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At least 1,063 records · Page 59Linked to original sources
PubMed1991

[Adhesiveness in Neisseria meningitidis. A virulence factor?].

The role of adhesivity as a factor of virulence in cases of N. meningitidis has not yet been established. Unlike other bacteria in which the presence of adhesivity reflects an enhanced virulence, a high capacity of adherence is associated with a low virulence and invasive capacity in cases of meningococcus. In order to gain more insight into the knowledge of this phenomenon we have studied the adhesivity of 109 strains of N. meningitidis to human pharyngeal epithelial cells. Twenty nine out of the 109 strains were isolated from blood or spinal fluid of patients with meningococcal infection (meningitis or septicemia), whereas the remaining 80 strains were obtained from pharyngeal smears of healthy carriers. The adhesivity was measured as the number of meningococci adhered to 50 epithelial cells according to Craven's scale. Strains of healthy carriers showed a greater adhesivity than that of patients (p less than 0.001). The relevance of the pharyngeal area in the evaluation of the adhesive capacity is in accordance with the hypothesis that meningococcal adhesivity decreases when the microorganism crosses the pharyngeal epithelium. The results would support the concept that the virulence of N. meningitidis is related to its adhesiveness.

Bacterial Adhesion↗
PubMed1977

[Post-meningococcal rheumatism].

Two cases of post-meningococcal inflammatory arthritis with a relapsing course in one case are reported. The authors then recall the characteristics of the joint manifestations during meningococcal infections in the light of other cases in the literature. These arthropathies are generally aseptic and their resistance to antibiotics is remarkable, whilst non- steroid anti-inflammatory drugs, even used alone as in one of the cases reported here, are remarkably effective. The pathogenesis of these cases of arthritis is not clear: it seems however according to Greenwood and Whittle that they are manifestations of immuno-allergic type. This "post-meningococcal rheumatism" may be compared to the gonococcal rheumatism of certain cases of Reiter's syndrome.

Adult↗
PubMedDate not supplied

Fever during treatment for bacterial meningitis.

The records of 476 infants and children with bacterial meningitis treated between 1979 and 1982 were reviewed. By the sixth hospital day 90% or more of children with pneumococcal or meningococcal infection compared with 72% of children with Haemophilus infection (P less than 0.001) were afebrile. The rates of prolonged fever for 10 days or more, persistent fever for 5 to 9 days and secondary fever were 13, 13 and 16%, respectively. The conditions associated with prolonged fever for 10 days or more were subdural effusion (27%), drug fever (23%) and concomitant arthritis or pneumonia (20%); 15% were of indeterminable cause. The principal conditions associated with persistent fever for 5 to 9 days were other foci of disease (17%), nosocomial infections (16%) and subdural effusion (14%); in 42% the cause was unknown. The conditions associated with secondary fever were nosocomial infections (27%) and subdural effusion (23%); 39% were of indeterminable cause. Neither the duration nor the patterns of fever correlated with neurologic abnormalities at discharge, including hearing deficit.

Child↗
PubMed2004

NadA diversity and carriage in Neisseria meningitidis.

NadA is a novel vaccine candidate recently identified in Neisseria meningitidis and involved in adhesion to host tissues. The nadA gene has been found in approximately 50% of the strains isolated from patients and in three of the four hypervirulent lineages of non-serogroup A strains. Here we investigated the presence of the nadA gene in 154 meningococcal strains isolated from healthy people (carrier strains). Only 25 (16.2%) of the 154 carrier isolates harbored the nadA gene. The commensal species Neisseria lactamica was also found not to have the nadA gene. Eighteen of the carrier strains belonged to the ET-5 and ET-37 hypervirulent clusters, indicating that only the 5.1% of the genuine carrier population actually harbored nadA (7 of 136 strains). Five of the seven strains harbored a novel allele of the nadA gene that was designated nadA4. The NadA4 protein was present on the bacterial surface as heat-stable high-molecular-weight oligomers. Antibodies against the recombinant NadA4 protein were bactericidal against homologous strains, whereas the activity against other NadA alleles was weak. In conclusion, the nadA gene segregates differently in the population of strains isolated from healthy individuals and in the population of strains isolated from patients. The presence of NadA can therefore be used as a tool to study the dynamics of meningococcal infections and understand why this bacterium, which is mostly a commensal, can become a severe pathogen.

Alleles↗
PubMed2003

Host genetic determinants of Neisseria meningitidis infections.

The clinical presentation of infections caused by Neisseria meningitidis is highly diverse. Some patients develop meningitis, and others present with sepsis or even septic shock. After invasion of the bloodstream by the bacteria, three main cascade pathways are activated. These are the complement system, the inflammatory response, and the coagulation and fibrinolysis pathway. These pathways do not act independently but are able to interact with each other. Genetic polymorphisms among components of these pathways have been shown to be involved in the susceptibility, severity, and outcome of meningococcal disease. We review knowledge of genetic variations associated with susceptibility to and severity of meningococcal infection. Complement deficiencies and defects in sensing or opsonophagocytic pathways, such as the rare Toll-like receptor 4 single nucleotide polymorphisms (SNPs) and combinations of inefficient variants of Fcgamma-receptors, seem to have the most important role in genetically established susceptibility. Effect on severity has repeatedly been reported for FcgammaRIIa and plasminogen activator inhibitor type 1 (PAI1) polymorphisms. Outcome effects have been confirmed for SNPs in properdin deficiencies, PAI1 and combination of the -511C/T SNP in interleukin 1beta, and the +2018C/T SNP in interleukin RN. Conflicting results are reported for the effect of the -308G/A promoter polymorphism in tumour necrosis factor (TNF) alpha. These differences may reflect discrepancies in group definitions between studies or the influence of additional SNPs in the TNFalpha promoter, which can form haplotypes representing different cytokine production capacity. For several SNPs, the potential effect on susceptibility, severity, or outcome has not yet been confirmed in an independent study.

Child↗
PubMed2006

Identification of Neisseria meningitidis nonlipopolysaccharide ligands for class A macrophage scavenger receptor by using a novel assay.

Macrophages (Mphi) may play an important role in the pathogenesis of invasive meningococcal infection. Previously, we have shown that the class A Mphi scavenger receptor (SR-A) is a major nonopsonic receptor for Neisseria meningitidis on Mphi. SR-A contributes to host defense by binding proinflammatory polyanionic ligands such as lipopolysaccharide (LPS) and by the uptake and killing of live organisms. SR-A-deficient mouse Mphi display a substantial reduction in the number of meningococci ingested compared to wild-type Mphi, and SR-A is required for meningococcal phagocytosis but not for the release of tumor necrosis factor alpha. Although soluble lipid A and lipid(IV)A are reported as ligands for SR-A, we demonstrated that LPS and LPS expression were not essential for the uptake of whole meningococci. In the present study, we set out to discover protein ligand(s) for SR-A in N. meningitidis lysates and outer membrane vesicles. Using various microbial mutant strains, we determined that molecules comprising the membrane capsule and pili, as well as the abundant surface Opa proteins were not essential for SR-A recognition. We developed a binding assay to detect SR-A ligands and identified three candidate proteins expressed on intact organisms, namely, NMB1220, NMB0278, and NMB0667. Soluble forms of these ligands were shown to block the binding of meningococci to CHO cells stably transfected with SR-A. Furthermore, NMB1220 was endocytosed by SR-A on Mphi and prevented internalization of soluble acetylated low-density lipoprotein. Thus, we have identified novel, unmodified protein ligands for SR-A that are able to inhibit meningococcal interactions with macrophages in vitro.

Animals↗
PubMed1991

Chemoprophylaxis of meningitis.

Chemoprophylaxis of meningitis caused by Neisseria meningitidis and Haemophilus influenzae may be determined by the epidemiology of transmission, the antibiotic susceptibility patterns of the organisms, and the usage of vaccines. A review of transmission in England distinguishes differences in sporadic and cluster meningococcal infections. Because of resistance to sulphadiazine, rifampicin and ciprofloxacin are prophylactic agents of choice. Vaccination can be a useful adjunct to antibiotic prophylaxis. Prophylaxis for meningitis due to H. influenzae type b can be provided by rifampicin and vaccination can also be an adjunct to antibiotic prophylaxis.

Ciprofloxacin↗
PubMed1999

Antigenic and molecular conservation of the gonococcal NspA protein.

A low-molecular-weight protein named NspA (neisserial surface protein A) was recently identified in the outer membrane of all Neisseria meningitidis strains tested. Antibodies directed against this protein were shown to protect mice against an experimental meningococcal infection. Hybridization experiments clearly demonstrated that the nspA gene was also present in the genomes of the 15 Neisseria gonorrhoeae strains tested. Cloning and sequencing of the nspA gene of N. gonorrhoeae B2 revealed an open reading frame of 525 nucleotides coding for a polypeptide of 174 amino acid residues, with a calculated molecular weight of 18,316 and a pI of 10.21. Comparison of the predicted amino acid sequence of the NspA polypeptides from the gonococcal strains B2 and FA1090, together with that of the meningococcal strain 608B, revealed an identity of 93%, suggesting that the NspA protein is highly conserved among pathogenic Neisseria strains. The level of identity rose to 98% when only the two gonococcal predicted NspA polypeptides were compared. To evaluate the level of antigenic conservation of the gonococcal NspA protein, monoclonal antibodies (MAbs) were generated. Four of the seven NspA-specific MAbs described in this report recognized their corresponding epitope in 100% of the 51 N. gonorrhoeae strains tested. Radioimmunobinding assays clearly indicated that the gonococcal NspA protein is exposed at the surface of intact cells.

Amino Acid Sequence↗
PubMed1995

The Neisseria meningitidis haemoglobin receptor: its role in iron utilization and virulence.

The Neisseria meningitidis haemoglobin receptor gene, hmbR, was cloned by complementation in a porphyrin-requiring Escherichia coli mutant. hmbR encodes an 89.5 kDa outer membrane protein which shares amino acid homology with the TonB-dependent receptors of Gram-negative bacteria. HmbR had the highest similarity to Neisseria transferrin and lactoferrin receptors. The utilization of haemoglobin as an iron source required internalization of the haemin moiety by the cell. The mechanism of haemin internalization via the haemoglobin receptor was TonB-dependent in E. coli. A N. meningitidis hmbR mutant was unable to use haemoglobin but could still use haemin as a sole iron source. The existence of a second N. meningitidis receptor gene, specific for haemin, was shown by the isolation of cosmids which did not hybridize with the hmbR probe, but which were able to complement an E. coli hemA aroB mutant on haemin-supplemented plates. The N. meningitidis hmbR mutant was attenuated in an infant rat model for meningococcal infection, indicating that haemoglobin utilization is important for N. meningitidis virulence.

Aldehyde Oxidoreductases↗
PubMed1988

Systemic meningococcal disease: a model infection to study acute endotoxinemia in man.

Plasma LPS were quantitated in 40 patients with bacteriological verified systemic meningococcal infection (SMD). Twenty-two patients (55%) demonstrated LPS greater than 25 pg/ml. Fourteen patients with initial plasma LPS levels greater than 700 pg/ml developed a severe septic shock, impaired renal function and extensive coagulopathy compared to 2 out of 26 patients with LPS levels below 700 pg/ml. Seven patients died due to the circulatory collapse and multiple organ failure all with initial LPS levels greater than 1,000 pg/ml. Initiation of antibiotic therapy did not result in further increase of plasma LPS concentration. LPS were cleared from the circulation with a half-life of 1.5-3 hours after initiation of antibiotic treatment with penicillin and chloramphenicol. The results suggest that plasma LPS are quantitatively related to the development of septic shock, multiple organ failure and death from these complications in SMD, making LPS measurement a direct prognostic marker.

Endotoxins↗
PubMed1981

Enhancement of recovery of Neisseria meningitidis by gelatin in blood culture media.

The efficacy of gelatin for the recovery of Neisseria meningitidis from blood cultures was evaluated in a clinical setting. The organism was isolated from seven patients with meningococcal infections in blood culture media containing 1% gelatin. In contrast, only two blood cultures from these patients were positive in media without gelatin (P less than 0.05). Gelatin did not influence the recovery of other organisms isolated during this study. Conventional blood culture media may be supplemented with gelatin when meningococcemia is suspected.

Blood↗
PubMed1990

Persistent low C3 levels associated with meningococcal meningitis and membranoproliferative glomerulonephritis.

Recurrent meningococcal meningitis is usually related to terminal complement factor deficiencies (C5-C8); however it is not frequent with isolated primary C3 deficiency. Similarly, membranoproliferative glomerulonephritis has been described in association with primary C3 deficiencies and the presence of C3 nephritic factor. We present a case of an 18-year-old woman with relapsing meningococcal meningitis in whom membranoproliferative glomerulonephritis and persistent low serum C3 levels were found. A detailed immunological study was performed, but no other abnormalities in the complement components were found. C3 Nef was also negative. Moreover, the familiar complement studies showed an asymptomatic C4 deficiency in her mother and borderline C3 levels in her sister. The presence of persistent low serum C3 levels in the absence of other immunological abnormalities suggests that this is the cause of the relapsing meningococcal infections and the glomerular disease of this patient. We suggest that a complement deficiency, including isolated C3 deficiency, should be ruled out in all cases of relapsing meningitis. Further, the possibility of glomerular disease should be carefully considered in these patients.

Adolescent↗
PubMed1987

Meningococcal disease in congenital absence of the fifth component of complement.

We describe a family in which 2 brothers had meningococcal infection, 1 of them twice. Their parents were first degree cousins. The brothers showed a complete, isolated deficiency of C5, both antigenic and functional. The parents had half-normal values, and the data are compatible with an inherited C5 deficiency where the defect is transmitted as an autosomal codominant trait.

Adult↗
PubMed1990

[Epidemiology and treatment of purulent meningitis in children].

The results are reported of the treatment of purulent meningitis in the years 1980-1987. The treated group comprised of 49 children aged from 2 months to 4 years. The most frequent cause was meningococcal infection. All children recovered, only in 6 youngest ones subdural hygroma remained and was emptied by punctures. The treatment included penicillin and sulphonamides, in normally used doses. Frequent lumbar taps were avoided since they traumatize the meninges. The treatment was continued 3 days after temperature fall. It was observed that bacteria attacked already in the perinatal period the damaged brain tissue.

Child, Preschool↗
PubMed2005

The establishment of Neisseria meningitidis serogroup W135 of the clonal complex ET-37/ST-11 as an epidemic clone and the persistence of serogroup A isolates in Burkina Faso.

We analyzed 48 invasive isolates of Neisseria meningitidis that were isolated from meningitis cases in Burkina Faso (April 2002 to April 2003). Thirty-nine of these isolates had the phenotype (serogroup:serotype:serosubtype) W135:2a:P1.5,2, eight isolates were A:4:P1.9 and one isolate was nongroupable:nonserotypable:nonserosubtypable. Genotyping of meningococcal isolates showed that W135 isolates belonged to the sequence type (ST)-11. The nongroupable isolate was of genogroup W135 and belonged to ST-192. Isolates of serogroup A belonged to ST-2859 (a member of the subgroup III/ST-5 clonal complex). W135 (ST-11) isolates involved in meningitis outbreaks in Burkina Faso differed from those involved in the Hajj-2000 associated outbreak by their pulsed-field gel electrophoresis profile. These data confirm the changing epidemiology of meningococcal infection in Burkina Faso with the establishment and expansion of serogroup W135 N. meningitidis strains of the ET-37/ST-11 clonal complex, as well as the emergence of a new clone within the subgroup III/ST-5 clonal complex.

Adolescent↗
PubMed2002

Outbreak of Neisseria meningitidis, Edmonton, Alberta, Canada.

From December 1999 to April 2001, the greater Edmonton region had 61 cases of invasive meningococcal infection, two fatal. The outbreak was due to Neisseria meningitidis serogroup C, electrophoretic type 15, serotype 2a. Analysis of the strains showed that 50 of 56 culture-confirmed cases were due to a single clone and close relatives of this clone. This strain had not been previously identified in the province of Alberta dating back to January 1997.

Adolescent↗