Journal articles: 'Meningococcie'

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Cartwright, K. A. V., J. M. Stuart, and P. M. Robinson. "Meningococcal carriage in close contacts of cases." Epidemiology and Infection 106, no. 1 (February 1991): 133–41. http://dx.doi.org/10.1017/s0950268800056491.

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SUMMARYBetween 1 October 1986 and 31 March 1987, 55 cases of meningococcal disease were identified in the South-West of England, an attack rate of 1·54 per 100000 during the study period. Antibiotics used in the treatment of the disease successfully eliminated nasopharyngeal carriage of meningococci in 13 out of 14 cases without use of rifampicin. The overall meningococcal carriage rate in 384 close contacts was 18·2% and the carriage rate of strains indistinguishable from the associated case strain was 11·1%. The carriage rate of indistinguishable strains in household contacts (16·0%) was higher than the carriage rate in contacts living at other addresses (7·0%, P > 0·05). A 2·day course of rifampicin successfully eradicated meningococci from 46 (98%) of 47 colonized contacts.In one third of cases groupable meningococci were isolated from at least one household contact; 92% of these isolates were of the same serogroup as the associated case strain. When a meningococcus is not isolated from a deep site in a clinical case of meningococcal disease, culture of serogroup A or C strains from nasopharyngeal swabs of the case or of household contacts is an indication that the close contact group should be offered meningococcal A + C vaccine in addition to chemoprophylaxis. The failure in this and other studies to isolate meningococci from any household contact in the majority of cases may be due either to the relative insensitivity of nasopharyngeal swabbing in detecting meningococcal carriage or to the acquisition of meningococci by most index cases from sources outside the household.

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Woodhams, Katelynn L., Jia Mun Chan, Jonathan D. Lenz, Kathleen T. Hackett, and Joseph P. Dillard. "Peptidoglycan Fragment Release from Neisseria meningitidis." Infection and Immunity 81, no. 9 (July 8, 2013): 3490–98. http://dx.doi.org/10.1128/iai.00279-13.

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ABSTRACTNeisseria meningitidis(meningococcus) is a symbiont of the human nasopharynx. On occasion, meningococci disseminate from the nasopharynx to cause invasive disease. Previous work showed that purified meningococcal peptidoglycan (PG) stimulates human Nod1, which leads to activation of NF-κB and production of inflammatory cytokines. No studies have determined if meningococci release PG or activate Nod1 during infection. The closely related pathogenNeisseria gonorrhoeaereleases PG fragments during normal growth. These fragments induce inflammatory cytokine production and ciliated cell death in human fallopian tubes. We determined that meningococci also release PG fragments during growth, including fragments known to induce inflammation. We found thatN. meningitidisrecycles PG fragments via the selective permease AmpG and that meningococcal PG recycling is more efficient than gonococcal PG recycling. Comparison of PG fragment release fromN. meningitidisandN. gonorrhoeaeshowed that meningococci release less of the proinflammatory PG monomers than gonococci and degrade PG to smaller fragments. The decreased release of PG monomers byN. meningitidisrelative toN. gonorrhoeaeis partly due toampG, since replacement of gonococcalampGwith the meningococcal allele reduced PG monomer release. Released PG fragments in meningococcal supernatants induced significantly less Nod1-dependent NF-κB activity than released fragments in gonococcal supernatants and tended to induce less interleukin-8 (IL-8) secretion in primary human fallopian tube explants. These results support a model in which efficient PG recycling and extensive degradation of PG fragments lessen inflammatory responses and may be advantageous for maintaining meningococcal carriage in the nasopharynx.

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Mowlaboccus, Shakeel. "Whole genome sequencing as a novel approach for characterising Neisseria meningitidis in Australia." Microbiology Australia 38, no. 3 (2017): 142. http://dx.doi.org/10.1071/ma17052.

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Neisseria meningitidis (meningococcus) is the causative agent of invasive meningococcal disease that manifests as life-threatening septicaemia and/or meningitis. This review provides a brief overview of the prevention of the disease and also highlights the importance of whole genome sequencing (WGS) in detecting outbreaks of meningococci in Australia. The use of WGS in identifying the emergence of a penicillin-resistant cluster of meningococci is Western Australia is used as an example for advocating the implementation of WGS on the routine surveillance in Australia.

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Newcombe, J., L. J. Eales-Reynolds, L. Wootton, A. R. Gorringe, S. G. P. Funnell, S. C. Taylor, and J. J. McFadden. "Infection with an Avirulent phoP Mutant of Neisseria meningitidis Confers Broad Cross-Reactive Immunity." Infection and Immunity 72, no. 1 (January 2004): 338–44. http://dx.doi.org/10.1128/iai.72.1.338-344.2004.

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ABSTRACT Successful vaccines against serogroup A and C meningococcal strains have been developed, but current serogroup B vaccines provide protection against only a limited range of strains. The ideal meningococcal vaccine would provide cross-reactive immunity against the variety of strains that may be encountered in any community, but it is unclear whether the meningococcus possesses immune targets that have the necessary level of cross-reactivity. We have generated a phoP mutant of the meningococcus by allele exchange. PhoP is a component of a two-component regulatory system which in other bacteria is an important regulator of virulence gene expression. Inactivation of the PhoP-PhoQ system in Salmonella leads to avirulence, and phoP mutants have been shown to confer protection against virulent challenge. These mutants have been examined as potential live attenuated vaccines. We here show that a phoP mutant of the meningococcus is avirulent in a mouse model of infection. Moreover, infection of mice with the phoP mutant stimulated a bactericidal immune response that not only killed the infecting strain but also showed cross-reactive bactericidal activity against a range of strains with different serogroup, serotype, and serosubtyping antigens. Sera from the mutant-infected mice contained immunoglobulin G that bound to the surface of a range of meningococcal strains and mediated opsonophagocytosis of meningococci by human phagocytic cells. The meningococcal phoP mutant is thus a candidate live, attenuated vaccine strain and may also be used to identify cross-reactive protective antigens in the meningococcus.

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O'Dwyer, Clíona A., Karen Reddin, Denis Martin, Stephen C. Taylor, Andrew R. Gorringe, Michael J. Hudson, Bernard R. Brodeur, Paul R. Langford, and J. Simon Kroll. "Expression of Heterologous Antigens in Commensal Neisseria spp.: Preservation of Conformational Epitopes with Vaccine Potential." Infection and Immunity 72, no. 11 (November 2004): 6511–18. http://dx.doi.org/10.1128/iai.72.11.6511-6518.2004.

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ABSTRACT Commensal neisseriae share with Neisseria meningitidis (meningococcus) a tendency towards overproduction of the bacterial outer envelope, leading to the formation and release during growth of outer membrane vesicles (OMVs). OMVs from both meningococci and commensal neisseriae have shown promise as vaccines to protect against meningococcal disease. We report here the successful expression at high levels of heterologous proteins in commensal neisseriae and the display, in its native conformation, of one meningococcal outer membrane protein vaccine candidate, NspA, in OMVs prepared from such a recombinant Neisseria flavescens strain. These NspA-containing OMVs conferred protection against otherwise lethal intraperitoneal challenge of mice with N. meningitidis serogroup B, and sera raised against them mediated opsonophagocytosis of meningococcal strains expressing this antigen. This development promises to facilitate the design of novel vaccines containing membrane protein antigens that are otherwise difficult to present in native conformation that provide cross-protective efficacy in the prevention of meningococcal disease.

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van Deuren, Marcel, Petter Brandtzaeg, and Jos W. M. van der Meer. "Update on Meningococcal Disease with Emphasis on Pathogenesis and Clinical Management." Clinical Microbiology Reviews 13, no. 1 (January 1, 2000): 144–66. http://dx.doi.org/10.1128/cmr.13.1.144.

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The only natural reservoir of Neisseria meningitidis is the human nasopharyngeal mucosa. Depending on age, climate, country, socioeconomic status, and other factors, approximately 10% of the human population harbors meningococci in the nose. However, invasive disease is relatively rare, as it occurs only when the following conditions are fulfilled: (i) contact with a virulent strain, (ii) colonization by that strain, (iii) penetration of the bacterium through the mucosa, and (iv) survival and eventually outgrowth of the meningococcus in the bloodstream. When the meningococcus has reached the bloodstream and specific antibodies are absent, as is the case for young children or after introduction of a new strain in a population, the ultimate outgrowth depends on the efficacy of the innate immune response. Massive outgrowth leads within 12 h to fulminant meningococcal sepsis (FMS), characterized by high intravascular concentrations of endotoxin that set free high concentrations of proinflammatory mediators. These mediators belonging to the complement system, the contact system, the fibrinolytic system, and the cytokine system induce shock and diffuse intravascular coagulation. FMS can be fatal within 24 h, often before signs of meningitis have developed. In spite of the increasing possibilities for treatment in intensive care units, the mortality rate of FMS is still 30%. When the outgrowth of meningococci in the bloodstream is impeded, seeding of bacteria in the subarachnoidal compartment may lead to overt meningitis within 24 to 36 h. With appropriate antibiotics and good clinical surveillance, the mortality rate of this form of invasive disease is 1 to 2%. The overall mortality rate of meningococcal disease can only be reduced when patients without meningitis, i.e., those who may develop FMS, are recognized early. This means that the fundamental nature of the disease as a meningococcus septicemia deserves more attention.

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SADLER, F., R. BORROW, M. M. DAWSON, E. B. KACZMARSKI, K. CARTWRIGHT, and A. J. FOX. "Improved methods of detection of meningococcal DNA from oropharyngeal swabs from cases and contacts of meningococcal disease." Epidemiology and Infection 125, no. 2 (October 2000): 277–83. http://dx.doi.org/10.1017/s0950268899004367.

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In the UK the increasing use of pre-admission parenteral antibiotic therapy in meningococcal disease has lessened the value of routine cultures as a tool to confirm diagnosis, and laboratory confirmation of invasive meningococcal infection is achieved increasingly by non-culture, nucleic acid amplification methods. The purpose of this study was to evaluate a DNA extraction and meningococcal-specific DNA amplification methodology for detection of meningococci from oropharyngeal swabs.One hundred and six swabs from suspected or confirmed cases of meningococcal disease, and 94 swabs from contacts of meningococcal disease cases were examined. Of laboratory-confirmed cases, 38/65 (58·5%) yielded a positive oropharyngeal swab PCR result and 5/24 (20·8%) swabs from suspected but laboratory-unconfirmed cases were PCR positive. No significant differences in PCR positivity rates were found between the types of swab transport systems utilized, but transport time to the testing laboratory was found to affect PCR positivity (P < 0·05).Application of meningococcus-specific PCR to oropharyngeal swabs, in addition to routine culture of swabs, can provide valuable epidemiological information as well as case confirmation for contact management. PCR amplification of meningococcal PCR from oropharyngeal swabs will also increase the ascertainment in swabbing surveys carried out as part of meningococcal disease outbreak investigation and management.

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Zhou, Jianwei, Frances Jamieson, Sharon Dolman, Linda MN Hoang, Prasad Rawte, and Raymond SW Tsang. "Genetic and Antigenic Analysis of Invasive Serogroup CNeisseria meningitidisin Canada: A Decrease in the Electrophoretic Type (Et)-15 Clonal Type and an Increase in the Proportion of Isolates Belonging to the Et-37 (But Not Et-15) Clonal Type During the Period from 2002 to 2009." Canadian Journal of Infectious Diseases and Medical Microbiology 23, no. 3 (2012): e55-e59. http://dx.doi.org/10.1155/2012/131328.

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BACKGROUND: Serogroup C meningococcal disease has been endemic in Canada since the early 1990s, with periods of hyperendemic disease documented in the past two decades. The present study characterized invasive serogroup C meningococci in Canada during the period from 2002 to 2009.METHODS: Serogroup C meningococci were serotyped using monoclonal antibodies. Their clonal types were identified by either multilocus enzyme electrophoresis or multilocus sequence typing.RESULTS: The number of invasive serogroup CNeisseria meningitidisisolates received at the National Microbiology Laboratory (Winnipeg, Manitoba) for characterization has dropped from a high of 173 isolates in 2001 to just 17 in 2009, possibly related to the introduction of the serogroup C meningococcal conjugate vaccine. Before 2006, 80% to 95% of all invasive serogroup C meningococci belonged to the electrophoreic type (ET)-15 clonal type, and the ET-37 (but not ET-15) type only accounted for up to 5% of all isolates. However, beginning in 2006, the percentage of the ET-15 clonal type decreased while the ET-37 (but not ET-15) type increased from 27% in 2006 to 52% in 2009. The percentage of invasive serogroup C isolates not belonging to either ET-15 or ET-37 also increased. Most ET-15 isolates expressed the antigenic formula of C:2a:P1.7,1 or C:2a:P1.5. In contrast, the ET-37 (but not ET-15) isolates mostly expressed the antigens of C:2a:P1.5,2 or C:2a:P1.2.CONCLUSION: A shift in the antigenic and clonal type of invasive serogroup C meningococi was noted. This finding suggests vigilance in the surveillance of meningoccocal disease is warranted.

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Borkowski, Julia, Horst Schroten, and Christian Schwerk. "Interactions and Signal Transduction Pathways Involved during Central Nervous System Entry by Neisseria meningitidis across the Blood–Brain Barriers." International Journal of Molecular Sciences 21, no. 22 (November 20, 2020): 8788. http://dx.doi.org/10.3390/ijms21228788.

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The Gram-negative diplococcus Neisseria meningitidis, also called meningococcus, exclusively infects humans and can cause meningitis, a severe disease that can lead to the death of the afflicted individuals. To cause meningitis, the bacteria have to enter the central nervous system (CNS) by crossing one of the barriers protecting the CNS from entry by pathogens. These barriers are represented by the blood–brain barrier separating the blood from the brain parenchyma and the blood–cerebrospinal fluid (CSF) barriers at the choroid plexus and the meninges. During the course of meningococcal disease resulting in meningitis, the bacteria undergo several interactions with host cells, including the pharyngeal epithelium and the cells constituting the barriers between the blood and the CSF. These interactions are required to initiate signal transduction pathways that are involved during the crossing of the meningococci into the blood stream and CNS entry, as well as in the host cell response to infection. In this review we summarize the interactions and pathways involved in these processes, whose understanding could help to better understand the pathogenesis of meningococcal meningitis.

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MARKOVA, K. V., E. Yu SKRIPCHENKO, N. V. SKRIPCHENKO, A. A. VILNITS, L. N. MAZANKOVA, S. V. SIDORENKO, E. A. MARTENS, and E. Yu GORELIK. "Clinical and microbiological features of meningococcal infection in children." Practical medicine 19, no. 2 (2021): 61–69. http://dx.doi.org/10.32000/2072-1757-2021-2-61-69.

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The threat of a pandemic of meningococcal infection, the severity of the disease and the unpredictability of outcomes necessitate monitoring of the characteristics of the disease course and the circulating serotypes of meningococcus. The purpose — to study the features of the clinical manifestations of meningococcal infection in children depending on the serogroup of N. meningitidis, as well as the phenotypic and genotypic characteristics of the pathogen. Material and methods. 97 children with invasive meningococcal infection with the established serogroup N. meningitidis, hospitalized in 2014–2020, were under observation at PRCCID. We also analyzed 15 discharge epicrises of children with invasive meningococcal infection caused by N. meningitidis W, hospitalized in hospitals in Moscow (Infectious Diseases Hospital No. 2 and Children’s City Clinical Hospital named after Z.A. Bashlyaeva) in 2017–2019. The study of the phenotypic and genotypic characteristics of the pathogen was carried out by the analysis of 34 strains of meningococcus isolated at PRCCID. Results. It was found that in the disease caused by NmW, in 29% of cases (n = 9), there was a subacute onset of the disease with a delayed appearance of an abundant hemorrhagic rash with a predominant localization on the distal extremities (p < 0,01). Also, with NmW in 22,6% (n = 7) cases, the development of convulsive syndrome is noted in 22,6% (n = 7) cases (p < 0,01). NmB is characterized (65,3%, n = 34) by multiple elements of hemorrhagic rash and the formation of soft tissue neuroses (46,2%, n = 24). Focal neurological symptoms were predominantly observed in children with HFMI caused by NmC (23,5%, n = 4) and NmW (13,3%, n = 4). It is noteworthy that among the atypical manifestations of meningococcal infection in NmW, diarrhea, pain in the abdomen and joints, myalgia were most often noted, and conjunctivitis in NmC. Intracranial complications are observed mainly in children with the disease caused by NmB (36,0%, n = 9) and NmC (24%, n = 6), extracranial — by NmB (50%, n = 5), and intracranial + extracranial — by NmW (26,8%, n = 11) and NmB (51,2%, n = 21). Analysis of the phenotypic and genotypic features of invasive meningococcal infection, depending on the pathogen, revealed meningococcal strains (54,1%, n = 20) with reduced sensitivity to antibacterial drugs, as well as 12 NmW strains (ST-11, cc11), closely located to Anglo-French and Swedish subgroup of the Hajj cluster. Conclusion. The features of the clinical manifestations of meningococcal infection in children largely depend on the serotype of the causally significant meningococcus, the timely diagnosis of which makes it possible to predict the course of the disease. It has been established that currently among circulating meningococci there are meningococcal strains with reduced sensitivity to antibacterial drugs (54,1%, n = 20), as well as NmW strains (ST-11, cc11), close to Anglo-French and Swedish subgroups of the Hajj cluster (35,3%, n = 12). This situation requires continuous monitoring of the phenotypic and genotypic characteristics of the microorganism to optimize management tactics.

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Claus, Heike, Alexander Friedrich, Matthias Frosch, and Ulrich Vogel. "Differential Distribution of Novel Restriction-Modification Systems in Clonal Lineages ofNeisseria meningitidis." Journal of Bacteriology 182, no. 5 (March 1, 2000): 1296–303. http://dx.doi.org/10.1128/jb.182.5.1296-1303.2000.

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ABSTRACT Using representational difference analysis, we isolated novel meningococcal restriction-modification (R-M) systems.NmeBI, which is a homologue of the R-M systemHgaI of Pasteurella volantium, was present in meningococci of the ET-5 complex and of lineage III. NmeAI was found in serogroup A, ET-37 complex, and cluster A4 meningococci.NmeDI was harbored by meningococci of the ET-37 complex and of cluster A4, but not by serogroup A meningococci. Two of the R-M systems, NmeBI and NmeDI, were located at homologous positions between the phenylalanyl-tRNA synthetase genespheS and pheT, which appeared to be a preferential target for the insertion of foreign DNA in meningococci. The distribution of the three R-M systems was tested with 103 meningococcal strains comprising 49 sequence types. The vast majority of the strains had either NmeBI, NmeAI, or bothNmeAI and NmeDI. Using cocultivation experiments, we could demonstrate that NmeBI, which was present in ET-5 complex meningococci, was responsible for a partial restriction of DNA transfer from meningococci of the ET-37 complex to meningococci of the ET-5 complex.

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Sharma, Supriya, Jyoti Acharya, Dominique A. Caugant, Jeewan Thapa, Manju Bajracharya, Madhusudan Kayastha, Saroj Sharma, et al. "Meningococcal Meningitis: A Multicentric Hospital-based Study in Kathmandu, Nepal." Open Microbiology Journal 13, no. 1 (December 11, 2019): 273–78. http://dx.doi.org/10.2174/1874285801913010273.

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Background: The global epidemiology of meningococcal disease varies markedly by region and over time. In Nepal, information on serogroup of meningococci is not available since the 1983 serogroup A epidemic in Kathmandu. Objective: To provide some fundamental data on the circulating serogroups of meningococci for potential meningococcal immunization programs in Nepal. Methods: This cross-sectional prospective study was conducted from January 2017 to December 2018 among 387 clinically suspected meningitis cases. Cerebrospinal fluid samples were collected by lumbar puncture technique at five referral hospitals of Kathmandu and processed by conventional cultural techniques. Neisseria meningitidis was identified by colony morphology, Gram staining and oxidase test. Serogrouping of meningococci was performed by slide agglutination test. Antibiotic susceptibility testing was done by the modified Kirby Bauer disc diffusion method. The data was entered into IBM SPSS Statistics 21 software and a p-value of <0.05 was considered significant. Results: Thirty-two samples were positive by culture for a bacterial pathogen with 2.3% of meningococci. All except one meningococcal meningitis cases were aged below 15 years. All N.meningitidis isolates belonged to serogroup A and were susceptible to ceftriaxone, chloramphenicol, meropenem and minocycline; however, 22% isolates showed resistance to cotrimoxazole and 11% intermediate resistance to ciprofloxacin. Conclusion: The circulating serogroup of N. meningitidis in Kathmandu has not changed over the past 35 years. The prevalence of meningococcal meningitis in Kathmandu is low but might be underestimated due to the sole use of culture-based diagnostic methods. Detection of meningococci by alternative methods may be useful in the precise estimation of actual disease burden.

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Barnier, Jean-Philippe, Daniel Euphrasie, Olivier Join-Lambert, Mathilde Audry, Sophia Schonherr-Hellec, Taliah Schmitt, Sandrine Bourdoulous, Mathieu Coureuil, Xavier Nassif, and Mohamed El Behi. "Type IV pilus retraction enables sustained bacteremia and plays a key role in the outcome of meningococcal sepsis in a humanized mouse model." PLOS Pathogens 17, no. 2 (February 16, 2021): e1009299. http://dx.doi.org/10.1371/journal.ppat.1009299.

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Neisseria meningitidis (the meningococcus) remains a major cause of bacterial meningitis and fatal sepsis. This commensal bacterium of the human nasopharynx can cause invasive diseases when it leaves its niche and reaches the bloodstream. Blood-borne meningococci have the ability to adhere to human endothelial cells and rapidly colonize microvessels. This crucial step enables dissemination into tissues and promotes deregulated inflammation and coagulation, leading to extensive necrotic purpura in the most severe cases. Adhesion to blood vessels relies on type IV pili (TFP). These long filamentous structures are highly dynamic as they can rapidly elongate and retract by the antagonistic action of two ATPases, PilF and PilT. However, the consequences of TFP dynamics on the pathophysiology and the outcome of meningococcal sepsis in vivo have been poorly studied. Here, we show that human graft microvessels are replicative niches for meningococci, that seed the bloodstream and promote sustained bacteremia and lethality in a humanized mouse model. Intriguingly, although pilus-retraction deficient N. meningitidis strain (ΔpilT) efficiently colonizes human graft tissue, this mutant did not promote sustained bacteremia nor induce mouse lethality. This effect was not due to a decreased inflammatory response, nor defects in bacterial clearance by the innate immune system. Rather, TFP-retraction was necessary to promote the release of TFP-dependent contacts between bacteria and, in turn, the detachment from colonized microvessels. The resulting sustained bacteremia was directly correlated with lethality. Altogether, these results demonstrate that pilus retraction plays a key role in the occurrence and outcome of meningococcal sepsis by supporting sustained bacteremia. These findings open new perspectives on the role of circulating bacteria in the pathological alterations leading to lethal sepsis.

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Kelleher, Julia A., and Marsha A. Raebel. "Meningococcal Vaccine Use in College Students." Annals of Pharmacotherapy 36, no. 11 (November 2002): 1776–84. http://dx.doi.org/10.1345/aph.1c024.

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OBJECTIVE: To discuss the role of meningococcal vaccine in prevention of meningococcal disease. DATA SOURCES: A MEDLINE search (1966–June 2001) was performed to identify key literature. Search terms included, but were not limited to, meningococcal vaccines, meningococcal meningitis, meningococcal infection, and meningococcus. The search was limited to English-language literature and references dealing with humans. The MEDLINE search was supplemented by a hand search of various bibliographies. DATA SYNTHESIS: The impact of meningococcal disease has caused national and regional organizations to develop recommendations for use of meningococcal vaccine. Even though the meningococcal vaccine can provide benefit, limitations exist. The available vaccine does not cover all meningococcal strains and is not useful in all age groups. The appropriate target groups for prevention of disease through vaccination have been difficult to determine; vaccine use in college students is especially controversial. CONCLUSIONS: Although a meningococcal vaccine is available, meningococcus causes significant morbidity and mortality. Controversy exists over the meningococcal vaccine and its use. Students entering college who will be living in dormitories should be informed of the increased risk of meningococcal disease and be offered vaccination.

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HILSE, R., J. STOEVESANDT, D. A. CAUGANT, H. CLAUS, M. FROSCH, and U. VOGEL. "Distribution of the meningococcal insertion sequence IS1301 in clonal lineages of Neisseria meningitidis." Epidemiology and Infection 124, no. 2 (April 2000): 337–40. http://dx.doi.org/10.1017/s0950268899003647.

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The distribution of the meningococcal insertion sequence IS1301 was analysed in 496 strains of different serogroups and clonal lineages of Neisseria meningitidis, and in 64 neisserial strains other than N. meningitidis. IS1301 was found in meningococci, but not in apathogenic Neisseria sp. and Neisseria gonorrhoeae. The copy numbers of IS1301 varied between 2 and 17 per genome. IS1301 positive strains were mostly found among the serogroups 29E, W135, X, and Y. Clonal lineages of serogroup A, B, and C meningococci associated with epidemic meningococcal disease were rarely positive for IS1301.

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Casey, Rosalyn, Jane Newcombe, JohnJoe McFadden, and Katherine B. Bodman-Smith. "The Acute-Phase Reactant C-Reactive Protein Binds to Phosphorylcholine-Expressing Neisseria meningitidis and Increases Uptake by Human Phagocytes." Infection and Immunity 76, no. 3 (January 14, 2008): 1298–304. http://dx.doi.org/10.1128/iai.00741-07.

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ABSTRACT Neisseria meningitidis is a global cause of meningitis and septicemia. Immunity to N. meningitidis involves both innate and specific mechanisms with killing by serum bactericidal activity and phagocytic cells. C-reactive protein (CRP) is an acute-phase serum protein that has been shown to help protect the host from several bacterial pathogens, which it recognizes by binding to phosphorylcholine (PC) on their surfaces. Pathogenic Neisseria species can exhibit phase-variable PC modification on type 1 and 2 pili. We have shown that CRP can bind to piliated meningococci in a classical calcium-dependent manner. The binding of CRP to the meningococcus was concentration dependent, of low affinity, and specific for PC. CRP appears to act as an opsonin for N. meningitidis, as CRP-opsonized bacteria showed increased uptake by human macrophages and neutrophils. Further investigation into the downstream effects of CRP-bound N. meningitidis may lead us to a better understanding of meningococcal infection and help direct more effective therapeutic interventions.

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Sasikumari, O., Angel Mary George, and K. L. Sarada Devi. "Extended Spectrum Beta Lactamase (ESBL) Producing Neisseria meningitidis – Isolated from a Case of Pneumonia." European Journal of Medical and Health Sciences 3, no. 3 (June 30, 2021): 75–77. http://dx.doi.org/10.24018/ejmed.2021.3.3.908.

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Neisseria meningitidis (meningococci) is the most common cause of bacterial meningitis in all age groups. Invasive meningococcal disease manifesting as meningococcal pneumonia is a very rare clinical condition. Here we have a 72 year old male who presented with meningococcal pneumonia and sepsis following a flu like illness. It is notable that he did not develop the syndrome of meningococcemia or its associated complications. This patient was treated with injections of Piperacillin-Tazobactum and Azithromycin because of the unusual antibiotic resistance pattern of the organism. He recovered completely without any sequelae. The meningococci isolated was an ESBL (extended spectrum beta lactamase) producing strain, hence it was resistant to Penicillin and third generation Cephalosporins which are usually used for the treatment of meningococcal infections .This strain was also resistant to Ciprofloxacin .This poses a threat to the community as well, especially because Ciprofloxacin is used as a chemo prophylactic drug by the contacts of the patient and the laboratory workers dealing with the patient’s clinical samples.

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Fijen, C. A. P., E. J. Kuijper, J. Dankert, M. R. Daha, and D. A. Caugant. "Characterization of Neisseria meningitidis Strains Causing Disease in Complement-Deficient and Complement-Sufficient Patients." Journal of Clinical Microbiology 36, no. 8 (1998): 2342–45. http://dx.doi.org/10.1128/jcm.36.8.2342-2345.1998.

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Serotyping and serosubtyping of meningococci showed no difference between isolates from 44 complement-deficient persons and from 50 complement-sufficient persons with meningococcal disease. Multilocus enzyme electrophoretic typing of the meningococci revealed 54 electrophoretic types that were equally distributed among isolates from complement-deficient and complement-sufficient patients. Analysis of strains isolated from eight complement-deficient persons with 11 recurrences of meningococcal disease showed that one strain was identical to the strain previously isolated from the same individual. Our results indicate that there are no differences between the clonal distributions of strains infecting complement-deficient and complement-sufficient patients. Most recurrences were infections caused by different strains.

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Nadel, Simon. "Prospects for eradication of meningococcal disease." Archives of Disease in Childhood 97, no. 11 (September 15, 2012): 993–98. http://dx.doi.org/10.1136/archdischild-2012-302036.

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Meningococcal meningitis and septicaemia remain a serious global health threat. This review focuses on the epidemiology of meningococcal disease following the recent implementation of effective vaccines and the potential utility of a vaccine against serogroup B meningococcus.

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Mairey, Emilie, Auguste Genovesio, Emmanuel Donnadieu, Christine Bernard, Francis Jaubert, Elisabeth Pinard, Jacques Seylaz, Jean-Christophe Olivo-Marin, Xavier Nassif, and Guillaume Duménil. "Cerebral microcirculation shear stress levels determine Neisseria meningitidis attachment sites along the blood–brain barrier." Journal of Experimental Medicine 203, no. 8 (July 24, 2006): 1939–50. http://dx.doi.org/10.1084/jem.20060482.

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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.

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Blackwell, C. C., D. M. Weir, V. S. James, W. T. A. Todd, N. Banatvala, A. K. R. Chaudhuri, H. G. Gray, E. J. Thomson, and R. J. Fallon. "Secretor status, smoking and carriage ofNeisseria meningitidis." Epidemiology and Infection 104, no. 2 (April 1990): 203–9. http://dx.doi.org/10.1017/s0950268800059367.

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SUMMARYA survey of ABO blood groups, secretor status and smoking habits among 389 students and staff of a school in which there was an outbreak of meningococcal disease found no difference in the distribution of the ABO blood groups but a significantly higher proportion of non-secretors (37·6%) in the population examined compared with that reported for previous surveys of the neighbouring population in Glasgow (26·2%) (P< 0·0005). There was also a significantly higher proportion of non-secretors among carriers of meningococci (47%) compared with non-carriers (32%). Increased carriage of meningococci among non-secretors might contribute to the increased susceptibility of individuals with this genetic characteristic to meningococcal disease observed in previous studies. Although passive exposure to cigarette smoke has been associated with meningococcal disease, there was no association between passive smoking and carriage. There was, however, a significant association between active smoking and carriage.

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TZENG, Y. L., L. E. MARTIN, and D. S. STEPHENS. "Environmental survival ofNeisseria meningitidis." Epidemiology and Infection 142, no. 1 (April 10, 2013): 187–90. http://dx.doi.org/10.1017/s095026881300085x.

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SUMMARYNeisseria meningitidisis transmitted through the inhalation of large human respiratory droplets, but the risk from contaminated environmental surfaces is controversial. Compared toStreptococcus pneumoniaeandAcinetobacter baumanni, meningococcal viability after desiccation on plastic, glass or metal surfaces decreased rapidly, but viable meningococci were present for up to 72 h. Encapsulation did not provide an advantage for meningococcal environmental survival on environmental surfaces.

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Filatova, T. G., A. I. Kovalenko, and M. M. Leri. "DYNAMICS OF MENINGOCOCCAL INFECTION RATE IN THE REPUBLIC OF KARELIA." Epidemiology and Infectious Diseases 18, no. 1 (February 15, 2013): 23–28. http://dx.doi.org/10.17816/eid40709.

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The paper presents the results of an epidemiological analysis of the incidence of meningococcal infection in the Republic of Karelia over epidemic and interepidemic periods. Year over year meningococcal infection rate in the Republic has been remaining to be higher than similar data in Russian Federation. In the years of epidemiological outbreak the number of regions being affected and the disease incidence in children under 14 increases. The largest lethality has been observed in the beginning of epidemiological outbreak. The results of the study indicate the exchange of the leader of meningococcus of serogroup В by meningococcus of serogroup C and A. In the absence of planned vaccinal prevention there remains the threat for the rise of meningococcal infection rate.

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Sharma, Supriya, Jyoti Acharya, Dominique A. Caugant, Shreedhar Aryal, Megha Raj Banjara, Prakash Ghimire, and Anjana Singh. "Meningococcal Carriage among Household Contacts of Patients with Invasive Meningococcal Disease in Kathmandu, Nepal: A Longitudinal Study." Pathogens 10, no. 7 (June 22, 2021): 781. http://dx.doi.org/10.3390/pathogens10070781.

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Because asymptomatic carriers are key source of transmission, information on meningococcal carriage in the community provides a scientific basis for appropriate preventive/control strategies. This longitudinal study (January 2017–December 2019) aimed to estimate carriage rate of meningococci among household contacts of meningococcal meningitis cases within Kathmandu Valley, Nepal. Throat swab samples were collected at first visit from each person in households, twice a month for up to 2 months and subsequently on a monthly basis for a further 4 months. Altogether, 1125 throat samples were processed by conventional culture for the identification of meningococci. To the best of our knowledge, this is the first longitudinal study on meningococcal carriage in Nepal. The meningococcal carriage rate among household contacts was 15%. All carriers were aged 19 years or older. There was no statistically significant gender difference. The duration of carriage was 60 days. Twenty of 36 isolates belonged to serogroup A, and 16 were non-serogroupable (NG). Serogroups isolated from the same individuals did not change within the follow-up period. All meningococcal isolates over the past 38 years in Nepal that have been reported in previous studies have belonged to serogroup A. The detection of NG meningococcal isolates in apparently healthy household contacts clearly indicates the importance of vigilance through surveillance and periodic in-depth studies.

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Yi, Kyungcheol, David S. Stephens, and Igor Stojiljkovic. "Development and Evaluation of an Improved Mouse Model of Meningococcal Colonization." Infection and Immunity 71, no. 4 (April 2003): 1849–55. http://dx.doi.org/10.1128/iai.71.4.1849-1855.2003.

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ABSTRACT Studies of meningococcal pathogenesis have been severely restricted due to the absence of an adequate animal model. Given the significance of iron in meningococcal pathogenesis, we developed a model of Neisseria meningitidis colonization in outbred adult mice that included daily administration of iron dextran. While receiving iron, the animals were inoculated intranasally with the initial doses of bacterial suspension. Meningococci were recovered from the animals by nasopharyngeal washes. Approximately half of the animals inoculated with 107 CFU remained colonized 13 days after the initial bacterial inoculation. The model was further evaluated with genetically defined isogenic serogroup B mutant strains, and the colonization capabilities of the mutants were compared to that of the wild-type parent. A mutant that produces truncated lipooligosaccharide (KDO2-lipid A) and a mutant defective in capsule transport were dramatically impaired in colonization. A mutant defective in pilus transport (pilQ) showed moderately impaired colonization. The immunological aspect of the model was also evaluated by challenging mice after immunization with homologous whole-cell meningococci. The immunized mice were protected from colonization of the homologous strain. In this model, long-term meningococcal colonization was maintained, allowing us to study the effects of specific genetic mutation on colonization. In addition, this model allows investigation of the role of active immune response against meningococci.

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Bratcher, Holly B., Charlene M. C. Rodrigues, Adam Finn, Mandy Wootton, J. Claire Cameron, Andrew Smith, Paul Heath, et al. "UKMenCar4: A cross-sectional survey of asymptomatic meningococcal carriage amongst UK adolescents at a period of low invasive meningococcal disease incidence." Wellcome Open Research 4 (August 6, 2019): 118. http://dx.doi.org/10.12688/wellcomeopenres.15362.1.

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Carriage of Neisseria meningitidis, the meningococcus, is a prerequisite for invasive meningococcal disease (IMD), a potentially devastating infection that disproportionately afflicts infants and children. Humans are the sole known reservoir for the meningococcus, and it is carried asymptomatically in the nasopharynx of ~10% of the population. Rates of carriage are dependent on age of the host and social and behavioural factors. In the UK, meningococcal carriage has been studied through large, multi-centre carriage surveys of adolescents in 1999, 2000, and 2001, demonstrating carriage can be affected by immunisation with the capsular group C meningococcal conjugate vaccine, inducing population immunity against carriage. Fifteen years after these surveys were carried out, invasive meningococcal disease incidence had declined from a peak in 1999. The UKMenCar4 study was conducted in 2014/15 to investigate rates of carriage amongst the adolescent population during a period of low disease incidence. The protocols and methodology used to perform UKMenCar4, a large carriage survey, are described here.

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Bratcher, Holly B., Charlene M. C. Rodrigues, Adam Finn, Mandy Wootton, J. Claire Cameron, Andrew Smith, Paul Heath, et al. "UKMenCar4: A cross-sectional survey of asymptomatic meningococcal carriage amongst UK adolescents at a period of low invasive meningococcal disease incidence." Wellcome Open Research 4 (October 28, 2019): 118. http://dx.doi.org/10.12688/wellcomeopenres.15362.2.

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Carriage of Neisseria meningitidis, the meningococcus, is a prerequisite for invasive meningococcal disease (IMD), a potentially devastating infection that disproportionately afflicts infants and children. Humans are the sole known reservoir for the meningococcus, and it is carried asymptomatically in the nasopharynx of ~10% of the population. Rates of carriage are dependent on age of the host and social and behavioural factors. In the UK, meningococcal carriage has been studied through large, multi-centre carriage surveys of adolescents in 1999, 2000, and 2001, demonstrating carriage can be affected by immunisation with the capsular group C meningococcal conjugate vaccine, inducing population immunity against carriage. Fifteen years after these surveys were carried out, invasive meningococcal disease incidence had declined from a peak in 1999. The UKMenCar4 study was conducted in 2014/15 to investigate rates of carriage amongst the adolescent population during a period of low disease incidence. The protocols and methodology used to perform UKMenCar4, a large carriage survey, are described here.

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KYAW, M. H., J. C. BRAMLEY, S. CLARKE, P. CHRISTIE, I. G. JONES, and H. CAMPBELL. "Prevalence of moderate penicillin resistant invasive Neisseria meningitidis infection in Scotland, 1994–9." Epidemiology and Infection 128, no. 2 (December 2001): 149–56. http://dx.doi.org/10.1017/s0950268801006549.

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We examined the serological characteristics of 774 invasive meningococcal isolates collected through an active laboratory-based surveillance system in Scotland from 1994 to 1999. Of these, 72–73% of isolates were tested for susceptibility to several antimicrobial agents. Meningococci with high-level resistance to sulphadiazine had a prevalence of 10% and incidence of 0·22 per 100000 population. High-level resistance to penicillin and other antibiotics was not detected. The prevalence of moderate penicillin resistant meningococci was 8·3%. There was no increase in moderate penicillin resistant meningococcal isolates during the study period, but there were temporal and geographic variations. The estimated incidence of moderate penicillin resistant meningococci was 0·15 per 100000 population. High and low incidence of moderate penicillin resistant meningococci appeared to correlate with the number of doses of penicillin prescribed in some geographic locations. The majority of moderate penicillin resistant isolates belonged to serogroups B (52·2%) and C (39·2%). However, the prevalence of moderate penicillin resistance in serogroup W135 was substantially higher (51·7%) than serogroups B (7·8%) and C (7·6%). Serogroup W135 accounted for a higher proportion of moderate penicillin resistance (8·7%) than disease (1%). There was no predominant penicillin resistant serotype/subtype within any serogroup. Constant surveillance is necessary to monitor the emergence and spread of resistance and to guide appropriate public health interventions in preventing drug resistant meningococci.

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Kotel’nikova, O. V., A. P. Alliluev, E. Yu Drozhzhina, I. S. Koroleva, E. A. Sitnikova, A. A. Zinchenko, E. A. Gordeeva, et al. "Protective properties of recombinant igA1 protease from meningococcus." Biomeditsinskaya Khimiya 60, no. 4 (2014): 479–86. http://dx.doi.org/10.18097/pbmc20146004479.

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The study of enzymatic and protective properties of recombinant IgA1 protease in active and mutant form showed that active form of IgA1 protease exhibited species – and type-specificity for mouse and human immunoglobulins. Mutant form, which did not exhibit enzymatic activity, had protective properties against meningococcal infection, induced by meningococcus serogroup A, B and C protecting the mice from lethal infection by living virulent culture of heterologous serogroups of meningococcus. Obtained results make it possible to consider IgA1 protease as a perspective preparation at the stages of development of polyvalent vaccine for protection the people from meningococcal infection of various etiology

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Zorina, L. M., F. V. Tarnopolskaya, Z. S. Minivarova, A. A. Dryakhlova, V. I. Tishinina, and F. K. Galeeva. "Application of thiamine-cystine-glutamine agar with feed yeast extract for the cultivation and isolation of meningococci." Kazan medical journal 66, no. 5 (October 15, 1985): 389–91. http://dx.doi.org/10.17816/kazmj62158.

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Colicchio, Roberta, Susanna Ricci, Florentia Lamberti, Caterina Pagliarulo, Chiara Pagliuca, Velia Braione, Tiziana Braccini, et al. "The Meningococcal ABC-Type l-Glutamate Transporter GltT Is Necessary for the Development of Experimental Meningitis in Mice." Infection and Immunity 77, no. 9 (June 15, 2009): 3578–87. http://dx.doi.org/10.1128/iai.01424-08.

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ABSTRACT Experimental animal models of bacterial meningitis are useful to study the host-pathogen interactions occurring at the cerebral level and to analyze the pathogenetic mechanisms behind this life-threatening disease. In this study, we have developed a mouse model of meningococcal meningitis based on the intracisternal inoculation of bacteria. Experiments were performed with mouse-passaged serogroup C Neisseria meningitidis. Survival and clinical parameters of infected mice and microbiological and histological analysis of the brain demonstrated the establishment of meningitis with features comparable to those of the disease in humans. When using low bacterial inocula, meningococcal replication in the brain was very efficient, with a 1,000-fold increase of viable counts in 18 h. Meningococci were also found in the blood, spleens, and livers of infected mice, and bacterial loads in different organs were dependent on the infectious dose. As glutamate uptake from the host has been implicated in meningococcal virulence, mice were infected intracisternally with an isogenic strain deficient in the ABC-type l-glutamate transporter GltT. Noticeably, the mutant was attenuated in virulence in mixed infections, indicating that wild-type bacteria outcompeted the GltT-deficient meningococci. The data show that the GltT transporter plays a role in meningitis and concomitant systemic infection, suggesting that meningococci may use l-glutamate as a nutrient source and as a precursor to synthesize the antioxidant glutathione.

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Alderson, Mark R., F. Marc LaForce, Ajoke Sobanjo-ter Meulen, Angela Hwang, Marie-Pierre Preziosi, and Keith P. Klugman. "Eliminating Meningococcal Epidemics From the African Meningitis Belt: The Case for Advanced Prevention and Control Using Next-Generation Meningococcal Conjugate Vaccines." Journal of Infectious Diseases 220, Supplement_4 (October 31, 2019): S274—S278. http://dx.doi.org/10.1093/infdis/jiz297.

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AbstractThe introduction and rollout of a meningococcal serogroup A conjugate vaccine, MenAfriVac, in the African meningitis belt has eliminated serogroup A meningococcal infections for >300 million Africans. However, serogroup C, W, and X meningococci continue to circulate and have been responsible for focal epidemics in meningitis belt countries. Affordable multivalent meningococcal conjugate vaccines are being developed to prevent these non-A epidemics. This article describes the current epidemiologic situation and status of vaccine development and highlights questions to be addressed to most efficiently use these new vaccines.

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33

Arreaza, L., L. de la Fuente, and J. A. Vázquez. "Antibiotic Susceptibility Patterns ofNeisseria meningitidis Isolates from Patients and Asymptomatic Carriers." Antimicrobial Agents and Chemotherapy 44, no. 6 (June 1, 2000): 1705–7. http://dx.doi.org/10.1128/aac.44.6.1705-1707.2000.

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ABSTRACT The activities of seven antimicrobial agents used for treatment and prophylaxis of meningococcal disease was investigated against 901Neisseria meningitidis isolates, 112 of which were recovered from patients and 789 of which were recovered from asymptomatic carriers. The proportions of isolates with decreased susceptibility to penicillin were 55.3 and 39.0%, respectively. Penicillin- and ampicillin-intermediate strains were more common among serogroup C meningococci than among non-serogroup C meningococci from both patients and carriers.

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Blackwell, C. C., D. M. Weir, V. S. James, K. A. V. Cartwright, J. M. Stuart, and D. M. Jones. "The Stonehouse study: secretor status and carriage of Neisseria species." Epidemiology and Infection 102, no. 1 (February 1989): 1–10. http://dx.doi.org/10.1017/s0950268800029629.

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SUMMARYThe genetically determined inability to secrete the water-soluble glycoprotein form of the ABO blood group antigens into saliva and other body fluids is a recognized risk factor for meningococcal disease. During a community-wide investigation of a prolonged outbreak of disease due to a B15: P1.16 sulphonamideresistant strain of Neisseria meningitidis in Stonehouse, Gloucestershire (the Stonehouse survey), the ABO blood group and secretor status of almost 5000 residents was determined.The proportion of non-secretors in the Stonehouse population was significantly higher than the proportion of non-secretors among blood donors in the South West Region and in England generally. Seven of 13 Stonehouse residents with meningococcal disease who were tested were found to be non-secretors, a high proportion. The outbreak in Stonehouse cannot be explained solely in terms of the increased proportion of non-secretors. There was no clear correlation between the proportions of non-secretors in different areas within the town and the incidence of cases of meningococcal disease.Carriers of meningococci, whether outbreak or other strains, were not more likely to be non-secretors. The reasons why non-secretors are more susceptible to meningococcal disease remain to be determined, but they do not appear to be related to carriage of meningococci.

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Newcombe, Jane, Tom A. Mendum, Chuan-peng Ren, and Johnjoe McFadden. "Identification of the immunoproteome of the meningococcus by cell surface immunoprecipitation and MS." Microbiology 160, no. 2 (February 1, 2014): 429–38. http://dx.doi.org/10.1099/mic.0.071829-0.

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Most healthy adults are protected from meningococcal disease by the presence of naturally acquired anti-meningococcal antibodies; however, the identity of the target antigens of this protective immunity remains unclear, particularly for protection against serogroup B disease. To identify the protein targets of natural protective immunity we developed an immunoprecipitation and proteomics approach to define the immunoproteome of the meningococcus. Sera from 10 healthy individuals showing serum bactericidal activity against both a meningococcal C strain (L91543) and the B strain MC58, together with commercially available pooled human sera, were used as probe antisera. Immunoprecipitation was performed with each serum sample and live cells from both meningococcal strains. Immunoprecipitated proteins were identified by MS. Analysis of the immunoproteome from each serum demonstrated both pan-reactive antigens that were recognized by most sera as well as subject-specific antigens. Most antigens were found in both meningococcal strains, but a few were strain-specific. Many of the immunoprecipitated proteins have been characterized previously as surface antigens, including adhesins and proteases, several of which have been recognized as vaccine candidate antigens, e.g. factor H-binding protein, NadA and neisserial heparin-binding antigen. The data demonstrate clearly the presence of meningococcal antibodies in healthy individuals with no history of meningococcal infection and a wide diversity of immune responses. The identification of the immunoreactive proteins of the meningococcus provides a basis for understanding the role of each antigen in the natural immunity associated with carriage and may help to design vaccination strategies.

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Konar, Monica, and Dan M. Granoff. "Eculizumab treatment and impaired opsonophagocytic killing of meningococci by whole blood from immunized adults." Blood 130, no. 7 (August 17, 2017): 891–99. http://dx.doi.org/10.1182/blood-2017-05-781450.

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Key Points Eculizumab, an anti–complement C5 mAb, blocked killing of meningococci by whole blood from healthy immunized adults. Blocking the AP with ACH-4471, a small molecule in development for PNH, had much less of an effect on meningococcal killing.

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Carr, Jeremy, Emma Plested, Parvinder Aley, Susana Camara, Kimberly Davis, Jenny M. MacLennan, Steve Gray, et al. "‘Be on the TEAM’ Study (Teenagers Against Meningitis): protocol for a controlled clinical trial evaluating the impact of 4CMenB or MenB-fHbp vaccination on the pharyngeal carriage of meningococci in adolescents." BMJ Open 10, no. 10 (October 2020): e037358. http://dx.doi.org/10.1136/bmjopen-2020-037358.

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IntroductionCapsular group B Neisseria meningitidis (MenB) is the most common cause of invasive meningococcal disease (IMD) in many parts of the world. A MenB vaccine directed against the polysaccharide capsule remains elusive due to poor immunogenicity and safety concerns. The vaccines licensed for the prevention of MenB disease, 4CMenB (Bexsero) and MenB-fHbp (Trumenba), are serogroup B ‘substitute’ vaccines, comprised of subcapsular proteins and are designed to provide protection against most MenB disease-causing strains. In many high-income countries, such as the UK, adolescents are at increased risk of IMD and have the highest rates of meningococcal carriage. Beginning in the late 1990s, immunisation of this age group with the meningococcal group C conjugate vaccine reduced asymptomatic carriage and disrupted transmission of this organism, resulting in lower group C IMD incidence across all age groups. Whether vaccinating teenagers with the novel ‘MenB’ protein-based vaccines will prevent acquisition or reduce duration of carriage and generate herd protection was unknown at the time of vaccine introduction and could not be inferred from the effects of the conjugate vaccines. 4CMenB and MenB-fHbp may also impact on non-MenB disease-causing capsular groups as well as commensal Neisseria spp. This study will evaluate the impact of vaccination with 4CMenB or MenB-fHbp on oropharyngeal carriage of pathogenic meningococci in teenagers, and consequently the potential for these vaccines to provide broad community protection against MenB disease.Methods and analysisThe ‘Be on the TEAM’ (Teenagers Against Meningitis) Study is a pragmatic, partially randomised controlled trial of 24 000 students aged 16–19 years in their penultimate year of secondary school across the UK with regional allocation to a 0+6 month schedule of 4CMenB or MenB-fHbp or to a control group. Culture-confirmed oropharyngeal carriage will be assessed at baseline and at 12 months, following which the control group will be eligible for 4CMenB vaccination. The primary outcome is the carriage prevalence of potentially pathogenic meningococci (defined as those with genogroups B, C, W, Y or X), in each vaccine group compared separately to the control group at 12 months post-enrolment, that is, 12 months after the first vaccine dose and 6 months after the second vaccine dose. Secondary outcomes include impact on carriage of: genogroup B meningococci; hyperinvasive meningococci; all meningococci; those meningococci expressing vaccine antigens and; other Neisseria spp. A sample size of 8000 in each arm will provide 80% power to detect a 30% reduction in meningococcal carriage, assuming genogroup B, C, W, Y or X meningococci carriage of 3.43%, a design effect of 1.5, a retention rate of 80% and a significance level of 0.05. Study results will be available in 2021 and will inform the UK and international immunisation policy and future vaccine development.Ethics and disseminationThis study is approved by the National Health Service South Central Research Ethics Committee (18/SC/0055); the UK Health Research Authority (IRAS ID 239091) and the UK Medicines and Healthcare products Regulatory Agency. Publications arising from this study will be submitted to peer-reviewed journals. Study results will be disseminated in public forums, online, presented at local and international conferences and made available to the participating schools.Trial registration numbersISRCTN75858406; Pre-results, EudraCT 2017-004609-42.

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Bergman, Peter, Linda Johansson, Hong Wan, Allison Jones, Richard L. Gallo, Gudmundur H. Gudmundsson, Tomas Hökfelt, Ann-Beth Jonsson, and Birgitta Agerberth. "Induction of the Antimicrobial Peptide CRAMP in the Blood-Brain Barrier and Meninges after Meningococcal Infection." Infection and Immunity 74, no. 12 (October 9, 2006): 6982–91. http://dx.doi.org/10.1128/iai.01043-06.

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ABSTRACT Antimicrobial peptides are present in most living species and constitute important effector molecules of innate immunity. Recently, we and others have detected antimicrobial peptides in the brain. This is an organ that is rarely infected, which has mainly been ascribed to the protective functions of the blood-brain barrier (BBB) and meninges. Since the bactericidal properties of the BBB and meninges are not known, we hypothesized that antimicrobial peptides could play a role in these barriers. We addressed this hypothesis by infecting mice with the neuropathogenic bacterium Neisseria meningitidis. Brains were analyzed for expression of the antimicrobial peptide CRAMP by immunohistochemistry in combination with confocal microscopy. After infection, we observed induction of CRAMP in endothelial cells of the BBB and in cells of the meninges. To explore the functional role of CRAMP in meningococcal disease, we infected mice deficient of the CRAMP gene. Even though CRAMP did not appear to protect the brain from invasion of meningococci, CRAMP knockout mice were more susceptible to meningococcal infection than wild-type mice and exhibited increased meningococcal growth in blood, liver, and spleen. Moreover, we could demonstrate that carbonate, a compound that accumulates in the circulation during metabolic acidosis, makes meningococci more susceptible to CRAMP.

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Peiser, Leanne, Katherine Makepeace, Annette Plüddemann, Silvana Savino, J. Claire Wright, Mariagrazia Pizza, Rino Rappuoli, E. Richard Moxon, and Siamon Gordon. "Identification of Neisseria meningitidis Nonlipopolysaccharide Ligands for Class A Macrophage Scavenger Receptor by Using a Novel Assay." Infection and Immunity 74, no. 9 (September 2006): 5191–99. http://dx.doi.org/10.1128/iai.00124-06.

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ABSTRACT Macrophages (Mφ) may play an important role in the pathogenesis of invasive meningococcal infection. Previously, we have shown that the class A Mφ scavenger receptor (SR-A) is a major nonopsonic receptor for Neisseria meningitidis on Mφ. 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 Mφ display a substantial reduction in the number of meningococci ingested compared to wild-type Mφ, and SR-A is required for meningococcal phagocytosis but not for the release of tumor necrosis factor alpha. Although soluble lipid A and lipidIVA 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 Mφ 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.

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Namork, Ellen, and Petter Brandtzaeg. "Fatal meningococcal septicaemia with “blebbing” meningococcus." Lancet 360, no. 9347 (November 2002): 1741. http://dx.doi.org/10.1016/s0140-6736(02)11721-1.

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Belkacem, Nouria, Eva Hong, Ana Antunes, Aude Terrade, Ala-Eddine Deghmane, and Muhamed-Kheir Taha. "Use of Animal Models To Support Revising Meningococcal Breakpoints of β-Lactams." Antimicrobial Agents and Chemotherapy 60, no. 7 (April 18, 2016): 4023–27. http://dx.doi.org/10.1128/aac.00378-16.

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ABSTRACTAntibiotic susceptibility testing (AST) inNeisseria meningitidisis an important part of the management of invasive meningococcal disease. It defines MICs of antibiotics that are used in treatment and/or prophylaxis and that mainly belong to the beta-lactams. The interpretation of the AST results requires breakpoints to classify the isolates into susceptible, intermediate, or resistant. The resistance to penicillin G is defined by a MIC of >0.25 mg/liter, and that of amoxicillin is defined by a MIC of >1 mg/liter. We provide data that may support revision of resistance breakpoints for beta-lactams in meningococci. We used experimental intraperitoneal infection in 8-week-old transgenic female mice expressing human transferrin and human factor H. Dynamic bioluminescence imaging was performed to follow the infection by bioluminescent meningococcus strains with different MICs. Three hours later, infected mice were treated intramuscularly using several doses of amoxicillin or penicillin G. Signal decreased during infection with a meningococcus strain showing a penicillin G MIC of 0.064 mg/liter at all doses. Signals decreased for the strain with a penicillin G MIC of 0.5 mg/liter only after treatment with the highest doses, corresponding to 250,000 units/kg of penicillin G or 200 mg/kg of amoxicillin, although this decrease was at a lower rate than that of the strain with a MIC of 0.064 mg/liter. The decrease in bioluminescent signals was associated with a decrease in the levels of the proinflammatory cytokine interleukin-6 (IL-6). Our data suggest that a high dose of amoxicillin or penicillin G can reduce growth during infection by isolates showing penicillin G MICs of >0.25 mg/liter and ≤1 mg/liter.

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Newcombe, J., J. C. Jeynes, E. Mendoza, J. Hinds, G. L. Marsden, R. A. Stabler, M. Marti, and J. J. McFadden. "Phenotypic and Transcriptional Characterization of the Meningococcal PhoPQ System, a Magnesium-Sensing Two-Component Regulatory System That Controls Genes Involved in Remodeling the Meningococcal Cell Surface." Journal of Bacteriology 187, no. 14 (July 2005): 4967–75. http://dx.doi.org/10.1128/jb.187.14.4967-4975.2005.

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ABSTRACT We previously identified and characterized a two-component regulatory system in the meningococcus with homology to the phoP-phoQ system in salmonella and showed that allele replacement of the NMB0595 regulator gene led to loss of virulence, sensitivity to antimicrobial peptides, perturbed protein expression, and magnesium-sensitive growth. On the basis of these findings we proposed that the system should be designated the meningococcal PhoPQ system. Here we further characterized the NMB0595 mutant and demonstrated that it had increased membrane permeability and was unable to form colonies on solid media with low magnesium concentrations, features that are consistent with disruption of PhoPQ-mediated modifications to the lipooligosaccharide structure. We examined the transcriptional profiles of wild-type and NMB0595 mutant strains and found that magnesium-regulated changes in gene expression are completely abrogated in the mutant, indicating that, similar to the salmonella PhoPQ system, the meningococcal PhoPQ system is regulated by magnesium. Transcriptional profiling of the mutant indicated that, also similar to the salmonella PhoPQ system, the meningococcal system is involved in control of virulence and remodeling of the bacterial cell surface in response to the host environment. The results are consistent with the hypothesis that the PhoP homologue plays a role in the meningococcus similar to the role played by PhoP in salmonella. Elucidating the role that the PhoPQ system and PhoPQ-regulated genes play in the response of the meningococcus to the host environment may provide new insights into the pathogenic process.

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Urwin, Rachel, Andrew J. Fox, Martin Musilek, Paula Kriz, and Martin C. J. Maiden. "Heterogeneity of the PorB Protein in Serotype 22Neisseria meningitidis." Journal of Clinical Microbiology 36, no. 12 (1998): 3680–82. http://dx.doi.org/10.1128/jcm.36.12.3680-3682.1998.

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The genetic diversity of porB genes from meningococcal isolates characterized as serotype 22 was investigated by gene sequencing. This procedure identified seven distinct porBsequences, demonstrating variation in the PorB protein recognized by the serotype 22 monoclonal antibody. This is consistent with the genetic heterogeneity of serotype 22 meningococci reported previously.

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Vazquez, J. A., C. Marcos, and S. Berron. "Sero/subtyping ofNeisseria meningitidisisolated from patients in Spain." Epidemiology and Infection 113, no. 2 (October 1994): 267–74. http://dx.doi.org/10.1017/s0950268800051694.

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SUMMARYTo know the types of meningococcal strains in Spain, we serotyped and subtyped 743Neisseria meningitidisisolates recovered between 1990 and 1992 from patients. A great number of serogroup B, serogroup C and non-groupable meningoccoci reacted with the serotyping reagents while many serogroup C and non-groupable isolates did not react with the serosubtyping reagents (78·2% and 54·8 % respectively); only 8·9 % of serogroup B meningococci were non-subtypeable (NST). Distribution of serotypes was similar in serogroup C and in non-groupable strains. Isolates showed great variability in antigenic phenotypes (71 in serogroup B, 20 in serogroup C and 25 in non-groupable meningococci). The most frequent antigenic combinations were 4:P1. 15 (39·8%) in serogroup B, 2b:NST (55·8%) in serogroup C and 2b:NST (35·6%) in non-groupable meningococci.

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Kahler, C. M., E. Blum, Y. K. Miller, D. Ryan, T. Popovic, and D. S. Stephens. "exl, an Exchangeable Genetic Island in Neisseria meningitidis." Infection and Immunity 69, no. 3 (March 1, 2001): 1687–96. http://dx.doi.org/10.1128/iai.69.3.1687-1696.2001.

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ABSTRACT The genetic structure and evolution of a novel exchangeable meningococcal genomic island was defined for the important human pathogen Neisseria meningitidis. In 125 meningococcal strains tested, one of three unrelated nucleotide sequences, designatedexl (exchangeable locus), was found between a gene required for heme utilization, hemO, andcol, encoding a putative Escherichia colicollagenase homologue. The 5′ boundary of each exlcassette was the stop codon of hemO, whereas the 3′ boundary was delineated by a 33-bp repeat containing neisserial uptake sequences located downstream of col. One of the three alternative exl cassettes contained the meningococcal hemoglobin receptor gene, hmbR (exl3). In other meningococcal strains, hmbR was absent from the genome and was replaced by either a nucleotide sequence containing a novel open reading frame, exl2, or a cassette containing exl3. The proteins encoded byexl2 and exl3 had no significant amino acid homology to HmbR but contained six motifs that are also present in the lipoprotein components of the lactoferrin (LbpB), transferrin (TbpB), and hemoglobin-haptoglobin (HpuA) uptake systems. To determine the evolutionary relationships among meningococci carryinghmbR, exl2, or exl3, isolates representing 92 electrophoretic types were examined.hmbR was found throughout the population structure ofN. meningitidis (genetic distance, >0.425), whereasexl2 and exl3 were found in clonal groups at genetic distances of <0.2. The commensal neisserial species were identified as reservoirs for all of the exl cassettes found in meningococci. The structure of these cassettes and their correlation with clonal groups emphasize the extensive gene pool and frequent horizontal DNA transfer events that contribute to the evolution and virulence of N. meningitidis.

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Tsang, Raymond S. W., and Wendell D. Zollinger. "Serological Specificities of Murine Hybridoma Monoclonal Antibodies against Neisseria meningitidis Serogroups B, C, Y, and W135 and Evaluation of Their Usefulness as Serogrouping Reagents by Indirect Whole-Cell Enzyme-Linked Immunosorbent Assay." Clinical Diagnostic Laboratory Immunology 12, no. 1 (January 2005): 152–56. http://dx.doi.org/10.1128/cdli.12.1.152-156.2005.

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ABSTRACT Murine hybridoma monoclonal antibodies (MAbs) were produced against the capsular antigens of serogroups B, C, Y, and W135 meningococci. Each serogroup-specific MAb reacted with the extracted capsular polysaccharide from its homologous serogroup only and did not react with capsules from the other three serogroups. The application of these MAbs for serogroup identification of meningococci was demonstrated by their abilities to correctly identify 183 clinical isolates of 185 meningococci recovered from individual invasive meningococcal disease (IMD) patients during routine surveillance in 2002. The remaining two meningococci were identified by PCR grouping as C in one case and Y in another, but neither isolate was positive by bacterial agglutination using rabbit antisera or by enzyme-linked immunosorbent assay using MAbs. The specificities of the anti-Y and anti-W135 MAbs were further assessed by tests with 37 serogroup W135 and 106 serogroup Y meningococci recovered from IMD cases during 1999 to 2001 and 2003. All 143 meningococci except one serogroup Y isolate were correctly identified by positive reactions with the corresponding MAbs that identified their homologous serogroups. The single serogroup Y isolate was received as nonagglutinable and tested as negative with both rabbit anti-Y antiserum and anti-Y MAb but was positive for the serogroup Y-specific siaD gene. The advantage of using MAbs for serogrouping of meningococci is discussed.

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47

Ren, Xiaoyun, and Joanna K. MacKichan. "Disease-Associated Neisseria meningitidis Isolates Inhibit Wound Repair in Respiratory Epithelial Cells in a Type IV Pilus-Independent Manner." Infection and Immunity 82, no. 12 (September 15, 2014): 5023–34. http://dx.doi.org/10.1128/iai.02001-14.

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ABSTRACTNeisseria meningitidisis the causative agent of meningococcal disease. Onset of meningococcal disease can be extremely rapid and can kill within a matter of hours. However, although a much-feared pathogen,Neisseria meningitidisis frequently found in the nasopharyngeal mucosae of healthy carriers. The bacterial factors that distinguish disease- from carriage-associated meningococci are incompletely understood. Evidence suggesting that disruptions to the nasopharynx may increase the risk of acquiring meningococcal disease led us to evaluate the ability of disease- and carriage-associated meningococcal isolates to inhibit cell migration, using anin vitroassay for wound repair. We found that disease-associated isolates in our collection inhibited wound closure, while carriage-associated isolates were more variable, with many isolates not inhibiting wound repair at all. For isolates selected for further study, we found that actin morphology, such as presence of lamellipodia, correlated with cell migration. We demonstrated that multiple meningococcal virulence factors, including the type IV pili, are dispensable for inhibition of wound repair. Inhibition of wound repair was also shown to be an active process, i.e., requiring live bacteria undergoing active protein synthesis.

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Sharabkhanov, V. V., K. V. Zhdanov, S. M. Zakharenko, N. I. L’vov, K. V. Kozlov, Yu I. Lyashenko, K. S. Ivanov, Yu I. Bulankov, and M. V. Yaremenko. "Meningococcal infection: clinical and epidemiological characteristics in modern conditions." Bulletin of the Russian Military Medical Academy 20, no. 4 (December 15, 2018): 186–91. http://dx.doi.org/10.17816/brmma12356.

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The problems of the incidence of meningococcal disease and the epidemiological situation in the world, in the Russian Federation and in the Armed Forces are consecrated. In the past decade, there has been a global decline in the incidence of meningococcal disease, but there is still the possibility of new outbreaks and epidemics. From 1996 to 2016, a decrease in the incidence of meningococcal disease was also noted in Russia. In certain regions of the Russian Federation, an increase in incidence was recorded, which did not affect the general trend. Against this background, the idea was formed that in the coming years, thanks to a favorable epidemiological situation and the possibility of preventing meningococcal infection with the help of a vaccine, it is possible to achieve control of this infection. However, meningococcus showed all the classic properties of variability and fitness. Changes in the structure of circulating serogroups of meningococcus led to the formation of a non-immune layer of the population in the face of increasing pathogenicity of the dominant serogroups. The activity of the epidemic process is indirectly indicated by the high diversity of genetic and serological clonal complexes, serogroups and serotypes of the pathogen. The incidence of meningococcal disease over the past ten years in the Armed Forces of the Russian Federation can be assessed as low, but mortality has high values. The peak incidence was in 2010, but the maximum percentage of mortality was in 2017-18,2%. The increase in mortality from invasive forms of meningococcal infection, on the one hand, is associated with an increase in the total number of sources of this infection, on the other hand, with errors in early diagnosis and, as a consequence, in the incorrect provision of emergency care at the prehospital stage, which recur from year to year and are of a similar nature.

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Plant, Laura, Hong Wan, and Ann-Beth Jonsson. "MyD88-Dependent Signaling Affects the Development of Meningococcal Sepsis by Nonlipooligosaccharide Ligands." Infection and Immunity 74, no. 6 (June 2006): 3538–46. http://dx.doi.org/10.1128/iai.00128-06.

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ABSTRACT 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.

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50

Lewis, L. A., M. H. Sung, M. Gipson, K. Hartman, and D. W. Dyer. "Transport of Intact Porphyrin by HpuAB, the Hemoglobin-Haptoglobin Utilization System of Neisseria meningitidis." Journal of Bacteriology 180, no. 22 (November 15, 1998): 6043–47. http://dx.doi.org/10.1128/jb.180.22.6043-6047.1998.

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ABSTRACT The meningococcal hemA gene was cloned and used to construct a porphyrin biosynthesis mutant. An analysis of thehemA mutant indicated that meningococci can transport intact porphyrin from heme (Hm), hemoglobin (Hb), and Hb-haptoglobin (Hp). By constructing a HemA− HpuAB− double mutant, we demonstrated that HpuAB is required for the transport of porphyrin from Hb and Hb-Hp.

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Journal articles on the topic 'Meningococcie'

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