Relevant bibliographies by topics / Meningococcie

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Meningococcie'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "Meningococcie"

1

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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Dissertations / Theses on the topic "Meningococcie"

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CADARS, LAURENCE. "Meningococcie benigne : a propos de deux cas pediatriques." Toulouse 3, 1993. http://www.theses.fr/1993TOU31005.

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PENARD, MARIE-CHRISTINE. "Prevention des infections a neisseria meningitidis et haemophilus influenzae : connaissances actuelles sur les vaccins polysaccharidiques." Nantes, 1989. http://www.theses.fr/1989NANT151M.

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Mölling, Paula. "Genetic characterisation of meningococci /." Linköping : Örebro : Univ. ; Örebro Medical Centre Hospital [Universitetssjukhuset], 2001. http://www.bibl.liu.se/liupubl/disp/disp2001/med697s.pdf.

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Urwin, Rachel. "Variation in meningococcal porb proteins." Thesis, Staffordshire University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246023.

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Suker, Janet. "Variation of meningococcal porin antigens." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264391.

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Moodley, Jennifer R. "Passive smoking and meningococcal disease." Master's thesis, University of Cape Town, 1997. http://hdl.handle.net/11427/27008.

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Neiserria meningitidis remains an important cause of morbidity and mortality in South Africa (SA). It is the sixth commonest cause of notified disease with a case fatality rate of 11% for the period 1990 1994. Identification of preventable risk factors is critical as no effective vaccine exists for serogroup B, the most prevalent serogroup in SA. A case control study was undertaken to determine the risk factors associated with meningococcal disease. The study population consisted of all children under the age of 14 years who were residents of the Cape Town City Council and Cape Metropolitan Council areas of jurisdiction. Cases were identified from weekly notification reports and from admissions to the City Hospital for Infectious Diseases. Controls were selected from the trauma wards at Red Cross War Memorial Children's Hospital. Data was analyzed using EPI INFO and SAS statistical software. During the period October 1993 to January 1995 70 cases and 210 controls were interviewed. Cases were significantly younger than controls (p = 0.0001). On univariate analysis significant risk factors for meningococcal disease included: a household where 2 or more members smoked (odds ratio (OR) =1.8), recent upper respiratory tract infection (OR= 1.8), poor nutritional status (OR= 3.6), being breastfed for less than 3 months (OR= 2.7) and overcrowding (OR= 2.8). After adjusting for confounders, the main force of passive smoking as a risk factor for meningococcal disease appeared to be in the presence of a recent upper respiratory tract infection. Other factors that remained significant after adjusting for confounders included: being breastfed for less than three months (adjusted OR= 2.4) and being less than 4 years old (adjusted OR= 2.3). This is the first case control study in South Africa examining risk factors associated with meningococcal disease. The study provides further evidence for the reduction of smoking, reduction of overcrowding and the promotion of breast-feeding as important public health measures. It also identifies children under the age of 4 years as an important target group should an effective vaccine become available.
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Dunlop, K. A. "Respiratory viruses and meningococcal disease." Thesis, Queen's University Belfast, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446133.

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El-Sheikh, Soliman M. "Resistance to sulphonamide and penicillin G in meningococci." Thesis, University of Manchester, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.237470.

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Abadi, Fariborz Jafari Rahmat. "Population genetic and epidemiological studies of Neisseria meningitidis." Thesis, University of Aberdeen, 1996. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU089864.

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The population structure of Neisseria meningitidis was investigated by MLEE and REA. Using MLEE 107 strains were characterised studying 6 loci. Clones were defined as 5 loci were identical in the strains studied. Seventy two strains fell into twenty six multimember clones. The clones identified contained between 2 and 6 members. The remaining (n=35) strains were regarded as unique. The genetic diversity of the population was estimated as 0.700. This high degree of diversity seems to be because the majority of the strains were isolated from sporadic cases. Isolates within multimember clones contain isolates of outbreaks and sporadic cases. Clones were also identified in a collection of serogroup C. Neisseria meningtidis (n=34) strains by REA using endonuclease StuI. Eleven multimember clones were recognised containing between 2 and 15 members. Seven strains were regarded as unique. The largest multimember clone (n=15) contained 6 rifampicin resistant meningococci and also strains sensitive to rifampicin. This finding seems to be in the favour of this hypothesis that the resistant phenotype arose once and spread through the United Kingdom. Similarly matrices between 11 serogroup C and 5 serogroup B meningococcal strains were determined. The extensive Dice similarity coefficient between strains of serogroup C and B and also close genetic distance between these two serogroups, on the one hand, and very low Dice similarity coefficient (>50%) and distant genetic relations between serogroups C meningococcal isolates, on the other, demonstrated serogrouping cannot be regarded as a reflection of overall genetic similarity; although its practicality in epidemics and its convenience renders it useful as a first step in hierarchical typing system.
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Vereen, Kalimah. "An SCIR Model of Meningococcal Meningitis." VCU Scholars Compass, 2008. http://scholarscompass.vcu.edu/etd/710.

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A model for meningitis is developed by adding a class of carriers to the basic SIR model. This model is used to analyze the impact a vaccination program can have on the health of the population of epidemic prone countries. Analysis of the model shows the local stability of the disease free equilibrium, the existence of an endemic equilibrium and computation of the reproduction number, ℜ0 . Using a MATLAB program we simulate a time course of the model using parameters gathered from the World Health Organization. The numerical solution demonstrates that our reproduction number was correct. We thenconcluded that a high infection transmission rate requires a high vaccine rate.
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Books on the topic "Meningococcie"

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Poolman, J. T., ed. Gonococci and Meningococci. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1383-7.

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Pollard, Andrew J., and Martin C. J. Maiden. Meningococcal Vaccines. New Jersey: Humana Press, 2001. http://dx.doi.org/10.1385/1592591485.

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Pollard, Andrew J., and Martin C. J. Maiden. Meningococcal Disease. New Jersey: Humana Press, 2001. http://dx.doi.org/10.1385/1592591493.

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Feavers, Ian, Andrew J. Pollard, and Manish Sadarangani, eds. Handbook of Meningococcal Disease Management. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28119-3.

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Félix, Balbina Ventura. Meningococcal meningitis in Angola: Outbreak investigation, 1995. [Luanda]: Monitoring Team, MHO--Angola/UNICEF[i.e MOH--Angola/UNICEF, 1995.

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Epidemiology of meningococcal disease in the Netherlands. [Amsterdam]: S. de Marie, 1985.

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Working Group for the Prevention and Control of Meningococcal Disease in California. Meningococcal disease prevention plan: Recommendations from the Working Group for the Prevention and Control of Meningococcal Disease in California. Sacramento: Division of Communicable Disease Control, California Dept. of Health Services, 2002.

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Félix, Balbina Ventura. Estudo sobre a epidemia de meningite meningococica em Angola: Relatório. Luanda: A Equipa, 1995.

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Pathogenic, Neisseria Conference (5th 1986 Noordwijkerhout Netherlands). Gonococci and meningococci: Epidemiology, genetics, immunochemistry, and pathogenesis : proceedings of the 5th International Pathogenic Neisseriae Conference, held in Noordwijkerhout, The Netherlands, 15-18 September, 1986. Dordrecht: Kluwer Academic Publishers, 1988.

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Akinwolere, Oladele Augustine Odunayo. Standardisation of ELISA for detecting human antibodies against meningococcal capsular polysaccharides. Birmingham: University of Birmingham, 1992.

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Book chapters on the topic "Meningococcie"

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Suryadevara, Manika. "Meningococcus." In Vaccines, 235–45. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-58414-6_19.

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Dudley, Matthew Z., Daniel A. Salmon, Neal A. Halsey, Walter A. Orenstein, Rupali J. Limaye, Sean T. O’Leary, and Saad B. Omer. "Meningococcal." In The Clinician’s Vaccine Safety Resource Guide, 95–101. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-94694-8_13.

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Demina, A. A., N. P. Devjatkina, Yu V. Martynov, I. S. Koroleva, H. T. Molinert, M. Valkarsel Novo, T. M. Martines, and A. C. Patton. "Two epidemiological types of meningococcal infection incidence caused by serogroup B meningococci." In Neisseriae 1990, edited by Mark Achtman, Peter Kohl, Christian Marchal, Giovanna Morelli, Andrea Seiler, and Burghard Thiesen, 43–48. Berlin, Boston: De Gruyter, 1991. http://dx.doi.org/10.1515/9783110867787-009.

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Treadwell, Patricia. "Meningococcal Infections." In Atlas of Adolescent Dermatology, 13–16. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-58634-8_3.

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Baltimore, Robert S. "Meningococcal Infections." In Bacterial Infections of Humans, 495–517. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-09843-2_24.

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Stewart, Campbell L. "Meningococcal Infections." In Inpatient Dermatology, 127–29. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-18449-4_26.

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Kreutner, A. Karen. "Meningococcal Infections." In Principles of Medical Therapy in Pregnancy, 447–49. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2415-7_53.

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Baltimore, Robert S., and Harry A. Feldman. "Meningococcal Infections." In Bacterial Infections of Humans, 425–42. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-1211-7_20.

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Pollard, Andrew J., Matthew D. Snape, and Manish Sadarangani. "Meningococcal Vaccines." In Pediatric Vaccines and Vaccinations, 215–24. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-59952-6_22.

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Pollock, Helen M. "Meningococcal Infections." In Laboratory Diagnosis of Infectious Diseases, 375–81. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3898-0_39.

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Conference papers on the topic "Meningococcie"

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Portilho, Amanda, Gabriela Lima, Gabrielle Lima, and Elizabeth De Gaspari. "Intranasal/subcutaneous prime-booster immunization with Outer Membrane Vesicles of Meningococci C elicits high-avidity, persistent antibodies against Meningococci B." In International Symposium on Immunobiological. Instituto de Tecnologia em Imunobiológicos, 2021. http://dx.doi.org/10.35259/isi.2021_46707.

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Souza, Iaralice, Priscila Guzzo, Renata Bastos, Fernanda Martins, Milton Silva, Elza Figueira, Ellen Jessouroun, Maria Leal, Eliana Bergter, and Ivna Silveira. "Development of a Meningococcal W Conjugate Vaccine." In IV International Symposium on Immunobiologicals & VII Seminário Anual Científico e Tecnológico. Instituto de Tecnologia em Imunobiológicos, 2019. http://dx.doi.org/10.35259/isi.sact.2019_32623.

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Castro-Rodriguez, Jose A., Leticia Jakubson, Oslando Padilla, Doris Gallegos, Rodrigo Fasce, Pablo Beltrand, Ignacio Sanchez, and Cecilia Perret. "Many Respiratory Viruses May Trigger Meningococcal Diseases." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4928.

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Bastos, Renata, Milton Silva, Iaralice Souza, Rafael Alves, José Silva Junior, Ricardo Medronho, and Ivna Silveira. "Brazilian meningococcal C conjugate vaccine: scaling up studies." In I Seminário Anual Científico e Tecnológico em Imunobiológicos. Instituto de Tecnologia em Imunobiológicos, 2013. http://dx.doi.org/10.35259/isi.sact.2013_26675.

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Simon, Michael, Anne Zomcik, Donald Brandon, Shane Christensen, Carmen Baccarini, Emilia Jordanov, and Mandeep S. Dhingra. "Safety and Immunogenicity Of A Quadrivalent Meningococcal Conjugate Vaccine (MenACYW-TT) Administered In Healthy Meningococcal Vaccine-Naïve Children (2-9 Years)." In AAP National Conference & Exhibition Meeting Abstracts. American Academy of Pediatrics, 2021. http://dx.doi.org/10.1542/peds.147.3_meetingabstract.309.

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Ramly, B. "G168(P) Meningococcal diseases: post men C vaccination era." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference and exhibition, 13–15 May 2019, ICC, Birmingham, Paediatrics: pathways to a brighter future. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-rcpch.163.

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Campbell, G., R. Bland, and S. Hendry. "G335(P) Fever after meningococcal b immunisation: a case series." In Royal College of Paediatrics and Child Health, Abstracts of the Annual Conference, 13–15 March 2018, SEC, Glasgow, Children First – Ethics, Morality and Advocacy in Childhood, The Journal of the Royal College of Paediatrics and Child Health. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2018. http://dx.doi.org/10.1136/archdischild-2018-rcpch.325.

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Catalin, Lungu Adrian, Capitanescu Andrei, Niculae Alexandra, Constantinescu Iulia, Negru Ileana, Pantoc Camelia, Marin Anca Elena, Baducu Diana Elena, Viziniuc Ana-Maria, and Stoica Cristina. "P255 Meningococcal vaccination in children with terminal complement complex deficiency." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.343.

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Pereira, Isabelly, Elezer Lemes, and Ana Santos. "Proposal of an intranasal formulation for meningococcal group C conjugate vaccine." In III Seminário Anual Científico e Tecnológico de Bio-Manguinhos. Instituto de Tecnologia em Imunobiológicos, 2016. http://dx.doi.org/10.35259/isi.sact.2016_27343.

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Silva, Milto, Iaralice Souza, Renata Bastos, Marilza Corrêa, Camila Faria, Ana Santos, and Ivna Silveira. "Thermostability Study of Meningococcal Conjugate Bulks produced for phase III clinical trials." In II Seminário Anual Científico e Tecnológico em Imunobiológicos. Instituto de Tecnologia em Imunobiológicos, 2014. http://dx.doi.org/10.35259/isi.sact.2014_26535.

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Reports on the topic "Meningococcie"

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Albornoz, Jorge T. Field Testing of Meningococcal Group B Vaccine and Oral Cholera Vaccine. Fort Belvoir, VA: Defense Technical Information Center, October 1995. http://dx.doi.org/10.21236/ada324898.

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Crum, Nancy F., Frank A. Chapman, Kevin L. Russell, and Braden R. Hale. The Many Faces of Meningococcal Disease: A Case Series and Review of Presentations and Treatment Options. Fort Belvoir, VA: Defense Technical Information Center, January 2004. http://dx.doi.org/10.21236/ada434380.

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Drabick, Joseph J., Brenda L. Brandt, Elizabeth E. Moran, Nancy B. Saunders, and David R. Shoemaker. Safety and Immunogenicity Testing of an Intranasal Group B Meningococcal Native Outer Membrane Vesicle Vaccine in Healthy Volunteers. Fort Belvoir, VA: Defense Technical Information Center, May 1998. http://dx.doi.org/10.21236/ada369066.

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Candrilli, Sean D., and Samantha Kurosky. The Response to and Cost of Meningococcal Disease Outbreaks in University Campus Settings: A Case Study in Oregon, United States. RTI Press, October 2019. http://dx.doi.org/10.3768/rtipress.2019.rr.0034.1910.

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Abstract:
Invasive meningococcal disease (IMD) is a contagious bacterial infection that can occur sporadically in healthy individuals. Symptoms are typically similar to other common diseases, which can result in delayed diagnosis and treatment until patients are critically ill. In the United States, IMD outbreaks are rare and unpredictable. During an outbreak, rapidly marshalling the personnel and monetary resources to respond is paramount to controlling disease spread. If a community lacks necessary resources for a quick and efficient outbreak response, the resulting economic cost can be overwhelming. We developed a conceptual framework of activities implemented by universities, health departments, and community partners when responding to university-based IMD outbreaks. Next, cost data collected from public sources and interviews were applied to the conceptual framework to estimate the economic cost, both direct and indirect, of a university-based IMD outbreak. We used data from two recent university outbreaks in Oregon as case studies. Findings indicate a university-based IMD outbreak response relies on coordination between health care providers/insurers, university staff, media, government, and volunteers, along with many other community members. The estimated economic cost was $12.3 million, inclusive of the cost of vaccines ($7.35 million). Much of the total cost was attributable to wrongful death and indirect costs (e.g., productivity loss resulting from death). Understanding the breadth of activities and the economic cost of such a response may inform budgeting for future outbreak preparedness and development of alternative strategies to prevent and/or control IMD.
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Gidengil, Courtney, Matthew Bidwell Goetz, Margaret Maglione, Sydne J. Newberry, Peggy Chen, Kelsey O’Hollaren, Nabeel Qureshi, et al. Safety of Vaccines Used for Routine Immunization in the United States: An Update. Agency for Healthcare Research and Quality (AHRQ), May 2021. http://dx.doi.org/10.23970/ahrqepccer244.

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Objective. To conduct a systematic review of the literature on the safety of vaccines recommended for routine immunization in the United States, updating the 2014 Agency for Healthcare Research and Quality (AHRQ) report on the topic. Data sources. We searched MEDLINE®, Embase®, CINAHL®, Cochrane CENTRAL, Web of Science, and Scopus through November 9, 2020, building on the prior 2014 report; reviewed existing reviews, trial registries, and supplemental material submitted to AHRQ; and consulted with experts. Review methods. This report addressed three Key Questions (KQs) on the safety of vaccines currently in use in the United States and included in the Centers for Disease Control and Prevention’s (CDC) recommended immunization schedules for adults (KQ1), children and adolescents (KQ2), and pregnant women (KQ3). The systematic review was supported by a Technical Expert Panel that identified key adverse events of particular concern. Two reviewers independently screened publications; data were extracted by an experienced subject matter expert. Studies of vaccines that used a comparator and reported the presence or absence of adverse events were eligible. We documented observed rates and assessed the relative risks for key adverse events. We assessed the strength of evidence (SoE) across the existing findings from the prior 2014 report and the new evidence from this update. The systematic review is registered in PROSPERO (CRD42020180089). Results. A large body of evidence is available to evaluate adverse events following vaccination. Of 56,608 reviewed citations, 189 studies met inclusion criteria for this update, adding to data in the prior 2014 report, for a total of 338 included studies reported in 518 publications. Regarding vaccines recommended for adults (KQ1), we found either no new evidence of increased risk for key adverse events with varied SoE or insufficient evidence in this update, including for newer vaccines such as recombinant influenza vaccine, adjuvanted inactivated influenza vaccine, and recombinant adjuvanted zoster vaccine. The prior 2014 report noted a signal for anaphylaxis for hepatitis B vaccines in adults with yeast allergy and for tetanus, diphtheria, and acellular pertussis vaccines. Regarding vaccines recommended for children and adolescents (KQ2), we found either no new evidence of increased risk for key adverse events with varied SoE or insufficient evidence, including for newer vaccines such as 9-valent human papillomavirus vaccine and meningococcal B vaccine. The prior 2014 report noted signals for rare adverse events—such as anaphylaxis, idiopathic thrombocytopenic purpura, and febrile seizures—with some childhood vaccines. Regarding vaccines recommended for pregnant women (KQ3), we found no evidence of increased risk for key adverse events with varied SoE among either pregnant women or their infants following administration of tetanus, diphtheria, and acellular pertussis vaccines during pregnancy. Conclusion. Across this large body of research, we found no new evidence of increased risk since the prior 2014 report for key adverse events following administration of vaccines that are routinely recommended. Signals from the prior report remain unchanged for rare adverse events, which include anaphylaxis in adults and children, and febrile seizures and idiopathic thrombocytopenic purpura in children. There is no evidence of increased risk of adverse events for vaccines currently recommended in pregnant women. There remains insufficient evidence to draw conclusions about some rare potential adverse events.
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