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PubMed1988

[A field trial with the liquid multicomponent meningococcal vaccine ABC].

The morbidity rates of generalized forms of meningococcal infection in persons immunized with different doses of liquid meningococcal vaccine ABC were compared. The vaccine was introduced subcutaneously by means of a jet injector. Altogether 3,920 males aged 18 years and older were immunized. 1,966 vaccinees received this vaccine in a dose of 200 micrograms and 1,954 vaccinees, in a dose of 400 micrograms. Meningococcal multicomponent vaccine ABC used in these doses showed moderate reactogenicity and did not prevent the development of generalized forms of meningococcal infection.

Adult↗
PubMed2005

4G/5G promoter polymorphism in the plasminogen-activator-inhibitor-1 gene in children with systemic meningococcaemia.

UNLABELLED: Meningococcal disease may present as sepsis, meningitis or a combination of both. Impaired fibrinolysis and massive elevation of the plasminogen activator inhibitor-1 (PAI-1) is a characteristic feature of meningococcal sepsis. Previously, an association between mortality and the functional 4G/5G promoter polymorphism of the PAI-1gene in a cohort of UK and Dutch children with meningococcal sepsis was reported. We carried out a prospective, multicentre study to investigate the association of the 4G/5G PAI-1 polymorphism, diagnosis, and outcome in meningococcal disease in a Central European and UK population. Blood samples and clinical information of 347 previously healthy children with meningococcal infection were collected from 95 paediatric hospitals in Germany, Switzerland, Italy, the United Kingdom, and Austria from 2000 until 2002. Mortality was significantly associated with the 4G/4G genotype (12 of 90 (13%) vs. 15 of 240 (6%), P = 0.037), resulting in an odds ratio of 2.31. The diagnosis of sepsis (independent of symptoms of meningitis) was significantly more frequent in carriers of the 4G/4G genotype (P = 0.01), resulting in an odds ratio of 2.21 to develop sepsis. Meningitis was not associated with the PAI-1 4G/5G polymorphism, and allele frequencies were similar in patient and control groups. CONCLUSION: Our data show a correlation between the 4G/4G genotype in the plasminogen activator inhibitor-1 gene and poor outcome in children with meningococcal infection. In addition, 4G homozygous patients were prone to develop sepsis. We found no influence of the plasminogen activator inhibitor-1 polymorphism on the susceptibility to invasive meningococcal infection.

Adolescent↗
PubMed1985

[Antigenic affinity of meningococci and human A- and B-group erythrocytes].

The use of the modified method of isohemagglutinin adsorption by microbial antigens in experiments with the causative agent of meningococcal infection has led, for the first time, to the detection of meningococcal antigens affined to the antigens of human erythrocytes, groups A and B. The antigenic affinity of group A erythrocytes and meningococci has proved to be more pronounced in meningococcal strains isolated from the spinal fluid of patients than in cultures obtained from the nasopharynx of healthy persons. The detection of the affinity of these antigens makes it possible to explain the mechanism of differences in the susceptibility of persons with different blood groups to meningococcal infection by "antigenic mimicry".

ABO Blood-Group System↗
PubMed1976

Acute bacterial meningitis in childhood. Incidence and mortality in a defined population.

Cases of acute bacterial (excluding tuberculous) meningitis and meningococcal infection, occurring in children under 10 years of age in the North-West Metropolitan region between 1969 and 1973 have been studied retrospectively by case-note review. The risk of having an acute meningococcal infection was estimated to be 1 in 1090, and that of having an attack of haemophilus meningitis to be 1 in 1500, but the age of 10 years. The case-fatality rates for meningococcal infection, haemophilus meningitis, and pneumococcal meningitis were 10.9%, 5.7%, and 16.4% respectively. Meningitis was not diagnosed in life in 26 of 94 fatal cases (28%).

Child↗
PubMed2004

Global epidemiology of meningococcal disease and vaccine efficacy.

BACKGROUND: Control of meningococcal infection has a high priority in many industrialized nations, because of the high mortality rates associated with invasive infection, the public health effects of disease outbreaks, and the position of Neisseria meningitidis as a leading infectious cause of death in childhood. Throughout the past 200 years, epidemics of meningococcal infection have been noted in Europe, Africa, Asia, the United States, and New Zealand. The proportions of cases caused by the 5 predominant capsular types (A, B, C, Y, and W135) associated with the disease vary among different regions and within specific geographic areas with time. Comprehensive disease control can be achieved only with the use of vaccines that target all of these disease-causing serogroups. METHODS: Routine immunization with a new generation of conjugate vaccines against serogroup C meningococci in the United Kingdom since 1999 has had a major effect on serogroup C disease in the region. The success of the vaccine involves 2 mechanisms, ie, (1) direct protective effects for vaccinated individuals through induction of bactericidal antibodies and (2) reductions in nasopharyngeal carriage of the organism and consequent generation of herd immunity through reductions in transmission to unimmunized individuals. CONCLUSIONS: Ongoing development of tetravalent A, C, Y, and W135 conjugate vaccines raises the hope that disease caused by these serogroups can be controlled in the near future. However, development of effective strategies to control serogroup B meningococcal disease is still needed for comprehensive control of meningococcal disease.

Global Health↗
PubMed2007

Diagnosis and management of meningococcal disease: the need for centralized care.

Meningococcal infection remains a significant health problem in children, with a significant mortality and morbidity. Prompt recognition and aggressive early treatment are the only effective measures against invasive disease. This requires immediate administration of antibiotic therapy, and the recognition and treatment of patients who may have complications of meningococcal infection such as shock, raised intracranial pressure (ICP) or both. Encouragingly, its mortality has fallen in recent years. This is the result of several factors such as the centralization of care of seriously ill children in paediatric intensive care units (PICUs), the establishment of specialized mobile intensive care teams, the development of protocols for the treatment of meningococcal infection, and the dissemination by national bodies and charities of guidance about early recognition and management. We will review the pathophysiology and management of the different presentations of meningococcal disease and examine the possible role of adjunctive therapies.

Anti-Bacterial Agents↗
PubMed1984

[Etiology of suppurative bacterial meningitis].

The results of the laboratory examination of 2034 patients with meningococcal infection and purulent meningitides, hospitalized during the period of June 1980 to October 1983, revealed that three main etiological agents were responsible for these diseases: meningococci, pneumococci and Haemophilus influenzae. The susceptibility of the patients to different etiological agents was found to depend on their age. Children aged up to 3 years constituted 75% of the patients with meningitis caused by H. influenzae; 50% of the patients with meningococcal infection were children aged up to 5 years; pneumococcal meningitis occurred more frequently in adults. Serogroup A meningococci were found to prevail in patients with meningococcal infection. Besides, in children serogroup C meningococci could be isolated in 24% of cases. Since 1983 the cases of the isolation of strains belonging to serogroup B increased in number. Among the pneumococci responsible for the disease serotypes 1, 19, 6 and in children serotype 12 occurred most frequently.

Adolescent↗
PubMed2004

Complement C7 deficiency presenting as recurrent aseptic meningitis.

BACKGROUND: Complement deficiency states are rare inherited disorders that may predispose affected individuals to angioedema, collagen vascular disease, or infection due to encapsulated organisms, especially Neisseria meningitidis. OBJECTIVES: To report the case of a 36-year-old man of Irish descent with recurrent culture-negative neutrophilic meningitis, to offer potential reasons for the inability to recover a causative pathogen, and to review the genetics and prevalence of complement deficiency states, the methods of screening for such deficiencies, the features of meningococcal infection as they relate to such deficiencies, and management strategies for clinicians caring for patients with such deficiencies. METHODS: The patient presented in 1988 and again in 2002 with culture-negative neutrophilic meningitis. His second episode was characterized by a rash suggestive of meningococcal infection, prompting immunologic evaluation. RESULTS: Immunologic evaluation revealed an undetectable CH50 level. Levels of C1, C2, and C5 through C9 were normal except for C7, which was undetectable. Further testing revealed that the patient's sister was also C7 deficient. CONCLUSIONS: Complement component deficiencies are relatively rare; individuals with collagen vascular disease and systemic neisserial infection should be screened using either the CH50 or the APH-50 assay. Key to the management of a late-complement component-deficient host is counseling, education about meningococcal infection, and discussions about the potential benefits of chemoprophylaxis and immunoprophylaxis. The ability to detect the bacterial cause of meningitis in such patients is organism dependent and may be influenced by factors such as cerebrospinal fluid bacterial concentration and previous antibiotic drug exposure.

Adult↗
PubMed2005

Candidacy of LPS-based glycoconjugates to prevent invasive meningococcal disease: developmental chemistry and investigation of immunological responses following immunization of mice and rabbits.

Glycoconjugates were prepared by covalently linking the immunogenic protein carrier CRM(197) to O-deacylated lipopolysaccharide (LPS) derived from Neisseria meningitidis (strain H44/76), immunotype L3 galE LPS. This mutant strain elaborates a truncated LPS structure that displays immunological epitopes characteristic of 76% of Group B meningococcal (NmB) strains. CRM(197) was covalently linked either to the reducing glucosamine residue of the lipid A region of the O-deacylated LPS or to a 2-keto-3-deoxy-octulosonic acid (Kdo) residue in the inner core region of the O-deacylated LPS. In both rabbits and mice a much stronger IgG response to the immunising antigen was generated in those animals that received conjugates linked via the lipid A region. Sera from mice that were immunized with these conjugates were assayed for their reactivity with LPS, both mutant and wild-type, of several homologous and heterologous NmB strains. Sera obtained from mice immunized with conjugates in which the carrier protein was linked via the Kdo moiety were only able to react with O-deacylated, but not fully acylated (native), LPS from the homologous strain. However, sera obtained from mice that were immunized with conjugates, in which the carrier protein was coupled to the lipid A region, reacted predominately with inner core epitopes that contained phosphoethanolamine at the same 3-position of the distal heptose residue (HepII) of the inner core LPS as was present on the immunising antigen. Additionally it was observed that sera from rabbits immunised with lipid A linked conjugates, unlike the mice responses, were generally not as specific for LPS antigens that contained phosphoethanolamine at the same 3-position as was present on the immunising antigen, but showed a broader inner core recognition, whereas those rabbits that received the Kdo-linked conjugates gave only a very weak non-specific response to all immunotypes. Finally, the sera from two out of six mice that had received lipid A linked conjugates had bactericidal activity against L3 wild-type NmB strain 8047 and one of these was able to passively protect against meningococcal infection in an infant rat model. This study demonstrates evidence towards the proof-in-principle that by using Nm inner core LPS conjugates coupled via the lipid A region with an intact phosphoethanolamine at the O-3 position of the HepII of the inner core LPS, it is possible to elicit functional and protective antibodies against meningococcal infection.

Animals↗
PubMed1991

Meningococcal chest infections in a general hospital.

In the course of one calendar year (1989-1990), 46 specimens of respiratory secretions (from 44 patients) cultured in the microbiology department of a large district general hospital in The Netherlands were found to yield Neisseria meningitidis. Twenty-eight of the 46 samples yielded pure cultures of meningococci and 18 yielded other recognised respiratory pathogens as well. Only one patient had pneumonia, whereas 19 had acute respiratory infections and 18 acute purulent exacerbations of chronic bronchitis. The remaining patients, who had a variety of symptoms, all had purulent sputum. Only 8 of the 44 patients were under 40 years of age; 21 were aged more than 60 years. Serological grouping and subtyping showed a predominance of group B strains (in 24 of 44 patients) and 13 strains were non-groupable. The importance of recognising or overlooking meningococci in cultures of respiratory secretions is discussed.

Acute Disease↗
PubMed2001

[Meningococcal W135 infection epidemics associated with pilgrimage to Mecca in 2000].

OBJECTIVES: On April 3 and 7, 2000, four cases of Neisseria meningitidis serogroup W135 infection were diagnosed in France in Raj pilgrims and their close relatives. Two cases were fatal. Due to the rarity of this strain in France, a strain belonging to a clonal complex implicated in several epidemics in Europe and North America, and it high mortality observed, The French General Direction of Heal issued recommendations on April 8th for rifampicin chemotherapy for all pilgrims and relatives living in their home. The national disease watch (Institut de Veille Sanitaire, InVS) conducted an investigation to describe the epidemic and follow the diffusion of the strain in the population and assess the impact of preventive measures taken as well as need for other specific measures. METHODS: A case was considered to be confirmed when the strain isolated from usually sterile media after March 22 was found to be identical to the epidemic strain (W135, 2a: P1-2.5--clonal complex ET37). A case was considered probable when a pilgrim or in a person in contact with a pilgrim had clinical meningitis (purulent cerebrospinal fluid or purpura fulminans) or when the identified strain was in the W135 serogroup but could not be further identified. A standardized questionnaire developed in collaboration with the European countries concerned by the epidemic was filled out. RESULTS: By November 20, 2000, 25 confirmed and 2 probable cases were identified; 85% of the cases occurred during the first 7 weeks of the epidemic. Mortality was 18%. Patients aged over 50 years accounted for 66% of the cases (6/9) occurring before April 9, 2000 and 17% of the cases (3/18) observed after this data. Four patients had single-joint arthritis. No cluster cases could be identified. Four cases occurred among 19,100 pilgrims (attack rate 21/100,000), 9 among persons living with pilgrims, 7 among subjects in direct contact with pilgrims but not living with them, and 7 among persons who had no identifiable contact with pilgrims. These last 7 cases occurred after the 3rd week of the epidemic. No cases occurred among persons who had taken rifampicin chemoprophylaxis. Eighteen cases occurred after diffusion of the prophylaxis recommendations including 5 in a population directly concerned by the recommendations. CONCLUSIONS: These data suggest that the epidemic strain is not different from other strains in terms of virulence and transmissibility. Eight months after the Raj, the number of cases related to the epidemic remained limited in France. The characteristics of the most recent cases do however suggest an epidemic clone persists in the general population. The Direction of Health recommends vaccination using the quadrivalent A,C,W135,Y vaccine for the 2001 Raj.

Aged↗
PubMed1998

Amplification of the meningococcal porB gene for non-culture serotype characterization.

Since 1992, the proportion of culture-confirmed meningococcal infections compared with numbers of notified cases of meningococcal disease has decreased in England and Wales. As most meningococcal strain characterization methods depend on a clinical isolate, this has resulted in a loss of epidemiological information. To address this problem, and to aid nonculture diagnosis, a semi-nested PCR protocol for the amplification of the meningococcal porB gene from clinical specimens was developed. This gene encodes the meningococcal serotyping antigen; strain typing data was provided by hybridization of allele-specific oligonucleotide probes to the digoxigenin-labelled porB amplicon in a 'PCR ELISA'. This assay was specific for meningococcal DNA and sensitivities of 0.81 for cerebrospinal fluid (CSF), 0.57 for serum, and 0.62 for whole blood taken from patients with proven meningococcal infection were obtained.

Bacterial Outer Membrane Proteins↗
PubMed2004

Surveillance of invasive meningococcal disease in the Czech Republic.

Routine notification of invasive meningococcal disease has a long tradition in the Czech Republic: mortality data are available from 1921 and morbidity data from 1943. The collection of Neisseria meningitidis strains kept in the NRL for Meningococcal Infections in Prague dates from 1970 onwards, and represents more than 3500 strains isolated from invasive disease and their contacts, from healthy carriers and from respiratory infection. Analysis of these strains showed that the Czech meningococcal population is different from that seen in western Europe. In 1993, the incidence serogroup C meningococcal disease increased and was associated with the emergence of the hypervirulent complex Neisseria meningitidis C, ST-11, ET-15/37, and caused an increase in the incidence of invasive meningococcal disease which peaked in 1995 (2.2/100,000). A vaccination strategy targeting the part of the population at highest risk of invasive meningococcal disease was adopted in the country.

Czech Republic↗
PubMed2004

[Meningococcal purpura fulminans in children].

In France, the incidence of meningococcal infections is increasing and the most severe presentation, called purpura fulminans, has still a death rate of 20-25%. Diagnosis of invasive meningococcal infection must be evoked in any child presenting with febrile purpura (vasculitic rash not disappearing with "tumbler test"); a fulminating form must be suspected in the presence of only one ecchymosis and signs of infection, remembering that recognition of shock is difficult in children. The Health Authority recommend to administer a third generation cephalosporin promptly for any child with signs of infection and an ecchymotic purpura (>3 mm of diameter), and then to refer the patient to the hospital. Children with purpura fulminans should be referred to a paediatric intensive care unit. Management includes antibiotics, steroids, fluid resuscitation and catecholamines (be aware of hypoglycaemia, particularly in infants, and hypocalcaemia). Treatment of cutaneous necrosis and distal ischemia is difficult and still controversial: antithrombin, protein C, tissue plasminogen activator and vasodilator infusion have no proved efficacy. Cases must be rapidly notified to the Public Health Service who will institute chemoprophylaxis for close contacts. Given the predominance of serogroup B in France, we hope that an efficient vaccine will soon become available.

Adolescent↗
PubMedDate not supplied

[Antibodies to meningococcal antibodies in the sera of patients and donors].

The comparative study of sera taken from healthy persons (pooled sera of 100 donors, 6 individual serum specimens) and sera taken from patients with meningococcal meningitis (pooled sera of 10 patients with meningococcal infection, group A, and 6 individual serum specimens from patients with meningococcal infection, groups A, B, C) was carried out by the method of immunoblotting. All proteins from healthy donors were found to contain antibodies to meningococcal iron-regulated protein (IRP) of 85 kD, designated as TbpB. In 30% of donor sera the presence of antibodies to meningococcal IRP of 34 kD (FbpA) was registered. Moreover, donor sera were found to contain antibodies to meningococcal IRP of 45 kD. The sera taken from convalescents were found to have the increased content of antibodies to IRP of 70 and 85 kD and somewhat lesser content of antibodies to proteins of 98, 44 and 34 kD. As regards other (non iron-regulated) proteins, in the process of convalescence the most intensive antibody production was observed with respect to minor protein with a molecular weight of 50 kD, as well as proteins of class 5, characterized by molecular weights of 30 kD and less.

Antibodies, Bacterial↗
PubMed1970

The relationship between group A and group C meningococcal polysaccharides and serum opsonins in man.

The interaction in vitro between human granulocytes and meningococci in the presence of sera from volunteers immunized by Gotschlich et al. with purified group A and group C meningococcal polysaccharides was studied. Phagocytosis of meningococci did not occur in the presence of preimmunization sera. In all volunteers tested, group-specific opsonins were detected in groups A and C polysaccharide antisera. Opsonic activity appeared within 1 wk after immunization and persisted for at least 14 months. Titers of opsonic activity ranged from 1:20 to 1:320; highest titers were noted in 2-4 wk antisera. Meningococcal opsonins were detected in both 19S and 7S immunoglobulins. Opsonic activity in low-titer antisera depended on heat-labile factors present in both normal and immune sera, whereas phagocytosis was observed in the presence of heat-inactivated high-titer antisera. Phagocytosis of group A meningococci in the presence of certain group A polysaccharide antisera was inhibited by N-acetyl mannosamine, but not by mannose, mannosamine, N-acetyl glucosamine, N-acetyl galactosamine, or N-acetyl neuraminic acid. Absorption studies with sera from patients with natural meningococcal infections revealed that these polysaccharides are the major antiphagocytic determinants for group A and group C meningococci. These studies are consistent with previous reports suggesting that immunization with group A and group C polysaccharides may well provide group-specific protection against meningococcal infections.

Antibodies↗
PubMed2001

[Treatment of meningococcal purpura fulminans].

In France, the incidence of meningococcal infections is increasing. The most severe presentation, called purpura fulminans, has a death rate of 20-25%; 5 to 20% of the survivors need skin grafts and/or amputations. Diagnosis of invasive meningococcal infection is very difficult when purpura and "toxic" appearance are absent: one should take into account parents' impression of their ill child. This diagnosis must be evoked in any child presenting with febrile purpura (like in the United Kingdom, parents should be encouraged to use the "tumbler test" to identify a vasculitic rash); a fulminant form is to be suspected in the presence of only one ecchymosis and signs of infection, remembering that recognition of shock is difficult in children. Recently, the Health Authority has recommended to administer a third generation cephalosporin promptly (before biological investigations) for any child with signs of infection and a necrotic or ecchymotic purpura (> 3 mm of diameter), and then to refer the patient to the hospital. By grouping the patients from 7 studies, it can be observed that preadmission antibiotic administration has a protective effect on mortality (odds ratio: 0.36; 95% confidence interval: 0.23-0.56); a negative effect was observed in only one of these series. Children with purpura fulminans should be referred to a paediatric intensive care unit. Management includes antibiotics, steroids, fluid resuscitation and catecholamines (be aware of hypoglycaemia, particularly in infants, and hypocalcaemia). Treatment of cutaneous necrosis and distal ischemia is difficult and still controversial: antithrombin, protein C, tissue plasminogen activator and vasodilator infusion have no proven efficacy. Cases must be rapidly notified to the Public Health Service who will institute chemoprophylaxis for close contacts. Given the predominance of serogroup B in France, we hope that an efficient vaccine will soon become available.

Anti-Bacterial Agents↗