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1
Flock, Margareta. "Development of a vaccine against strangles /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-500-3/.
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Unnikrishnan, Meera. "Streptococcal superantigens in Group A streptococcal infections." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248185.
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Smith, Jennifer Marie. "Characterization of host-bacteria interactions contributing to group B streptococcus colonization." Huntington, WV : [Marshall University Libraries], 2002. http://www.marshall.edu/etd/descript.asp?ref=64.
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Ihendyane, Nahla. "Pathogenesis and immunotherapy of streptococcal septicemia and shock /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-599-9/.
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De, Winter Leanne Marie. "Characteristics of Streptococcus canis from canine streptococcal toxic shock syndrome and necrotizing fasciitis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ33219.pdf.
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Garcia, Febres Julio Carib. "A comparative investigation of Streptococcus agalactiae isolates from fish and cattle." Auburn, Ala., 2007. http://repo.lib.auburn.edu/2007%20Spring%20Dissertations/GARCIA_JULIO_46.pdf.
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Davies, Frances Joan. "Superantigen interactions in streptococcal tonsillitis." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9660.
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Streptococcus pyogenes is the commonest cause of bacterial throat infections, and asymptomatic throat carriage acts as an important reservoir for invasive soft tissue infections. Despite the high rates of infection little is known about the immunology of streptococcal throat infections. Superantigens have been identified as one of the bacterial virulence factors associated with the establishment of streptococcal throat infections. This PhD investigates superantigen expression both in vitro and in clinical disease, and the immune effects of superantigens in human tonsils. Results: The production of superantigens was assessed using quantitative RT-PCR and biological assays both directly from patient samples and from the corresponding strain in vitro. The presence of superantigens was demonstrated in tissues which cultured live bacteria. In vitro production of the superantigen SMEZ from throat strains was higher than from invasive strains. Human tonsils were cultured as cell suspensions or solid block histocultures and stimulated with recombinant superantigens. There was a marked clonal T cell expansion and pro-inflammatory cytokine release in the presence of superantigens. There was apoptosis of tonsil B cells during co-culture with superantigens, with inhibition of IgG, IgA and IgM production. This corresponded with an alteration of the tonsil T cell phenotype from CXCR5 expressing T follicular helper cells to proliferating cells expressing high levels of the TNF receptor superfamily members OX40 and ICOS and the immune synapse signalling molecule SLAM. Conclusions: Superantigens are actively produced during clinical infection with S. pyogenes. They profoundly alter the functions of tonsil B and T cells in vitro, resulting in impaired immunoglobulin production.
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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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Sriskandan, Shiranee. "A study of the superantigen streptococcal pyrogenic exotoxin A in invasive group A streptococcal disease." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266009.
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Persson, Jenny. "Streptococcal M protein and human C4BP." Lund : Faculty of Medicine, Lund University, 2006. http://theses.lub.lu.se/scripta-archive/2006/04/04/med_1287/Jenny_Persson_kappa.pdf.
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Law, Vicky Wai-Kee. "Oral colonization of mutans streptococci in young children : a longitudinal study /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19176.pdf.
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Westling, Katarina. "Viridans group streptococci septicaemia and endocarditis : molecular diagnostics, antibiotic susceptibility and clinical aspects /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-364-7/.
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Lindsay, Anna-Marie. "Characterisation of hyaluronate lyases from streptococcal species." Thesis, Northumbria University, 2008. http://nrl.northumbria.ac.uk/1505/.
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Previously cloned bacteriophage encoded HyIP 1 from the genome sequenced organism Streptococcus pyogenes SF370 was expressed in Escherichia coli and purified to homogeneity. The protein, previously assigned to glycoside hydrolase family 69 (GH69) was biochemically recharacterised as a polysaccharide lyase and reassigned to family 16 (PL16). The enzyme demonstrated a Km of 1.47 mg m1-1 and a kcat of 7.2 s-1. Biochemically the enzyme had an optimum pH of 6.5 and temperature of 37 °C. The enzyme required no additional divalent ions for catalysis. The enzyme demonstrated strict substrate specificity only degrading hyaluronate and with no activity against related substrates chondroitin 4 sulphate and chondroitin 6 sulphate. HPAEC indicated the HylP1 had an endo mechanism of cleavage producing a range of differently sized oligosaccharides with the smallest being a tetramer. Site directed mutagenesis revealed a role for residues D157 and Y169 with substitution of these residues with alanine resulted in a 88.5% and 91.9 % loss of activity respectively. The location of these residues within the solved structure of HylP1 falls within the triple stranded (3 helix formed by the trimerised protein. This region of the protein was cloned, expressed and characterised and demonstrated similar kinetics as the full length protein (Km of 0.53 mg m1-1 and keat of 11.1 s-1). The activity of the enzyme when compared to other hyaluronate lyases shows it to be relatively inefficient yet when compared to other bacteriophage encoded hyaluronate lyases, HylP 1 was very similar. The proposed role of these bacteriophage encoded hyaluronate lyases is one of degradation of the hyaluronate capsule surrounding the streptococcal cells to allow for penetration of the bacteriophage during infection. Using the sequence of HylP1 the recently completed genome of Streptococcus equi was searched using bioinformatics tool BLAST. This revealed the presence of a protein, SEQ2045, sharing 85 % identity with HylPl. The protein was cloned and expressed in E. colt and biochemically characterised as a hyaluronate lyase. The enzyme demonstrated a Km of 2.05 mg m1-1 and a kcat of 6.2 s-1 which when compared to those of Hy1P 1 is suggestive that the two enzymes are strongly related. The enzyme had an optimum pH of 6.5 and temperature of 37 °C and like Hy1P 1 demonstrated only activity against hyaluronate and had an endo mechanism of cleavage with the smallest product of digestion being a tetramer. Site directed mutagenesis of the same residues as in HylP1 again yielded reduced activity (91.3 % and 87.6 % respectively). Bioinformatic analysis of the genome of S. equi was performed by BLAST searching with the proposed gene sequences of S. equi flanking SEQ2045. This allowed for the production of a prophage map which shows distinct similarities to the prophage map of S. pyogenes suggesting both may be of the same origin. Purified SEQ2045 was used in western blot analysis with S. equi convalescent horse serum. A strong positive reaction demonstrated a possible role for SEQ2045 during an infection suggesting that the bacteria have acquired this enzyme as a potential virulence factor by horizontal gene transfer. This presents a useful opportunity for the study of both S. pyogenes and S. equi infection process and the role of bacteriophage by the use of S. equi as a model for S. pyogenes.
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Power, Daniel Aaron, and n/a. "Non-culture based studies of the human upper respiratory tract microbiota and preliminary considerations of the influence of bacteriocin producing commensal and pathogenic oral streptococci." University of Otago. Department of Microbiology & Immunology, 2007. http://adt.otago.ac.nz./public/adt-NZDU20070620.160726.
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The upper respiratory tract (URT) of humans is complex and interconnected region and comprises several major ecosystems including the oral cavity, oropharynx, nasal cavity, sinuses, nasopharynx and middle ear. Most of the anatomical locations within the URT are colonised with a normal bacterial microbiota, within which are often organisms having the potential to cause disease. The diseases of the URT are both varied and frequent in their occurrence, and conditions such as otitis media, rhinosinusitis and pharyngitis are sources of morbidity and mortality in adults and children in both developing and developed countries.
The study of diseases of the URT has traditionally been based on application of culture-based methods in which the infection-implicated organisms are first grown in vitro and then studied further. Ongoing advances in DNA-based techniques have led to the development of new molecular tools for the study of infectious diseases. One such technique is PCR-denaturing gradient gel electrophoresis (PCR-DGGE). This is a PCR-based tool that allows the investigation of microbial communities independent of culture. Although this technique has been applied extensively in the study of the gastrointestinal tract, the vagina and endodontic infections in humans, there have been few reports of its application to URT infections. PCR-DGGE was applied in the present study to investigate (a) the bacteria present in the middle ear of children suffering from otitis media with effusion (OME), (b) the microbiota associated with the sinuses in patients with chronic rhinosinusitis (CRS) and (c) perioperative changes in the bacterial population of the middle meatus of patients undergoing nasal or sinus surgery. The analysis of the middle ear fluid samples indicated an increased role in OME for the newly-discovered pathogen Alloiococcus otitidis and also the possible involvement of certain coryneform bacteria and coagulase-negative staphylococci in the aetiology of this condition. PCR-DGGE analysis of patients with CRS revealed a polymicrobial disease with considerable variability in the predominant species detected when multiple, serial samples were evaluated. The perioperative audit showed that when good clinical practice is adhered to, there was no apparent introduction of potentially-harmful organisms into the middle meatus.
Streptococcus salivarius is a common, commensal inhabitant of the oral cavity of humans and has also been shown to inhabit the nasopharynx of infants. S. salivarius is also a well known producer of bacteriocins with activity directed against Streptococcus pyogenes. One such strain, S. salivarius K12, is now marketed in New Zealand as the probiotic, K12 Throat Guard[TM]. In the present study, S. salivarius K12 was compared with two additional strongly-inhibitory S. salivarius (strains T18A and T30A) for activity against the common causative pathogens of otitis media. A paediatric formulation of strain K12 was also tested in a pilot clinical trial for its ability to colonise the URT of young children. Although the levels of colonisation of these subjects was not as high as typically obtained with use of the K12 Throat Guard[TM] formulation, it was considered that further development of the paediatric formulation is warranted, particularly with respect to use of a different pre-treatment regimen. In other studies, the molecular basis for the unusual in vitro inhibitory activity of S. salivarius strain T30A was investigated. Although this still remains unresolved, other observations made during the course of this study have led to the introduction of a schema for the division of inhibitory S. salivarius into three groups based on (a) their sensitivity to the lantibiotic salivaricin A and (b) the structure of their salivaricin A genetic locus. This grouping is analogous to the "rock-paper-scissors" system previously described for colicin-producing strains of E. coli.
Streptococcus pneumoniae is a major human pathogen responsible for a variety of diseases in humans. There have been very few reports of bacteriocin production by S. pneumoniae when compared to other streptococcal species. In the present study a putative cluster of bacteriocins encoded by the blp locus has been investigated. The distribution of the individual blp determinants within this locus was evaluated in a collection of S. pneumoniae strains using PCR. The blp genes were detected in 92% of 57 tested strains and a variant form (termed the B-form) of the cluster was identified that appeared to have arisen due to a genetic recombination event. In this case an approximately 250 bp portion of the blpMNO cluster appears to have recombined into blpK of the blpIJK cluster. Attempts were made to express the putative bacteriocin peptide genes in an Escherichia coli expression system. Failure to achieve expression was taken to indicate that these bacteriocin-like peptides may be toxic for the host producer cells under these test conditions. Future attempts to achieve expression of the Blp peptides, could explore the use of different fusion proteins, a Gram-positive expression host or a cell-free protein expression system.
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Jarvis, Christopher D. "Mouse Antibody Response to Group A Streptococcal Carbohydrate: A Thesis." eScholarship@UMMS, 1989. https://escholarship.umassmed.edu/gsbs_diss/227.
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In an attempt to more fully understand the generation of antibody diversity to carbohydrate antigens, we produced and characterized a panel of hybridoma cell lines specific for group A streptococcal carbohydrate from mice injected with the intact bacteria (minus the hyaluronic acid capsule and cell wall protein antigens). We have analyzed the use of heavy and light chain variable region genes in the early (day 7) and late response (hyperimmune) and have determined the nucleotide sequence of the dominant VH gene used in several of our hybridomas. Our data allowed us to assess the extent to which the recombination of various V, D, and J gene segments and somatic mutation contribute to antibody diversification in this system. In this report we confirm that a minimum of two VH and four VK gene segments are used to encode this response. We extend this analysis to show that multiple D and J gene segments are used and that a significant amount of junctional variability is tolerated in CDR 3. Our results also suggest that there is a positive selection for somatic mutation in CDR 1 during the hyperimmune response to group A streptococcal carbohydrate.
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Buschman, Heather Clair. "Novel roles for surface pili in streptococcal pathegenesis /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3311960.
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Nylander, Åsa. "Structural and functional studies of streptococcal surface adhesins." Doctoral thesis, Umeå universitet, Tandläkarutbildning, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-78920.
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The oral cavity is home to an array of microorganisms that are associated with dental plaque. Some Gram-positive bacteria are common inhabitants of the oral cavity and in order to colonize such a unique environment adhesion becomes essential and is accomplish by adhesins expressed on the bacterial surface. Adhesins can interact with host molecules or with structures on the resident oral microbial flora. Members of the antigen I/II (AgI/II) protein family are commonly found on the surface of oral streptococci and have the unique feature that their putative adhesin domain is located in the centre of the primary sequence. Crystal structures representing parts of the C-terminal domains from two AgI/II members, SpaP from Streptococcus mutans and AspA from Streptococcus pyogenes, were determined to 2.2 and 1.8 Å resolution respectively. The structures are very similar and consist of two domains with DEv-IgG folds. The proteins are stabilized by intramolecular isopeptide bonds and tightly coordinated metal ions. Another group of surface proteins is the microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) that have their putative adhesin domain in the N-terminal, presented on a stalk formed by multiples of repeated C-terminal domains. Sgo0707 from Streptococcus gordonii is an example of this group of proteins and its N-terminal domain was determined to 2.1 Å resolution. The structure consists of two domains, N1 and N2, both of which adopt β-sandwiches. In the Sgo0707 structure no isopeptide bonds or metal ions were detected. A putative binding cleft is present in the N1 domain. Functional studies revealed collagen type-1 and keratinocytes as possible binding partners. In order to further characterize the AgI/II protein AspA from S. pyogenes a long form of the protein, AspA-AVPC, was expressed and purified. During the purification process it was observed that the protein fragmented into two major parts. This process could be inhibited by the addition of 0.5 mM EDTA during protein purification. In conclusion, these studies have resulted in adding to the knowledge of protein structures and function of streptococcal surface proteins.
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Grahn, Eva. "Bacteriological aspects of treatment failures in streptococcal tonsillitis." Doctoral thesis, Umeå universitet, Klinisk bakteriologi, 1986. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-99340.
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ß-hemolytic streptococci persist in 10-25% of patients with acute streptococal tonsillitis (about 10.000-25.000 per year in Sweden) in spite of treatment with a recommended dosage and schedule of Phenoxymethylpenicillin. The aim of the study was to investigate different bacteriological factors involved in treatment failures of streptococcal tonsillitis. Patients included in the study were 33 patients who underwent tonsillectomy, 62 persons included in a tonsillitis epidemic outbreak, 267 tonsillitis patients contacting the ENT-clinic, Sahlgrenska Hospital, Göteborg, and 20 healthy volunteers taking Phenoxymethylpenicillin. It was found that the Steer's steel pin replicator was a useful tool to study interference between a- and ß-hemolytic streptococci and a guantitative differen ce in. the inhibitory capacity of the different a-strains was noted, a-streptococci with a strong inhibitory capacity on ß-streptococci were isolated mainly from individuals seemingly resistant to ß-streptococcal tonsillitis, while from patients with repeated tonsillitis no or low numbers of inhibiting a-streptococci were demonstrated. Patients with clinical treatment failure had less a-streptococci with inhibiting capacity on their own ß-streptococcal strain compared with the healthy carriers. These treatment failures also showed beta-lactamase activity in their saliva pellet significantly more often than patients in the control groups. In volunteers penicillin was released from ordinary sugar coated tablets already in the mouth resulting in a decrease of the a-strep- tococcal flora. A synergistic effect on ß-hemolytic killing by low concentration of penicillin and inhibition of a-streptococci was noted in vitro and in vivo. Penicillin tolerance was registered in most strains from the treatment failure group, but in none of the strains from the group of successfully treated patients. A co-operation between different bacteriological factors (bacterial interference, beta-lactamase production, penicillin tolerance) seems to be important in treatment failures of streptococcal tonsillitis.Diss. (sammanfattning) Umeå : Umeå universitet, 1986, härtill 6 uppsatser
digitalisering@umu
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Charlton, Fraser Graham. "Structure-function relationships of streptococcal pyrogenic exotoxin A." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285321.
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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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Dwivedi, Gaurav Dutta. "Cloning and Expression of Streptococcal Recombinant Protein G." Thesis, Umeå universitet, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet), 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-106723.
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Recombinant Protein G (rPG), an engineered form of streptococcal protein G with a theoretical molecular weight of 22.26 kDa was successfully cloned and expressed in E.coli BL 21(DE3) cells. The albumin binding domain was removed during the gene synthesis to avoid unspecific binding. This recombinant form of protein G contains only the IgG binding domains along with the 6X histidine tag at the N terminal. The removal of non-specific domains maximizes the specificity of IgG binding through the Fc region. The recombinant protein G was purified through heat treatment and using immobilized metal affinity chromatography (IMAC). On an SDS-PAGE gel there was only a single band of the purified preparation which migrated at 32 KDa, however when analyzed by mass spectrometry it was ~22.4 kDa, this phenomenon of retarded migration on SDS-PAGE has been known from previous studies. The production of recombinant protein has also been optimized. The effects of expression temperature, inducer type, inducer concentration and media composition have been investigated. The expression was done at 10 liter scale using the best expression conditions, and the protein was purified to homogeneity, dialyzed and lyophilized. The pure protein was immobilized on a POROS AL (Self Pack® POROS® 20 AL, Applied Biosystems, USA). The immobilized protein IgG binding has been monitored using a VersAFlo system. This system allowed real time monitoring of IgG binding characteristics.
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Orrling, Arne. "Recurrent streptococcal pharyngotonsillitis studies on etiology and treatment /." Lund : The Faculty of Medicine Lund University, 2006. http://theses.lub.lu.se/scripta-archive/2006/03/08/med_1274/arne_kappa.pdf.
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Bwanika, Harry Colyn. "Purification and crystallisation of streptococcal collagen binding proteins." Thesis, Umeå universitet, Kemiska institutionen, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-160858.
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Langshaw, Emma. "The immunopathogenesis of group A streptococcal skin disease." Thesis, Griffith University, 2017. http://hdl.handle.net/10072/373963.
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Group A Streptococcus (GAS, Streptococcus pyogenes) is a Gram-‐positive bacterial pathogen exhibiting human host exclusivity. GAS is responsible for a wide array of non-‐ invasive suppurative infections of the throat and skin, such as pharyngitis and pyoderma respectively. GAS is also capable of causing severe invasive diseases and post-‐streptococcal complications, each with high rates of morbidity and mortality. Epidemiological studies have demonstrated a high prevalence of pyoderma in tropical regions such as in northern Australia. Streptococcal skin infections are thought to be a significant risk factor for the development of rheumatic fever in Indigenous Australians within these tropical regions. The skin is also a common portal of entry for invasive GAS disease. The ability of GAS to cause these invasive diseases relies upon the timely expression of specific virulence factors enabling the bacteria to evade host immune responses. Several important virulence factors are under the transcriptional control of the CovR/S operon. GAS strains possessing a mutation within their CovR/S regulatory system are particularly adept at evading host immunity resulting in hypervirulence and an increased capacity for invasive disease. CovR/S wild-‐type (WT) and mutant (MT) GAS pairs were identified from a panel of clinical and laboratory isolates. Each CovR/S MT assessed possessed a different mutation within their CovR or CovS gene. It was observed that mice immunised with the M protein-‐derived vaccine candidate J8-‐DT/Alum were protected from local and systemic infections by the CovR/S WT strains; however, protection was significantly compromised for all mice infected with the CovR/S MT strains. Analysis of gene expression via RT-‐PCR revealed that each of the CovR/S MT isolates were up-‐regulating specific virulence factors, namely streptolysin O (SLO), SpyCEP, and the hyaluronic acid capsule, that enhanced their immune evasion capabilities. The increased gene expression by CovR/S MT strains observed using in vitro assays with increased red blood cell lysis, increased IL-‐8 chemokine degradation, and a greater production of hyaluronic acid. The virulence of these CovR/S mutant strains was then tested in the context of the redesigned J8-‐DT vaccine (J8-‐DT combined with an inactive 20-‐mer fragment from SpyCEP, ‘S2’). The J8 CombiVax (comprising J8 and S2 with four lysine residues, ‘K4S2’) afforded significantly better protection compared to J8-‐DT, as each of the CovR/S MT strains were unable to cause a systemic infection in a murine model of pyoderma in the immunised cohorts. The combination of two minimal epitopes provided a synergistic effect through the opsonic J8-‐specific antibodies and the S2-‐ specific antibodies neutralizing SpyCEP, and thus preserving IL-‐8-‐mediated neutrophil chemotaxis. Further investigation into the altered virulence profile of CovR/S mutants underscored SLO as an essential virulence factor for the pathogenesis of these hypervirulent strains. Utilising the CovR/S mutant 5448 (5448 MT) as a representative M1T1 GAS isolate, we generated several additional CovR/S mutants lacking SLO (ΔSLO) to investigate the contribution of this toxin to GAS virulence. The up-‐regulation of SLO by 5448 MT resulted in increased SLO-‐mediated hemolysis, decreased dendritic cell (DC) viability post-‐infection, and an increased production of pro-‐inflammatory cytokines TNF and MCP-‐1 under in vitro conditions. Further to this, it was observed that when SLO was absent from the isolate, the viability of infected DCs improved whilst inflammatory cytokine production decreased. This was despite the observation that infecting isolates still exhibited the characteristic CovR/S mutant virulence factor up-‐regulation of SpyCEP and the hyaluronic acid capsule. Moreover, histological analyses showed that DC presence was restored in murine skin post-‐infection with 5448 MT if SLO was absent from the strain. The presence of SLO correlated with systemic infection and severe pathology at the site of infection in a murine model of pyoderma. Conversely, the absence of SLO significantly attenuated the virulence of 5448 MT in vivo. J8 CombiVax immunisation was effective against all CovR/S mutant infections and provided significant systemic protection. Neutrophils have been shown to be critical in controlling GAS infection, and also for the protective efficacy of J8 CombiVax. Therefore, we sought to investigate the main cellular source of CXCL2, the primary murine neutrophil chemoattractant (a homologue of human IL-‐8) and target of SpyCEP-‐mediated proteolysis. We used a clinical isolate (NS88.2 MT) sourced from the Northern Territory of Australia that possessed a natural CovS mutation, in parallel with the genetically repaired isogenic CovR/S wild-‐type strain (NS88.2 Rep). Following cutaneous infection in a murine model, we observed hypervirulence of the NS88.2 MT strain and differential interactions with neutrophils between the NS88.2 MT and NS88.2 Rep strains. The NS88.2 Rep strain was observed via immunofluorescence analysis interacting with neutrophils in skin sections in vivo and also being killed by human neutrophils in vitro. Conversely, NS88.2 MT appeared to inhibit neutrophil ingress in vivo and proliferated in the presence of human neutrophils in vitro. RT-‐PCR revealed that NS88.2 MT significantly up-‐regulated its SpyCEP expression compared to NS88.2 Rep providing a likely causative factor for the observed differential neutrophil interactions. To specifically target the up-‐regulated expression of SpyCEP, mice were immunised with K4S2-‐DT/Alum. Whilst there was no significant protection against NS88.2 Rep or MT infection with K4S2 alone, spleen samples of immunised mice showed evidence of germinal centre formation post-‐infection, particularly in the context of NS88.2 MT, which was consistent with immunological boosting of K4S2-‐specific B cells by MT infection. Investigation into the cellular response of infection using intracellular staining (ICS) revealed that neutrophils were the primary source of CXCL2 in the skin. This in turn, enabled further recruitment of neutrophils to the site of the infection. This was highlighted by the significant increase in neutrophil abundance in K4S2-‐immunised cohorts compared to the non-‐immunised cohorts, suggesting that protection against SpyCEP-‐mediated cleavage through K4S2 antibodies in vivo contributes to the adaptive immune response against GAS skin infections. ICS also revealed that CXCL2+ve neutrophils were more abundant in the skin of CovR/S WT-‐infected mice compared to the skin of mice infected with the CovR/S MT NS88.2. Similarly, significantly higher levels of CXCL2 protein were found in the skin of mice infected with the CovR/S WT compared to those infected with the CovR/S MT by day 3 post-‐infection. The degradation of CXCL2 in vitro by NS88.2 Rep or NS88.2 MT supernatant was effectively inhibited by the addition of K4S2 anti-‐sera. Overall, the studies within this thesis highlight the hypervirulent nature of CovR/S mutant GAS and some of the mechanisms by which each strain can evade the host immune system. Gaining a greater understanding of host-‐pathogen interactions during GAS infections has enabled improved vaccine design strategies, such as the generation of vaccine candidate J8 CombiVax from J8-‐DT/Alum. J8, being a highly conserved cryptic epitope, in synergy with a 20-‐mer epitope from SpyCEP, provides protective coverage against GAS by neutralizing two of their most important virulence factors.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Institute for Glycomics
Science, Environment, Engineering and Technology
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Sanderson-Smith, Martina Louise. "Investigation of the role of the plasminogen-binding group A streptococcal M-like protein (PAM) in the pathogenesis of Streptococcus pyogenes." Access electronically, 2006. http://www.library.uow.edu.au/adt-NWU/public/adt-NWU20070821.125843/index.html.
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Filipe, Soares Renata. "Proteomic analysis of post-translational modification of streptococcal proteins." Thesis, King's College London (University of London), 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.618344.
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Eriksson, Björn K. G. "Invasive group A streptococcal infection : host and pathogen interactions /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3609-9/.
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Pointon, Jonathan Anthony. "Structure-function studies of group A streptococcal pilus subunits." Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1125.
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Streptococcus pyogenes (Group A Streptococcus, GAS) is an important Gram positive human pathogen that produces a multitude of virulence factors, including cell-surface pili that were first described shortly before the beginning of this project. Pili in M1 GAS strain SF370 mediate adhesion to human tonsil and skin and are composed of a single major protein subunit (Spy0128) forming the pilus shaft and two minor subunits (Spy0125 and Spy0130), whose roles had not been defined. This thesis reports combined molecular microbiology and protein structure studies that provide insights in to the structures and functions of the M1 GAS strain SF370 pilus subunits. Recombinant Spy0125 (rSpy0125), rSpy0128 and rSpy0130 were purified to apparent homogeneity and low resolution structures were obtained using a combination of biophysical techniques. Novel intra-molecular isopeptide bonds discovered in the Spy0128 crystal structure, reported by others during this project, were examined here for their affects on GAS adhesion. This was achieved by combining site-directed and allele replacement mutagenesis to introduce point mutations into the spy0128 gene in the GAS chromosome. Comparison of parent and mutant strains showed that these bonds were not essential for adhesion of GAS to human keratinocytes in vitro, though the pattern of adhesion appeared altered. Most of the work in this project focused on Spy0125, which was first localized at the tip of the pilus and shown to act as the adhesin. Allele replacement mutagenesis confirmed that the adhesin resided within a stable c. 50 kDa polypeptide corresponding to the Cterminal 2/3 of intact Spy0125. A recombinant version of this region, rSpy0125-CTR, was produced and its high resolution crystal structure determined. In addition to internal intra-molecular bonds similar to those recently found by others in Spy0128, the rSpy0125-CTR structure revealed an internal thioester bond between a Cys and a Gln residue that is unprecedented outside of complement and complement-like proteins. Whereas current paradigms of bacterial-host interactions suggest non-covalent forces are involved, the presence of a thioester in Spy0125 reveals for the first time that strong covalent forces may also play a role.
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Shahbazi, Daniel. "Investigating streptococcal biodiversity in sepsis using next-generation sequencing." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-16248.
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Sepsis is one of the leading causes for fatalities in the intensive care unit, and also one of the biggest health problems worldwide. It is a disease caused primarily by bacterial infections but can also be caused by viral or fungal infections. Since it is such a big health problem being associated with increased risk of sepsis, coupled with longer stays in the intensive care unit, the need for fast diagnosis and treatment is very important. Currently, culture is the leading diagnostic method for identification of bacteria, although other methods are currently being tested to improve identification time and decrease cost and workload. Next generation sequencing (NGS) has the capacity to output several million reads in a single experiment, making it very fast and relatively cheap compared to other older sequencing methods such as Sanger sequencing. The ability to analyze genes and even whole genomes, opens the possibilities to identify factors such as bacterial species, virulence genes and antibiotic resistance genes. The aim of this study was to find any possible correlations between 16 species of streptococci and clinical data in patients with suspected sepsis. Initial species identification was performed using MALDI-TOF before the samples were sequenced using NGS. Sequence files were then quality controlled and trimmed before being assembled. Following assembly, coverage was controlled for all assembled genomes before the downstream analysis started. Different tools such as 16S RNA species identification, multi locus sequence typing and antibiotic resistance finder were used, among other tools. The results were extremely mixed, with the overall quality of the data being of good quality, but the assembly and downstream analysis being worse. The most consistent species was S. pyogenes. No correlation between sepsis patients and relevant clinical data was found. The mixed quality of results from assembly and downstream analysis were most likely contributed to difficulties in culturing and sequencing of the streptococci. Finding ways to circumvent these problems would most likely aid in general sequencing of streptococcal species, and hopefully in clinical applications as well.
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Christie, Julie. "Fibronectin-interacting proteins in Streptococcus gordonii." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324360.
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Crowley, Ian F. "Intranasal Vaccination to Boost Equine Immunity to Uterine Streptococcal Infection." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/CrowleyIF2007.pdf.
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Ghassemifar, Sara. "Streptococcal mAb10F5 interacts with synaptic vesicles due to antiphospholipod activity." Virtual Press, 2008. http://liblink.bsu.edu/uhtbin/catkey/1398710.
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Hypermetabolism, observed in Sydenham's chorea (SC); a complication of acute rheumatoid fever (ARF) involving binding of streptococcal M protein antibodies in the brain, may result from an increase in glutamate release. The interaction of mAb 1 OF5, a specific M protein antibody subtype, with brain proteins (e.g. Rabphilin-3A), synaptic vesicles (SVs) and synaptosomal fraction (SF) was examined. Rat brain slices immunostained with mAb l OF5 revealed an interaction with choroid plexus and elements appearing to be neuropils. Dot blotting demonstrated an interaction of mAb I OF5 with both SVs and SFs. Western blotting revealed a smear from mAb 10F5 against the SF fraction. However, both modified SVs and pure liposomes examined by fluorescent and confocal microscopy bound mAbl0F5 suggesting a direct interaction with phospholipids. ELISA demonstrated binding of mAb1OF5 with negatively charged phospholipids involved in antiphospholipid syndrome (APS). Hypermetabolism and binding at the choroid plexus is observed in SC and APS supporting the connection between these disorders.Department of Physiology and Health Science
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Kennedy, Helen F. "Viridans streptococcal bacteraemia in paediatric immunocompromised patients with malignant disease." Thesis, University of Glasgow, 2001. http://theses.gla.ac.uk/2214/.
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Amongst the paediatric haematology/oncology patients attending the Royal Hospital for Sick Children, Glasgow, episodes of viridans streptococcal bacteraemia increased from 12% of al microbiologically documented bacteraemias (i.e. 10/81) in 1993 to 22% (18/83) in 1994. During the first year of this project (which started in December 1994), ITU support was required following the development of viridans streptococcal bacteraemia on 6 occasions, and of these, there were two fatalities. The overall aim of this study was to improve the management of this infection and to explore preventative strategies. Three different approaches were adopted: (1) an extensive epidemiological analysis was undertaken - to include all episodes of viridans streptococcal bacteraemia from December 1994 to December 2000. (2) Phenotypic, followed by genotypic analyses of isolates of viridans streptococci from mouth swabs and blood cultures were carried out to determine whether the mouth was in fact the source of organisms responsible for this infection. (3) Extensive antibiotic susceptibility studies were performed on all isolates of viridans streptococci from blood culture. In total, 69 episodes of viridans streptococcal bacteraemia occurred in 54 children. The infection was more often associated with patients with haematological malignancy (particularly AML), than those with solid tumours, and in the majority (84%) of episodes, the patients suffered from chemotherapy-induced mucositis or other forms of oral compromise. Forty-eight episodes of infection (70% of total) responded well to antimicrobial therapy with no evidence of additional clinical complications. However, in 21 cases (30% of total), pulmonary complications developed, with 8 of these requiring mechanical ventilation and supplemental oxygen. Five of these 8 cases also developed septic shock. S. oralis was the species most commonly isolated from blood culture (63% of total isolates of viridans streptococci) and S. mitis represented 25% of total isolates. Polymicrobial bloodstream infection occurred in 23% of episodes.
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Smith, Wendy D. "A functional genomic analysis of group A streptococcal virulence factors." Thesis, University of Newcastle Upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413953.
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Lau, Roxanne. "Characterisation of the streptococcal DNA polymerase I flap endonuclease domain." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/19951/.
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Spoerry, Christian. "Streptococcal immunoglobulin degrading enzymes of the IdeS and IgdE family." Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-134552.
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Bacteria of the genus Streptococcus are common asymptomatic colonisers of humans and animals. As opportunistic pathogens they can however, depending on their host’s immune status and other circumstances, cause mild to very severe infections. Streptococci are highly intertwined with specific host species, but can also cause zoonosis or anthroponosis in more uncommon hosts. Prolonged and reoccurring infections require immune evasion strategies to circumvent detection and eradication by the host’s immune defence. A substantial part of the immune defence against bacterial pathogens is mediated by immunoglobulins. This thesis is based on work to identify and characterise immunoglobulin degrading enzymes secreted by different Streptococcus species as a means to sabotage and evade antibody-mediated immune responses. Stoichiometric and kinetic analysis of the IgG degrading enzyme IdeS from the important human pathogen S. pyogenes revealed that IdeS cleaves IgG, opposed to previous publications, as a monomer following classical Michaelis-Menten kinetics. The IdeS homologue of S. suis, IdeSsuis, did however not cleave IgG, but was highly specific fo rporcine IgM. S. suis was found to possess yet another protease, IgdE, capable of cleaving porcine IgG. Both of these proteases were shown to promote increased bacterial survival in porcine blood during certain conditions. IgdE is the founding member of a novel cysteine protease family (C113). Novel streptococcal members of this protease family were shown to specifically degrade certain IgG subtypes of the respective Streptococcus species’ main host. The observed substrate specificity of IgdE family proteases reflects the host tropism of these Streptococcus species, thereby giving insights into host-pathogen co-evolution. The abundance of immunoglobulin degrading enzymes among Streptococcus species indicates the importance of evasion from the antibody mediated immune responses for streptococci. These novel identified immunoglobulin degrading enzymes of the IdeS and IgdE protease families are potential valid vaccine targets and could also be of biotechnological use.
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Pratt, Stephanie Ann. "Immunoglobulin A1 protease of Streptococcus pneumoniae." Thesis, University of Leicester, 1988. http://hdl.handle.net/2381/35410.
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The aim of this project was to examine the Streptococcal IgA1 proteases, with particular interest on the Streptococcus pneumoniae enzyme. IgA1 protease of S. pneumoniae was identified and characterised. A non-reducing polyacrylamide gel system was employed to screen clinical isolates for IgA1 protease activity. Of 187 isolates tested 18% were found to be IgA1 protease negative, there was no correlation with the site of isolation of the organism and its ability to produce the enzyme. Attempts were made to clone the pneumococcal IgA1 protease gene using the cosmid pEMBLcos4, the plasmid vector pLG339 and the ? replacement vector ?EMB4. Libraries were screened for pneumolysin and IgA1 protease activity. Clones that expressed pneumolysin were identified by overlaying with sheep red blood cells. One haemolytic clone was not inhibited in the presence of cholesterol. Screening for IgA1 protease activity identified clones with IgA1 protease-ike activity but this activity was not stably expressed. Closer analysis of the libraries suggested that pneumococcal DNA was highly unstable when cloned into E. coil plasmid and cosmid vectors.
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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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Hanage, William Paul. "Host microbial interactions in the pathogenesis of Viridans streptococcal septic shock." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272512.
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Lamb, Lucy Elizabeth Moffatt. "Group A streptococcal necrotising fasciitis and its association with blunt trauma." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/55260.
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Necrotising fasciitis (NF) due to invasive Group A streptococcus (iGAS) is frequently associated with emm1 isolates, with an attendant mortality of approximately 40%. Cases occur in previously healthy individuals with a history of upper respiratory tract infection, soft tissue contusion and no obvious portal of entry. Using a new model of mild contusion injury, we set out to determine the impact of contusion on iGAS bacterial burden, phenotype and host cytokine response. Firstly invasive bioluminescent GAS strains were developed using a replicative plasmid pTHLK but these were unstable in vivo. A stably bioluminescent M89 iGAS strain was developed using a plasmid pICL18Lux and characterised in vitro and in vivo models of invasive infection. Bioluminescence measured in vivo correlated with bacterial quantity but practical application to produce a lower respiratory tract infection or prolonged soft tissue infection was limited by detection of light production during infection. The new isolate was attenuated in growth and virulence and it could not be used to study the interaction of contusion and virulence. A new model of soft tissue contusion was developed that resulted in local soft tissue neutrophilic inflammation, no bony injury, systemic cytokine production or weight loss. The model of mild contusion was used to determine the impact of trauma on emm1 iGAS. Surprisingly, mild contusion did not provide a focus for initiation or seeding of bacteraemic GAS infection, but instead provided an environment that enhanced GAS dissemination to local lymph nodes. Dissemination was linked to a phenotypic change with the emergence of mucoid GAS colonies in lymphoid tissue, bloodstream and spleen. The mucoid GAS colonies in the lymph node demonstrated a significant increase in production of capsular hyaluronan and were not associated with covRS mutations. Whole genome sequencing was applied to understand the genetic change responsible, a selection of mutations occurring in the spleen and lymph node were discovered. The exact role of some of the mutations in the pathogenesis of dissemination of GAS and the influence of trauma is not entirely known and the subject of on-going investigation.
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Teles, Cristina Alexandra Ribeiro. "Antibiotic induced modulation of virulence factors associated with viridans streptococcal endocarditis." Thesis, Glasgow Caledonian University, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.547437.
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Kong, Fanrong. "Integrated study of group B streptococcus and human ureaplasmas � the paradigm shifts." University of Sydney. Medicine, 2004. http://hdl.handle.net/2123/592.
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Group B streptococcus (GBS, S. agalactiae) and human ureaplasmas (U. parvumand U. urealyticum) are two clinically and phylogenetically related, potential perinatal pathogens. Their relationships between genotypes and pathogenesis of GBS and ureaplasma infection were still not well understood, one of the reason is that both of them are still short of a very practical genotyping system. In the study, to solve the above problem we developed genotyping systems for the organisms (the second section). For human ureaplasmas, based on four genes/gene clusters (rRNAgene clusters, the elongation factor Tu genes, urease gene complexes and multiplebanded antigen genes), we designed many primer pairs suitable for developing species identification assays for the two newly established human ureaplasma species (U. parvum and U. urealyticum). Further, based on the heterogeneity of ureaplasma multiple banded antigen gene (which contains species- and serovar-specific regions), we developed genotyping methods for each ureaplasma species.For GBS, based on three sets of molecular markers (capsular polysaccharidesynthesis gene clusters, surface protein antigen genes and mobile genetic elements),we developed a genotyping system. The primary evaluation of the genotyping systems showed that the genotyping systems were practical alternative assays for the conventional serotyping and they will be useful to further explore the relationships between genotypes and pathogenesis of GBS and ureaplasma infection. In the study, we introduced novel data and tools into GBS and ureaplasma studies especially from genomic- and bioinformatics-based molecular microbiology(the third section). For two newly established human ureaplasma species, based on the U. parvum serovar-3 genome, and using the above four important genes/geneclusters, we exposed some interesting problems in the understanding of newureaplasma taxonomy especially in the post genomic era. For GBS, we studied the two published full genomes and exposed some new problems or possible future new research fields. In particular we found the two finished and one ongoing GBS genomes were all non-typical and suggest that future genomic project had better have genetic population structure viewpoint. Finally, we suggested that integrated studies of the two potential or conditional perinatal pathogens, from the viewpoint of evolution, would provide a new understanding angle of the pathogenesis of the two organisms. Studies suggested that during coevolution, human ureaplasmas(especially U. parvum) became friendlier than their ancestors to their human host (by losing most of its virulence genes); however, GBS tried to increase its invasive abilities (by getting more virulence genes) to fight against the human host attack.
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Leung, Chin-pang, and 梁展鵬. "Characterization of group a streptococcus in Hong Kong." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B3196963X.
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Stofile, P. Z. "Prevalence of Group B streptococcus and staphylococcus aureus colonization in the anogenital tract of pregnant women in the Eastern Cape Province, South Africa." Thesis, University of Fort Hare, 2017. http://hdl.handle.net/10353/5983.
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Neonatal sickness and death is increasingly becoming a public health problem worldwide. The colonization of Group B Streptococcus and Staphylococcus in the rectovaginal area is among the sources of infections in neonates which can result in illness and mortality. The over exposure of humans to antibiotics is the possible cause of resistance in bacteria. These resistant strains can be passed onto offspring, leading to resistant infections and increasing the morbidity of neonates because of treatment failures. Many people, including healthcare personnel are not aware of the effect of these bacteria, and informing clinics and hospitals can help create awareness and monitoring the levels of resistance among bacteria can assist in preventing the transference of the bacteria. In this study we investigated the prevalence of group B Streptococcus (GBS) and Staphylococcus aureus in the anogenital tract of pregnant women in the Eastern Cape Province, South Africa. A total of 49 isolates from 25 (30.5 percent) pregnant women colonized with GBS were isolated from vaginal and rectal swabs of 82 pregnant women at 25-37 gestation who participated in this study. These isolates were obtained using standard microbiological methods and confirmed by polymerase chain reaction (PCR) technique aimed at the ScpB gene. The isolates were further screened for the presence of 9 serogroups (Ia, Ib, II, III, IV, V, VI, VII, VII) and serogroups Ib 2 (4.8 percent), II 20 (40.8 percent) and IV 5 (10.2 percent) and 22 non-typable (44.9 percent) were identified. Susceptibility profiling of the isolates to 12 antibiotics (tetracycline, clindamycin, erythromycin, gentamycin, naladixic acid, norfloxacin, chloramphenicol, cefuroxime, cefotaxime, imipenem, penicillin and vancomycin) was tested in vitro by the standardized disc diffusion method. All the confirmed GBS isolates (49) were resistant to erythromycin, tetracycline and clindamycin. A higher percentage of the isolates were resistant to gentamycin 44 (90 percent), nalidixic acid 41 (84 percent), penicillin 41 (84 percent), chloramphenicol 38 (78 percent), cefuroxime 36 (74 percent), imipenem 36 (74 percent), cefotaxime 35 (71 percent), norfloxacin 32 (65 percent) and vancomycin 31 (78 percent). Multiple antimicrobial resistance patterns ranged from 9‒11 and indices ranged from 0.7‒0.9, respectively. Among the antimicrobial resistance determinants examined, genes encoding for resistance to erythromycin ermB 25 (51 percent), tetracycline tetM 32 (65 percent) and penicillin bla-Z 4 (8 percent) only were identified. On the other hand, screening for S. aureus yielded a total of 7 isolates from 4 study participants as confirmed by PCR based on staphylococcal, nuc gene. The isolates were further screened for the presence of six virulence genes (Hla, Hlb, LUKM, LUKED, PVL, Eta and Etb) and antibiotic susceptibility pattern by the disc diffusion method using 12 (penicillin, vancomycin, tetracycline, rifampicin, imipenem, gentamycin, chloramphenicol, norfloxacin, oxacillin, erythromycin and sulfamethoxazole-trimethoprim) antibiotics that are adopted in the treatment of infections caused by the organism. PVL 6 (85.7 percent) and eta 1 (14.3 percent) were the two virulence genes detected. The following percentages of antibiotics resistance among the isolates were observed; penicillin G 7 (100 percent), clindamycin 7 (100 percent), vancomycin 5 (100 percent), rifampicin 5 (71 percent), oxacillin 5 (71 percent), erythromycin 5 (71 percent) gentamycin 3 (43 percent), norfloxacin 3 (43 percent), sulfamethoxazole-trimethoprim 3 (43 percent), chloramphenicol 2 (29 percent), imipenem 1 (14 percent). Multiple antimicrobial resistance patterns ranged from 7‒8 and indices ranged from 0.6‒0.7, respectively. Genetic profiling of the resistance genes identified erythromycin ermB 5(71.4 percent), tetracycline tetM 5(71.4 percent) and penicillin bla-Z 1(14.3 percent) only. The findings from the study have revealed GBS and S. aureus colonization of pregnant women in the Eastern Cape Province, and these have great public health implications especially for the neonates who are mostly likely to be infected during birth. The unidentifiable multidrug resistant serogroups of GBS as well as resistant S. aureus limit the choice of drugs in the management of infections caused by these pathogens more so if transmitted to infants. Therefore asymptomatic pregnant women needed to be properly educated about the bacteria as well as the precautions that need to be taken.
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Herting, Egbert. "Surfactant treatment in neonatal group B streptococcal pneumonia : experimental and clinical studies /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3691-9/.
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Rox, Katharina [Verfasser], and Rolf [Akademischer Betreuer] Müller. "Natural compounds as pathoblockers of streptococcal infections / Katharina Rox ; Betreuer: Rolf Müller." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2015. http://d-nb.info/1165573938/34.
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Raja, Khairuddin Raja Farhana. "A computational approach to studying the evolution of streptococcal quorum sensing systems." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/a-computational-approach-to-studying-the-evolution-of-streptococcal-quorum-sensing-systems(85598abb-8085-4777-885b-160e99466148).html.
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For many years, researchers have studied the social lives of bacteria to understand intra- and inter-species interactions. Cell-cell communication, also known as quorum sensing (QS), is used by bacteria to coordinate their behaviour in response to environmental conditions. The QS system in Streptococcus species is well known to regulate competence. Studies show that Streptococcus pneumoniae has two homologous QS systems: 1) the competence (Com) system that regulates competence; and 2) a bacteriocin-like peptide (Blp) system that regulates the production of bacteriocins. Both functions are widespread in the genus. In S. pneumoniae, the Blp QS system shares a common ancestor and has similar features to the Com QS system. However, the evolutionary relationship between these QS systems remains obscure. SUCRE methodology was developed to identify the QS homologous genes in the streptococcal species. SUCRE uses four complementary approaches: homology search, putative gene finding, regulon construction, and evolutionary analysis. The performance of SUCRE was assessed in comparison with other orthology detection methods. SUCRE is precise in identifying the QS homologous genes and has similar performance to OrthoMCL. The QS system structures are found to be conserved across the streptococcal species. A streptococcal species phylogeny was constructed from the ribosomal and tRNA synthetase gene families. Using the QS genes identified from SUCRE and the streptococcal species phylogeny, the study infers the evolution of the QS systems in Streptococcus species. The study shows that the QS systems evolved as a regulon unit. The paralogous relationship between each of the QS systems suggests that duplication has a huge influence on functional divergence of the QS systems in the genus. Although, horizontal gene transfer (HGT) is commonly found in bacteria, little evidence is found to support that the effect of HGT on the functional divergence of the QS systems in this genus. However, the QS regulon genes of the same QS system are found to be non- vertically transferred across species that signifies that the HGT event promotes the sequence variation between these genes.
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Kan, Su-Yin. "The proline-rich repeat and thioester domains of streptococcal fibronectin-binding proteins." Thesis, University of St Andrews, 2014. http://hdl.handle.net/10023/6134.
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Streptococcus pyogenes is an important human pathogen. One of the most prominent virulence factors produced by S. pyogenes is SfbI, a surface adhesin composed of three domains: thioester domain (TED), proline-rich repeat domain (PRR) and fibronectin-binding repeat domain (FnBD). The structures and functions of TED and PRR and their contributions to the pathogenesis of streptococcal diseases are unknown. The interaction between PRR and its putative target, the intracellular actin cytoskeleton regulator Arp2/3, was investigated by both in vitro and in vivo studies. PRR was shown to inhibit Arp2/3-dependent actin polymerisation. The expression of PRR in HeLa cells caused disruption to the cytoskeleton of the cells. All data point towards a role of PRR in inhibiting the Arp2/3 complex but more evidence is needed to support this. The N-terminal domain of SfbI (TED) and four homologous domains from S. pyogenes, group G streptococci and Streptococcus pneumoniae were characterised by mass spectrometry, NMR spectroscopy and biochemical assays. All were shown to possess intramolecular thioester bonds, spontaneously formed between sides chains of Cys and Gln residues. Fibrinogen (Fg) was identified as the first binding target of bacterial TEDs with direct evidence that the thioester bond was involved in the interaction with Fg. A pull-down experiment using human plasma showed Fg is a specific binding partner of SfbI-TED. The binding sites were narrowed down to the thioester-forming Gln of SfbI-TED and Lys residues in the Fg-Aα chain, and binding potentially occurred via covalent isopeptide linkage. The data presented here suggest two new roles for SfbI, previously unknown in bacterial pathogenesis. The PRR may be the first bacterial inhibitor of the actin cytoskeleton acting by inhibiting the Arp2/3 complex. Thioester domains appear to be a shared common feature of surface proteins of many Gram-positive pathogens. They may form covalent crosslinks between bacteria and host tissue.
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Nooh, Randa M. S. "Maternal group B streptococcal colonization and preterm premature rupture of the fetal membranes." Thesis, University of Ottawa (Canada), 1994. http://hdl.handle.net/10393/9609.
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The problem. Group B Streptococci (GBS) are one of the most frequent causes of life-threatening infections in newly born infants, who acquire the micro-organism while passing through the genital tracts of their asymptomatic colonized mothers. Some previous studies have suggested that maternal genital colonization by GBS is associated with preterm rupture of the fetal membranes and preterm delivery. In this thesis both a prevalence study and a historical cohort study were conducted, to investigate the prevalence of maternal GBS colonization at 28 weeks of gestation, and whether there is an association between colonization and preterm rupture of the fetal membranes. Background information. Different rates for maternal GBS colonization during pregnancy have been reported, ranging from 4.6% up to 40%. The association between maternal GBS colonization and preterm rupture of the membranes has been reported in some studies, but other studies have not supported this view, which led to differsnces in opinions and the lack of a specific conclusion. The variations in the findings of these studies may have been due to several factors, which include differences in cultured sites and phase of pregnancy at which culture was obtained, in addition to the wide variations in the definition of premature rupture of the membranes used by various authors. (Abstract shortened by UMI.)
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Norton, Robert. "The detection of antibodies to group a streptococcal M protein in rheumatic fever /." Title page, table of contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09MD/09mdn887.pdf.
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