PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “MENINGOCOCCUS INFECTIONS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1997

[Meningococcal infection: changes in serogroups and penicillin resistance].

OBJECTIVE: There has been an increasing number of strains of meningococcus with reduced susceptibility to penicillin in Spain during the past few years. The serogroup distribution has also changed during this period. The objective of this study was to estimate the incidence of different N. meningitidis serogroups, the penicillin susceptibility and the clinical and laboratory data from the patients with meningococcal disease in our hospital. PATIENTS AND METHODS: A retrospective study of the patients admitted to the hospital during a 4 year period (1993-1996) with bacteriological data of meningococcal sepsis/meningitis was performed. Serogroup and penicillin minimum inhibitory concentration (MIC) were determined. Analysis of the clinical data from the patients with disease due to serogroups B or C was also performed. RESULTS: The incidence of serogroups C and B was 47% and 51.6%, respectively. There were 5 cases of decreased susceptivility to penicillin (MIC 0 0.25 microgram/ml). There were no clinical differences between the two groups of patients. CONCLUSIONS: There was a progressive increase in the incidence of serogroup C, while the incidence of serogroup B remained stable, as did the cases of meningococci with reduced susceptibility to penicillin. Although this study did not suggest a modification in the initial treatment, every strain of meningococci must be studied to show penicillin MIC to avoid treatment failure.

Child, Preschool↗
PubMed1991

A cluster of meningococcal disease on a school bus following epidemic influenza.

An outbreak of meningococcal disease among children on a school bus offered the opportunity to study a proposed association between this infection and preceding influenza infection. Five students who rode the bus became ill with invasive group C meningococcus. Transmission was limited to the bus; there was no evidence for school transmission. All five students reported influenza-like symptoms within several weeks before the development of meningococcal disease. School absenteeism, principally due to upper respiratory tract illness, was higher during the 3 weeks before the outbreak of meningococcal disease than during any period in the preceding 3 1/2 years, suggesting an unusually severe outbreak of respiratory illness. A case-control study comparing students with and without influenza symptoms revealed that the outbreak of respiratory disease was due to B/Ann Arbor/1/86 influenza (geometric mean titers, 86 for 80 patients and 33 for 47 controls [P = .0007]). These data add to the evidence suggesting that influenza respiratory infection predisposes to meningococcal disease.

Absenteeism↗
PubMed1979

[Meningococcus profilaxis (author's transl)].

In a General Hospital in San Sebastian, 96 cases of Neisseria meningitidis infections were detected in a two years period. By the use of the disk diffusion method, we found that all causative meningococcal strains but 4 were resistant to sulfonamide (with a 300 microgram sulfadiazine disk, all isolates with a zone diameter of less than 20 mm were considered to be resistant of sulfadiazine, whereas those with zone diameters of greater than 30 mm were considered susceptible). No rifampin nor minocycline-resistant meningococci were isolated. All strains had a disk zone diameter (30 micrograms rifampin and 30 micrograms tetracycline) of greater than 20 mm. The serogroups of meningococcal strains were as follows: group A, 1; group B, 67; group C, 5 and 23 were no typed. Children less than four years of age were most frequently attacked (67,7%). The attack rate was only slightly higher in males than in females (52 and 44).

Anti-Bacterial Agents↗
PubMed2003

The iron-responsive regulator fur is transcriptionally autoregulated and not essential in Neisseria meningitidis.

Fur is a well-known iron-responsive repressor of gene transcription, which is used by many bacteria to respond to the low-iron environment that pathogens encounter during infection. The fur gene in Neisseria meningitidis has been described as an essential gene that may regulate a broad array of genes. We succeeded in obtaining an N. meningitidis mutant with the fur gene knocked out and used it to undertake studies of fur-mediated iron regulation. We show that expression of both Fur and the transferrin binding protein Tbp2 is iron regulated and demonstrate that this regulation is Fur mediated for the Tbp2 protein. Footprinting analysis revealed that Fur binds to two distinct sites upstream of its coding region with different affinities and that these binding sites overlap two promoters that differentially control transcription of the fur gene in response to iron. The presence of two independently regulated fur promoters may allow meningococcus to fine-tune expression of this regulator controlling iron homeostasis, possibly during infection.

Bacterial Proteins↗
PubMed1985

Prevention and therapy of experimental Escherichia coli infection with monoclonal antibody.

Mouse hybridoma antibody of immunoglobulin class M prepared with live group B meningococci was evaluated for its ability to protect against and treat Escherichia coli infections in a newborn-rat model. In these studies, antibody was administered intraperitoneally and bacteria were administered subcutaneously to avoid introducing the antibody and bacteria to the same site. The activity of this hybridoma antibody was specific; the antibody provided protection against the K-1 strain, but not against the K-92 strain. In addition, the amount of the antibody required for protection was dependent upon the size of bacterial challenge. With an increase of the bacterial inocula from the 100% lethal dose to 10 times the 100% lethal dose there was a threefold increase in the amount of the antibody required for 50% protection. Similarly, therapeutic efficacy of the antibody was also dependent upon the magnitude of bacteremia before therapy. The antibody successfully cleared the bacteremia only when the pretherapy bacterial counts in blood were less than 10(4) CFU/ml. These findings suggest that the monoclonal immunoglobulin M antibody against the capsular polysaccharide of the group B meningococcus may be useful in the prevention and treatment of K-1 E. coli infections.

Animals↗
PubMed2001

[Impact of bacterial resistance on severe infections].

Since many years, the antimicrobial resistance increases as well as for community-acquired as for nosocomial infections. Antibiotic-resistant pneumococci are neither more nor less virulent susceptible strains. Except for immunocompromised patients, the outcome of penicillin-resistant pneumococcal infections have been similar to those in patients who are infected by susceptible ones. Current levels of S. pneumoniae resistance to penicillin and cephalosporin are not associated to an increase in mortality in children with meningitis if adequate doses of antibiotics are given. Because empiric therapy has changed, antibiotic resistance has not been associated with increased mortality. This statement can be extended to Meningococcus, for which 32 to 50% of the strains have a decreased susceptibility to penicillin. For nosocomial infections, S. aureus is the main studied pathogen. Several studies report that in patients with severe diseases (bacteremia or pneumonia) methicillin resistance of S. aureus had no significant impact on patient outcome after adjustment for different confounders. The main risk factor for mortality is the severe underlying diseases rather than the resistance as well for methicillin--resistant S. aureus, as for vancomycin resistant enterococci, Klebsiella with extended spectrum beta lactamase and Enterobacters. Recommendations for controlling epidemiologic surveillance, using barrier precautions and limiting the use of antibiotics as well in the hospital as in the community must be undertaken.

Anti-Bacterial Agents↗
PubMed2006

Cerebral microcirculation shear stress levels determine Neisseria meningitidis attachment sites along the blood-brain barrier.

Neisseria meningitidis is a commensal bacterium of the human nasopharynx. Occasionally, this bacterium reaches the bloodstream and causes meningitis after crossing the blood-brain barrier by an unknown mechanism. An immunohistological study of a meningococcal sepsis case revealed that neisserial adhesion was restricted to capillaries located in low blood flow regions in the infected organs. This study led to the hypothesis that drag forces encountered by the meningococcus in the bloodstream determine its attachment site in vessels. We therefore investigated the ability of N. meningitidis to bind to endothelial cells in the presence of liquid flow mimicking the bloodstream with a laminar flow chamber. Strikingly, average blood flows reported for various organs strongly inhibited initial adhesion. As cerebral microcirculation is known to be highly heterogeneous, cerebral blood velocity was investigated at the level of individual vessels using intravital imaging of rat brain. In agreement with the histological study, shear stress levels compatible with meningococcal adhesion were only observed in capillaries, which exhibited transient reductions in flow. The flow chamber assay revealed that, after initial attachment, bacteria resisted high blood velocities and even multiplied, forming microcolonies resembling those observed in the septicemia case. These results argue that the combined mechanical properties of neisserial adhesion and blood microcirculation target meningococci to transiently underperfused cerebral capillaries and thus determine disease development.

Animals↗
PubMed1995

Interaction of pathogenic neisseriae with nonphagocytic cells.

The ability to interact with nonphagocytic cells is a crucial virulence attribute of the meningococcus and the genococcus. Like most bacterial pathogens, Neisseria meningitidis and Neisseria gonorrhoeae initiate infections by colonizing the mucosal epithelium, which serves as the site of entry. After this step, both bacteria cross the intact mucosal barrier. While N. gonorrhoeae is likely to remain in the subepithelial matrix, where it initiates an intense inflammatory reaction, N. meningitidis enters the bloodstream, and eventually the cerebrospinal fluid to cause meningitis. Both pathogens have evolved very similar mechanisms for interacting with host cells. Surface structures that influence bacterium-host interactions include pili, the meningococcal class 5 outer membrane proteins or the gonococcal opacity proteins, lipooligosaccharide, and the meningococcal capsule. This review examines what is known about the roles these structures play in bacterial adhesion and invasion, with special emphasis, on pilus-mediated adhesion. Finally, the importance of these structures in neisserial pathogenesis is discussed.

Amino Acid Sequence↗
PubMed1995

Novel lipoprotein expressed by Neisseria meningitidis but not by Neisseria gonorrhoeae.

The ppk gene, which codes for the enzyme polyphosphate kinase in Neisseria meningitidis strain BNCV, is preceded by an open reading frame coding for a protein with a predicted size of 19.2 kDa with a typical lipoprotein signal sequence of 21 amino acids. The protein has significant homology to the N-terminal portion of an outer membrane protein from Haemophilus somnus (J. Won and R. W. Griffith, Infect. Immun. 61:2813-2821, 1993). Sequencing of the same open reading frame from meningococcus strain M1080 predicted an almost identical protein. Antisera were raised against the lipoprotein, expressed in Escherichia coli as a fusion protein with glutathione S-transferase. The antisera reacted with meningococcal membrane fractions on a Western blot (immunoblot) but did not elicit complement-dependent bactericidal activity. Restriction enzyme digestion demonstrated conservation of this portion of the meningococcal and gonococcal chromosomes. However, antisera raised to the recombinant protein showed that the protein was absent from all strains of gonococcus tested. The sequences of the gene from several strains of Neisseria gonorrhoeae and N. meningitidis were compared and found to be almost identical, except that the coding sequences from all of the gonococcal strains were terminated prematurely as a result of a frameshift mutation. The significance of the remarkable conservation of these gonococcal genes is discussed.

Amino Acid Sequence↗
PubMed1986

A neonatal mouse model of meningococcal disease.

Neisseria meningitidis, the meningococcus, remains a major cause of bacterial meningitis. Previously developed animal models for this infection do not adequately mimic its natural pathogenesis in humans. We have investigated a number of different potential animal models and describe a neonatal mouse model. Meningococci were instilled intranasally into five-day-old mice; invasiveness was measured by blood cultures and cisternal puncture, and colonization was determined by nasal cultures. Fifty two percent of mice became bacteremic after instillation of strains which are virulent for humans. Human carrier strains were avirulent in this model. Iron dextran enhanced the nasal colonization, invasiveness and mortality due to disease-associated isolates but had no effect on carrier strains. Colonization rates were similar for all strains. There was a marked age-related change in susceptibility to infection which was inversely correlated with levels of serums C3. Immunization of Swiss CD1 dams with N. meningitidis serotype 2 vaccine protected their litters from meningococcal infection. Protective levels of serum antibody were acquired by neonatal mice after suckling immunized dams. The neonatal mouse meets most of the criteria for an appropriate animal model for meningococcemia.

Aging↗
PubMed2005

Binding of the complement inhibitor C4bp to serogroup B Neisseria meningitidis.

Neisseria meningitidis (meningococcus) is an important cause of meningitis and sepsis. Currently, there is no effective vaccine against serogroup B meningococcal infection. Host defense against neisseriae requires the complement system (C) as indicated by the fact that individuals deficient in properdin or late C components (C6-9) have an increased susceptibility to recurrent neisserial infections. Because the classical pathway (CP) is required to initiate efficient complement activation on neisseriae, meningococci should be able to evade it to cause disease. To test this hypothesis, we studied the interactions of meningococci with the major CP inhibitor C4b-binding protein (C4bp). We tested C4bp binding to wild-type group B meningococcus strain (H44/76) and to 11 isogenic mutants thereof that differed in capsule expression, lipo-oligosaccharide sialylation, and/or expression of either porin (Por) A or PorB3. All strains expressing PorA bound radiolabeled C4bp, whereas the strains lacking PorA bound significantly less C4bp. Increased binding was observed under hypotonic conditions. Deleting PorB3 did not influence C4bp binding, but the presence of polysialic acid capsule reduced C4bp binding by 50%. Bound C4bp remained functionally active in that it promoted the inactivation of C4b by factor I. PorA-expressing strains were also more resistant to C lysis than PorA-negative strains in a serum bactericidal assay. Binding of C4bp thus helps Neisseria meningitidis to escape CP complement activation.

Amino Acid Sequence↗
PubMed1993

Complement deficiency states and meningococcal disease.

Analysis of complement deficiency states has supported the role of complement in host defense and elucidated diseases associated with defective complement function. Although neisserial infection plays a prominent role in these deficiency states, examination of individuals with late complement component deficiency (LCCD) reveals a particular propensity for recurrent meningococcal disease and provides important clues to the role of complement in neisserial infections. In response to meningococcal disease, LCCD individuals produce significantly greater amounts of antilipooligosaccharide (LOS) antibody which can kill group B meningococcus in a complement-sufficient in vitro system. Further studies of antibody cross-reactivity to other meningococci has led to a clearer understanding of its epitopic specificity. Nevertheless, epidemiologic evidence is consistent with the relative absence of protective immunity in LCCD persons following an episode of infection and supported by quantitation of antibody to capsular polysaccharide. However, compared to anti-LOS antibodies, anticapsular antibodies can offer immune protection to LCCD individuals via complement-dependent opsonophagocytosis--the only form of complement-mediated killing available to these persons. Thus vaccination of LCCD persons with capsular antigens is considered an important means of protecting these high-risk individuals against meningococcal disease.

Complement System Proteins↗