) and TNF alpha production as markers of neutrophil and monocyte activation respectively, plasma levels of elastase-alpha 1-AT and TNF alpha were found to increase in a dose-dependent manner. Elastase-alpha 1-AT was detected early, with most release occurring between 15-30 min whereas TNF alpha was detected later, between 120-180 min. Dexamethasone, prostacyclin and pentoxifylline caused a dose-dependent inhibition of TNF alpha release but had no effect on elastase release. HA-1A had no effect on either TNF alpha or elastase release. This model may be useful in determining the sequence of inflammatory cell activation and in selecting candidate anti-inflammatory agents for evaluation in clinical trials.

Anti-Inflammatory Agents↗

PubMed1991

Clonal properties of meningococci from epidemic meningitis.

Methods from the field of population genetics now enable the classification of epidemic strains of Neisseria meningitidis and have resolved the relationships between apparently distinct epidemics. The diversity of serogroup A bacteria seems quite limited and only a few strains have been responsible for the epidemics of recent decades. Meningococci express both constant and highly variable antigens, the variability of which is determined by the clonal background of the epidemic strain. The development of an improved vaccine is being pursued but still faces technical problems.

Antigens, Bacterial↗

PubMed2006

Genetic mechanisms for loss of encapsulation in polysialyltransferase-gene-positive meningococci isolated from healthy carriers.

Encapsulated Neisseria meningitidis expressing serogroups A, B, C, W-135, or Y remain a major cause of morbidity and mortality globally. This bacterium is, however, a common commensal inhabitant of the human nasopharynx that causes disease infrequently. Isolates obtained from healthy carriers are frequently unencapsulated and therefore essentially avirulent. The lack of capsule can be due to inactivation of capsule synthesis genes by a variety of genetic mechanisms, or the absence of capsule synthesis genes. Analysis of inactivation mechanisms was undertaken in a diverse but representative set of 166 acapsulate meningococci isolated from carriage that possessed capsule synthesis genes. Slipped strand mispairing in the siaA and siaD genes of the capsule synthesis locus was observed in 39 isolates. Insertion sequence (IS) elements (IS1016-like, IS1106 and IS1301) were responsible for the loss of encapsulation in 46 isolates. Irreversible gene silencing events (insertions, deletions, base exchanges) were found in 47 isolates. Two non-synonymous mutations were identified in close vicinity of the putative active site of the UDP-N-acetylglucosamine 2-epimerase encoded by the siaA gene. The mechanisms for loss of encapsulation were not associated with particular meningococcal genotypes. There was no evidence for successive gene silencing events in the capsule genes, suggesting that the irreversible inactivation events observed were the result of short-term, within-host evolution. These observations are consistent with the postulate that particular meningococcal clonal complexes are associated with possession of a capsule and that this association is important for transmission success.

Adolescent↗