Dissertations / Theses: 'Meningococcie'

1

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

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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Tzanakaki, Georgina. "Meningococcal disease and carriage in Greece." Thesis, University of Edinburgh, 1996. http://hdl.handle.net/1842/21580.

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The objectives of the thesis were to answer the following questions: 1. Are genetic and environmental factors associated with carriage among Greek children and young adults similar to those found in northwest Europe? 2. Are strains with serogroups, serotypes and subtypes associated with disease in northwest Europe isolated from patients and carriers in Greece? 3. Are the antibiotic sensitivities of meningococci isolated from patients and carriers in Greece similar to those observed in northwest Europe? 4. Are the genetic clones associated with disease in northwest Europe present among meningococcal strains in Greece and other Balkan countries? Among military recruits and primary and secondary school children active smoking or exposure to cigarette smoke were significantly associated with carriage of meningococci. In both populations the rate of carriage was higher among the 15-19 year age range; similar results were reported for studies in Britain and the Faroe islands. The results obtained from the epidemiological studies (recruits and schoolchildren) showed that viral upper respiratory tract infection in general is not a predisposing factor for colonisation and that specific viral infections (e.g., RSV and influenza) need to be investigated. Lower socio-economic group was not associated with carriage in Greek school children but with smoking habits of members of the house closely involved in child care. While the subtype reagents were able to differentiate strains from both patients and carriers, the serotype antibodies did not react with the majority of strains. The serogroup, serotype and subtype combinations associated with outbreaks in northwest Europe were not found among over 500 isolates examined. The studies on meningococcal strains isolated from patients in Greece and Romania were the first to identify significant phenotypic and genetic differences between meningococcal strains isolated in northwest and southeast European countries.

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12

Thiru, Yamuna. "Myocardial function in paediatric meningococcal disease." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251576.

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13

Marshall-Jones, Zoe Victoria. "Molecular analysis of neisserial pilins." Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.369116.

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14

Mackenzie, Joanne Emily. "Immunomodulatory properties of meningococcal outer membrane vesicles." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444979/.

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Neisseria meningitidis (Nm) causes potentially fatal bacterial sepsis and meningitis in susceptible individuals, but induces protective immunity in asymptomatic carriers. Nm naturally sheds outer membrane vesicles (NOMVs) that contain a high proportion of lipopolysaccharide (LPS) and outer membrane proteins. NOMVs are known to induce serum bactericidal antibodies in mice and humans, but their inherent adjuvanticity of humoral responses toward protein and carbohydrate antigens has not been studied in detail. This thesis investigation has determined that NOMVs are potent intraperitoneal and intranasal adjuvants for model T-dependent antigens such as Ovalbumin and T-independent antigens such as dinitrophenol-ficoll. Surprisingly NOMVs had little or no effect on the primary antibody responses towards several clinically relevant capsular polysaccharides from Streptococcus pneumoniae regardless of the route of immunisation. NOMVs induced the proliferation of splenic B cells, and the production of cytokines from splenocytes and bone marrow-derived dendritic cells from not only wild-type but also LPS-hyporesponsive mice which indicates that both LPS and non-LPS components have immunomodulatory properties. Despite the potential of NOMVs inducing proinflammatory responses, preliminary results showed that intranasally applied NOMVs suppressed allergen induced or respiratory syncytial virus-induced airway eosinophilia in mouse models. Together our results provide important insights into the role of NOMVs in inducing protective immunity against meningococcal diseases, and their immunomodulatory properties that could be useful separately or synergistically in adjuvant development or immunotherapy.

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15

Guthrie, Terry. "Characterisation of immune responses toward meningococcal antigens." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397615.

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16

Halem, Annelise Jeannette van. "W135 meningococcal disease associated with the Hajj pilgrimage." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/71618.

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17

Harrison, Odile Barbara. "Meningococcal gene expression in children with Purpura fulminans." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269687.

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18

Taylor, Stephen. "Development of predictors of protection from meningococcal disease." Thesis, Open University, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.524790.

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19

Boulton, Ian Charles. "In vitro characterisation of the meningococcal transferrin receptor." Thesis, Birkbeck (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266085.

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20

Oakhill, Jonathan Stuart. "Structural studies of meningococcal transferrin-binding protein A." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271430.

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21

Bradley, Christopher James. "Molecular determinants of host susceptibility to meningococcal infection." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289627.

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22

Du, Plessis Jean-Pierre. "Orthopaedic implications of physeal arrest following meningococcal septicaemia." Master's thesis, University of Cape Town, 2010. http://hdl.handle.net/11427/10387.

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Includes bibliographical references (leaves 45-46).
Thirteen patients seen at Red Cross Children's and Maitland Cottage hospitals have under gone complex treatment for the significant deformities caused by meningococcal septicaemia. These patients underwent 62 surgical procedures between them. These procedures were directed at the treatment of sequelae of growth arrest alone and excluded amputations, contracture releases, skin grafts and flaps. The extent of the surgical problems caused by this disease brought about the realisation that a thorough review of the literature and follow up of these patients was required. This would hopefully be of use in assessing the outcomes of various surgical treatment options employed and in developing guidelines for the future management of physeal arrest in these patients.

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23

Coen, Pietro G. "Mathematical models of Haemophilus influenzae type b and Neisseria meningitidis." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298260.

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24

Potts, Wendy Jane. "Molecular analysis of pilus expression in Neisseria meningitidis." Thesis, University of Liverpool, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.237534.

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25

MacKinnon, Fiona Gwynneth. "An investigation into the virulence components of Neisseria meningitidis." Thesis, Open University, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387274.

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26

Russell, Joanne. "Variation in the PorA protein, and clonal diversity within the UK Neisseria meningitidis population over a twenty year period (1975-1995)." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368014.

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27

McGuinness, Brian Timothy. "Immunochemistry and structural variation of the class 1 outer membrane protein of Neisseria meningitidis." Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386663.

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28

Sadler, Francesca. "Enhanced detection and assessment of virulence status in carrier and case isolates of Neisseria meningitidis." Thesis, Manchester Metropolitan University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248811.

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29

Daramola, Olufunmilayo Adetokunbo. "An investigation of the effect of Nimeningitidis on endothelial cell proteins." Thesis, Imperial College London, 2000. http://hdl.handle.net/10044/1/8470.

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30

Mavromatis, Charalampos. "Modeling large scale epidemics of meningococcal disease in Europe." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18760.

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Meningococcal disease is a severe acute infectious disease caused by the bacterium Neisseria meningitidis (aka meningococcus). The infectious agent affects mainly children and young adults. Neisseria meningitidis belongs to a specific class of pathogens, accidental pathogens, since the disease results in the death of both the host and the infectious agent. Epidemics of meningococcal disease happen sporadically, in small clusters, and disease incidence has been reported from all the European countries. Since 1999, a surveillance network for meningococcal disease is monitoring the activity of the infectious agent in 17 of these countries. In our study, we combine empirical information on the incidence and death rate due to meningococcal disease with data on demographics, socio-economics and health care resources in an attempt to develop a statistical model that can describe the patterns observed. Furthermore, we expand an already developed model for meningococcal disease to a metacommunity to theoretically study how patch dynamics change when more than one patch is connected in a network topology. The results of our study can have important implications in the control and prevention of future epidemics in newly built networks such as that of the European Union.
La méningite est une maladie infectieuse aiguë et sévère causée, entre autres, par la bactérie Neisseria meningitidis (le méningocoque). Cet agent infectieux touche principalement les enfants et les jeunes adultes. Neisseria meningitidis appartient à une classe particulière de pathogènes, pathogènes accidentels, puisque la maladie entraîne tant la mort de l'hôte que de l'agent infectieux. Les épidémies de méningites apparaissent sporadiquement, sous formes de petits groupes de cas, et son incidence est rapportée par tous les pays européens. Depuis 1999, un réseau de surveillance international sur la méningite assure le monitorage de l'activité de l'agent infectieux parmi 17 de ces pays. Dans notre étude, nous combinons l'information empirique sur l'incidence et le taux de mortalité par méningite avec des données démographiques, socio-économiques et les ressources de santé en vue de développer un modèle qui décrit les profils observés. De plus, nous adaptons un modèle déjà existant pour la méningite à une métapopulation pour étudier théoriquement comment la dynamique des petits groupes change lorsque plus d'un groupe est connecté dans un réseau topologique. Les résultats de notre étude auront des retombées importantes pour le contrôle et la prévention d'épidémies futures dans de nouveaux réseaux tels que celui de l'Union européenne.

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31

Thompson, Emily A. L. "Antigenic variation in the potential meningococcal vaccine candidate FetA." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393450.

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32

Correia, Jailson de Barros. "Contrasting features of meningococcal disease in Brazil and Ethiopia." Thesis, University of Liverpool, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410646.

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33

Riordan, Frederick Andrew Ian. "Factors associated with mortality from meningococcal disease in children." Thesis, University of Liverpool, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284153.

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34

Baines, Paul Bruce. "Factors determining the severity of meningococcal disease in childhood." Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250450.

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35

Marzouk, Omnia. "Clinical and laboratory aspects of meningococcal disease in children." Thesis, University of Liverpool, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295945.

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36

Ramasamy, Maheshi Nirmala. "B cell responses to conjugate and polysaccharide meningococcal vaccines." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:0086ad26-89c4-4234-a02f-f0e7f50e4551.

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The primary approach to the control of meningococcal disease remains effective vaccination programmes in susceptible populations. Vaccines against serogroups A, C, W and Y offer broad protection against meningococci and both polysaccharide and conjugate quadrivalent vaccines are licensed for use in the UK. Previous studies have assessed the antibody response to meningococcal polysaccharide and conjugate vaccines, but there is limited information on the nature of the B cell response to these antigens. As part of a clinical trial using both polysaccharide (MenACWY-PS) and conjugate (MenACWY-CRM) vaccines in adult volunteers, this DPhil reports the analysis of subsets of antigen specific B-cells produced in response to either vaccine. Prior MenACWY-PS impaired the response to a subsequent dose of MenACWY-CRM. This may be due to MenACWY-PS driving terminal differentiation of antigen specific cells into plasma cells, without replenishment of the memory B cell pool. In addition, despite prior data indicating that it may act as a thymus dependent antigen, the serogroup A polysaccharide component of MenACWY-PS appears to behave in the same way as serogroup C, W & Y polysaccharide components. Antibody molecules recognise and bind to a multitude of conformational epitopes. This variability is enabled by the complexities of immunoglobulin variable domain gene recombination which can generate a vast potential repertoire of unique antibody molecules. However, the diversity of the antibody repertoire is more restricted against specific antigens and within defined B cell subsets. In this DPhil, ‘next generation’ sequencing technologies were used to investigate the diversity of the B cell variable domain before and after vaccination of adult volunteers. Individuals at baseline were found to have distinct antibody repertoires. Vaccination with a Haemophilus influenzae type b (Hib) conjugate vaccine resulted in an oligoclonal antibody response, with enrichment for Hib specific canonical antibody sequences.

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37

Webb, Steven Anthony Rochford. "Evaluation of differential gene expression in Neisseria meningitidis using a Green Fluorescent Protein reporter sytem." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246674.

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38

Pollard, Andrews John. "Age-related changes in immunity to Neisseria meningitidis." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314059.

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39

Limas, François. "Purpura fulminans et méningococcémies : expérience d'un service de réanimation." Montpellier 1, 2000. http://www.theses.fr/2000MON11062.

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40

Wang, Xiao. "Macrophage programming and host responses to bacterial infection." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-129243.

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Macrophages are dynamic, plastic, and heterogeneous immune cells that play an important role in host immune defense against bacterial infection. Various bacterial pathogens, such as Neisseria meningitidis and Mycobacterium tuberculosis, can modulate host immune responses by interfering with macrophage differentiation and polarization. The focus of this thesis was to understand the role of macrophages in the pathogenesis of bacteria-induced diseases, which has important implications in the search for novel therapeutic strategies to control those infectious diseases. In Paper I, we found that NhhA, a conserved meningococcal outer membrane protein, can activate macrophages through both Toll-like receptor 4 (TLR4)-dependent and -independent pathways. In Paper II, we demonstrated that NhhA activates monocytes through TLR2 and triggers autocrine IL-10 and TNF production through the ERK and JNK pathways, which skew monocyte differentiation into CD200Rhi macrophages. These immune homeostatic macrophages are associated with nasopharyngeal carriage of meningococci. In Paper III, we examined the role of human CD46, a ubiquitous transmembrane protein, in regulating macrophage apoptosis, differentiation, and functional polarization. We revealed that macrophages expressing CD46 exhibit an M1 phenotype and are prone to generate proinflammatory cytokines, such as IL-6, TNF, and IL-12, upon lipopolysaccharide challenge or meningococcal infection. The important role of these macrophages in the development of septic shock was further confirmed by in vivo studies using a CD46 transgenic mouse disease model. M. tuberculosis, a gram-positive bacterium, remains an important cause of death in developing countries. In Paper IV, we reported that murine macrophages expressing human CD46 exhibit enhanced viability and bactericidal capacity and are prone to form granulomas following chronic mycobacterial infection. Increased understanding of host factor roles in the physiopathology of tuberculosis is critical for the design of effective vaccines and new drugs.

At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 3: Manuscript. Paper 4: Manuscript.

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41

Erickson, Lonny James. "Complications and sequelae of meningococcal disease in Québec, 1990-1994." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0008/MQ35672.pdf.

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42

Pathan, Nazima. "Characterisation of a myocardial depressant factor in meningococcal septic shock." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412281.

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Irving, Thomas J. "Mathematical modelling of meningococcal meningitis in the African meningitis belt." Thesis, University of Bristol, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.617595.

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Meningococcal meningitis is a major public health problem in an area of sub-Saharan Africa known as the meningitis belt. In this region, thousands of people fall ill each year during highly seasonal meningitis outbreaks. At frequent but unpredictable times, large epidemics of meningitis sweep the belt. Despite the gravity of the problem, much is still unknown about what drives this pattern of epidemics. The aim of this thesis is to use mathematical models to gain insights into the epidemiology of meningococcal meningitis in the meningitis belt. Firstly, several simple deterministic models are analysed. They highlight the importance of immunity following both asymptomatic carriage and invasive meningitis. For a broad range of plausible parameter values, seasonal variation of the rate of meningococcal transmission results at long, irregular intervals. Realistic sized repeated epidemics are not possible if only the ration of cases to carriers changes seasonally.

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Erickson, Lonny. "Complications and sequelae of meningococcal disease in Québec, 1990-1994." Sherbrooke : Université de Sherbrooke, 1998.

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45

Dufailu, Osman Adamu. "Role of meningococcal Neisserial autotransporter lipoprotein (NalP) in host pathogenesis." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/41127/.

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Neisseria meningitidis (Nm) can cause life-threatening bacterial meningitis and septicaemia. The high mortality of meningitis is associated with meningococcal invasion of the central nervous system (CNS) by breaching of the blood-brain barrier (BBB). Nm elaborates several cell-surface and secreted virulence factors that promote host invasion and colonisation. One important class are the autotransporter proteins. Adhesion and penetration protein (App), meningococcal serine protease A (MspA), Immunoglobulin A1 protease (IgA1p) and Neisserial autotransporter lipoprotein (NalP) are serine protease autotransporters of Nm; all have previously been demonstrated to have roles in meningococcal virulence. For App and MspA, uptake by host cells, nuclear localisation, histone clipping and induction of apoptosis have been described in our laboratory. However, a time course for the efficient uptake and nuclear localisation of these proteins into human brain microvascular endothelial cells (HBMECs) and details regarding the mechanism for histone clipping remained unknown. To address these points, both App and MspA and proteolytically-inactive mutant derivatives were expressed using the pColdTF vector system and purified under native conditions. Using confocal scanning microscopy optimal uptake and nuclear localisation of recombinant fusion proteins containing the functional passenger domains of both App and MspA in HBMECs was shown to occur 8 h-post exposure. Furthermore, the requirement for the active site serine residue in both autotransporters for H3.1 clipping was demonstrated, and human coagulation factor V (FV) was shown to be an additional substrate for both proteins. NalP is a cell-surface maturation protease which processes App, MspA and other meningococcal surface proteins such as IgA1P, LbpB and NhbA, and thus modulates the cell surface and secretome of the organism. Previous studies aimed at functional characterisation of NalP have typically relied on the phenotypic comparison of wild-type and nalP-mutant derivatives. Here an active recombinant NalP was expressed and purified, and used to investigate the interaction of NalP with host cells in order to more comprehensively elucidate the role of NalP during meningococcal interaction with the host. A recombinant NalP (rNalP) passenger domain was purified under non-denaturing conditions using immobilized nickel chromatography. Although rNalP had apparent molecular weight 8-10 kDa less than that of NalP secreted by wild-type meningococci, it was functional as determined by its ability to process human complement 3 (C3). rNalP was shown to cleave human coagulation factor V (FV), a proteolytic event which is likely to contribute to bacterial pathogenesis. Binding and uptake of rNalP into human cells was demonstrated by flow cytometry and confocal microscopy. Interestingly, rNalP was differentially localised to different cellular compartments in different cell types. Treatment of HBMECs with rNalP resulted in increased levels of IL-6 and IL-8, and decreased levels of TNF-α in culture supernatants. rNalP was shown to clip histone 2B but not other histone proteins. Using a re-tagging approach a number of rNalP-interacting host proteins were identified. These included proteins of the candidate membrane, cytoplasm, cytoskeleton endoplasmic reticulum, mitochondrion, and nucleus. Some of these proteins are likely to be involved in trafficking of NalP and the cellular response to this protein. Overall, the findings of this study expand our knowledge on the contribution of three autotransporters to meningococci pathogenesis and provide a platform to further explore the host response to NalP uptake and the epigenetic changes associated with autotransporter host interactions, which may guide the development of future therapeutic interventions.

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46

Haque, Md Risat Ul. "Bacterial nitric oxide metabolism in the pathogenesis of meningococcal sepsis." Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/12201/.

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Neisseria meningitidis is the causative agent of fatal meningococcal sepsis in humans, characterised by high bacterial loads in blood, and collapse of the microcirculatory system. The organism is adapted to colonise the human nasopharynx, an environment which is oxygen poor but rich in nitric oxide (NO), a gas vital for the regulation of essential physiological processes such as vasorelaxation, antimicrobial and innate immune responses by the host. Furthermore, during sepsis caused by meningococcaemia, high concentrations of nitrite can be measured in the blood, derived from activated circulating monocytes and endothelial cells. Meningococci express a partial denitrification pathway comprising of a nitrite reductase (AniA) and a nitric oxide reductase (NorB) to survive and thrive in an oxygen deficient niche such as the nasopharynx. The aniA and norB genes are negatively regulated by an NO sensitive repressor, NsrR. Studies from our group have shown that NorB is critical for counteracting the antimicrobial and innate immune response of the host. As NO based regulation requires a tightly regulated equilibrium, this could have far reaching consequences on the NO mediated signalling processes, and is likely to be relevant to survival of the organism within NO-enriched nasopharyngeal mucosae and blood. Previously, it was shown that bacterial NO detoxification reduces the concentration of host-cell S-nitrosothiol (SNO), a vital post-translational modification akin to phosphorylation, in murine macrophages in vitro. To investigate if similar meningococcal NO metabolism mediated SNO depletion persists in vivo, we established a murine model of early acute meningococcal sepsis. We showed that bacterial burden correlates positively with plasma SNO and hepatic NO2- but negatively with hepatic NOx. However, bacterial NO metabolism did not differentially modulate SNO and other NO metabolite profile of murine blood and liver tissue. Since there is no information to date on the effect of multiple meningococcal denitrification genes (aniA and norB) on the cellular pathology of meningococcal sepsis, we constructed and characterised a combination of NO metabolising gene mutants (ΔaniA/ΔnorB, ΔnsrR/ΔnorB, ΔaniA/ΔnorB/ΔnsrR) using the isocloning method. Differentiated human primary bronchial airway epithelial cells cultured at an air-liquid interface (HPEC-ALI) are polarised cells with tight junctions, possessing similar characteristics to the nasopharyngeal epithelial cells with which meningococci have to interact during colonisation and pathogenesis. HPEC-ALIs were infected with the newly created mutants (ΔaniA/ΔnorB and ΔaniA/ΔnorB/ΔnsrR) to examine the role of bacterial NO metabolism on the barrier function and immune response, functions known to be modulated by high concentrations of NO present in the airway epithelium. We demonstrated bacterial burden inversely correlates with the barrier function (TER) but positively with the cytokine profile (IL-8, TNFα). However, meningococcal denitrification does not have any differential role in the regulation of barrier function and cytokine profile of the HPEC-ALIs in the experimental system we used. The role of meningococcal denitrification in biofilm formation in vitro was also investigated. Preliminary data showed when biofilm formation was induced by nutrient starvation, ΔaniA/ΔnorB showed a significantly reduced biofilm forming ability compared to the Wt strain measured by the crystal violet staining. To investigate the role of aniA in differential regulation of biofilm formation, reverse complemented strains (ΔaniA/aniAIPTG+ and ΔaniA/aniA+) were created. Characterisation data showed functional activation was restored in ΔaniA when aniA was complemented along with the upstream regulatory elements such as the endogenous promoter (ΔaniA/aniA+) but not when aniA coding region was complemented under the control of an IPTG inducible lac promoter (ΔaniA/aniAIPTG+).

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47

Erickson, Lonny. "Complications and sequelae of meningococcal disease in Québec, 1990-1994." Mémoire, Université de Sherbrooke, 1998. http://savoirs.usherbrooke.ca/handle/11143/3134.

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Objectif : To determine the frequency and the nature of complications and sequelae of serogroup B and serogroup C meningococcal disease, during a recrudescence caused by a virulent clone of serogroup C, serotype 2a Neisseria meningitidis. To evaluate the quality of life of survivors. Methods. The study population included all cases of culture-proven serogroup B and C meningococcal disease reported in the province of Quebec, Canada, between 1 January 1990 and 31 December 1994. Complications and sequelae were assessed by review of medical files, postal questionnaires, and telephone interviews. Results. There were 167 cases of serogroup B and 304 cases of serogroup C infection. The largest number of cases was observed in the under 1 year age group for serogroup B and in the 10-19 year age group for serogroup C. Fatality rates were 7% for serogroup B and 14% for serogroup C. %). Only 3% of survivors of serogroup B cases had physical sequelae. 15% of survivors of serogroup C infection had one or more significant physical sequelae (skin scars 12%, amputations 5%, significant sensorineural hearing loss 2%, renal failure 1%, other sequelae 4%. Among cases without identified physical sequelae who completed the questionnaire, 19% reported a reduction in their quality of life attributable to the disease. Conclusions. These results confirm the gravity of disease caused by serogroup C, serotype 2a Neisseria meningitidis and support vaccination for control of outbreaks and epidemics of disease caused by this particular strain.

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48

Deus, Aline Anne Ferreira. "Avaliação do Impacto Epidemiológico da Vacina Meningocócica C conjugada no Estado da Bahia." Instituto de Saúde Coletiva-ISC, 2014. http://repositorio.ufba.br/ri/handle/ri/18268.

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A gravidade da gravidade da doença meningocócica (DM) e seu seu seu potencial para causar surtos e epidemias conferem a esta infecção a condição importante problema de Saúde Pública, demandando esforços para a sua prevenção e controle. No Brasil, a vacina meningocócica C Conjugada (Men C) foi introduzida no Programa Nacional introduzida no Programa Nacional de Imunização em 2010. Esse estudo avaliou o impacto dessa vacina, na Bahia, de 2010 a 2014. Foi realizada análise da tendência temporal da incidência de DM, no período de 1980 a 2013, mediante Regressão Polinomial.O impacto da vacina Men C foi avaliado pela Redução Relativa do Risco/RRR para menores de 5 anos em 2010, menores de 1 ano em 2010-2013 e para uma coorte retrospectiva (2010 a 2014) de crianças que, em 2010, tinham menos de 1 ano idade e que receberam a 2ª dose da vacina neste ano. As fontes de dados de foram Sistemas Nacionais de Informação em Saúde, Bancos Paralelos da Vigilância Epidemiológica, Laboratório Central/Bahia, e IBGE. A tendência da incidência DM C foi decrescente....

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49

Sullivan, Christopher B. "A molecular epidemiological analysis of meningococcal isolates within Scotland 1972-1998." Thesis, University of Glasgow, 2008. http://theses.gla.ac.uk/657/.

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Neisseria meningitidis is an important cause of meningitis and bacteraemia worldwide and is associated with high case-fatality rates. Meningococcal disease continues to remain a public health issue in Scotland and the rest of Europe. Typing methods are used for epidemiological purposes to investigate outbreaks and the spread of meningococci and to examine the population structure of the organism in order to better understand its variation and evolution. Reference institutes have employed such methods for a number of decades for the diagnosis and detection of meningococci. However, phenotypic methods for serogrouping, serotyping and serosubtyping meningococci, although providing good strain information, can lead to endemic strains appearing identical using these methods when they are in fact quite different. More recently methods have been developed to further characterise bacteria. These methods have included PCR for the detection of meningococcal disease within blood, serogrouping and sequencing of housekeeping genes (MLST) and antigen genes such as PorA. These molecular epidemiological methods were used for the retrospective typing of invasive meningococci in Scotland, 1972-1998, using a fully automated procedure. The results of these were then analysed using statistical packages to examine the population structure of the organism. In total there were 2517 invasive isolates, received by the Scottish Meningococcus and Pneumococcus Reference Laboratory (SMPRL) from the start of 1972 to the end of 1998. Serogroup distribution changed from year to year during the time period 1972-1998 but serogroups B and C were dominant throughout this period. Serogroup B was the dominant serogroup throughout the seventies and early eighties until serogroup C became dominant during the mid 1980s. This increase in dominance of serogroup C has been found in this study not to be associated with one particular sequence type (ST) but is associated with a number of STs, which include ST-8, ST-11, ST-206 and ST-334. This is in contrast to the increase in serogroup C disease in the 1990s that was due to the ST-11 clonal complex. While there was much diversity in the STs (309 different STs among the 2517 isolates), only ten accounted for 1562 isolates (59.9%). These were ST-11, ST-8, ST-41, ST-153, ST-1, ST-32, ST-33, ST-269, ST-334 and ST-60. There were 177 new STs found during the time period. The STs were further differentiated into 31 clonal complexes, with 57 singleton types. As with the STs, although there was much diversity in the clonal complexes, only seven accounted for 1993 isolates. It was found that with PorA variable region (VR) types there were certain combinations significantly more common than others. There was a strong link with PorA type and ST and more so with clonal complex. This link was evident with the PorA type 5, 2-1, 36-2, which occured in 70 isolates representing the ST-11 complex and in all but two isolates representing ST-11. Similarly PorA type 18-3, 1, 35-1 was associated with 15 isolates belonging to the ST41-44 complex. However, this was not the case with all PorA combinations as the PorA type 19, 15, 36 was associated with 10 different complexes. There was some association between serogroup and PorA VR types. There was strong evidence of certain VR1, 2 and 3 regions being associated with certain serogroups, although this was not definitive. For example, of 192 isolates with PorA type 19, 15, 36, 85.4% were associated with serogroup B. Genosubtyping of the porA gene has been shown to increase the power of differentiation within clonal meningococcal populations. For, example, seven isolates that had the same serogroup, ST, VR1 and VR2 could be differentiated by their VR3 type. Using cluster detection software SaTScan to analyse all isolates, it was found there were 29 clusters in Scotland, from 1972-1998. These clusters included 63 cases, which accounted for 2.5% of all cases. A range of different strains caused the clusters that were identified in this study, some caused by hypervirulent strains. These strain types were responsible for a number of cases throughout the world as well as in Scotland during the period of this study. However it was also shown that there were clusters identified in this study caused by lesser-known strain types that were not responsible for many cases and that appear to be unique to Scotland or the UK. This study is the first to look at the detection of clusters over a time period of 26 years and to identify clusters that would have previously been unidentified due to lack of suitable characterisation techniques. The results in this study indicate that the multivalent preparation produced by the Netherlands Vaccine Institute (Nonavalent vaccine) had the potential, based on the PorA types that it contains, to prevent the majority of serogroup B infection that had occurred in Scotland, from 1972-1998. It also had the potential, although not to the same extent as serogroup B, to protect against other serogroups. For the age groups that would potentially have been the first to be immunised with any vaccine as part of the childhood vaccination programme, the 0-4 years old group, the potential coverage was over 92% which is comparable with the coverage seen with the serogroup C meningococcal conjugate (MCC) vaccine, of approximately 90%.

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50

Christensen, Hannah. "Modelling the impact of vaccination targeted against serogroup B meningococcal disease." Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539763.

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Dissertations / Theses on the topic 'Meningococcie'

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