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PubMed2006

MyD88-dependent signaling affects the development of meningococcal sepsis by nonlipooligosaccharide ligands.

The Toll-like receptors (TLRs) and the adaptor myeloid differentiation factor 88 (MyD88) are important in the innate immune defenses of the host to microbial infections. Meningococcal ligands signaling via TLRs control inflammatory responses, and stimulation can result in fulminant meningococcal sepsis. In this study, we show that the responses to nonlipooligosaccharide (non-LOS) ligands of meningococci are MyD88 dependent. An isogenic LOS-deficient mutant of the serogroup C meningococcal strain FAM20 caused fatal disease in wild type C57BL/6 mice that was not observed in MyD88-/- mice. Fatality correlated with high proinflammatory cytokine and C5a levels in serum, high neutrophil numbers in blood, and increased bacteremia at 24 h postinfection in the wild-type mice. Infection with the parent strain FAM20 resulted in fatality in 100% of the wild-type mice and 50% of the MyD88-/- mice. We conclude that both LOS and another neisserial ligand cause meningococcal sepsis in an in vivo mouse model and confirm that meningococcal LOS can act via both the MyD88- dependent and -independent pathways, while the non-LOS meningococcal ligand(s) acts only via the MyD88-dependent pathway.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Neisseria meningitidis sequence type and risk for death, Iceland.

Invasive meningococcal infections are hyperendemic in Iceland, a relatively isolated country in the mid-Atlantic. We performed a nationwide study on all viable meningococcal strains (N = 362) from 1977 to 2004. We analyzed the association of patient's age and sex, meningococcal serogroups, and sequence types (STs) with outcomes. Overall, 59 different STs were identified, 19 of which were unique to Iceland. The most common STs were 32 (24.6%), 11 (19.9%), and 10 (10.2%). The unique ST-3492 ranked fourth (7.7%). The most common serogroups were B (56.4%), C (39.8%), and A (2.2%). Age (p < 0.001) and infection with a unique ST (p = 0.011) were independently associated with increased death rates, whereas isolation of meningococci from cerebrospinal fluid only was associated with lower death rates (p = 0.046). This study shows evolutionary trends of meningococcal isolates in a relatively isolated community and highlights an association between unique STs and poor outcome.

Adolescent↗
PubMed1991

Influenza A and meningococcal disease.

There are several anecdotal accounts of the association between outbreaks of influenza and meningococcal disease. The exceptional increase in the number of cases of meningococcal infection 2 weeks after an influenza A outbreak in England and Wales during November and December, 1989, provided an opportunity to investigate the relation between the two events. Patients with meningococcal disease in December, 1989, were more likely than age-matched controls to show serological evidence of recent influenza A infection (odds ratio 3.9, 95% Cl 1.2-13.9). The most likely explanation for the association is immune suppression induced by influenza A, though a lowering of mucosal resistance to meningococcal invasion may also be a factor. Public health authorities should be aware of the association and should be prepared to alert medical practitioners and the public to the increased risk of meningococcal disease when influenza A outbreaks occur.

Adult↗
PubMedDate not supplied

[Meningococcal disease caused by Neisseria meningitidis: epidemiological, clinical, and preventive perspectives].

Bacterial meningitis constitutes a significant global public health problem. In particular, Neisseria meningitidis continues to be a public health problem among human populations in both developed and developing countries. Meningococcal infection is present as an endemic and an epidemic disease. Meningococcal disease is manifested not only as meningitis, but also as meningococcemia. The latter is usually fulminant. The global persistence of N. meningitidis is due to the significant number of carriers and the dynamics of transmission and disease. Approximately 500 million people worldwide are carriers of the bacterium in their nasopharynx. Multiple factors have been identified that predispose to the transmissibility of N. meningitidis, including active or passive inhalation tobacco smoking, upper viral respiratory tract infections, drought seasons, and overcrowding. These factors explain the frequent occurrence of outbreaks in military barracks, schools, prisons, and dormitories. Some of the determinants of invasiveness of the bacteria include nasopharyngeal mucosal damage in colonized individuals, virulence of the strains, absence of bactericidal antibodies, and deficiencies of the complement system. During both endemic and epidemic scenarios of meningococcal disease, control measures should include treating the cases with appropriate antimicrobial therapy (penicillin, ceftriaxone, or chloramphenicol); providing chemoprophylactic drugs to contacts (rifampin or ciprofloxacin), and close observation of contacts. Nevertheless, the key to effective control and prevention of meningococcal disease is immunoprophylaxis. Available vaccines include the polysaccharide monovalent, bivalent (serogroups A, C), or tetravalent (A, C, Y, W-135 serogroups) vaccines; conjugate vaccine (serogroup C); and the combined vaccine with outer membrane proteins and polysaccharide (serogroups B, C). Due to a recent increase in case reporting of serogroup C N. meningitidis in Mexico, we have developed a national response strategy that includes availability of vaccines and medications for chemoprophylaxis. This review aims at providing health care workers with updated information regarding the epidemiological, clinical, and preventive aspects of meningococcal disease. The English version of this paper is available at: http://www.insp.mx/salud/index.html.

Humans↗
PubMed2003

Low utilisation of unactivated protein C in a patient with meningococcal septic shock and disseminated intravascular coagulation.

BACKGROUND: Activated protein C has recently been shown in a multicentre trial to significantly reduce mortality in patients with septic shock. There are also some case reports and minor studies demonstrating promising results with the unactivated form of protein C. However, in children with severe meningococcal infection, skin biopsies have demonstrated low expression of endothelial thrombomodulin and protein C receptors, suggesting low protein C activation capacity in severe meningococcal sepsis. METHODS: A patient with meningococcal septic shock was treated with two doses of the unactivated form of protein C, the first during intense activation of the coagulation system and the second during a phase of low grade or no activation. Repeated plasma samples were analysed for protein C concentration, which made it possible to compare pharmacokinetics and half-lives of the two administrations. A shorter half-life during intense coagulation was expected if there was an activation and consumption of the protein C administered. RESULTS: The calculated half-lives of protein C during intense and low grade activation were 32 h and 19 h, respectively, a magnitude similar to that reported in protein C-deficient patients without infection. CONCLUSION: The result indicates that whole body utilisation of the unactivated protein C was low. Endothelial impairment of protein C activation does not seem to be restricted to the skin vessels only.

Adult↗
PubMed1984

Outbreak of infection caused by Neisseria meningitidis group C type 2 in a nursery.

An outbreak of meningococcal infection which took place in a nursery in Rioja, Spain, is reported. Between November 1981 and February 1982, 11 patients had meningitis with or without septicaemia. Two died. Three meningococcal strains from the patients isolated were studied. All three were group C type 2 and were resistant to sulphadiazine (MIC 50 mg/l) but susceptible to penicillin, ampicillin, chloramphenicol, rifampicin and spiramycin. This outbreak took place during an epidemic in which serogroup B was the most prevalent in Spain. Two surveys before and after chemoprophylaxis were made to determine the carrier rate in the nursery population. The strain causing the outbreak was found in 2.5 and 4 per cent of persons respectively. Rifampicin was administered to all carriers after the first survey and to carriers of the virulent strain after the second survey. The remaining children were given polysaccharide C vaccine. No more cases arose after this last prophylactic measure.

Adult↗
PubMed1993

Management of bacterial meningitis.

In developed countries the mortality from bacterial meningitis acquired outside the neonatal period is relatively low. In contrast, in developing countries it is often higher (20%-40%). In developed countries despite (and perhaps because of) the introduction of increasingly potent antimicrobials, the morbidity of bacterial meningitis has remained high. For example, up to 25% of patients with Haemophilus influenzae meningitis have some form of neurological deficit. Neisseria meningitidis is the major cause of bacterial meningitis in many areas of the world. A clone of Group A meningococcus has spread from China to cause the most recent major epidemic in Sub-Saharan Africa. Group B meningococcal infections causing sporadic meningitis are increasing in parts of Europe and South America. The mortality from meningococcal disease is greatest when there is a septicaemic component to the infection. Although antimicrobial chemotherapy is of major importance some adjuncts to therapy are beneficial. High dose corticosteroid therapy has been shown to decrease mortality in pneumococcal meningitis in an uncontrolled study and to speed recovery and decrease neurological sequelae in H. influenzae meningitis. Nevertheless to prevent infection would be of greater benefit. Prevention can be achieved by either chemoprophylaxis or immunoprophylaxis. Although safe and effective vaccines are available to prevent pneumococcal, H. influenzae (Hib) and Groups A and C meningococcal meningitis; apart from the protein conjugate Hib vaccine they are less effective in children under two years of age. There is no effective vaccine to protect against group B meningococcal meningitis.

Adolescent↗
PubMed1977

[Prevention of meningococcal meningitis].

Meningococcal meningitis as well as meningococcal sepsis must be regarded as complications of an otherwise mild meningococcal infection of the nasopharynx. Only individuals without antibodies against a given meningococcal type will contract the above-mentioned diseases. Causal prophylactic measures have proved to be ineffective because of the great number of "carriers" of meningococci. Immunprophylaxis with specific polysaccharides is effective and presently available for use against types A and C but not against type B. Chemoprophylaxis is most effective when administered to those living in close quarters. Sulfonamides are the prophylaxis of choice agianst meningococci sensitive to sulfonamides. With the appearance of sulfonamide-resistant meningococci, the sulfonamide must be replaced by rifamycin or minocyclin. Though treatment with penicillin gives protection against infection, it does not eradicate the carrier state.

Adult↗
PubMed2002

Retinal hemorrhages in meningococcal septicemia.

PURPOSE: Meningococcal septicemia is associated with coagulopathy and hemorrhagic tendency. We carried out this study to determine the incidence of retinal hemorrhages in meningococcal septicemia. METHODS: This was a prospective study involving all children admitted to the Sheffield Children's Hospital, Sheffield, England, with a diagnosis of meningococcal septicemia. Confirmation of meningococcal infection was by blood culture or DNA analysis using polymerase chain reaction. The children underwent ocular examination including dilated fundus examination by direct and indirect ophthalmoscopy. Details of their coagulation status were also obtained. RESULTS: Twelve children (mean age, 4.5 years) with a confirmed diagnosis of meningococcal septicemia were included. All children had coagulopathy. Retinal hemorrhages were found in 5 children (42%). The disease was fatal in 3 children. Group C meningococcus was responsible for the infection in all those with retinal hemorrhages and those with fatal outcome. CONCLUSIONS: Retinal hemorrhage is a common feature in meningococcal septicemia. Ophthalmic evaluation should be part of the assessment of children with meningococcal septicemia. Future studies on meningococcal disease should include retinal hemorrhage as another parameter in the assessment. This should help us to understand the role of retinal hemorrhage in the prognosis of this serious disease.

Bacteremia↗
PubMed1996

Polymerase chain reaction for case ascertainment of meningococcal meningitis: application to the cerebrospinal fluids collected in the course of the Norwegian meningococcal serogroup B protection trial.

To improve the diagnosis of systemic meningococcal disease we used a nested polymerase chain reaction (nPCR) test to detect meningococcal DNA in cerebrospinal fluid (CSF) samples from patients. The nPCR test was based on the gene coding for the PorA outer membrane protein, a major antigen of Neisseria meningitidis, which is the basis for determining the subtype of the strains. The method was tested on CSF samples from 87 patients with various disease aetiology, including 37 patients with systemic meningococcal disease. It was also applied to all 67 CSF samples from culture-negative patients with suspected meningococcal disease which were collected in the course of the Norwegian serogroup B vaccination trials, between 1987 and 1993. Of the 67 culture-negative CSF samples, 10 were nPCR positive. Two of the 67 CSF were positive with the antigen test, and both of these were nPCR positive. Serum pairs from 46 of the 67 culture-negative patients were analysed for serological serogroup response in an enzyme-linked immunosorbent assay (ELISA) against meningococcal capsular polysaccharides. Nine of the 10 nPCR-positive CSF samples belonged to patients with serological response judged as either typical of, or compatible with systemic meningococcal disease. Sequence analysis of the nPCR products was performed to determine the subtype of the infecting meningococcal strains. Four of the 10 positive CSF samples were infected with a strain of subtype P1.7,16, which is similar to the epidemic strain used to produce the vaccine. Inclusion of nPCR for diagnosis of meningococcal meningitis did not significantly alter the results of the vaccination trial, but added important information about the strain causing disease in 5 of 13 serogroup B cases without preserved isolates.

Base Sequence↗
PubMed1994

[Gram-negative coccus infection].

The main pathogens of gram-negative infections are Neisseria gonorrhoeae, Neisseria meningitidis and Moraxella catarrhalis infection. N. Gonorrhoeae infection is one of the STD, but the chemotherapy for this infection is very easy because this pathogen is very susceptible to new quinolones. Meningococcal infection is very rare in Japan. Since 1980, M. catarrhalis is one of the important pathogen of respiratory infections such as acute bronchitis, pneumonia, chronic bronchitis. This pathogen also causes acute sinusitis and otitis. Most pathogenic strains of M. catarrhalis are beta-lactamase producing.

Animals↗
PubMed1989

Sequence of the structural gene (rmpM) for the class 4 outer membrane protein of Neisseria meningitidis, homology of the protein to gonococcal protein III and Escherichia coli OmpA, and construction of meningococcal strains that lack class 4 protein.

The structural gene (rmpM) of the class 4 outer membrane protein of Neisseria meningitidis has been cloned and sequenced. The derived amino acid sequence reveals a 218-amino-acid protein following a 22-amino-acid signal peptide. The protein shows 94.2% homology with protein III of Neisseria gonorrhoeae and shares its two potential disulfide loops. The protein also shares limited homology with Escherichia coli OmpA. N. gonorrhoeae protein III has been shown to elicit blocking antibodies that prevent the killing of serum-resistant strains by immune sera (P. A. Rice, H. E. Vayo, M. R. Tam, and M. S. Blake, J. Exp. Med. 164:1735-1748, 1986). The very close homology of meningococcal class 4 protein with gonococcal protein III suggests that meningococcal outer membrane preparations containing class 4 protein may similarly stimulate blocking antibodies. In order to investigate the role of the class 4 protein in the pathogenesis of meningococcal infection, we have used an erythromycin resistance gene in developing two meningococcal strains that lack class 4 protein.

Amino Acid Sequence↗
PubMed1989

[The role of cellular and humoral factors of body resistance in the development of experimental influenza-staphylococcal infections in mice].

The clinico-experimental studies of mixed influenza-staphylococcal infection constantly point to the development of the aggravation of the infectious process due to the synergic action of the bacterial and viral infective agents. But, as shown by the authors of the present work, in those cases when the experimental infection with the virus was preceded by staphylococcal infection by 72 hours no synergism was observed. In cases of infection with adaptogenic virus the mortality rate of mice resulting from meningococcal infection was twice as low. The possible explanation of this fact is discussed.

Animals↗
PubMed1989

Comparison of the abilities of different protein sources of iron to enhance Neisseria meningitidis infection in mice.

This study was done primarily to determine whether the previously observed specificity of the meningococcal transferrin and lactoferrin receptors for human proteins was maintained in vivo during meningococcal infection in mice. Preliminary experiments evaluating the choice of host strain, the age and sex of mice, and the growth conditions of the meningococci indicated that 45-day-old female Swiss Webster mice challenged with meningococci grown on low-pH, low-iron Mueller-Hinton agar plates were appropriate for this study. The comparison of transferrins and lactoferrins from different species demonstrated that only the human forms of these proteins were utilized by meningococci; there was significantly greater mortality among mice treated with iron-saturated human transferrin or lactoferrin (93 and 100%, respectively) than among those not treated or treated with iron-saturated bovine transferrin or bovine lactoferrin (0%). Provision of exogenous hemoglobin also resulted in increased mortality, although not as great as that observed with amounts of transferrin with equivalent iron content, which parallels the more effective utilization of transferrin and lactoferrin in in vitro growth experiments. In addition, unlike with transferrin and lactoferrin, there was no difference in utilization of human and bovine hemoglobin in vitro or in vivo.

Animals↗
PubMed2005

Complement levels in Brazilian children during and after meningococcal meningitis.

PURPOSE: To evaluate the functional activity of the classical and alternative pathways of the complement system and the levels of C3, C4, and factor B during the first episode of meningococcal infection and during the convalescence period. PATIENTS AND METHODS: Ten Brazilian children ranging in age from 8 months to 8 years, admitted from 1991 to 1993 with a clinical-laboratory diagnosis of meningococcal meningitis, were studied during acute infection (up to 7 days from diagnosis) and during the convalescence period (1 to 6 months after the acute episode). C3, C4, and Factor B were measured using nephelometry, and the lytic activity of classical and alternative pathways were evaluated by a kinetic method and expressed as the time needed to lyse 50% of an erythrocyte suspension (T1/2, expressed in seconds). Low T1/2 values for classical and alternative pathways correlate with high activities of the classical and alternative complement pathways, respectively. RESULTS: A significant difference was observed between the alternative pathway lytic activity during infection and the convalescence period (282 vs 238 seconds, respectively, P = .01). No differences were detected in the other complement parameters analyzed. CONCLUSIONS: In the presence of meningococcal meningitis, the alternative pathway is preferentially activated. This is probably due to the greater ability of the meningococcal endotoxin to activate this pathway in vivo.

Acute Disease↗
PubMed2006

Clonal spread of serogroup W135 meningococcal disease in Turkey.

Six cases of Neisseria meningitidis serogroup W135 meningococcal infection have been reported in Turkey since 2003. Seven isolates recovered from four meningococcal meningitis patients and two asymptomatic carriers produced three distinct pulsed-field gel electrophoresis (PFGE) patterns. Multilocus sequence typing and antigen gene sequencing showed that five isolates were indistinguishable from ST-11 (ET-37) serogroup W135 meningococci, which were first isolated in Saudi Arabia and were responsible for the worldwide outbreak among Hajj pilgrims and their contacts in 2000. The remaining two isolates, which had related PFGE patterns, differed from each other at only one of the genetic loci characterized but were not related to the ST-11 clonal complex. None of the six individuals recalled contact with a pilgrim or had traveled on the Hajj. These six individuals exhibited no time or place relationships to each other, except for the two asymptomatic carriers, who were soldiers and served in the same military unit. These data demonstrate that serogroup W135 meningococci with different genotypes, including the Hajj epidemic strain, are endemic in Turkey.

Bacterial Typing Techniques↗
PubMed1998

Failure of mass antibiotic prophylaxis to control a prolonged outbreak of meningococcal disease in an Israeli village.

In January 1994 mass antibiotic prophylaxis was undertaken in the contiguous villages of Deir el-Asad and B'ine in northern Israel (combined population of 11600) in response to a prolonged outbreak of serogroup B meningococcal infection with an overall annual rate of 37.4 cases of infection per 100000 residents. The average case fatality rate in the villages was 23% compared with 11% in Israel during the same period. Neisseria meningitidis group B was identified in 9 of 13 (69%) cases. Seven of these were subtype P1.7,16. The persistence of the outbreak with its accompanying public reaction prompted the establishment of an intervention programme that included antibiotic prophylaxis for the whole community with monitoring for pharyngeal carriage of meningococci in a stratified sample of the population. The objectives were to achieve a reduction of carriage of the outbreak strain and to reduce morbidity and mortality. A total of 1036 pharyngeal swabs were taken 1 day before and 6 weeks after treatment. Antibiotic prophylaxis was administered in one dose: children under 5-years-old received ceftriaxone i.m.; all others received oral ciprofloxacin. Overall, 96% of the population received treatment. The carriage rate was 8.3% prior to treatment (three serogroup B:14:P1.7,16), and 1.3% afterwards (one serogroup B:14:P1.7,16). The intervention failed to eradicate carriage of the putative outbreak strain, or to reduce the incidence and fatality rates in the villages. The outbreak finally terminated in late 1996. Public health professionals should bear this experience in mind when faced with prolonged, localized, nonexplosive outbreaks of meningococcal disease associated with low carriage rates of the outbreak strain.

Adolescent↗