Dissertations / Theses: 'Pyogenes'

1

Berge, Andreas. "Molecular analysis of Streptococcus pyogenes and its interactions with the human host." Lund : Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/68945123.html.

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2

Zhang, Meng. "Proteomic analysis of streptococcus pyogenes." Thesis, Northumbria University, 2007. http://nrl.northumbria.ac.uk/842/.

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Streptococcus pyogenes (group A streptococcus, GAS) is a major human Gram-positive pathogen that causes infections that normally occur in the respiratory tract, the skin, the wound, the lung, the bloodstream and/or muscle tissues and result in millions of deaths every year. To cause such infections, S. pyogenes produces a wide range of virulence factors. The destruction of connective tissue and the hyaluronic acid therein plays an important role in pathogenesis. S. pyogenes was propagated in hyaluronic acid rich growth media in an attempt to create a simple biological system that could reflect some elements of the pathogenesis. The growth of bacteria was analyzed in the hyaluronic acid rich media and control media and a proteomic approach was applied to identify those proteins that were differentially expressed by the streptococcal pathogens growing in the different media. The techniques of two dimensional gel electrophoresis and static nanospray mass spectrometry were optimized and proteome maps for S. pyogenes grown in both media were constructed. The differentially expressed proteins by S. pyogenes were identified and analyzed using bioinformatics. Our results showed that several recognized virulence factors of S. pyogenes were upregulated in hyaluronic acid rich media, including the Ml protein, a collagen-like surface protein and the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase, which has been shown to play important roles in streptococcal pathogenesis. Interestingly, two hypothetical proteins of unknown function were also up-regulated and detailed bioinformatics analysis showed that at least one of these hypothetical proteins is likely to be involved in GAS pathogenesis. It was therefore concluded that this simple biological system provided a valuable tool for the identification of potential streptococcal pathogens virulence factors.

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Thern, Anette. "Interactions between Streptococcus pyogenes and the human immune system with special reference to C4b-binding protein /." Lund : Dept. of Medical Microbiology, Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/39224761.html.

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4

Desai, Meeta. "Molecular epidemiological typing of Streptococcus pyogenes." Thesis, Open University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299021.

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Becherelli, Marco <1979&gt. "Functional characterization of Streptococcus pyogenes pili." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/3015/.

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Group A Streptococcus is a Gram-positive human pathogen able to colonize both upper respiratory tract and skin. GAS is responsible for several acute diseases and autoimmune sequelae that account for half a million deaths worldwide every year (Cunningham et al., 2000). As other bacteria, GAS infections requires the capacity of the pathogen to adhere to host tissues and to form cell aggregates. The ability to persist in distinct host niches like the throat and the skin and to trigger infections is associated with the expression of different GAS virulence factors. GAS pili has been described as important virulence factors encoded by different FCT-operon regions. Based on this information, we decided to study the possible effect of environmental conditions that could regulate the pili expression. In this study we reported the influence of pH environment variations in biofilm formation for strains pertaining to a panel of different GAS FCT-types. The biofilm formation was promoted, excepted in the FCT-1 strains, by a changing in pH from physiological to acidic condition of growth in in vitro biofilm assay. By analyzing the possible association between biofilm formation and pH dependence, we have found that in FCT-2 and FCT-3 strains, the biofilm is promoted by pH reduction leading to an increase of pili expression. These data confirmed a direct link between pH dependent pilus expression and biofilm formation in GAS. As pili are a multi component structure we decided to investigate the functional role of one of its subunits, the AP-1 protein. AP-1 is highly conserved through the different FCT-types and suggests a possible essential role for the pili function. We focused our attention on the AP-1 protein encoded by the FCT-1 strains (M6). In particular this AP-1 protein contains the von Willebrand Factor A (VWFA) domain, which share an homology with the human VWFA domain that has been reported to be involved in adhesion process. We have demonstrated that the AP-1 protein binds to human epithelial cells by its VWFA domain, whereas the biofilm formation is mediated by the N-terminal region of AP-1 protein. Moreover, analyzing the importance of AP-1 in in vivo experiments we found a major capacity of tissue dissemination for the wild-type strain compared to the isogenic AP-1 deletion mutant. Pili have been also reported as potential vaccine candidates against Gram positive bacteria. For these reason we decided to investigate the relationship between cross reaction of sera raised against different GAS and GBS pilin subunits and the presence of a conserved Cna_B domain, in different pilin components. Our idea was to investigate if, using pilus conserved domains, a broad coverage vaccine against streptococcal infection could be possible.

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Broglia, Laura. "Regulating with ribonucleases in Streptococcus pyogenes." Doctoral thesis, Humboldt-Universität zu Berlin, 2020. http://dx.doi.org/10.18452/21573.

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Bakterien haben eine Vielzahl an Strategien entwickelt, um sich an ständig wechselnde Umweltbedingungen anzupassen, darunter auch post-transkriptionelle regulatorische Mechanismen. Die Genexpression kann hierbei durch gezielten Abbau oder Stabilisierung von RNA durch Ribonukleasen (RNasen) reguliert werden. RNasen weisen je nach Spezies allerdings unterschiedliche Effekte auf Genexpression und bakterielle Physiologie, sowie verschiedene Strategien der Substraterkennung auf. Dies zeigt, dass unser Verständnis des RNA-Abbaus bei weitem nicht vollständig ist. Ziel dieser Arbeit ist es, die Eigenschaften und Funktionen der endoRNase Y des humanpathogenen Bakteriums Streptococcus pyogenes zu studieren. Um Einblick in Funktion und Spezifität dieser RNase zu gewinnen, wurden deren genomweite Schnittpositionen (“targetome”) mit Hilfe von RNA-Sequenzierung identifiziert. Zur weiteren Analyse des RNase Y-abhängigen RNA-Abbaus wurde dieses Ergebnis mit dem “targetome” der drei 3′-5′-Exoribonukleasen (ExoRNasen) PNPase, YhaM und RNase R verglichen. Schließlich wurden die Anforderungen für die Prozessierung durch RNase Y und deren Rolle in der Regulation von Virulenzgenen in vivo anhand der speB mRNA, die einen wichtigen Virulenzfaktor codiert, untersucht. Wir konnten in dieser Arbeit zeigen, dass RNase Y Substrate bevorzugt nach einem Guanosin schneidet und dieses Nukleosid essenziell für die Prozessierung der speB mRNA in vivo ist. Obwohl RNase Y die speB mRNA schneidet, unterstützen die Daten ein Modell nach dem RNase Y die Expression von speB auf transkriptioneller Ebene reguliert. Mit Hilfe des “targetome”-Vergleichs konnten wir ferner zeigen, dass RNase Y den RNA-Abbau in S. pyogenes initiiert und die dabei generierten 3′-Enden der RNA hauptsächlich von den 3′-5′-exoRNasen PNPase und/oder YhaM prozessiert werden. Zusammenfassend erweitern diese Erkenntnisse unser Verständnis der Funktionalität von RNase Y und des RNA-Abbaus in Gram-positiven Bakterien.
Bacteria have developed a plethora of strategies to cope with constantly changing environmental conditions, including post-transcriptional regulatory mechanisms. With this regard, regulation of gene expression can be achieved by either the rapid removal or stabilization of RNA molecules by ribonucleases (RNases). RNases exhibit species-specific effects on gene expression, bacterial physiology and different strategies of target recognition, indicating that our understanding of the RNA degradation machinery is not yet complete. The aim of this thesis was to investigate the features and functions of endoRNase Y from the strict human pathogen Streptococcus pyogenes. To gain insight into the role and specificity of this RNase, we identified RNase Y cleavage positions (i.e. targetome) genome-wide by RNA sequencing. Next, to investigate the RNA degradation pathway depending on RNase Y, we compared the RNase Y targetome with the ones of the three 3′-to-5′ exoribonuclease (exoRNases), namely PNPase, YhaM and RNase R. Finally, to dissect the requirements for RNase Y processing and to decipher the role of RNase Y in virulence gene regulation, we studied the impact of RNase Y on speB mRNA, encoding a major virulence factor. This study reveals that RNase Y preferentially cleaves RNAs downstream of a guanosine and for the first time we were able to show that the presence of a guanosine residue is essential for the processing of speB mRNA, in vivo. Although RNase Y cleaves the speB mRNA, our data underpin a model in which RNase Y-mediated regulation of speB expression occurs at the transcriptional level. Using the targetome comparative approach, we demonstrated that RNase Y initiates RNA decay in S. pyogenes and that the RNase Y-generated RNA 3′ ends are usually further trimmed by PNPase and/or YhaM. Overall, these findings increase our understanding of RNase Y functionality and RNA degradation in Gram-positive bacteria.

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Siou, GeÌrard Paul Serge. "Streptococcus pyogenes interactions with human tonsils." Thesis, University of Newcastle upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424082.

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8

McNamara, Case W. "Molecular analysis of Streptococcus pyogenes M1 protein." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2006. http://wwwlib.umi.com/cr/ucsd/fullcit?p3230034.

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Thesis (Ph. D.)--University of California, San Diego, 2006.
Title from first page of PDF file (viewed November 17, 2006). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.

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Dixon, Emma Victoria. "Mechanisms of immunoglobulin deactivation by Streptococcus pyogenes." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:ec80e3f9-0c73-4d39-bc68-c39b927365d4.

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The bacteria Streptococcus pyogenes produces a multitude of proteins which interact with and alter the functions of the host immune system. Two such proteins, Endoglycosidase S (EndoS) and Immunoglobulin G-degrading enzyme from S. pyogenes (IdeS) are able to specifically alter the effector functions of immunoglobulin G (IgG). EndoS is a glycoside hydrolase which removes the conserved N-linked glycan from IgG Fc whereas IdeS is a cysteine protease that cleaves the exible protein hinge of IgG. The activity of both proteins results in the reduced ability of IgG to elicit immune responses through Fc receptor binding and complement activation. Amongst other applications, both EndoS and IdeS are actively being explored as new therapeutics for IgG-mediated autoimmune diseases. Given the therapeutic potential of EndoS and IdeS, experiments were designed to investigate the structural and functional characteristics of these enzymes in an effort to understand their specficity for and activity against IgG. Here, bioinformatic and biophysical characterisation of EndoS identified subdomains outside of the catalytic domain which contribute to glycoside hydrolase activity. The substrate specificity of EndoS was also explored and showed that EndoS hydrolyses a broad range of glycans from the IgG scaffold. EndoS was also shown to have activity against alternative glycoprotein substrates, however, this non-specific activity was negligible in the context of whole serum. The effect of EndoS-mediated deglycosylation on the structure of the IgG Fc domain was explored using both X-ray crystallography and small-angle X-ray scattering. Small angle X-ray scattering was also used to characterise both EndoS and IdeS in complex with IgG Fc. Solution-state models of each complex were produced providing preliminary data towards how these enzymes interact with IgG. Overall, the results presented here contribute to our understanding of these enzymes which is of importance as they go forward into clinical applications.

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10

Caswell, Clayton Christopher. "The SCL1 protein of Streptococcus pyogenes a structure-function analysis /." Morgantown, W. Va. : [West Virginia University Libraries], 2008. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=6026.

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Thesis (Ph. D.)--West Virginia University, 2008.
Title from document title page. Document formatted into pages; contains xi, 190 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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11

Meinhart, Anton. "Kristallstrukturanalyse des e, z-Proteinkomplexes [Epsilon, zeta-Proteinkomplexes], kodiert vom Plasmid pSM19035 aus Streptrococcus pyogenes." [S.l.] : [s.n.], 2001. http://www.diss.fu-berlin.de/2001/188/index.html.

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12

Russell, Hugh Hayden. "Molecular basis of epithelial internalisation of Streptococcus pyogenes." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423540.

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13

Le, Rhun Anaïs. "Multifaceted RNA-mediated regulatory mechanisms in Streptococcus pyogenes." Doctoral thesis, Umeå universitet, Molekylär Infektionsmedicin, Sverige (MIMS), 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-111090.

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Bacterial pathogens rely on precise regulation of gene expression to coordinate host infection processes and resist invasion by mobile genetic elements. An interconnected network of protein and RNA regulators dynamically controls the expression of virulence factors using a variety of mechanisms. In this thesis, the role of selected regulators, belonging to the class of small RNAs (sRNAs), is investigated. Streptococcus pyogenes is a pathogen responsible for a wide range of human diseases. Genome-wide screenings have indicated that S. pyogenes encodes numerous sRNAs, yet only a limited number have been characterized. A major goal of this study was to identify and characterize novel sRNAs and antisense RNAs (asRNAs) using RNA sequencing analysis. We validated 30 novel sRNAs and asRNAs, and identified 9 sRNAs directly cleaved by the ribonucleases RNase III and/or RNase Y. Previous work from the laboratory has highlighted the role of sRNAs from the type II Clustered Regularly Interspaced Short Palindromic Repeats-CRISPR associated proteins (CRISPR-Cas) systems in S. pyogenes. CRISPR-Cas systems provide adaptive immunity to prokaryotes against infection by mobile genetic elements. Two sRNAs, forming a complementary duplex (dual-RNA), are effectors of this system: the mature CRISPR RNAs (crRNAs) and the trans-activating crRNA (tracrRNA). The dual-RNA guides the Cas9 endonuclease to cleave both strands of the invading DNA in a sequence-specific manner. This RNA-programmable CRISPR-Cas9 system is now utilized for genome editing and engineering in a wide range of cells and organisms. To expand the potentialities of this tool, we both, searched for Cas9 orthologs and predicted numerous tracrRNA orthologs. We defined tracrRNA as a new family of sRNAs sharing the ability to base-pair to cognate crRNAs, without conservation of structure, sequence or location. We show that Cas9 and the dual tracrRNA:crRNAs are only interchangeable between closely related type II CRISPR-Cas systems. In summary, this thesis presents new insights into RNA-mediated regulatory mechanisms in S. pyogenes. We identified and described the expression of novel sRNAs, highlighting potential antisense RNAs. Focusing on the dual-RNA programmable type II CRISPR-Cas system, we provided evidence for co-evolution of the Cas9 enzyme with tracrRNA:crRNA, a basis for Cas9 multiplexing in genome editing.

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14

Sethman, Chad Robert. "Attachment of Streptococcus pyogenes to Host Epithelial Cells." Miami University / OhioLINK, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=miami1071776892.

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15

Cunningham, Cynthia A. "Induction of myosin cross-reactive antibody and cytolytic T cell responses in mice with Streptococcus pyogenes." Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1530.

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16

Smeesters, Pierre. "Epidémiologie, pathogénie et prise en charge des infections à Streptococcus pyogenes touchant les enfants de Bruxelles et de Brasília." Doctoral thesis, Universite Libre de Bruxelles, 2007. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210620.

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Les Streptocoques Béta-hémolytiques du groupe A (GAS) sont responsables de manifestations cliniques variées et de séquelles non suppuratives comme notamment le rhumatisme articulaire aigu (RAA). Les affections sévères à GAS tuent plus de 500.000 personnes chaque année. Le pouvoir pathogène du GAS est encore mal compris. Il semble être notamment lié à la présence de nombreux gènes codant pour des facteurs de virulence dans le génome du GAS, dont celui codant la protéine emm. La protéine transmembranaire M joue un rôle essentiel dans la virulence du GAS. Le typage moléculaire des GAS se base sur la séquence de la partie hypervariable de ce gène (emm-typing). L’épidémiologie du GAS semble varier au cours du temps et en fonction de la localisation géographique et/ou du contexte socio-économique. Cependant, les différences dans les critères d’inclusion des différentes études épidémiologiques disponibles dans la littérature rendent les comparaisons difficiles.

Pour mieux évaluer ces variations, nous avons mené une analyse prospective de l’épidémiologie clinique et moléculaire d’isolats de GAS provenant d’enfants présentant une infection à GAS, simultanément en deux localisations géographiques différentes (Bruxelles et Brasília, Brésil).

Un des points importants de notre étude a été la mise en évidence de la diversité génétique de la protéine M des isolats belges et brésiliens. Alors que de nombreux emm-types différents sont retrouvés à Brasília (48 emm-types sur 128 isolats), ceux retrouvés à Bruxelles sont relativement peu nombreux (20 emm-types sur 200 isolats) et sont ceux communément retrouvés dans les pays industrialisés. Afin de mieux comprendre les bases moléculaires de cette différence, une analyse phylogénétique basée sur la quasi-totalité de la séquence de la protéine M exposée à la surface de la bactérie a été réalisée. Cette analyse a permis de montrer que les emm-types belges sont génétiquement éloignés les uns des autres alors que les emm-types brésiliens sont génétiquement plus proches. De manière intéressante, cette analyse a montré que les souches belges présentent une grande diversité au niveau de la région de la protéine M dite ‘constante’. En conséquence, la diversité génétique globale des protéines M belges et brésiliennes est similaire, mais elle se situe dans des régions différentes de la protéine M, ce qui pourrait indiquer l’existence de pressions de sélection différentes entre les deux pays. D’un point de vue vaccinal, ces résultats indiquent qu’un vaccin dirigé contre certaines des parties constantes de M présenterait une bonne couverture théorique dans les deux pays. Par contre, le vaccin 26-valent, en cours d’évaluation clinique, aurait une couverture théorique de 76% à Bruxelles et de 32% à Brasília.

Notre analyse phylogénétique a également permis de montrer que la non-sensibilité à la ciprofloxacine (observée dans 22,5 % et 9% des souches belges et brésiliennes respectivement) survient dans des souches génétiquement éloignées, contrairement à ce qui est proposé actuellement dans la littérature. De plus, nous avons mis en évidence un polymorphisme au sein des gènes codant les topoisomérases cibles de la ciprofloxacine. L’identification de mutations responsables du phénotype de non-sensibilité nécessite par conséquent une confirmation expérimentale.

Les manifestations cliniques sont assez différentes entre Bruxelles et Brasília. Les infections cutanées sont beaucoup plus fréquentes à Brasília. De manière intéressante au Brésil, des souches de GAS présentant un tropisme cutané sont isolées du pharynx. Ces souches ‘cutanées’ pourraient avoir acquis des déterminants génétiques leur permettant de se développer dans des tissus pharyngés. De plus, ces résultats pourraient remettre en question le postulat que seules les souches de tropisme pharyngé sont impliquées dans le développement du RAA. D’autres études épidémiologiques dans des pays où le RAA est endémique devront être réalisées afin de préciser nos résultats et de mieux comprendre les mécanismes moléculaires menant au développement du RAA.

Cependant, étant donné la prévalence du RAA et l’accès limité au diagnostic microbiologique des pharyngites dans le réseau public de soins au Brésil, nous avons développé un score clinique permettant de limiter les traitements antibiotiques chez les enfants probablement atteints de pharyngites virales. L’utilisation de ce score permettrait de réduire le nombre de prescriptions antibiotiques dans les pharyngites de l’enfant de 41 à 55% à Brasília.

Le choc toxi-infectieux est une pathologie relativement rare et le RAA n’est quasi plus décrit dans les pays développés. Cependant, deux nourrissons ont présenté un choc toxi-infectieux suivi d’un RAA (HUDERF, Bruxelles). A notre connaissance, cette association clinique n’a jamais été décrite. L’analyse de ces deux cas du point de vue de la virulence bactérienne a révélé la présence de nombreux gènes de facteurs de virulence, portés par des phages et différents dans les deux souches. Nos résultats illustrent la complexité de la relation hôte-pathogène.

La capacité des bactéries à s’adapter à leurs hôtes et à causer des pathologies dépend de nombreux facteurs, qui varient d’un isolat à l’autre, et dont l’importance varie d’un hôte à l’autre. Notre travail a permis d’exemplifier la diversité génétique des GAS, aussi bien au niveau du gène emm qu’au niveau des facteurs de virulence, et de l’implication de ceux-ci dans le développement de pathologies streptococciques rares.

Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished

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17

Delgado, Giselle M. "SIAA and Neat2 Heme Binding Proteins from Streptococcus Pyogenes." Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/chemistry_theses/24.

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The bacterium Streptococcus pyogenes requires heme, which is taken up via an ABC transporter. An understanding of this pathway may result in new approaches to antibacterial agents. Both SiaA and NEAT2 (NEAr Transporter 2) are proteins involved in heme binding. One of the axial ligands of SiaA, His 229, was purified to study how mutagenesis affects heme binding. UV-visible studies showed a small band at 420 nm with respect to the protein band at 288 nm which probably indicates that heme was lost easily from this mutant. We have also worked to optimize the yield of Shr-NEAT2 by changing different variables. For each of the batches, the yield of holoNEAT2 was calculated by UV-visible spectroscopy. Increasing oxygen during growth did not improve holoNEAT2 yield. On the other hand, lower temperature, decrease in time after induction, and addition of ALA all increased the protein production.

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18

Galeas, Pena Trilce Michelle. "Thermoregulation of capsule production of Streptococcus pyogenes strain HSC5 /." Available to subscribers only, 2009. http://proquest.umi.com/pqdweb?did=1967978671&sid=7&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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19

Calusni, Ana Lucia Roscani. "Interação entre o Streptococcus pyogenes e a hemoglobina S." [s.n.], 1994. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316745.

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Orientador: Antonio Sergio Ramalho
Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-07-19T08:31:44Z (GMT). No. of bitstreams: 1 Calusni_AnaLuciaRoscani_M.pdf: 1715301 bytes, checksum: acd3974eacbc813ea7e1416eeec145b7 (MD5) Previous issue date: 1994
Mestrado
Genetica
Mestre em Ciências Biológicas

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Galeas, Trilce Michelle. "Thermoregulation of Capsule Production of Streptococcus pyogenes Strain HSC5." OpenSIUC, 2009. https://opensiuc.lib.siu.edu/theses/122.

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Group A Streptococcus (GAS) is responsible for mild and common infections like tonsillitis and pharyngitis, and more serious invasive disorders like necrotizing fasciitis and glomerulonephritis. The ability to invade tissues is closely linked to the virulence factors expressed by the bacterium. Hyaluronic acid capsule expression is variable among all the strains in S. pyogenes and confers the capacity to evade the immune response. In a previous study, it was found that capsule production in CovR mutants was temperature-regulated, showing no capsule production at 37℃ but increased production was observed at 25℃. In this study, the objective is to ﬁnd the elements involved in the thermoregulation using a genetic approach. First, mutants were created by knocking-out CovR, the response regulator of the CovRS two-component system that controls about 15% of GAS genome. Transposon mutants were screened to ﬁnd changes in capsular phenotype. Colonies expressing capsule at 37℃ were selected for sequencing. The sequencing revealed three different events in different mutants. Two of them pointed at hypothetical proteins, one of them, SpyM3_1255, was phage associated protein with a DnaD domain and the other one, SpyM3_1377, encoded cvfA. A third over-producer mutant showed an insertion in the promoter area of the has operon, the operon that encodes for hyaluronan synthase production, upstream from other disruptions in the promoter area that generated non-producing mutants. This suggest that there is more than one factor involved in thermoregulation of capsule production.

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Wright, Jordan. "Capsule Thermoregulation and Non-Coding RNA in Streptococcus pyogenes." OpenSIUC, 2014. https://opensiuc.lib.siu.edu/theses/1505.

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Streptococcus pyogenes is a re-emerging pathogen that produces superficial and life threatening invasive diseases. One important virulence factor in S. pyogenes is hyaluronic acid capsule which has been shown to increase expression at sub-body temperatures in certain strains. This study showed that thermoregulation is common in invasive clinical isolates. Regulation was shown to occur independent of the CovRS two-component regulator in a post transcription manner and before protein level regulation. The endoribonuclease, CvfA, was also confirmed to be required for capsule thermoregulation. The search for a regulator lead to the discovery of the 1st antisense RNAs in S. pyogenes found opposite the capsule synthesis genes. Its role if any in capsule has not been discovered. Finally, a group of sRNAs were characterized adding to the knowledge of this layer of regulation in S. pyogenes.

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LE, BOUGUENEC-BRIVE CHANTAL. "Etude d'un element genetique mobile (tn3701) chez streptococcus pyogenes." Paris 7, 1989. http://www.theses.fr/1989PA077082.

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Mise en evidence chez streptococcus pyogenes d'un element transposable (tn3701) capable de conferer la resistance aux antibiotiques erythromycine, tetracycline et microcycline. Une carte de restriction de la region contenant cet element a ete etablie. Par hybridation moleculaire il a ete possible de reveler une forte homologie entre tn3701 et d'autres elements chromosomiques transferables par conjugaison decrits dans d'autres souches de streptococcus

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23

Steinberg, Gregory. "Long-term Stationary Phase Behavior of Streptococcus pyogenes Biofilms." Master's thesis, Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/170151.

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Microbiology and Immunology
M.S.
Long-term Stationary Phase Behavior of Streptococcus pyogenes Biofilms Department of Microbiology and Immunology Streptococcus pyogenes is the etiological agent of many human diseases ranging from mild superficial skin infections and pharyngitis to life-threatening necrotizing fasciitis. There can be several complications as a result of S. pyogenes infection including post-streptococcal glomerulonephritis and rheumatic fever, which leads to rheumatic heart disease. Despite the significant virulence associated with the pathogen, the bacteria can also persist asymptomatically in human host carriers. S. pyogenes is characterized by significant strain-to-strain variation with many single nucleotide polymorphisms and differences in genetic content of up to 33% of the genome. Active infection is associated with the rapid growth of the pathogen, whereas survival or carriage is associated with slow growth. Our laboratory has demonstrated that during survival in long-term stationary phase cultures and in eukaryotic cells, S. pyogenes diversifies into a mixed population. Isolates from this population show diversification in their proteome, in metabolism, and in virulence factor transcription patterns. These are stable, heritable changes with unique mutations in global gene regulators in some isolates, suggesting that an accumulation of genetic mutations leads to diversification. There are two proposed modes of survival in the human host; by taking residence intracellularly in host cells and as biofilms. Previous studies showed that isolates surviving within eukaryotic cells acquire heritable changes in metabolism and virulence factor expression. Biofilms are highly organized structures formed by many bacteria, which provide resiliency to harsh environmental conditions. It has been demonstrated that S. pyogenes form biofilms in vivo and in vitro, and up to 90% of clinical isolates can form biofilms. Considering the resiliency of biofilms, and the organized roles played by individual cells in biofilms, we hypothesized that biofilms may provide S. pyogenes with a niche for persistence and diversification. Despite the capacity for survival of planktonic cells, we have found that viable cells could not be isolated from static biofilms after 10 days. No metabolic variants were found among biofilm isolates prior to loss of biofilm viability. Biofilm structure was examined using confocal microscopy to image cells after LiveDead® staining. These experiments revealed that the biofilms lost viability rapidly, and also appeared to disperse. Dispersion of 2-day old biofilms could be induced with culture supernatants collected from 7-day old planktonic cells. Overall, the results of these studies suggest that secreted factors from late stationary phase cultures induce biofilm dispersion and biofilms do not serve as a niche for long-term survival and diversification of S. pyogenes. Therefore, S. pyogenes biofilms may be more critical for initial colonization of the oropharynx. These studies may provide a valuable insight to the role of biofilms in S. pyogenes infections.
Temple University--Theses

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Weinstein, Kathryn Elizabeth. "Generation of Diversity During the Survival of Streptococcus pyogenes." Diss., Temple University Libraries, 2010. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/105846.

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Microbiology and Immunology
Ph.D.
Streptococcus pyogenes is a human-specific pathogen that can cause a wide variety of diseases. These diseases range from the relatively mild pharyngitis and impetigo to invasive diseases such as necrotizing fasciitis to post-streptococcal sequelae such as rheumatic heart disease. The bacteria are frequently carried asymptomatically and may cause recurrent disease. Corresponding with their etiologic variation amongst diseases, clinical isolates demonstrate diverse virulence factor expression and random genetic mutations. In these studies, we examine the role of intracellular residence during survival as a niche for the diversification of S. pyogenes. Survival was previously studied using two in vitro systems: long-term stationary phase survival in culture and survival within epithelial cells in the presence of extracellular antibiotics. The surviving populations diversified, giving rise to stable strains with alternate colony morphologies, distinct proteomes, and altered metabolic properties. Further analysis in these studies showed that alterations in colony morphology were not solely observed during survival, but could also be induced in models mimicking acute infection. However, diversification in certain metabolic pathways occurred only during survival, and this metabolic diversification was observed at the transcriptional level. Further, one of three clinical isolates from patients with recurrent pharyngitis was altered in its metabolic profile, suggesting metabolic diversification may be occurring in vivo. The survivor strains had varied transcriptional changes in the genes encoding the virulence factors emm, slo, and speB. All of the stationary phase-derived survivor strains and two intracellular survival-derived strains had attenuated virulence in zebrafish. Most of the attenuated strains disseminated to the spleen and were cleared within three days. A whole blood killing assay showed a strong correlation between bacterial killing and emm expression. While the diversification appeared random, these strains retained their multilocus sequence type (MLST). These results suggest S. pyogenes strains with the same MLST, but diverse virulence properties, may arise during survival in the host.
Temple University--Theses

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Miller, Aleisha Nadine Altovese. "The effect of arcanobacterium pyogenes in the bovine uterus." Thesis, Royal Veterinary College (University of London), 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522690.

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Johansson, Söderberg Jenny. "The streptococcal IgG degrading enzyme IdeS : studies on host-pathogen interactions." Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-53706.

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The important human pathogen Streptococcus pyogenes causes both mild infections such as pharyngitis and impetigo but also severe life threatening invasive infections. Specific antibodies (IgG) recognize pathogens and are important mediators for pathogen clearance by the immune defence. S.ipyogenes expresses a highly effective and specific IgG endopeptidase called IdeS (immunoglobulin degrading enzyme of S.ipyogenes). IdeS rescues bacteria from opsonising IgG by cleavage of IgG generating two fragments F(ab´)2 and ½Fc. Moreover, IdeS block ROS production by neutrophils. In this thesis I have studied (i) allelic variants of IdeS and their biological potential, (ii) consequences of ½Fc production for host-pathogen interactions and (iii) IdeS processing by streptococcal and neutrophil proteases. When investigating the allelic variants of IdeS we could show that in respect to IgG degradation and inhibition of ROS production the allelic variants where indistinguishable, however the allelic variant of serotype M28 appears to be an unique exception as this protein was deficient in IgG cleavage but still inhibited ROS production. Further, the ½Fc fragments produced when IgG is cleaved by IdeS were shown to prime human neutrophils and under ex vivo experimental conditions this increased the bactericidal activity of the neutrophils. Finally, we made the interesting finding that IdeS is N-terminally processed by neutrophil proteases and by the streptococcal protease SpeB, but retain enzymatic activity and was less immunogenic compared to the full length protein.

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Libkind, Marianna. "SiaA, a heme protein." unrestricted, 2006. http://etd.gsu.edu/theses/available/etd-02192007-092252/.

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Thesis (honors)--Georgia State University, 2006.
Title from title screen. Under the direction of Dabney White Dixon. Electronic text (46 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed Aug. 1, 2007. Includes bibliographical references (p 45-46).

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Fontaine, Michael Christopher. "Allel-replacement mutagenesis of group A streptococci." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285338.

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Abe, Lucienne M. "Adhesion and internalization of group A streptococcus isolates found in Hawaii." Thesis, University of Hawaii at Manoa, 2003. http://proquest.umi.com/pqdweb?index=0&did=764803591&SrchMode=2&sid=1&Fmt=2&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1233167604&clientId=23440.

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Parks, Thomas Edward. "Host genetic susceptibility to group A streptococcal disease." Thesis, University of Cambridge, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709471.

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FERNANDEZ, FRANCK. "Les infections humaines a actinomyces pyogenes : a propos de deux cas rencontres en france." Aix-Marseille 2, 1993. http://www.theses.fr/1993AIX20911.

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Almengor, Audry C. "Transcriptional regulation of the MGA virulence regulon in Streptococcus pyogenes." Access to abstract only; dissertation is embargoed until after 12/19/2006, 2005. http://www4.utsouthwestern.edu/library/ETD/etdDetails.cfm?etdID=115.

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Anderton, Stephen M. "A study of murine T lymphocyte responses to Streptococcus pyogenes." Thesis, University of Newcastle Upon Tyne, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287332.

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Al-Jeldah, Mohammed M. "Investigating pathogenesis of streptococus pyogenes using molecular and cellular methods." Thesis, University of Manchester, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517722.

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Turner, Claire Elizabeth. "SpyCEP : The Interleukin 8 Cleaving Streptococcus pyogenes Cell Envelope Proteinase." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501216.

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Tesorero, Melendez Rafael Angel. "Experimental validation for computationally predicted small RNAs of Streptococcus pyogenes." OpenSIUC, 2011. https://opensiuc.lib.siu.edu/theses/769.

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The human pathogen Streptococcus pyogenes (Group A Streptococcus or GAS) are a versatile Gram-positive cocci that havw shown complex modes of regulation of its different virulence factors. Discoveries of a few small non-coding RNAs (sRNAs) in S. pyogenes and their influence on the expression of virulence factors revealed an important role of sRNAs on S. pyogenes virulence. The genome-wide analysis of bacterial genomes for the discovery of sRNAs through computational methods has become an effective way to discover new sRNAs. In this study we provided a computational scheme where three different algorithms (RNAz, eQRNA, and sRNAPredict) were combined to increase the probabilities of predicting putative sRNAs within S. pyogenes' intergenic regions (IGR). A total of 46 candidates were chosen based on our criteria, and through Northern blot we analyzed each candidate. We obtained hybridization signals from twelve newly discovered sRNAs in S. pyogenes. Subsequently, we analyzed their sequence and their location within the IGR to find a putative -10 promoter region and possible Rho-independent terminator site, and their possible targets through computational methods. We further expanded our analysis of the new sRNAs by using Real-Time RT-PCR to determine the expression of sRNAs during different phases of growth. Our results showed that our computational scheme and experimental method was effective in predicting sRNAs previously undiscovered in S. pyogenes, and that more sRNAs are yet to be discovered and characterized, helping to further understand the regulation of virulence factors in S. pyogenes

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Abou, El Enien Ibrahim. "Caractérisation des propriétés biologiques du facteur d'opacité de Streptococcus pyogenes." Lyon 1, 1991. http://www.theses.fr/1991LYO1T067.

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Zarate, Bonilla Lina Johana. "Characterization of Chromosomally Encoded Toxin-Antitoxin Systems in Streptococcus pyogenes." Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/20547.

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Streptococcus pyogenes ist ein humanpathogenes Bakterium, welches verschiedene Gewebe besiedeln kann und dadurch unterschiedliche Krankheiten verursacht. Die enorme Anpassungsfähigkeit des Bakteriums beruht auf dessen Fähigkeit, verschiedene, vom Wirt induzierte Stresskonditionen zu ertragen. Genetische Faktoren, die in diesem Zusammenhang eine Rolle spielen, sind Toxin-Antitoxin (TA) Systeme. Typ II TA Systeme kodieren für zwei Proteine, ein Toxin und ein Antitoxin, die einen stabilen TA Komplex bilden. Verschlechtern sich die Wachstumsbedingungen, kann das Antitoxin proteolytisch abgebaut werden, wodurch das freigesetzte Toxin essentielle zelluläre Prozesse des Bakteriums inhibiert. In dieser Studie charakterisierte ich zwei chromosomal kodierte ParDE TA Systeme des pathogenen Bakteriums S. pyogenes. Ähnlich zu anderen Systemen werden das Toxin und das Antitoxin beider hier charakterisierten Systeme co-transkribiert und durch Stresseinwirkung (z.B. Aminosäure-mangel) induziert. Zudem konnten weitere posttranskriptionelle bzw. posttranslationale Mechanismen zur Regulierung der Genexpression beider Systeme nachgewiesen werden. Die extrachromosomale Expression der Toxine ParE1 und ParE2 führten in S. pyogenes und Escherichia coli zum Zelltod, wobei die Co-expression der entsprechenden Antitoxine ParD1 und ParD2 die Toxizität minderte. Allerdings verursachte die Überexpression der Antitoxine allein ebenfalls eine Inhibierung des Zellwachstums. ParD1 hemmte die Zellteilung in E. coli, wobei der N-Terminus des Proteins entscheidend für diesen Effekt zu sein schien. Zusammengefasst erweitern die Ergebnisse dieser Arbeit unser Verständnis von ParE Toxinen und verdeutlichen die diversen Mechanismen, welcher sich TA Systeme bedienen, um die bakterielle Physiologie zu beeinflussen. Zusätzlich gibt diese Arbeit einen Einblick in mögliche Mechanismen, die S. pyogenes implementiert, um Stresskonditionen im Wirt zu überdauern.
Streptococcus pyogenes is a human pathogen with a remarkable ability to colonize different tissues and to endure diverse host-induced stress conditions through mechanisms that have yet to be fully understood. One strategy employed by bacteria to cope with changing environments are toxin-antitoxin (TA) genetic modules. Under non-ideal conditions, the antitoxin is subject to proteolysis and thus the freed toxin protein can target crucial pathways in the cell modulating bacterial growth. This study, describes the characterization of two chromosomally encoded ParDE-like TA systems from the human pathogen S. pyogenes. The antitoxin-toxin genes of the parDEF1 and parDE2 TA systems are co-transcribed and triggered by stress-induced conditions. The parDE2 TA showed an inspected mRNA processing under amino acid starvation which suggest a putative post-transcriptional regulation. At the post-translational level, both systems are controlled by ClpXP antitoxin-protein degradation in vivo, an important factor for TA triggering. Furthermore, bacterial plasmid-based expression of the toxins ParE1 and ParE2 resulted in effects in cell viability while the antitoxin molecules ParD1 and ParD2 were able to prevent the toxins lethality, respectably. Unlike canonical antitoxins, both ParD1 and ParD2 molecules also displayed deleterious effects, which seemed to be exclusive and related with the N-terminus domain potentially involved in DNA-interaction. Finally, the ParE toxins presented remarkable plasticity, able to harm not only gyrase but also topoisomerase IV, two important bacterial drug targets that modulate DNA-topology. These results expand the view on the ParE molecular targets and highlight the diverse mechanisms TAs employ to modulate bacterial physiology. We also provide more insights into possible mechanisms that S. pyogenes employs to endure stress in the host and efficiently cause disease.

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Swe, Pearl M., and n/a. "Mode of action of dysgalacticin and mechanism of its producer cell immunity." University of Otago. Department of Microbiology & Immunology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20081119.111402.

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Dysgalacticin is a large, 21.5 kDa bacteriocin that belongs to subgroup B of the class III bacteriocins. It is ribosomally produced by Streptococcus dysgalactiae subsp. equisimilis strain W2580 and exerts inhibitory activity mainly against the medically important pathogen Streptococcus pyogenes by a "non-lytic" mechanism. Despite numerous studies of the mechanisms of action of a wide variety of bacteriocins and of the basis of their producer strain self-immunity, relatively little is known about the "non-lytic" class of bacteriocins. The structural gene encoding for dysgalacticin (dysA) was known to be carried on a small, rolling circle plasmid pW2580 (3.04 kb) (Heng et al., 2006). However, the dysgalacticin immunity gene (dysI) had not been identified prior to the present study. The aims of this research were to elucidate the mechanism of action of dysgalacticin against S. pyogenes and to identify the genetic basis and the mechanism of producer strain self-immunity. Recombinantly-produced dysgalacticin was used to determine the mode of action against S. pyogenes. Dysgalacticin was bactericidal for S. pyogenes, increasing the permeability of the cytoplasmic membrane and ultimately leading to leakage of intracellular potassium ions. Moreover, dysgalacticin dissipated the membrane potential and inhibited [�⁴C]serine uptake, a membrane potential-dependent process in S. pyogenes. Interestingly, dysgalacticin inhibited glucose fermentation by non-growing cell suspensions and blocked transport of both glucose and the nonmetabolisable analogue 2-deoxyglucose. This finding indicates that dysgalacticin may target the phosphophenolpyruvate (PEP)-dependent glucose and mannose phosphotransferase system (PTS) of S. pyogenes. Taken together, these data suggest that dysgalacticin targets the glucose-PTS and/or mannose-PTS as a receptor, leading to inhibition of sugar uptake, and a subsequent dissipation of the membrane potential leading to cell death. Complementation studies demonstrated that dysI is located on pW2580. RNA analysis showed that dysI is co-transcribed with genes encoding for the plasmid copy control protein, copG and replication initiation protein, repB. S. pyogenes transformed with a plasmid containing dysI displayed a markedly higher dysgalacticin MIC (1024 nM) than the corresponding dysgalacticin-sensitive, plasmid-negative strain (8 nM). Further studies of this DysI-expressing S. pyogenes showed that membrane integrity, glucose fermentation and [�H]2DG uptake were not affected by dysgalacticin treatment. These findings are consistant with a mechanism whereby the immunity peptide binds to the target-binding site of dysgalacticin, effectively blocking access by the bacteriocin. H₆DysI was found to localise to the cytoplasmic membrane, further indicating that DysI may bind to the proposed target of dysgalacticin, i.e., the membrane-bound glucose-PTS and mannose-PTS. Thus both the mode of action and the producer strain self-immunity of dysgalacticin are likely to be cytoplasmic-membrane based. Homology searching revealed that the bacteriocin SA-M7 produced by M-type 57 S. pyogenes has structural similarities to dysgalacticin, as do two hypothetical proteins, EF1097 and YpkK, of Enterococcus faecalis and Corynebacterium jeikeium, respectively (Heng et al., 2004, 2006). These proteins were all predicted to contain relatively unstructured N-termini and helix-loop-helix structured C-termini. In each case the C-termini contain two conserved cysteine residues that are predicted to form a disulphide bridge. Heterologous expression of SA-M57, EF1097 and YpkK in Escherchia coli demonstrated that all three proteins have antimicrobial activity, but of differeing activity spectra. Reductive-alkylation of SA-M57, EF1097 and YpkK confirmed that their predicted disulphide bonds were essential for biological activity. These proteins were later renamed streptococcin A-M57, enterococcin V583 and corynicin JK respectively. The outcome of preliminary domain-swapping experiments supported the existence of functional domain-type segments in streptococcin A-M57, enterococcin V583, corynicin JK and dysgalacticin. The N-terminal domain of each of these proteins and also the C-terminal domain of corynicin JK were successfully expressed in E. coli. The failure to express the C-termini of the remaining proteins was thought possibly due to toxicity of thses pepetides for the E. coli host. Nevertheless, the C-terminus of corynicin JK displayed an inhibitory spectrum apparently identical to that of the full-length corynicin, indicating that the N-terminus may not always be required for target binding of this class of antimicrobials. Preliminary mode of action studies revealed that streptococcin A-M57, enterococcin V583 and corynicin JK all resemble dysgalacticin in that they exert inhibitory activity by non-lytic means. These results, in combination with the protein structural predictions indicate that dysgalacticin, streptococcin A-M57, enterococcin V583 and corynicin JK are all members of the same basic class of "non-lytic" bactericoicns.

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Sylla, Maguette Dème. "Contribution à l'étude de l'action opsonisante des immunoglobulines sur les streptocoques du groupe A." Lyon 1, 1987. http://www.theses.fr/1987LYO1T126.

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Rivera, Martínez M. Alba. "Estudi epidemiològic d'infeccions invasives i no invasives produïdes per Streptococcus pyogenes." Doctoral thesis, Universitat Autònoma de Barcelona, 2008. http://hdl.handle.net/10803/3920.

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Streptococcus pyogenes és un patogen humà responsable d'un ampli ventall d'infeccions que varien des d'infeccions superficials com faringitis i impetigen a formes sistèmiques greus com fascitis necrosant (FN) i síndrome del xoc tòxic estreptocòccic (SSTS). El ressorgiment i persistència de formes invasives greus descrit des de mitjans dels anys 1980 ha motivat una intensa recerca sobre els aspectes epidemiològics, microbiològics i clínics d'aquestes infeccions.
S'ha realitzat un estudi retrospectiu de base hospitalària que inclou 126 soques de S. pyogenes (27 procedents d'infeccions invasives i 99 d'infeccions no invasives) aïllades entre gener de 1999 i juny de 2003. Les soques de S. pyogenes es van caracteritzar en base a la distribució de tipus i subtipus emm i els perfils genètics de superantígens (SAgs) (speA-C, speF-J, speL, speM, ssa i smeZ). Tanmateix, es va determinar la prevalença i els mecanismes de resistència a macròlids, tetraciclina i levofloxacino.
Les formes clíniques més freqüents d'infecció invasiva van ser les infeccions de la pell i teixits tous (40,7%). La SSTS es va registrar en quatre (14,8%) dels casos invasius i es va associar a FN en la meitat dels casos. La majoria dels pacients afectats de quadres invasius eren adults, en particular d'edat avançada i de mitjana edat, i una elevada proporció presentaven factors predisposants, destacant l'alteració de la barrera cutània, la infecció per HIV, l'ús de drogues per via parenteral, i les neoplàsies.
En la col·lecció de 126 soques analitzada es van identificar un total de 29 tipus emm amb una distribució encapçalada pel tipus emm1 (17,5%), seguit d'emm3 (8,7%), emm4 (8,7%), emm12 (7,1%), emm28 (7,1%), emm11 (6,3%) i emm77 (6,3%). Aquests set tipus van constituir el 61,9% del total de soques. No es van observar diferències significatives en la distribució de tipus emm entre soques aïllades d'infeccions invasives i no invasives amb l'única excepció del tipus poc freqüent emm25 que es va trobar associat a infeccions invasives en addictes a drogues per via parenteral. Es va trobar una forta correlació entre el patró de SAgs i el tipus emm independentment del tipus d'infecció.
La resistència a eritromicina va mostrar un increment anual progressiu del 16,6% (1999) al 38,8% (2003) i va estar causada per soques pertanyents a 11 tipus emm. Les soques mef(A) positives dels tipus emm4, emm12 i emm75 i erm(B) positives dels tipus emm11 i emm25 constituïren el 80% de les soques resistents. La freqüència de resistència a tetraciclina va fluctuar durant el període estudiat (màxim 34,6% el 2002 i mínim 15,8% el 2001) i va ser superior en les soques resistents a eritromicina que en les soques sensibles (42,8% vs 18,7%). En les soques resistents a tetraciclina el gen tet(M) va ser el predominant i es va trobar en soques pertanyents a 14 tipus emm, mentre que el gen tet(O) només es va trobar en soques emm77. No es van observar diferències significatives en la prevalença de resistència a eritromicina ni a tetraciclina en el grup invasiu respecte del no invasiu.
La prevalença de resistència a levofloxacino fou del 3,2%, incloent quatre soques amb sensibilitat reduïda o resistència intermèdia (CIM 2-4 µg/ml) i dues soques amb resistència d'alt nivell (CIM >32 µg/ml). La resistència de baix nivell es va associar a substitucions únicament en ParC (Ser80Pro, Ser79Ala, Ser79Phe i Ala121Val), mentre que la resistència d'alt nivell es va relacionar amb mutacions en ParC (Ser79Phe i Ala121Val) i GyrA (Ser81Tyr).
Streptococcus pyogenes (GAS) is a human pathogen responsible for a wide array of infections, ranging from pharyngitis and impetigo to severe invasive infections such as necrotizing fasciitis (NF) and streptococcal toxic shock syndrome (STSS). The resurgence and persistence of severe forms of GAS diseases reported since the mid 1980s have motivated intensive research on epidemiological, microbiological and clinical aspects of these diseases.
A retrospective hospital-based study was conducted including 126 GAS isolates (27 from invasive infections and 99 from non-invasive infections) collected from January 1999 to June 2003. GAS isolates were characterized by emm type and subtype and superantigen (SAg) gene profile (speA-C, speF-J, speL, speM, ssa and smeZ). The prevalence and mechanisms of macrolide, tetracycline and levofloxacin resistance were also determined.
The most common clinical presentations of invasive cases were skin and soft-tissue infections (40.7%). SSTS occurred in four cases (14.8%) and was associated to NF in half of the cases. Most invasive cases were found in adults, in particular among the elderly and the middle-aged, and a large proportion had underlying conditions, the most frequent being skin lesions, HIV infection, injection drug use, and malignancy.
A total of 29 emm types were identified among the 126 isolates; the most prevalent were emm1 (17.5 %), followed by emm3 (8.7 %), emm4 (8.7 %), emm12 (7.1 %), emm28 (7.1 %), emm11 (6.3 %) and emm77 (6.3 %). These seven emm types accounted for 61.9 % of isolates. There were no differences in the emm type distribution between invasive and non-invasive infections, except for emm25 isolates, which were associated with invasive infections in injecting drug users. The SAg gene profiles were closely associated with the emm type and were independent of the disease type.
The prevalence of erythromycin resistance showed an annual progressive increase from 16.6% (1999) to 38.8% (2003) and was caused by isolates belonging to 11 emm types. mef(A)-positive emm types 4, 12 and 75, and erm(B)-positive emm types 11 and 25 were responsible for up to 80% of the erythromycin-resistant isolates. The prevalence of tetracycline resistance fluctuated over the period studied (maximum 34.6% in 2002 and minimum 15.8% in 2001) and was higher in erythromycin-resistant isolates than in susceptible isolates (42.8% vs 18.7%). Among the tetracycline-resistant isolates, the tet(M) determinant was the most prevalent and was distributed in isolates belonging to 14 emm types, whereas tet(O) was only found in emm77 isolates. No significant differences in resistance rates to erythromycin or tetracycline were found between invasive and non-invasive isolates. The rate of resistance to levofloxacin was 3.2%, encompassing four isolates with reduced susceptibility or intermediate resistance (MIC 2-4 µg/ml) and two isolates with a high level of resistance (MIC >32 µg/ml). Low-level resistance was associated with alterations in ParC (Ser80Pro, Ser79Ala, Ser79Phe and Ala121Val), while high-level resistance was associated with alterations involving both ParC (Ser79Phe and Ala121Val) and GyrA (Ser81Tyr).

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42

Darenberg, Jessica. "Streptococcus pyogenes infections and toxic shock syndrome : molecular epidemiology and immunotherapy /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-676-X/.

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43

Vindebro, Reine. "Studies on secreted cysteine proteases of Streptococcus pyogenes : IdeS and SpeB." Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-88223.

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The pathogen Streptococcus pyogenes is a significant cause of human morbidity and mortality. Most of the work in this thesis is focused on streptococcal virulence factor IdeS, but the thesis also features work on SpeB, another streptococcal virulence factor. Both IdeS and SpeB are secreted cysteine proteases and both have previously been shown to degrade human IgG. IgG is the only known substrate for IdeS while SpeB is a more promiscuous protease with a larger number of identified substrates. A significant part of the data presented in this thesis is the result of designing and optimizing methods to detect and accurately measure the proteolytic degradation of IgG. Methods aimed at measuring the binding interactions between enzyme and substrate have also been frequently utilized. I show that IdeS is a monomeric protease, as opposed to previously published data that suggested it to be dimeric. IdeS cleaves the two heavy chains of IgG in a two-step reaction and I demonstrate that the first cleavage is magnitudes faster than the second one. This means that IdeS is a more efficient enzyme than previously thought. The difference in rate cannot completely be explained by a loss of affinity between IdeS and IgG after the cleavage of the first heavy chain. The velocity of IdeS is further increased by the presence of human Cystatin C, via an unknown mechanism. Cystatin C is normally a protease inhibitor and it having an opposite effect is puzzling.The synthesis and evaluation of novel inhibitors are also described. Peptide analogues mimicking the sequence surrounding the scissile bond on IgG - with an amino acid replaced with a more rigid motif - act as specific, but low-affinity, inhibitors of IdeS. The peptide analogues’ inhibitory capacity for SpeB and papain was also assayed.When it comes to SpeB, I show that it does not have IgG as a substrate under physiological conditions, in contrast to what was previously thought. This thesis does not only present findings on the IgG degrading capacity of IdeS and SpeB but also include data on fundamental enzymatic properties for these proteases.

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Whatmore, Adrian Mark. "Sequence analysis of the emm-like gene family of Streptococcus pyogenes." Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357642.

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Alam, Faraz Mainul. "Modelling nasopharyngeal colonisation by Streptococcus pyogenes : bioluminescence and other longitudinal techniques." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/14463.

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Streptococcus pyogenes causes an estimated 616 million pharyngitis cases per year and a variety of invasive diseases such as necrotising fasciitis and toxic shock syndrome. The human nasopharynx is the major reservoir for all S. pyogenes infection, including severe invasive disease. A combination of biophotonic imaging (BPI) and direct nasal sampling techniques were used to longitudinally measure the in vivo carriage of S. pyogenes, looking at the effects of virulence factor expression on carriage and transmission and to enable vaccine evaluation. Direct nasal sampling demonstrated that the two component regulatory system, CovR/S, is required for infection and transmission from the nasopharynx. The fitness cost conferred by covR/S mutation in the nasopharynx may explain why S. pyogenes with altered covR/S have not become prevalent in community infections despite conferring a selective advantage in invasive infection. Bioluminescent S. pyogenes strains expressing the luxABCDE operon demonstrated a growth deficit independent of the target site for integration in vitro that manifested as a fitness cost during infection in vivo. Notwithstanding this, bioluminescence expression permitted longitudinal quantitation of S. pyogenes within the nasopharynx using BPI. Intramuscular vaccination with heat killed streptococci or the streptococcal chemokine protease SpyCEP conferred protection against pharyngeal infection in this model. These longitudinal techniques allow for S. pyogenes to be tracked in the nasopharynx non-invasively, and allow for new insights into the pathogenesis of this disease.

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Luis, Philippe Renard Vincent. "Le TDR modifie-t-il la pratique des médecins généralistes d'Ile de France ?" Créteil : Université de Paris-Val-de-Marne, 2006. http://doxa.scd.univ-paris12.fr:80/theses/th0240166.pdf.

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Fischer, Christian Ansgar Alexander. "Resistenzentwicklung von S. pneumoniae, S. pyogenes und anderer Streptokokken-Spezies gegenüber Fluorchinolonen." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972397817.

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Enlund, Åström Caroline, and Sandra Gullström. "Omvårdnad av nyförlöst kvinna som har infektion av Streptococcus pyogenes : En litteraturstudie." Thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-241448.

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Bakground: Puerperal fever caused by group A Streptococcus is in a global context seen as a common cause of death in childbirth. Aim: To examine the consequences of group A streptococcus infections in women postpartum and to see what a nurse can do to stop the infection with adequate nursing interventions. Method: This is a review built on 15 articles. These articles were read in full and audited with a suitable template. Result: Women postpartum has 20 times higher risk to get group A stretococcus infection as compared to non pregnant. The consequences of Group A Streptococcus infection can lead to high fever, abscesses around the uterus, sepsis, acute respiratory distress syndrome (ARDS), hysterectomy and death. Patients who share room with infected patients carries an increased risk to be infected. Curtains between patient beds can be colonized by Group A Streptococcus. Nursing interventions such as good hand hygiene and sanitized equipment in the patient room are important since Group A Streptococcus can survive for a long time on different surfaces. A woman who recently gave birth should have her body temperature monitored. In an outbreak of Group A Streptococcus, healthcare workers can be carriers. It is therefore important for a nurse to educate other healthcare workers about the importance of good hand hygiene. Conclusion: A woman infected by Group A Streptococcus can in several cases suffer serious consequences. In the worst case, death can occur as a cause of non adequate treatment. A nurse should work preventively to limit spreading of the infection. Nurses need knowledge in this area to prevent propagation of the infection and to reduce suffering. A nurse is responsible for establishing a work environment where patient safety comes first.
Bakgrund: Barnsängsfeber, som orsakas av grupp A streptokocker, är globalt sett en vanlig dödsorsak i samband med förlossningar. Syfte: Att undersöka vad grupp A streptokocker har för konsekvenser för nyförlöst kvinna postpartum, samt att se vad sjuksköterskan kan göra för att sätta in rätt omvårdnadsåtgärder och undvika eventuell smittspridningen mellan patienter. Metod: Detta är en litteraturstudie som innefattar 15 artiklar. Dessa lästes i sin helhet och granskades enligt strukturerad mall. Resultat: Kvinnor postpartum löper 20 gånger ökad risk att smittas av grupp A streptokocker än ickegravida. Konsekvenserna för nyförlöst kvinna som drabbas av Grupp A streptokockinfektion kan leda till hög feber, abscesser kring uterus, sepsis, acute respiratory distress syndrom (ARDS), hysterektomi och dödsfall. Patienter som delar rum med smittade patienter löper ökad risk att drabbas av en infektion. Gardiner mellan patienternas sängar kan vara koloniserade av grupp A streptokocker. Sjuksköterskans omvårdnadsåtgärder är god handhygien och desinficering och rengöring av inredningen på patientrummet, eftersom grupp A streptokocker kan leva länge på olika ytor. Den nyförlösta kvinnans temperatur ska mätas. Vid ett utbrott av bakterien kan vårdpersonal vara bärare och det är viktigt att sjuksköterskan informerar personal om vikten av god hygien. Slutsats: En kvinna som drabbas av grupp A streptokocker postpartum får i flera fall allvarliga konsekvenser av detta. Om inte adekvat behandling sätts in kan hon i värsta fall avlida. En sjuksköterska ska arbeta preventivt för att förhindra smittspridning. Sjuksköterskor behöver kunskap inom ämnet för att förhindra smittspridning och minska lidandet. Sjuksköterskan är ansvarig för att organisera arbetet på avdelningen och ska undervisa personalen så att de arbetar på ett patientsäkert sätt

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Johansson, Björn. "Analysis of the molecular interplay between Streptococcus pyogenes and its human host." Lund : Lund University, 2006. http://theses.lub.lu.se/scripta-archive/2006/04/24/med_1300/Johansson_Kappa.pdf.

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Bruner, Patricia Jane. "A role for Streptococcus pyogenes in apoptotic dysregulation of neutrophilic polymorphonuclear leukocytes /." Connect to Digital dissertations. Restricted to UC campuses. Access is free to UC campus dissertations, 2002. http://uclibs.org/PID/11984.

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Dissertations / Theses on the topic 'Pyogenes'

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