Dissertations / Theses on the topic 'Campylobacter jejuni'
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Pratt, Alisa Annabelle. "Antibiotic Resistance Determinants of Australian Campylobacter Jejuni & Campylobacter Coli Isolates." Thesis, Griffith University, 2008. http://hdl.handle.net/10072/366198.
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Campylobacter species are the most common cause of foodborne disease in Australia and many countries throughout the World. Although campylobacteriosis is usually self-limiting, severe cases and those in the young, elderly and immunocompromised require antibiotic therapy. Antibiotic resistant Campylobacter isolates however may prolong illness and increase the risk of invasive disease. Antibiotic resistance in Campylobacter is thought to have arisen through the selective pressure of exposure to antimicrobial agents in veterinary medicine or animal husbandry, leading to the acquisition and dissemination of antibiotic resistance determinants, and genetic elements that harbour such genes, amongst isolates.
Little was known about tetracycline and trimethoprim resistance in Australian campylobacters, including the presence of resistance genes and associated genetic elements. Aims of this study were therefore to identify in Australian Campylobacter jejuni and Campylobacter coli isolates i). Tetracycline resistant determinants and associated genetic elements, ii). Trimethoprim resistant determinants and associated genetic elements, and iii). Integron like structures and associated genetic elements.
High-level tetracycline resistance was observed in 46 C. jejuni and C. coli isolates, with MICs ranging from 32 to >256mg/ml. All isolates examined harboured the tetO gene, confirming that tetracycline resistance in Australian campylobacters is also due to the previously reported TetO determinant. While several studies have described a significant role for plasmids in tetracycline resistance, this study demonstrated that in the majority of isolates (78%), including two thirds of strains that harboured plasmids, resistance was due to chromosomally encoded tetO. Six C. jejuni isolates were able to transfer a tetO harbouring plasmid to another C. jejuni strain. Plasmids were detected in approximately 74% of resistant strains, and ranged in size from small to larger plasmids (21 - 50kb). ClaI profiling of plasmids revealed genetic diversity and indicated that the tetO gene may be carried by a variety of plasmids.
High level trimethoprim resistance (MICs of 1000mg/ml and >1000mg/ml) was observed in all isolates (>100) examined from a second collection of C. jejuni, C. coli and non-C. jejuni/coli spp. Just over half of isolates harboured plasmids indicating that plasmids may not be involved in trimethoprim resistance in campylobacters. Isolates were also examined for the presence of the previously identified Campylobacter associated trimethoprim resistance genes dfr1 and dfr9. Although these genes play a significant role in this resistance, only approximately 16% of strains examined putatively harboured dfr1, and dfr9 was not detected.
Integrons, antibiotic resistance gene acquisition and expression systems, play an important role in trimethoprim resistance due to carriage of dfr genes as inserted gene cassettes. Trimethoprim resistant Campylobacter isolates were examined for the presence of the intI1 and intI2 genes, encoding the class 1 and class 2 integrons. Only 5.56% of strains examined for intI1 putatively carried this gene, and only 1.67% of isolates examined for intI2 putatively carried intI2. Both putative intI1 positive and negative isolates produced a variety of amplicons, ranging in size from »210bp to >1.5kb, when analysed for gene cassette sequences inserted into class 1 integrons.
This study has contributed to the knowledge of tetracycline and trimethoprim resistance, including the presence of resistance genes and associated genetic elements, in Australian isolates of C. jejuni and C. coli.Thesis (Masters)
Master of Philosophy (MPhil)
Griffith University. School of Medical Science.
Griffith Health
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Deibel, Kurt Eugene. "A study of Campylobacter jejuni /." The Ohio State University, 1985. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487260135358.
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Guthrie-Irons, Colette. "Biofilm formation in `Campylobacter jejuni'." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.536794.
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Semchenko, Evgeny A. "Characterisation of Campylobacter jejuni Lipooligosaccharides." Thesis, Griffith University, 2012. http://hdl.handle.net/10072/366659.
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Campylobacter jejuni is a major bacterial cause of food-borne enteritis, and its lipooligosaccharide (LOS) plays an initiating role in the development of the autoimmune neuropathy, Guillain-Barré syndrome, by induction of anti-neural cross-reactive antibodies through ganglioside molecular mimicry. Herein we describe the existence and heterogeneity of multiple LOS forms in C. jejuni strains of human and chicken origin grown at 37°C and 42°C. The C. jejuni NCTC 11168 original isolate (11168-O) was compared to the genome-sequenced variant (11168-GS), and both were found to have a lower-Mr LOS form, which was different in size and structure to the previously characterized higher-Mr form bearing GM1 mimicry. The lower-Mr form production was found to be dependent on the growth temperature as the production of this form increased from ~5 %, observed at 37°C to ~35 % at 42°C. The structure of the lower-Mr form contained a Galβ1,3GalNAc disaccharide moiety which is consistent with the termini of the GM1, asialo-GM1, GD1, GT1 and GQ1 gangliosides, however, it did not display GM1 mimicry as assessed in blotting studies but was shown by NMR analysis to resemble asialo-GM1. The production of multiple LOS forms and lack of GM1 mimicry was not a result of phase variation in the genes tested for NCTC 11168 and was also observed in most of the human and chicken isolates of C. jejuni tested.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Institute for Glycomics
Science, Environment, Engineering and Technology
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Pacheco, Sophia A. "Identification of Campylobacter jejuni secreted proteins." Pullman, Wash. : Washington State University, 2010. http://www.dissertations.wsu.edu/Thesis/Spring2010/s_pacheco_021610.pdf.
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Hani, Eric. "Hippurate hydrolase gene of Campylobacter jejuni." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0001/NQ27943.pdf.
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Zilbauer, Matthias. "Innate immune defence to Campylobacter jejuni." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445170/.
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Campylobacter jejuni is the most prevalent cause of bacterial diarrhoea worldwide and is frequently associated with severe post-infectious complications such as the Guillain-Barre syndrome. Despite the serious health burden caused by the bacterium disease pathogenesis remains ill defined. Human (3-defensins (hBDs)), a family of epithelial antimicrobial peptides, are a major component of host innate defence at mucosal surfaces. In the present study we investigated the effect of C. jejuni on intestinal epithelial innate responses. Up-regulation of IL-8, hBD-2 and hBD-3 gene and peptide expression was observed in Caco-2 and HT-29 cell-lines in response to C. jejuni strains 11168H and 81-176. Furthermore, recombinant hBDs were found to exhibit potent bactericidal activity against C. jejuni suggesting a major role for these peptides in disease pathogenesis. Secondly, we aimed to identify host receptor(s) involved in sensing of C. jejuni and initiating innate defence. Given the invasive nature of infection, we investigated the potential role of cytoplasmic nucleotide-binding oligomerisation domain (NOD) proteins. Using small interfering (si) RNA targeting NODI and transfection of NOD2 overexpression plasmids, we identified NODI as a major pattern recognition receptor involved in mediating innate host defence to C. jejuni while NOD2 was found to play a minor role. Additionally, reduced NODI expression resulted in an increased number of intracellular C. jejuni thus highlighting a critical role for NODI mediated antimicrobial defence in limiting infection. In the final part of the study an ex-vivo model of C. jejuni infection using human intestinal biopsies was developed. Additionally, a vertical diffusion chamber system was utilised to improve culture conditions in C. jejuni infection models. In conclusion, this study highlights the important role of intestinal innate host defence to C. jejuni. The development of new and improved models of infections has the potential to provide previously unavailable opportunities to study C. jejuni disease pathogenesis.
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Wainwright, Laura. "The truncated haemoglobin of Campylobacter jejuni." Thesis, University of Sheffield, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419585.
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Ainsworth, Paul. "Chemotaxis signal transduction in Campylobacter jejuni." Thesis, University of Leicester, 2014. http://hdl.handle.net/2381/28667.
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The bacterium Campylobacter jejuni is the most common cause of food borne disease in the UK, causing a 5-7 day enteritis including profuse watery diarrhoea, abdominal pain, fever, headache and occasionally vomiting. In rare cases leading to the paralysing autoimmune disease, Guillain-Barré syndrome. C. jejuni are highly motile cells, propelled through the environment by flagella, their motility is directed through a behaviour called chemotaxis. Cells are able to detect attractants or repellents and reposition the cell accordingly. Chemotaxis is central to C. jejuni colonisation as non-motile and non-chemotactic mutant strains poorly colonise their usual hosts. In Escherichia coli chemotaxis is regulated by the Che proteins which form a two component phospho relay system. In previous studies In silico comparison of E. coli Che proteins identified homologues in C. jejuni, which display altered chemotactic phenotypes in Δche mutant strains. Studies of interactions between the Che proteins using bacterial and yeast two hybrid systems, suggested ways in which the homologues may interact, but to further discern these mechanisms required in vitro study. For the purpose of this study the C. jejuni Che homologues were cloned, expressed and purified, for use in in vitro experiments. Radiolabelled Phosphotransfer assays confirmed CheA as a histidine kinase, and demonstrated Pi transfer to the response regulators of CheY, CheV and CheA, in that order of preference. Affinity tag pull-down assays found the predicted decrease in affinity between phosphorylated CheY and CheA, but also an increase in the affinity of phosphorylated CheV for the receptor, TLP[subscript 1]. The results of this study confirm the two component backbone of the C. jejuni Che model, and suggest how CheV may regulate methylation adaption in a system devoid of a CheB response regulator.
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Morley, L. "Niche-adaptive evolution in Campylobacter jejuni." Thesis, Nottingham Trent University, 2014. http://irep.ntu.ac.uk/id/eprint/27913/.
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Campylobacter jejuni is the leading causative agent of human bacterial gastroenteritis. Human C. jejuni infection (campylobacteriosis) is frequently associated with poultry; through consumption of undercooked products, cross contamination from raw meats, or through direct contact with birds or their faecal matter, however it is established that poultry is not the sole cause of C. jejuni infection in humans. This research reveals new information on the MLST ST403 Clonal Complex, a previously identified C. jejuni lineage associated with the porcine host. ST403CC C. jejuni have also been linked with other mammalian hosts to a lesser degree, and have been implicated in human campylobacteriosis, however to date this clonal complex has not been linked to poultry. The original hypothesis of this research predicted that due to sharing a host niche commonly associated with C. coli, the porcine ST403CC may show evidence of increased recombination with C. coli, however this was not observed. Six ST403CC isolates of porcine origin were subjected to phenotype testing and whole genome sequencing; these isolates were capable of invasion in vitro, and were revealed both to have acquired seemingly lineage specific content, in the form of Restriction-Modification (R-M) system associated genes, and to have undergone degredation of certain loci. The ST403CC isolates also exhibited a distinct pattern of reduced genomic recombination compared to non-ST403CC C. jejuni, with evidence of lineage specific recombination events. Both generalist & specialist lineages have previously been revealed in C. jejuni. The research presented here identifies a new specialist lineage which is associated with mammalian hosts, and not found in poultry.
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Hartley, Lauren Elizabeth. "Characterisation of the Aspartate Chemosensory Receptor of Campylobacter jejuni." Thesis, Griffith University, 2009. http://hdl.handle.net/10072/366822.
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Campylobacter jejuni is a highly motile bacterium that responds via chemotaxis to environmental stimuli to migrate towards favourable conditions. Previous in-silico analysis of the C. jejuni strain NCTC 11168 genome sequence identified ten open reading frames, tlp1-10, that encode putative chemosensory receptors. This study describes the characterisation of the role and ligand specificity of the Tlp1 chemoreceptor of C. jejuni 11168-0 (Cj1506c).Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Shaheen, Bashar Wajeeh. "In vitro survival of Campylobacter jejuni and Campylobacter coli at low Ph." Auburn, Ala., 2006. http://repo.lib.auburn.edu/2006%20Spring/master's/SHAHEEN_BASHAR_0.pdf.
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Stiller, Christiane. "Zum Vorkommen von Campylobacter jejuni und Campylobacter coli in Rohmilch von Erzeugerbetrieben in Nordbayern mit Versuchen zur Überlebensfähigkeit von Campylobacter jejuni in Milch." [S.l. : s.n.], 1999. http://www.diss.fu-berlin.de/1998/88/index.html.
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Esson, Diane Alison Ross. "Genetic basis of spirality in Campylobacter jejuni." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708477.
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Gormley, Fraser James. "The epidemiology of Campylobacter jejuni and Campylobacter coli in north east Scotland." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25813.
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Adler, Linda [Verfasser]. "Autoinducer 2 in Campylobacter jejuni / Linda Adler." Berlin : Freie Universität Berlin, 2016. http://d-nb.info/1096221179/34.
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Flint, Annika. "The Oxidative Stress Defenses of Campylobacter jejuni." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32073.
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Campylobacter jejuni infection is one of the leading causes of gastroenteritis in humans worldwide. During colonization of the gastrointestinal tract, C. jejuni will be unavoidably exposed to reactive oxygen species (ROS) produced by the host immune system and other intestinal microbiota. Identification of defenses against ROS is therefore important for understanding how Campylobacter survives this environmental stress during infection. Construction of isogenic deletion mutants into genes encoding potential oxidative stress defense systems followed by phenotypic screening revealed genes important for oxidant defense within C. jejuni. Surprisingly, genes involved in motility were found to play an indirect role in resistance to oxidative stress. Deletion of the flagellar motor apparatus genes, motAB, resulted in increased sensitivity towards superoxide which could be restored by fumarate supplementation or tandem deletion of motAB with ccoQ (cytochrome c oxidase). This finding suggested that disruption of the proton gradient across the inner membrane resulted in increased superoxide production in non-motile flagellar mutants. Phenotypic screening of the mutant library also identified a novel gene (cj1386) specifically involved in hydrogen peroxide defense within the cell. Hydrogen peroxide detoxification within living organisms is predominantly carried out by catalase enzymes. Interestingly, cj1386 is located directly downstream from katA (catalase) in the C. jejuni genome and it was found that a ∆cj1386 mutant had reduced catalase activity relative to wild-type C. jejuni. Immunoprecipitation of KatA from ∆cj1386 revealed a significant reduction in hemin content associated with KatA suggesting a role for cj1386 in hemin trafficking to KatA. Hemin binding experiments with purified Cj1386 demonstrated the ability of Cj1386 to bind hemin with a 1:1 hemin-to-protein binding ratio. Furthermore, co-immunoprecipitation experiments revealed an interaction between KatA and Cj1386. Mutagenesis of conserved amino acids in Cj1386 demonstrated that tyrosine 57 plays an important role in hemin affinity and is required for proper hemin content of KatA within the cell. Overall, this work provides a global characterization of key oxidant defenses within C. jejuni and provides one of the first studies investigating hemin trafficking to KatA.
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Bras, Ana Maria Leao da Silva. "Campylobacter jejuni virulence mechanisms : characterisation and regulation." Thesis, University of Leicester, 1998. http://hdl.handle.net/2381/30303.
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Campylobacter jejuni is a major cause of gastrointestinal illness throughout the world. Despite its importance as a human pathogen, the current understanding of C. jejuni virulence mechanisms or the means by which the bacterium regulates the expression of virulence remains limited. In this thesis, two different areas were investigated and are presented separately. In Part I, studies focused on the characterisation of C. jejuni translocation across an epithelial-like barrier. It was previously demonstrated that many strains of C. jejuni are able to translocate across polarised Caco-2 cell monolayers. A small number of these strains are not detectable within cells but are nevertheless able to translocate across the monolayer, presumably using a paracellular route. The possibility of paracellular translocation (without invasion) was investigated by looking at changes in the permeability across differentiated Caco-2 cell monolayers. The data obtained suggest that C. jejuni does not significantly alter the permeability of the monolayer, causing no permanent damage to the host cells, at least in the short term. In the long term, however, C. jejuni infection leads to a drop in the monolayer resistance, suggesting host cell damage. Although paracellular translocation seems unlikely to occur in the early stages of infection, it may occur later as consequence of host cell damage caused during invasion. In Part n, studies focused on the role played by the environment on the regulation of C. jejuni virulence. Two-component regulatory systems are involved in the regulation of numerous cell functions in response to environmental stresses, including virulence. Recently, the polymerase chain reaction with degenerate oligonucleotide primers was used to isolate regulatory genes responsive to environmental stimuli. The fragment isolated was identified as homologous to the members of the family of response regulators. The DNA fragment was subsequently used to probe a genomic library. The complete gene, regXl, was isolated, sequenced and mutated. In order to determine the role of regXl in C. jejuni, the phenotype of two regXl mutants was investigated. The results suggest that RegXl may respond to changes in temperature and that RegXl may be involved in the control of genes related to growth, host cell interaction and in vivo colonisation. Furthermore, a putative histidine protein kinase partner to RegXl was identified downstream regXl.
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Lodge, Karen, and karen lodge@rmit edu au. "A Molecular Investigation of Campylobacter jejuni Pathogenesis." RMIT University. Applied Sciences, 2007. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080229.151747.
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Campylobacter jejuni is one of the leading bacterial causes of human gastroenteritis world wide and has been linked to several severe complications including autoimmune syndromes which can result in paralysis. Despite being the subject of much study, C. jejuni remains a major public health burden in both developing and developed nations. There is currently no vaccine available for protection against this pathogen and the mechanisms important for C. jejuni pathogenesis are not fully defined. This study has employed a range of experimental approaches to investigate the molecular mechanisms involved in C. jejuni pathogenesis. Lipooligosaccharides (LOSs) are surface structures and known virulence factors of C. jejuni which are involved in serum resistance, resistance to phagocytic killing, endotoxicity and adhesion. Mutagenesis studies targeting the putative LOS biosynthesis genes wlaRF, wlaTA, wlaTB, wlaTC and waaV were performed in order to characterise the proteins encoded by each of these six genes and assess their potential role in C. jejuni pathogenesis in vitro. The gene product of wlaTA was found to be essential for C. jejuni survival and therefore a knock out mutant could not be generated. Phenotypic characterisation of four knock-out mutants confirmed that each gene contributed to the construction of the LOS molecule as all four mutants produced a truncated LOS moiety and altered their immunoreactivity. Further analysis determined that the production of complete LOSs was important for C. jejuni to invade and adhere to both human and chicken cells in vitro. This study identified a link between the inactivation of two LOS biosynthesis genes and the loss of motility, another important virulence factor. A major source of human C. jejuni infection is contact with contaminated poultry. However, C. jejuni exists as a commensal in chickens. It is currently not known why C. jejuni is pathogenic to humans and not to chickens and the differences between these two hosts represent pathogenic and non-pathogenic environments respectively. These environmental differences were exploited in this study. The four conditions investigated were temperature, blood, bile and host cells in vitro. Five different C. jejuni strains (NCTC11168, 81116, HB93-13, a recent human enteritis isolate and a recent chicken isolate) were subjected to modelled
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Phongsisay, Vongsavanh, and vongsavang@yahoo com au. "Campylobacter jejuni and the Guillain-Barré syndrome." RMIT University. Applied Sciences, 2006. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20061221.100446.
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Campylobacter jejuni is an enteric bacterium that causes human gastroenteritis worldwide. Some C. jejuni strains exhibiting human ganglioside-like lipooligosaccharide (LOS) structures, such as GM1 ganglioside, can induce an autoimmune neuropathy of the peripheral nervous system known as the Guillain-Barré syndrome (GBS). This GBS-inducible determinant is encoded by a gene cluster, which shows a high degree of variation among C. jejuni strains. The experiments presented in this thesis were conducted to give a better insight into the LOS synthesis genes in relation to the pathophysiology of C. jejuni. Firstly, a C. jejuni strain without GM1-like molecules was shown to be able to take up large DNA fragments, including LOS synthesis genes, from a strain expressing GM1-like molecules and consequently be transformed into a number of potential GBS-inducible transformants, which exhibited a high degree of genetic and phenotypic diversity. The ability of C. jejuni to take up and integrate foreign DNA explains the genome plasticity observed in this pathogen. Secondly, while attempting to analyse transcription of the LOS gene cluster, neither published methods nor any commercially available kits for RNA isolation could produce DNA-free RNA from C. jejuni. Combinations of these methods were trialled and only the combination of RNAzolB, TURBO DNase treatment, and acid phenol extraction was able to produce DNA-free RNA. The RNA isolated from most C. jejuni strains showed different RNA patterns to that of other bacteria. In addition the RNA from C. jejuni seemed closely associated with DNA compaired to RNA from other organisms. This might be caused by species-specific DNA conformation or chromatin structure. Thirdly, bidirectional transcription was observed in the LOS gene cluster. Both DNA strands were transcribed but transcription of the non-coding strands was at a lower rate, and both sense and antisense transcripts of each LOS gene tested were responsive to acid stress. This unusual transcription might have a potential effect on the expression of the GBS-inducing determinant. Finally, one of the LOS genes, the htrB gene, was further analysed. It was shown that expression of the htrB gene affects morphology, viability, growth ability, and sensitivity to stress environments. These results showed that the LOS molecule of C. jejuni is involved in many processes and is an important molecule for survival.
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Szymanski, Christine Mary. "Interactions between Campylobacter jejuni and the host." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21644.pdf.
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Marchant, Joanna Elizabeth. "Studies into the chemotaxis of Campylobacter jejuni." Thesis, Queen Mary, University of London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313661.
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Miller, Claire Elizabeth. "Iron acquisition from transferrins by Campylobacter jejuni." Thesis, University of Leicester, 2009. http://hdl.handle.net/2381/9918.
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Iron acquisition is vital for intestinal colonisation by Campylobacter jejuni. Characterisation of a number of iron uptake systems has occurred recently, allowing advancement in the understanding of the iron sources that C. jejuni utilises and how this occurs; however, the molecular basis of iron uptake from host iron-binding glycoproteins, the transferrins, is not known. The research presented here confirms that C. jejuni can use iron from the transferrins for growth and further characterises this process and the factors involved. Iron uptake from the transferrins requires proximity and appears to be receptor specific. Binding of lactoferrin to the cell surface is iron-responsive. Cj0178, a protein similar to TonB-dependent receptors, is required and the involvement of the enterochelin outer membrane receptor protein CfrA, FeoB, the ferrous iron inner membrane transporter, and the ABC transporter system Cj0175c-Cj0173c was also indicated. Less lactoferrin bound to cells without Cj0178 and complementation of the cj0178 mutation was successful. A role for Cj0178 in the uptake of haem was not demonstrated. Regulation of the genes cj0176c-cj0173c and cj0177-tonB1 was shown to require Fur and promoter activity levels increased under iron-restriction. The presence of two Fur-boxes indicated separate regulation of the operons. The catecholamine stress hormone noradrenaline augmented the growth of C. jejuni in the absence and presence of iron and in the presence of the transferrins, but was non-essential. A model is proposed of how transferrin-bound iron is used by C. jejuni. The process appears to be novel, involving a number of systems, but further work is required to confirm how they interact. The system through which noradrenaline may supply iron was investigated; however the mechanisms involved require further characterisation. The involvement of Cj0178 implies that the uptake of transferrin-derived iron is important for successful colonisation, which is vital for establishing an infection.
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Sandhu, Randeep. "The transducer-like proteins of Campylobacter jejuni." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/9910.
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Campylobacter jejuni is the leading cause of gastrointestinal disease in the developed world. Chemotactic motility is a pre-requisite for intestinal colonisation by C. jejuni. In silico analysis of the C. jejuni NCTC 11168 genome identified homologues of 10 chemotaxis receptor and two aerotaxis genes. Six of the ten putative Transducer-like proteins (Tlp 1, 2, 3, 4, 7 and 10) resemble chemoreceptors of Escherichia coli. The aim of this project is to characterise the C. jejuni Tlp1-4 chemoreceptors. The genes encoding the Tlps were inactivated using an insertional inactivation strategy. Isogenic mutants were made in tlp1, tlp2 and tlp4; a final mutant in tlp3 could not be obtained. A tlp1 complement was also constructed in this work. The tlp1 mutant showed reduced chicken colonisation ability when tested by our collaborators. Chemotactic phenotypes of the tlp mutants were determined in the swarm assay; the tlp mutants appeared defective for chemotaxis when compared with the wild-type and non-motile flaAB mutant. The Capillary assay and Hard-Agar Plug (HAP) assay were developed as methods to ascertain the ligand specificities of the Tlp chemoreceptors under study. Unfortunately, the Capillary assay proved to be insufficiently reproducible for effective use with C. jejuni. The HAP procedure was optimised using a C. jejuni wild-type motile variant. Positive chemoattractant responses were observed in NCTC 11168 for the first time towards a range of chemicals. Data derived from the modified HAP assay indicated that Tlp1 may be the receptor for serine. Chemotactic responses could not be detected in the tlp2 and tlp4 mutants in the HAP assay. The signalling domain of Tlp1 was purified using a polyhistidine tag and used to produce a polyclonal antibody. The Tlp1 primary antibody and immunofluorescence labeling has shown for the first time that the Tlps cluster at the cell poles in C. jejuni.
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Jennings, Claire Elizabeth. "Recovery of Campylobacter jejuni from cold storage." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323454.
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Kelly, Alison Faith. "The survival and recovery of Campylobacter jejuni." Thesis, University of Reading, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312567.
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Kamal, Nahid. "Regulation of flagellar biogenesis in Campylobacter jejuni." Thesis, University of Birmingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422295.
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Campylobacter jejuni, the cause of acute bacterial enteritis, is a Gram-negative, microaerophilic, spiral bacterium. The single polar flagellum of the organism has an important role inc ausing disease. In the published genome a nnotation of C. j ejuni some of the key regulatory flagellar genes are missing. Therefore the regulatory control of flagellar biogenesis is still not clear in the organism. FliK, the protein that controls the length of the flagellar hook and is also involved in switching of secretory pathway specificity in Salmonella, is among the regulatory proteins missing in the organism. We have identified the missingjliK gene in C. jejuni, which is Cj0041, and the homologue in its close relative Helicobacter pylori, HP0906. Although the protein encoded by Cj0041 is not readily identified by BLAST search against the major databases, a BLAST query of the C. jejuni genome database (Sanger Institute) with the FliK sequence from Aeromonas hydrophila identifies the Cj0041 gene product at E=0.056. Cj0041 knock-out mutants in two strains (NCTC11168 and 81116) 0 f C. jejuni were non-motile and showed a polyhook phenotype, which is in line with that of FliK mutants in Salmonella. SDS PAGE and mass spectrometry analysis with 'flagellar' filament proteins from Cj0041 mutants revealed increased production of FlgE hook protein in mutants compared to wild-type and indicated the synthesis of these polyhooks with mainly FlgE proteins. Microarray analysis of these mutants, verified by real-time PCR, showed overexpression of flagellar and other regulatory genes dependent on cr54 , one of the sigma factors involved in flagellar biogenesis, and provided a clear delineation of the cr54-dependent regulon. These results established the importance of Cj0041 or jliK in regulation of flagellar biogenesis in C. jejuni. We also have established by two-hybrid analysis the roles of Cj 1464 as jlgM and Cj 1465 asjlgN, two other key missing genes in the gene annotation of the organism. The roles of other flagellar genes such asjliS,jliD and Cj0848c were also studied to get a clear picture of flagellar biogenesis in C. jejuni. This study established that the organism shares most of the key regulatory flagellar genes found in model organisms like Salmonella and made it possible to define the regulation of flagellar biogenesis in C. jejuni more clearly than it has been described to date.
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Vaz, Diana Filipa Pereira. "Insights into Campylobacter jejuni Desulforubrerythrin catalytic mechanism." Master's thesis, Faculdade de Ciências e Tecnologia, 2013. http://hdl.handle.net/10362/10812.
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Dissertation presented to obtain the Master Degree in Molecular Genetics and BiomedicineThe following work aims to contribute to a better understanding of systems involved in resistance to oxidative stress species, namely hydrogen peroxide. The work is focused in one protein from the pathogen Campylobacter jejuni: desulforubrerythrin. Desulforubrerythrin is a non-heme iron protein in which the catalytic centre harbours a diiron cluster. Besides, the protein has a desulforedoxin domain at the N-terminal and a rubredoxin domain at the C-terminal. With the objective of understanding the protein catalytic mechanism three site-directed mutants, as well the wild type protein, were over expressed in Escherichia coli, purified and studied through biochemical and spectroscopic techniques. The amino acid residues selected for mutations are two tyrosines near the catalytic centre (residues 59 and 127). These residues are strictly conserved in rubrerythrins; moreover in diiron centres containing proteins tyrosines play a role in dissipating oxidizing species of iron (IV) by forming a tyrosil radical. The selected residues were replaced by a phenalanine residue which gave rise to three mutants: Y59F, Y127F and Y59F Y127F. These were characterized having as reference the wild type protein. All proteins have a molecular mass of 24 kDa and are tetramers in solution. The EPR and UV-visible techniques confirmed the presence of the three metallic domains in the wild type and Y59F mutant. The Y127F mutant was successfully used to test a protocol for diiron centre reconstitution in desulforubrerythrin. Finally, crystals of the wild type and, for the first time, of the Y59F and double mutants were obtained. The X-ray data for the mutants were collected with a resolution of 1.9 Å and its structure will be determined.
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Mustafa, Kasem Hamed. "Survival of Campylobacter jejuni in the environment." Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3000171/.
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Campylobacter jejuni is an emerging food borne pathogen and a successful human pathogen, with the infection mostly transmitted to humans through consumption of contaminated under-cooked poultry meat. However, the environment can also play a role in transmission either directly or indirectly to humans. The microorganism has reservoirs in water and various animals. Its survival outside the host is generally thought to be poor, but the organism survives well in poultry meat. Previous studies have suggested that the ability to survive may vary between different strain types of C. jejuni. A number of survival experiments were conducted, based on the ability of different C. jejuni strains to retain culturability in sterile distilled water. These experiments demonstrated that survival varies between different strains of C. jejuni and that the retention of culturability was much better at low temperatures (4 °C) than higher temperatures (25 °C). Survival was also better in non-autoclaved natural water. One strain, C. jejuni M1, lost culturability more quickly at both temperatures than the others tested. However, cells remained viable in these samples, suggesting that the bacteria had entered into a viable but non-culturable (VBNC) state under stress conditions. These variations may contribute to the transmission of C. jejuni from the environment to humans or farm animals. Using end-point and Q-PCR assays, a set of stress response genes, including genes implicated previously in the formation of VBNC cells, were targeted for different C. jejuni strains during survival in sterile distilled water. Differences in gene expression between different strains of C. jejuni were identified, including in key genes (luxS, htrA, ppk1), suggesting that these genes might have contributed to strain M1 switching to a VBNC state in response to starvation (sterile distilled water). This is the first report suggesting a role for the C. jejuni luxS (a gene likely to be involved in quorum sensing) in the formation of VBNC state and survival in water. Co-existence with other microorganisms, such as Pseudomonas spp., is one of the suggested survival strategies of C. jejuni in the environment. In a small study using environmental PCR assays, it was demonstrated that when C. jejuni is present in the farm environment, Pseudomonas spp. are also always present. In preliminary in vitro experiments, we demonstrated that some fluorescent Pseudomonas spp. could secret proteinaceous products that enhance the growth of Campylobacter. In natural environments, it is likely that interactions with other species, such as Pseudomonas, play an important role in C. jejuni survival and subsequent transmission to humans or animals.
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Turonova, Hana. "Adaptation de Campylobacter jejuni à l’environnement alimentaire." Nantes, 2015. http://www.theses.fr/2015NANT071F.
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C. Jejuni est couramment rapporté comme l’agent majeur responsable d’entérites bactériennes d’origine alimentaire dans les pays développés. En dépit de ses exigences pour sa croissance et son génome de petite taille, C. Jejuni développe des stratégies pour contourner les stress rencontrés lors de la transformation des aliments et limiter ainsi une perte de viabilité et de virulence. . Contrairement à d’autres pathogènes Campylobacter est dénué du facteur RpoS intervenant dans la réponse globale aux stress et dans la transition vers la phase stationnaireC. Jejuni has been continuously reported as the major cause of foodborne bacterial enteritis in developed countries. Despite its fastidious growth requirements and relatively small genome, C. Jejuni has developed strategies to overcome stress during food processing without permanent loss of viability and virulence. Unlike other pathogens, Campylobacter lacks the sigma factor RpoS responsible for global stress response and switch to stationary phase
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Bronnec, Vicky. "Etude de la réponse au stress oxydant chez Campylobacter jejuni : exemple de la souche aérotolérante C. Jejuni Bf : Approches phénotypique, génomique et de ChIP-Seq intégrées pour mieux comprendre l’aérotolérance de cette souche." Nantes, 2016. http://www.theses.fr/2016ONIR084F.
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Campylobacter jejuni est la première cause mondiale de toxi-infections bactériennes d'origine alimentaire. Ce pathogène est en mesure de survivre dans des environnements divers. Du tube digestif des volailles, son réservoir naturel, jusqu'à l'assiette du consommateur, C. Jejuni doit développer divers mécanismes afin de survivre aux environnements hostiles. Le développement d'un biofilm représente une stratégie adaptative pour survivre dans ces environnements et en aérobiose. Une souche clinique, C. Jejuni Bf, isolée au laboratoire, présente la particularité unique dans l'espèce de croître en aérobiose. Elle a donc été utilisée comme modèle pour mieux décrire les mécanismes de résistance au stress de C. JejuniCampylobacter jejuni is leading cause of bacterial foodborne infections in the world. This pathogen is able to survive in various environments. From the digestive tract of poultry, its natural reservoir, to the consumer's plate, C. Jejuni must develop several mechanisms to survive in hostile environments. Biofilm formation is an adaptative strategy to survive in these environments and under aerobic conditions. A clinical strain, C. Jejuni Bf, isolated in our laboratory, has the unique feature in the species to grow aerobically. It has been used as a model to better describe the mechanisms of stress resistance in C. Jejuni
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McTavish, Sharla. "Comparative analysis of New Zealand campylobacter isolates using MLST, PFGE and flaA PCR RFLP genotyping : a thesis submitted to the Victoria University of Wellington in partial fulfilment of the requirements for the degree of Master of Science in Molecular Microbiology /." ResearchArchive@Victoria e-Thesis, 2008. http://hdl.handle.net/10063/413.
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Lewis, Sally O'Donovan Gerard A. "Development of a real-time PCR assay for the detection of Campylobacter jejuni and Campylobacter coli." [Denton, Tex.] : University of North Texas, 2009. http://digital.library.unt.edu/permalink/meta-dc-9840.
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Calderon-Gomez, Lirio I. "Characterisation of Campylobacter jejuni Genes Involved in Aerobic Respiration." Thesis, Griffith University, 2012. http://hdl.handle.net/10072/365229.
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Campylobacter jejuni is an important pathogen that causes human bacterial gastroenteritis worldwide and can colonise the intestinal mucosa of all food-producing animals. Under such conditions C. jejuni is able to tolerate a variety of stresses, which they must in order to permit their transmission to a suitable environment for growth. C. jejuni is an obligate microaerophile, with the ability to survive in oxygen conditions and the natural environment indicating a potential to carry out aerobic respiration. This, in principle, allows growth in the absence and presence of oxygen. Despite its importance, effective control of Campylobacter spp. in the food chain and the design of disease prevention strategies are restricted by a poor understanding of the genetics, physiology and virulence of this organism. Therefore, to gain a greater understanding of its survival in different environments, it is important to understand how the respiratory pathway functions in C. jejuni in order to gain a greater
understanding of its physiology.
C. jejuni encodes a large respiratory enzyme complex, named NDH-I or complex I, which is composed of 14 different genes designated as the nuo operon. These genes are clustered in a conserved order in bacteria like Escherichia coli and Paracoccus denitrificans, however in C. jejuni the subunits nuoE and nuoF have been replaced by two subunits of unknown function, designated NuoX and NuoY (encoded by cj1575c and cj1574c genes respectively).Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Institute for Glycomics
Science, Environment, Engineering and Technology
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de, Mello Indaue Ieda Giriboni. "Factors affecting growth and culturing of campylobacter jejuni." [Gainesville, Fla.]: University of Florida, 2002. http://purl.fcla.edu/fcla/etd/UFE0000575.
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Bolton, Frederick James. "Isolation, growth and epidemiology of Campylobacter jejuni/coli." Thesis, University of Central Lancashire, 1985. http://clok.uclan.ac.uk/20060/.
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A selective blood agar (SBA) and a selective blood enrichment broth (SBEB) containing polymyxin (5,000 iu/l), trimethoprim (10 mg/i), rifampicin (10 mg/l) and cyclohexamide (100 mg/l) have been developed. Results from a comparison with four other media showed that the SBA gave the most isolations and was the most selective. Enrichment culture using SBEB achieved additional isolations. The SBEB was used in a most probable number (MPN) method which detects as few as 10 campylobatters/tOO ml of water. A glass microfibre filtration system was even more sensitive. A blood-free non-selective agar (BFNSA) containing charcoal (0.4%), ferrous sulphate (0.025%) and sodium pyruvate (0.025%) was also developed. These supplements were shown to detoxify rather than enrich the basal medium. A blood-free selective agar (BFSA) was produced by incorporating cephazolin (10 mg/i) and sodium deoxycholate (0.1%). This medium and the SBA gave similar isolation rates from faecal specimens when incubated at 42 0C for 42h but the BFSA was less selective. A blood-free selective enrichment broth (BFSEB) containing sodium metabisulphite (0.05%) gave slightly fewer Campylobacter isolations than the SEES when evaluated with various types of specimens and was also less selective. Maximum isolation rates were achieved by incubating broths at 42 0C and subculturing after 24h and 42h. Growth studies of three Campylobacter strains in four enrichment brothc incubated at 37 0C and 420C produced different growth curves. However, the mean generation time (approx 90 mins) was fairly constant. Studies on the gaseous requirements of campylobacters showed that atmospheres. containing S - 10% 02 and 1 - 10% CO2 facilitate growth. Satisfactory microaerobic conditions were produced by the evacuation-replacement technique and gas generating envelopes but not by candle jars. A biotyping scheme has been developed which differentiates Campylobacter spp. and is useful for epidemiological purposes. Environmental surveys have shown: i) that animal carcasses and equipment in abattoirs were frequently contaminated with campylobacters whilst similar samples from butchers' shops were free from campylobacters; ii) that frozen chickens were the main source of campylobacters in a hospital kitchen and that environmental contamination was uncommon; and iii) river water frequently contains Campylobacter spp., serotypes and biotypes associated with human infection and sewage effluent discharge is an important source of these organisms.
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Hayek, Nabil. "Campylobacter jejuni NCTC 11168 response to protamine sulfate." Thesis, University of Ottawa (Canada), 2009. http://hdl.handle.net/10393/28385.
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Campylobacter jejuni is the principal cause of gastroenteritis worldwide. Contaminated chickens is the most important source of human infection by Campylobactor. In its hosts, C. jejuni colonizes the gastrointestinal tract despite the constitutive and induced secretion of cationic antimicrobial peptides (CAMPs). These peptides are a major component of the host's innate immune system and have been found to be effective against different bacterial species including Campylobacter . These observations suggest that Campylobacter has developed mechanisms to evade CAMPs. To test this hypothesis and identify genes presumably involved in adaptation and/or resistance to CAMPs, two approaches were pursued. In the first approach, the transcriptome profile of C. jejuni NCTC 11168 was analyzed upon exposure to increasing concentrations of protamine sulfate, which is a known antimicrobial peptide. In the second approach, a Campylobacter transposon mutant library was screened against two concentrations of protamine. The data obtained from both approaches revealed genes that could be important to overcome the effect of the studied antimicrobial agent and potentially other antimicrobial peptides. The transcriptome profile study unveiled the importance of two genes Cj1721c and Cj0355c, Cj1721c is an outer membrane protein with an unknown function, and Cj0355c, is an essential two-component system regulator. Phenotypic studies demonstrated that the Cj1721c knockout was more resistant to protamine, more motile, and had reduced biofilm-forming ability compared to the wild-type strain. In contrast, the strain that overexpresses Cj0355c was more sensitive to protamine and had greater biofilm-forming ability compared to the wild-type strain. Furthermore, it was attenuated in its ability to colonize the gastrointestinal tract of new born piglets. Moreover, transcriptome profiling of the strain that overexpresses Cj0335c in MH and MEM medium revealed potential pathways that could be regulated by this regulator. This observation suggests that membrane integrity could be sensed by a still unknown sensor and then the signal transferred to Cj0355c, which affects the expression of key genes that are involved in resistance to protamine sulfate.
In summary, this study identifies previously uncharacterized genes (CJ1721c and Cj035c) that are involved in the resistance to protamine sulfate and potentially to other antimicrobial peptides. In addition, the performed transposon mutants library screening indicates that Campylobacter jejuni NCTC 11168 can intrinsically evade the effect of protamine sulfate. On the other hand, we showed that C. jeuni does not use the multidrug efflux pump (MATE) to resist the effect of protamine.
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Cantu, Deborah. "Characterisation of the Campylobacter jejuni PEB3 and GlpT." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/characterisation-of-the-campylobacter-jejuni-peb3-and-glpt(75754190-96b3-46e7-9239-fe5bb9557dd8).html.
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The pathogen C. jejuni is now recognised as the leading cause of bacterial foodborne enteritis in the industrial world. The yearly estimate for Campylobacter infections in the United States alone is 2.4 million people or 1% of the population. Illness caused by C. jejuni is self-limiting, however, some individuals develop complications resulting in autoimmune responses. Despite being a major health burden, the pathogenic process is not fully understood. One aspect of importance is the ability of C. jejuni to adhere to glycosaminoglycans (GAGs), such as heparin. GAGs, sulphated carbohydrates expressed on or in host cells, can serve as receptors for bacterial proteins. In the first study, five heparin-binding proteins of C. jejuni NCTC 11168H were identified. For PEB3 (Cj0289c), this work showed that native wild-type PEB3 and purified recombinant PEB3 produced in E. coli bind heparin. The location of two PEB3 heparin-binding clusters: 62KAKKD65 and 122NKKVRI127, was investigated via site-directed mutagenesis, resulting in impaired heparin-binding. These data suggest GAG-protein-binding may play a role in the pathogenesis of C. jejuni. As well as GAG-binding PEB3 binds 3-PG. Though its exact in vivo role remains unclear, it may act to deliver 3-PG. Scrutiny of the C. jejuni NCTC 11168H genome revealed an uncharacterised gene next to peb3 encoding glpT, or a putative 3-PG transporter. The location of glpT adjacent to peb3 may suggest a related function for the corresponding proteins with PEB3 as the periplasmic binding partner for the transport of 3-PG via GlpT. In this thesis, the roles of peb3 and glpT for two independent phenotypes, 3-PG dependent growth and fosfomycin sensitivity was studied in vitro. The findings indicate glpT has an effect on both, but not peb3. Furthermore, the NCTC 11168H glpT pseudogene, despite containing two frameshift mutations, has the capacity to encode a functional protein. Lastly, the NCTC 11168H peb3/glpT locus was compared with other C. jejuni strains and closely related species C. coli, C. lari and C. upsaliensis genome sequences. The majority of strains peb3/glpT locus followed the gene arrangement lpxB, peb3, glpT, surE. However, the findings indicate the gene loci between lpxB/surE in remaining strains to be hypervariable. Further analysis shows peb3 to be relatively conserved, whereas, the majority of glpT genes display genetic diversity due to interruptions such as indels and deletion. Lastly, I display the organisation of the peb3/glpT locus and glpT structure in their evolutionary context through MLST. In summary, the findings provide for further characterisation of the PEB3 protein and explores the importance of the uncharacterised GlpT of C. jejuni.
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Rock, Jonathan D. "Iron acquisition from host molecules by Campylobacter jejuni." Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/30349.
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The ability of pathogenic organisms to obtain iron in the host is critical for pathogenesis. Limited research has been carried out into iron acquisition from host molecules by the important gastro-intestinal pathogen Campylobacter jejuni. The objective of this study was to investigate the ability of C. jejuni to acquire iron from host molecules and the nature of iron responsive regulation of gene expression in C. jejuni. Four C. jejuni genes encoding putative haem uptake proteins are arranged in a predicted operon. Data presented in this study confirms that ChuA, a protein similar to haem receptors, functions as an outer membrane haem receptor in C. jejuni and is expressed from a promoter in the region upstream of chuA, under iron-responsive control by Fur. The chuB, C and D genes are non-essential for iron acquisition from haem, however involvement of chuB, C and D in haem uptake cannot be dismissed due to the possible complementation of chu mutation by another system. Identification of alternative haem uptake systems in C. jejuni was unsuccessful. For the first time it was demonstrated that C. jejuni can acquire iron from both transferrin (Tf) and lactoferrin (Lf) in a contact dependent, substrate specific manner which does not require noradrenaline. Iron acquired from Tf and Lf accumulates in the soluble cellular fractions and is utilised for cellular growth. The molecular basis of iron acquisition from Tf or Lf has not been elucidated. C. jejuni fur is co-transcribed with the lysS and glyA housekeeping genes from two distal promoters (adjacent to the gatC and Cj0399 genes). Expression from either promoter is not controlled by Fur in response to iron and therefore is not autoregulated. This study demonstrates the presence of several sytems involved in iron acquisition from host molecules. Future research is essential to investigate the importance of these systems during host colonisation.
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Pope, Christopher E., and n/a. "Campylobacter jejuni : virulence, dosage, survival, and colonisation characteristics." University of Otago. Department of Microbiology and Immunology, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070501.141243.
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In a previous study, twenty-five flaA types were detected among 200 Campylobacter jejuni isolates obtained from clinical and poultry meat sources.
The most common flaA type detected among poultry isolates was flaA-3 at a frequency of 23%. In contrast, flaA-3 constituted 5% of the clinical isolates. FlaA-15 was detected most frequently among clinical isolates (31%) but rarely among poultry isolates (5%). Purchasers of poultry meat were therefore commonly exposed to flaA-3 yet most of the human infections were due to flaA type 15. The prevalence of different flaA types in poultry and humans might have been due to: FlaA-15 was more virulent for humans than flaA-3 (infection more likely to result). There were more C. jejuni flaA-15 cells on poultry meat (dose effect). Better survival of flaA-15 cells when freeze/thawed or when stored at +4�C (survival in kitchen). Ecological performance of flaA-3 strains in chicken gut better than that of flaA-15 (more flaA -3 cells in gut therefore greater chance of carcass contamination)?
Eleven strains representing flaA types 3, 13, and 15 were tested for their ability to invade cultured human epithelial cells (HEp-2). Invasiveness was considered to reflect virulence. FlaA-15 isolates were more invasive in comparison to flaA-3 and flaA-13 isolates (p<0.0001).
Washings from chicken portions were cultured to enumerate Campylobacter cells present on the meat. C. jejuni isolates were flaA typed and the numbers were related to FlaA type. A correlation was not detected.
The eleven representative strains were used to inoculate 1 cm� sections of chicken skin which were stored at -20�C or +4�C over a five day period. The samples stored at -20�C were thawed and held either overnight at 25�C, overnight at +4�C or for thirty minutes at 25�C. The numbers of viable Campylobacter cells on the sections were determined. Survival ability differed from strain to strain but was not associated with flaA type.
The most invasive C. jejuni strain (T1016; flaA-15) and the least invasive strain (Pstau; flaA-3) were assessed for their ability to colonise the intestinal tract of one-day-old chicks. The dynamics of colonisation, after inoculation of the birds with pure cultures or with mixtures, was monitored by real-time quantitative PCR. Strain-specific primers based on the variable region of the nucleotide base sequence of flaA genes were derived for this work. This enabled the individual strains to be enumerated in gut contents from colonized chickens. Both strains could colonise the chick intestinal tract but C. jejuni strain T1016 (flaA-15) could competitively exclude PStau (flaA-3).
It was concluded that the higher prevalence of flaA-15 strains among the clinical isolates was due to its higher virulence for humans. In other words, despite a low prevalence of flaA-15 on poultry meat, infection was more likely to result when C. jejuni flaA-15 cells were consumed.
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Zheng, Jie. "Campylobacter jejuni/coli - host intestinal epithelial cell interaction." College Park, Md. : University of Maryland, 2006. http://hdl.handle.net/1903/3931.
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Thesis (Ph. D.) -- University of Maryland, College Park, 2006.Thesis research directed by: Food Science. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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Cawthraw, Shaun Allan. "Human and chicken immune responses to Campylobacter jejuni." Thesis, Queen Mary, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420102.
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Grove-White, David Hugh. "The molecular epidemiology of Campylobacter jejuni in ruminants." Thesis, University of Liverpool, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501729.
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The prunary objective of this study was to describe the temporal and spatial aspects of the epidemiology of ruminant Campylobacter jejuni. The work presented in this thesis is nested within a larger multidisciplinary study investigating the epidemiology of human campylobacteriosis in Lancashire and will be used to quantify and descnbe the contribution ot ruminant derived Campylobacters to the human disease burden.
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Albaridi, Najla. "The antibacterial activity of honey against Campylobacter jejuni." Thesis, University of Surrey, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616479.
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Honey is a food with high popularity, consumption and availability. The effective antibacterial activity of honey, without any reported bacterial resistance or side effects, increases its use in traditional medicine for treating many different kinds of infections. Initially, this study examined the antibacterial activity of honey against Campylobacter jejuni. Six different types of honey, which were commercially available in the UK, Saudi Arabia and New Zealand, were assessed. Honey samples were introduced to Muller Hinton media in three different ways: filtration, autoclaving honey alone and autoclaving honey with media. C. jejuni NCTC 11168 showed good sensitivity to all six investigated honey samples. The minimum inhibitory concentrations ranged between 2 and 10 % for filtered honey. Thermal treatment increased the activity of some honey types and the MIC was 4% for all honey samples, except for clear honey (C.) Heating honey (2 %, v/v) with the medium resulted in an increase in antibacterial activity with C. jejuni, reducing to detectable levels after 6 hours of incubation. A similar result was observed when honey was mixed with casein, followed by thermal treatment. This result indicates that thermal treatment generates a selection of new antibacterial agents in the honey-casein mixture (honey-casein MRPs).
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Hepworth, Philip John. "Genomic variation in the zoonotic pathogen Campylobacter jejuni." Thesis, University of Liverpool, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502305.
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The zoonotic bacterium Campylobacterjejlllli is the major cause of gastrointestinal disease in developed countries. The source ofhuman infections is believed to be animal food products, but the relative contributions ofdifferent sources to the overall burden of disease remain unclear. By improving our knowledge ofthe variable genome of Campylobacterjejlllli it may be possible to uncover links between variable gene distribution and strain phenotypes such as host preference or virulence. Our current knowledge ofvariable genes may be unrepresentative of strains from potential disease reservoirs such as ruminants and wildlife species. The technique of suppression subtraction hybridization can be used to identify gene fragments present in the genome of a strain of interest (tester strain) but absent from the genome ofa reference strain (driver strain). We carried out subtractions using strains from novel hosts, and various MLST clonal complexes. The distribution ofeight subtracted sequences was analysed using PCR and dot blot hybridization. These sequences included four with putative roles in the use of alternative electron acceptors, which have been hypothesized to contribute to selective advantages in specific ecological niches. For these eight subtracted sequences there was no evidence for a link between sequence distribution and host species. However, there was a clear correlation between subtracted sequence distribution and clonal complex, suggesting minimal transfer ofthese genes between clonal complexes. To further characterise genomic variation in C. jejzl11i populations, comparative genomic hybridization was carried out on a panel of C. jejlllli isolates representing diverse host species and MLSTs. DNA from these isolates was interrogated using a newly developed oligonucleotide microarray based on the genomes of C. jejllni strains NCTC11168, RM1221 and 81-176. The microarray also included strain variable genes from other strains and genetic loci in the database, and a selection of genes from our subtractions. The strain panel included several isolates from wildlife and water sources with unusual MLST genotypes not currently found in clinical isolates from humans (WW isolates). . Clustering analysis ofM-CGH data confirmed that genomic content was assocfated with the MLST rather than the host species ofthe isolates. Strikingly the WW isolates had a number of genes deleted or significantly divergent from the arrayed genes, which were present in all or most other isolates. Many ofthese genes had functions which related to colonisation, invasion and virulence. This suggests that the WW strains may reach humans but may be unable to colonise or cause disease in humans. The genome sequence of a WW isolate revealed several novel genomic insertions not present in the genome of C. jejzl11i NCTC11168. These novel insertions may contain genes which contribute to the colonisation of water and wildlife sources, or the unusual epidemiology of the WW strains. Further studies will include the genome sequencing of several more WW isolates and characterisation oftheir colonisation phenotypes using a chick colonisation model, expression M-CGH, and defined gene mutants.
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Al-Obaidi, A. S. R. "The colonization of young chicks with Campylobacter jejuni." Thesis, University of Bristol, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235177.
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Jackson, Colin John. "The typing and environmental detection of Campylobacter jejuni." Thesis, Manchester Metropolitan University, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262007.
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Corcionivoschi, Nicolae. "A novel cytochrome P450 from Campylobacter jejuni 11168." Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/13463.
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Campylobacter jejuni is the most commonly recognized cause of bacterial gastroenteritis in man and also infects cattle, sheep and poultry. Publishing of the genome sequence of Campylobacter jejuni 11168 (Parkhill, 2000) revealed the presence of only one cytochrome P450. Its coding sequence (Cj411c) is located in an operon involved in sugar and cell surface biosynthesis. The gene name is Cj1411c, is 1359 bp long and encodes 453 aa. The sequence is strictly conserved in Campylobacter jejuni RM221. Recombinant P450 was expressed in E. coli and showed the 450 nm peak in the presence of CO indicating the correct folding. The protein was partially purified to about 70% purity. By deleting the P450 gene from the Campylobacter jejuni 11168 genome clear changes in cell morphology were identified, cells becoming wider and shorter. The capsular sugar profile of the NC1 knockout strain reveals the presence of arabinose which was not found in the wild type strain. The arabinose was identified by both HPLC and NMR. The phenotype studies showed clear differences between NC1 and WT cells: NC1 cells are less resistant to starvation in the stationary phase; by exposure to the atmospheric oxygen 36.47% of the wild type cells survived after 24 hours and only 16.61% of the NC1 cells survived; by growing the NC1 cells in competition with the WT cells the growth rate of NC1 cells approximately 10x lower than the WT; NC1 cells were proved to be less resistant to high temperature, more resistant to low temperatures and pH. By analysing the results obtained with NaC1 and glycerol we have determined that it is not the osmotic pressure that is affecting the growth of Campylobacter and the differences between the WT and NC1 strain might be related with changes in cell surface components.
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Jowiya, C. W. J. "The response of Campylobacter jejuni to pancreatic enzymes." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1428632/.
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Campylobacter jejuni is an important food-borne pathogen, and a major cause of bacterial gastroenteritis. Despite this, relatively little is known regarding the way in which C. jejuni colonises hosts, causes disease or survives in the environment during transmission between hosts. C. jejuni responds to a number of biological molecules found in the human intestinal environment such as bile salts leading to the induction of Campylobacter invasion antigens (Cia), and norepinephrine in response to which the bacterium shows increased virulence. In this study we investigated the response of C. jejuni to mammalian pancreatic α-amylase. The results of this study show that C. jejuni responds to pancreatic α-amylase with production of a mucoid colony phenotype that results from increased secretion of extracellular polysaccharide (EPS) identified as an α-dextran, further to this it was found that the amount of extracellular protein produced by C. jejuni was also increased, the proteins where identified using liquid chromatography mass spectrometry (LC-MS), a number of proteins associated with virulence were identified in the samples grown in the presence of α-amylase. In response to pancreatic α-amylase C. jejuni forms significantly increased biofilm and exhibits increased virulence in the Galleria mellonella and Caco-2 epithelial cell models. Furthermore C. jejuni pre exposed to amylase show significantly increased colonisation of chickens and increased resistance to stresses. It is also shown that C. jejuni is able to utilise α-amylase as a nutrient source, this was determined by growing the bacterium on a defined minimal media with the α-amylase as the only source of carbon present. The ability of C. jejuni to respond pancreatic amylase was shown to require proteolytic activity of Cj0511.
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Baig, A. "Genome sequence of the hyperinvasive Campylobacter jejuni strains." Thesis, Nottingham Trent University, 2012. http://irep.ntu.ac.uk/id/eprint/96/.
Full textAbstract:
Campylobacter jejuni is the world’s major cause of gastroenteritis in humans. Although motility, toxin production, adhesion and invasion are some of the key factors associated with C. jejuni pathogenesis, their mechanism in the disease process remains unclear. The key aim of this project is to study the genetic basis of hyperinvasiveness in a group of six C. jejuni strains which have been reported as hyperinvasive into human intestinal cell lines. Here, genomotyping of the hyperinvasive C. jejuni was performed by comparative genomic hybridization (CGH) against four low invasive C. jejuni strains. A group of 67 genes were identified as being present or highly divergent/absent in the hyperinvasive versus low invasive C. jejuni strains. Of these, nine genes were present and six genes were highly divergent/absent in all hyperinvasive C. jejuni. The PCR screening of these 15 genes in nine additional low invasive C. jejuni strains showed a significant association with the hyperinvasive phenotype. The majority of identified genes encoded proteins with essential cellular and metabolic functions along with some genes with known virulence related roles. Thus, the hyperinvasive phenotype is characterised by different functional networks rather than a single gene or gene cluster. All strains showed an overall genetic variability and the capsule, lipooligosaccharide, flagellar biosynthesis and restriction modification regions were the most diverse. The hierarchical clustering based on comparative genomic hybridization (CGH) did not group together the hyperinvasive C. jejuni as a single group and these strains possessed different MLST profiles. The hyperinvasive C. jejuni strains were shown to contain additional genetic content by pooled suppressive subtractive hybridization (PSSH). Eleven inserts were identified in total which were variably distributed in the hyperinvasive C. jejuni strains. Of these four sequences were specific to the hyperinvasive C. jejuni as these were absent from all thirteen low invasive C. jejuni strains tested. The majority of sequences matched with genes in Campylobacter and other bacteria and one sequence had no homology with anything in the databases today. Since, there is no insert identified as present in all the hyperinvasive C. jejuni strains it can be suggested that each strain might have evolved a different mechanism for hyperinvasiveness and that this phenotype is a multifactorial process. C. jejuni 01/10 and 01/51 whole genome sequences identified no unique genetic content in either strain except for a prophage in C. jejuni 01/51. C. jejuni 01/10 was found to contain two prophages. C. jejuni 01/51 has a highly mosaic capsule locus with genes similar to C. jejuni subsp. doylei and C. lari capsular polysaccharide genes. Some genes with homology to the C. jejuni subsp. doylei capsule genes were also identified in C. jejuni 01/10 capsule region. This is evidence of genetic recombination with capsule genes from other pathogenic Campylobacter species which is not reported in the capsule region of other Campylobacter strains sequenced to date. This suggests that the highly diverse capsule in C. jejuni 01/10 and 01/51 is required for the hyperinvasive phenotype in these strains. This study has provided detailed insight into the genomic structure of the hyperinvasive C. jejuni strains and has highlighted genetic factors involved in their hyperinvasive phenotype.