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Relevant bibliographies by topics / Escherichia coli infections Pathogenesis

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Academic literature on the topic 'Escherichia coli infections Pathogenesis'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 January 2023

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Journal articles on the topic "Escherichia coli infections Pathogenesis"

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Hacker, Jörg. "Role of fimbrial adhesins in the pathogenesis of Escherichia coli infections." Canadian Journal of Microbiology 38, no. 7 (July 1, 1992): 720–27. http://dx.doi.org/10.1139/m92-118.

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Escherichia coli strains are able to cause intestinal (enteritis, diarrhoeal diseases) and extraintestinal (urinary tract infections, sepsis, meningitis) infections. Most pathogenic E. coli strains produce specific fimbrial adhesins, which represent essential colonization factors: intestinal E. coli strains very often carry transferable plasmids with gene clusters specific for fimbrial adhesins, like K88 and K99, or colonization factor antigens (CFA) I and II. In contrast, the fimbrial gene clusters of extraintestinal E. coli strains, such as P, S, or F1C fimbriae, are located on the chromosomes. The fimbrial adhesin complexes consist of major and minor subunit proteins. Their binding specificity can generally be assayed in hemagglutination tests. In the case of fimbrial adhesins of intestinal E. coli strains, the major subunit proteins preferentially represent the hemagglutinating adhesins, whereas minor subunit proteins are the hemagglutinins of extraintestinal E. coli strains. Recently "alternative" adhesin proteins were identified, which have the capacity to bind to eukaryotic structures different from the receptors of the erythrocytes. Fimbrial adhesins are not constitutively expressed but are stringently regulated on the molecular level. Extraintestinal E. coli wild-type strains normally carry three or more fimbrial adhesin determinants, which have the capacity to influence the expression of one another (cross talk). Furthermore the fimbrial gene clusters undergo phase variation, which seems to be important for their contribution to pathogenesis of E. coli. Key words: fimbriae, adhesins, Escherichia coli, pathogenicity.

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Paton, James C., and Adrienne W. Paton. "Pathogenesis and Diagnosis of Shiga Toxin-Producing Escherichia coli Infections." Clinical Microbiology Reviews 11, no. 3 (July 1, 1998): 450–79. http://dx.doi.org/10.1128/cmr.11.3.450.

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SUMMARY Since their initial recognition 20 years ago, Shiga toxin-producing Escherichia coli (STEC) strains have emerged as an important cause of serious human gastrointestinal disease, which may result in life-threatening complications such as hemolytic-uremic syndrome. Food-borne outbreaks of STEC disease appear to be increasing and, when mass-produced and mass-distributed foods are concerned, can involve large numbers of people. Development of therapeutic and preventative strategies to combat STEC disease requires a thorough understanding of the mechanisms by which STEC organisms colonize the human intestinal tract and cause local and systemic pathological changes. While our knowledge remains incomplete, recent studies have improved our understanding of these processes, particularly the complex interaction between Shiga toxins and host cells, which is central to the pathogenesis of STEC disease. In addition, several putative accessory virulence factors have been identified and partly characterized. The capacity to limit the scale and severity of STEC disease is also dependent upon rapid and sensitive diagnostic procedures for analysis of human samples and suspect vehicles. The increased application of advanced molecular technologies in clinical laboratories has significantly improved our capacity to diagnose STEC infection early in the course of disease and to detect low levels of environmental contamination. This, in turn, has created a potential window of opportunity for future therapeutic intervention.

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Serna, Antonio, and Edgar C. Boedeker. "Pathogenesis and treatment of Shiga toxin-producing Escherichia coli infections." Current Opinion in Gastroenterology 24, no. 1 (January 2008): 38–47. http://dx.doi.org/10.1097/mog.0b013e3282f2dfb8.

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Vel, W. A. C., A. M. J. J. Verweij-Van Vught, F. Namavar, and D. M. MacLaren. "Pathogenesis of mixed infections by Escherichia coli and Bacteroides species." Antonie van Leeuwenhoek 51, no. 5-6 (1985): 598. http://dx.doi.org/10.1007/bf00404584.

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Servin, Alain L. "Pathogenesis of Afa/Dr Diffusely Adhering Escherichia coli." Clinical Microbiology Reviews 18, no. 2 (April 2005): 264–92. http://dx.doi.org/10.1128/cmr.18.2.264-292.2005.

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SUMMARY Over the last few years, dramatic increases in our knowledge about diffusely adhering Escherichia coli (DAEC) pathogenesis have taken place. The typical class of DAEC includes E. coli strains harboring AfaE-I, AfaE-II, AfaE-III, AfaE-V, Dr, Dr-II, F1845, and NFA-I adhesins (Afa/Dr DAEC); these strains (i) have an identical genetic organization and (ii) allow binding to human decay-accelerating factor (DAF) (Afa/DrDAF subclass) or carcinoembryonic antigen (CEA) (Afa/DrCEA subclass). The atypical class of DAEC includes two subclasses of strains; the atypical subclass 1 includes E. coli strains that express AfaE-VII, AfaE-VIII, AAF-I, AAF-II, and AAF-III adhesins, which (i) have an identical genetic organization and (ii) do not bind to human DAF, and the atypical subclass 2 includes E. coli strains that harbor Afa/Dr adhesins or others adhesins promoting diffuse adhesion, together with pathogenicity islands such as the LEE pathogenicity island (DA-EPEC). In this review, the focus is on Afa/Dr DAEC strains that have been found to be associated with urinary tract infections and with enteric infection. The review aims to provide a broad overview and update of the virulence aspects of these intriguing pathogens. Epidemiological studies, diagnostic techniques, characteristic molecular features of Afa/Dr operons, and the respective role of Afa/Dr adhesins and invasins in pathogenesis are described. Following the recognition of membrane-bound receptors, including type IV collagen, DAF, CEACAM1, CEA, and CEACAM6, by Afa/Dr adhesins, activation of signal transduction pathways leads to structural and functional injuries at brush border and junctional domains and to proinflammatory responses in polarized intestinal cells. In addition, uropathogenic Afa/Dr DAEC strains, following recognition of β1 integrin as a receptor, enter epithelial cells by a zipper-like, raft- and microtubule-dependent mechanism. Finally, the presence of other, unknown virulence factors and the way that an Afa/Dr DAEC strain emerges from the human intestinal microbiota as a “silent pathogen” are discussed.

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Tang, Fengyi, and Milton H. Saier. "Transport proteins promoting Escherichia coli pathogenesis." Microbial Pathogenesis 71-72 (June 2014): 41–55. http://dx.doi.org/10.1016/j.micpath.2014.03.008.

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Neill, Marguerite A. "Pathogenesis of Escherichia coli O157:H7 infection." Current Opinion in Infectious Diseases 7, no. 3 (June 1994): 295–303. http://dx.doi.org/10.1097/00001432-199406000-00003.

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Nicholson, Tracy F., Kristin M. Watts, and David A. Hunstad. "OmpA of Uropathogenic Escherichia coli Promotes Postinvasion Pathogenesis of Cystitis." Infection and Immunity 77, no. 12 (September 21, 2009): 5245–51. http://dx.doi.org/10.1128/iai.00670-09.

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ABSTRACT Type 1 pilus directs bladder epithelial binding and invasion by uropathogenic Escherichia coli (UPEC) in the initial stage of cystitis, but the bacterial determinants of postinvasion events in the pathogenesis of cystitis are largely undetermined. We show here that the UPEC outer membrane protein A (OmpA), a monomeric, major, integral protein component of the bacterial outer membrane, functions as a critical determinant of intracellular virulence for UPEC, promoting persistent infection within bladder epithelium. Using a murine urinary tract infection (UTI) model, we demonstrate that whereas deletion of the UPEC ompA gene did not disrupt initial epithelial binding and invasion by UPEC, it did preclude completion of the intracellular bacterial community (IBC) pathway, accompanied by diminishing bacterial loads in the bladder. This defect in epithelial persistence of the ompA mutant was enhanced in competitive infections with wild-type UPEC. Microscopic examinations revealed that the ompA mutant formed significantly fewer IBCs, and those that were initiated were unable to progress past the early stages of maturation. These defects could be corrected by complementation of ompA. In addition, expression of ompA during wild-type UTI was sharply increased at time points correlated with IBC development and the arrival of host immune effector cells. Our findings establish OmpA as a key UPEC virulence factor that functions after epithelial invasion to facilitate IBC maturation and chronic bacterial persistence.

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Herthelius, B. M., K. G. Hedström, R. Möllby, Lena Pettersson, J. Winberg, and C. E. Nord. "Pathogenesis of urinary tract infections — Amoxicillin induces genital escherichia coli colonization." Infection 16, no. 5 (September 1988): 263–66. http://dx.doi.org/10.1007/bf01645066.

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Bogdanos, Dimitrios P., Harold Baum, Diego Vergani, and Andrew K. Burroughs. "The Role ofE. coliInfection in the Pathogenesis of Primary Biliary Cirrhosis." Disease Markers 29, no. 6 (2010): 301–11. http://dx.doi.org/10.1155/2010/595078.

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Among various infectious agents possibly involved in the pathogenesis of primary biliary cirrhosis (PBC),Escherichia Coli (E. coli)has received special attention because of epidemiological and experimental evidence linking this bacterium with the disease's development. This review discusses early and more recent epidemiological studies associating recurrent urinary tract infections withE. coliand the development of PBC. We also critically review data provided over the years demonstrating disease-specific humoral and cellular immune responses againstE. coliantigens in patients with PBC. Finally, we assess the relevance of experimental findings reporting cross-reactive immunity between mimicking sequences ofE. coliand the major PBC mitochondrial antigens in the pathogenesis of the PBC. We also address the extent to which molecular mimicry and immunological cross-reactivity can be considered as a critical pathogenic process linking infection with self destruction.

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Dissertations / Theses on the topic "Escherichia coli infections Pathogenesis"

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Paton, Adrienne Webster. "Molecular characterization of variant shiga-like toxin genes of Escherichia coli /." Title page, contents and abstract only, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09php3118.pdf.

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Srimanote, Potjanee. "Analysis of putative virulence factors of a locus of enterocyte effacement-negative shiga-toxigenic Escherichia coli O113:H21 strain." Title page, contents and abstract only, 2003. http://web4.library.adelaide.edu.au/theses/09PH/09php863.pdf.

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"February 2003." Addendum and corrigenda inserted at back Includes bibliographical references (leaves 249-272) Aims to identify and characterise potential virulence-associated factors from the locus of enterocyte effacement-negative shiga-toxigenic Escherichia coli O113:H21 strain 98NK2 which was responsible for an outbreak of haemolytic uremic syndrome. Particular attention was focused on putative virulence genes encoded on the megaplasmid of this strain.

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Rodrigues, Ângela Maria Gonçalves. "Patogénese das infeções entéricas por escherichia coli." Master's thesis, [s.n.], 2014. http://hdl.handle.net/10284/4840.

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Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências Farmacêuticas
As estirpes de E. coli podem ser agrupadas em estirpes comensais, patogénios extraintestinais e patogénios intestinais. É um relevante patogénio intestinal que causa infeções entéricas com grandes taxas de morbilidade e mortalidade em todo o mundo. O desenvolvimento da infeção depende da dose infeciosa ingerida pelo indivíduo, da sua susceptibilidade à doença, da interação entre o patogénio e os enterócitos e virulência do patogénio. E. coli induz diarreia através de diversos mecanismos, entre os quais a produção de adesinas, produção de toxinas, indução de alterações celulares nas células do hospedeiro e invasão da mucosa intestinal. As estirpes diarreiogénicas foram agrupadas em seis principais categorias, baseadas nos seus factores de virulência e mecanismos através dos quais provocam doença: E. coli enteropatogénicas (EPEC), enterohemorrágicas (EHEC), E. coli enterotoxicogénicas (ETEC), E. coli enteroagregativas (EAEC), E. coli enteroinvasivas (EIEC) e E. coli de adesão difusa (DAEC). As EPEC são caracterizadas pela formação de lesões histopatológicas nos enterócitos com posterior secreção de proteínas que causam alterações celulares. As EHEC têm um mecanismo semelhante, além disso, produzem toxinas Shiga, responsáveis por casos severos como diarreia sanguinolenta, colite hemorrágica (HC), síndrome hemolítico-urémico (HUS) e púrpura trombocitopénica trombótica (TTP). Quanto a estirpes de ETEC, podem produzir e libertar duas toxinas diferentes: LT e ST, que causam o desequilíbrio da homeostase intestinal por aumento do AMPc e GMPc, respetivamente. EAEC formam um biofilme e libertam toxinas como EAST1 e Pet que estimulam a secreção de fluídos e eletrólitos. EIEC são capazes de invadir enterócitos e replicarem-se. Em relação às DAEC, a infeção é caracterizada pelo crescimento de projeções em forma de “dedo” da superfície dos enterócitos. Para reduzir as taxas de morbilidade e de mortalidade, ter acesso a informação sobre as infeções entéricas causadas por E. coli e aplicar a prevenção primária são essenciais. Escherichia coli (E. coli) strains can be grouped as commensal strains, extraintestinal pathogens and intestinal pathogens. It is a relevant intestinal pathogen which causes enteric infections with high morbidity and mortality rates around the world. The development of the infection depends on the infectious dose ingested by an individual, his susceptibility to the disease, enterocytes and pathogens interaction and pathogen’s virulence. E. coli induces diarrhea through several mechanisms, among them are production of adhesins, production of toxins, induction of cellular alterations in host cells and invasion of intestinal mucosa. Diarrheagenic strains were grouped into six main categories, based on their virulence factors and mechanisms by which they provoke disease: enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli (EHEC), enterotoxigenic E. coli (ETEC), enteroaggregative E. coli (EAEC), enteroinvasive E. coli (EIEC) and diffusely adherent E. coli (DAEC). EPEC are characterized by the formation of histopathological lesions in the enterocytes with posterior secretion of proteins that cause cellular alterations. EHEC have a similar mechanism, besides, they produce Shiga toxins, responsible for severe cases as bloody diarrhea, hemorrhagic colitis (HC), hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP). As for ETEC strains, they can produce and release two different toxins: LT and ST, which cause intestinal homeostatic disequilibrium by increasing AMPc and GMPc levels, respectively. EAEC form a biofilm and release toxins as EAST1 and Pet that stimulate fluid and electrolyte secretion. EIEC are capable of invading enterocytes and replicate. Regarding to DAEC strains, the infection is characterized by the growth of finger-like projections of the enterocytes’ surface that wrap around the bacteria. To reduce morbidity and mortality rates, having access to information about enteric infections caused by E. coli and applying primary prevention are essential.

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Hostetter, Shannon Jones. "Role of Shiga toxin dissemination and inflammation in the pathogenesis of Shiga toxin-producing Escherichia coli infection." [Ames, Iowa : Iowa State University], 2009.

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Walz, Paul S. "Influence of pathogenic bacterial determinants on genome stability of exposed intestinal cells and of distal liver and spleen cells." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Biology, c2011, 2011. http://hdl.handle.net/10133/3405.

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Most bacterial infections can be correlated to contamination of consumables such as food and water. Upon contamination, boil water advisories have been ordered to ensure water is safe to consume, despite the evidence that heat-killed bacteria can induce genomic instability of exposed (intestine) and distal cells (liver and spleen). We hypothesize that exposure to components of heat-killed Escherichia coli O157:H7 will induce genomic instability within animal cells directly and indirectly exposed to these determinants. Mice were exposed to various components of dead bacteria such as DNA, RNA, protein or LPS as well as to whole heat-killed bacteria via drinking water. Here, we report that exposure to whole heat-killed bacteria and LPS resulted in significant alterations in the steady state RNA levels and in the levels of proteins involved in proliferation, DNA repair and DNA methylation. Exposure to whole heat-killed bacteria and their LPS components also leads to increased levels of DNA damage.
xiv, 132 leaves : ill. (chiefly col.) ; 29 cm

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Lekmeechai, Sujinna. "The role of EspO1 in Escherichia coli pathogenesis." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/58146.

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Enterohaemorrhagic E. coli (EHEC) has been the causative agent of diarrhoeal outbreaks for decades. EHEC virulence relies on a type 3 secretion system (T3SS), which directly translocates T3SS effectors into the host cell cytoplasm. Once translocated, T3SS effectors alter various host cell functions, including manipulating the cell death response, in order to facilitate bacterial colonisation. EHEC is equipped with at least 40 effector proteins; however, not all identified effectors are fully characterised. This study set out to investigate the role of EspO during EHEC infection. EHEC O157:H7 strain EDL933 carries 2 EspO homologs: EspO1 and EspO2. EspO homologs are also found in several enteric pathogens including Shigella flexneri (OspE1 and OspE2), Salmonella enterica serovar Typhi and Typhimurium (SopD), Citrobacter rodentium (EspO), and some enteropathogenic E. coli (EPEC) clinical isolates (EspO). It has previously been established that the EspO effector family interacts with integrin linked kinase (ILK) via a conserved tryptophan residue: W68 for OspE1 and W77 for EspO1. EspO1 and EspO2 co-operatively inhibit cell detachment by blocking focal adhesion disassembly, via their interactions with ILK and EspM2, respectively. In a previous study, HAX-1 was identified as the novel interaction partner of EspO1 by a yeast 2 hybrid (Y2H) screen. HAX-1 is an ubiquitiously expressed anti-apoptotic protein that localises to mitochondria. In this study, the EspO1-HAX-1 interaction was confirmed by direct Y2H. Functionally, EspO1 and OspE1 were shown to protect HeLa cells from staurosporine-induced apoptosis during transfection and EspO1 was able to inhibit cell death during in vitro infection. Additionally it was established that the EspO1 and OspE1 anti-apoptotic activity is HAX-1 dependent, but ILK independent. To summarise, this study reported that EspO1 displays anti-apoptotic activity in a HAX-1 dependent manner. Therefore, EspO1 serves 2 main functions: inhibition of apoptosis through HAX-1 and blocking of cell detachment through ILK.

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Burke, Denis Anthony. "Ulcerative colitis and Escherichia coli." Thesis, University of Newcastle Upon Tyne, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309075.

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Wu, Gilbert Kar Po. "Signal transduction responses to enteropathogenic Escherichia coli and Shiga toxin-producing Escherichia coli infections." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0007/MQ46054.pdf.

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Solecki, Olivia. "Explaining the urban and rural differences of Escherichia coli 0157 human infection in Grampian." 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=25203.

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Kimmitt, Patrick Thomas. "Expression of Shiga toxin genes in Escherichia coli." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299614.

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Books on the topic "Escherichia coli infections Pathogenesis"

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International Symposium on Pyelonephritis (4th 1986 Göteborg, Sweden). Host-parasite interactions in urinary tract infections: Proceedings of the Fourth International Symposium on Pyelonephritis held in Göteborg, Sweden, 23-25 June 1986. Chicago: University of Chicago Press, 1989.

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Wiwanitkit, Viroj. Escherichia coli Infections. North Charleston: CreateSpace Independent Publishing Platform, 2011.

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Hilary, Babcock, ed. Escherichia coli infections. 2nd ed. New York: Chelsea House, 2010.

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Manning, Shannon D. Escherichia coli infections. Edited by Alcamo I. Edward and Heymann David L. Philadelphia: Chelsea House, 2005.

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Manning, Shannon D. Escherichia coli infections. Edited by Babcock Hilary. 2nd ed. New York: Chelsea House, 2010.

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Kay, Miller Ellen. Escherichia coli O157. Beltsville, Md: National Agricultural Library, 1993.

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Kay, Miller Ellen. Escherichia coli O157. Beltsville, Md: National Agricultural Library, 1992.

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United States. Animal and Plant Health Inspection Service. Veterinary Services. Centers for Epidemiology and Animal Health. Escherichia coli O157:H7: Issues and ramifications : executive summary. Fort Collins, Colo: USDA:APHIS:VS, Centers for Epidemiology and Animal Health, 1994.

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Wu, Gilbert Kar Po. Signal transduction responses to enteropathogenic Escherichia coli and Shiga toxin-producing Escherichia coli infections. Ottawa: National Library of Canada, 1999.

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Kay, Miller Ellen. Escherichia coli O157: January 1994 - July 1995. Beltsville, Md: National Agricultural Library, 1995.

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Book chapters on the topic "Escherichia coli infections Pathogenesis"

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Gyles, C. L., and J. M. Fairbrother. "Escherichia Coli." In Pathogenesis of Bacterial Infections in Animals, 267–308. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9780470958209.ch15.

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Rabinowitz, Ronald P., and Michael S. Donnenberg. "Escherichia coli." In Infectious Agents and Pathogenesis, 101–31. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0313-6_6.

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Knutton, S. "Intestinal Colonization by Enteropathogenic Escherichia coli." In Molecular Pathogenesis of Gastrointestinal Infections, 93–102. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5982-1_13.

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Benz, Inga, and M. Alexander Schmidt. "Diffuse Adherence Of Enteropathogenic Escherichia coli Strains." In Molecular Pathogenesis of Gastrointestinal Infections, 103–5. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5982-1_14.

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Klemm, Per, and Karen A. Krogfelt. "Molecular Biology of Escherichia coli Type 1 Fimbriae." In Molecular Pathogenesis of Gastrointestinal Infections, 87–92. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5982-1_12.

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Scotland, Sylvia M. "Vero Cytotoxins (Shiga-Like Toxins) of Escherichia coli." In Molecular Pathogenesis of Gastrointestinal Infections, 155–60. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5982-1_20.

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Ørskov, Ida, and Frits Ørskov. "The Clone Concept and Enteropathogenic Escherichia Coli (EPEC)." In Molecular Pathogenesis of Gastrointestinal Infections, 49–53. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5982-1_7.

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McConnell, Moyra M. "Newly Characterized Putative Colonization Factors of Human Enterotoxigenic Escherichia coli." In Molecular Pathogenesis of Gastrointestinal Infections, 79–85. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5982-1_11.

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Svennerholm, Ann-Mari, Christina Åhrén, Christine Wennerås, and Jan Holmgren. "Development of an Oral Vaccine Against Enterotoxigenic Escherichia coli Diarrhea." In Molecular Pathogenesis of Gastrointestinal Infections, 287–94. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5982-1_37.

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Gaastra, Wim, Anja M. Hamers, Bart J. A. M. Jordi, Paul H. M. Savelkoul, Geraldine A. Willshaw, Moyra M. McConnell, Johannes G. Kusters, Arnoud H. M. van Vliet, and Bernard A. M. van der Zeijst. "Regulation of Expression of Fimbriae of Human Enterotoxigenic Escherichia Coli." In Molecular Pathogenesis of Gastrointestinal Infections, 61–70. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5982-1_9.

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Conference papers on the topic "Escherichia coli infections Pathogenesis"

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Al-Asmar, Jawaher, Sara Rashwan, and Layla Kamareddine. "The use of Drosophila Melanogaster as a Model Organism to study the effect of Bacterial Infection on Host Survival and Metabolism." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0186.

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Enterobacteriaceae, a large family of facultative anaerobic bacteria, encloses a broad spectrum of bacterial species including Escherichia coli, Salmonella enterica, and Shigella sonnei, that produce enterotoxins and cause gastrointestinal tract diseases. While much is known about the regulation and function of enterotoxins within the intestine of the host; the lack of cheap, practical, and genetically tractable model organisms has restricted the investigation of others facets of this host-pathogen interaction. Our group, among others, has employed Drosophila melanogaster, as a model organism to shed more light on some aspects of host-pathogen interplays. In this project, we addressed the effect of Escherichia coli, Salmonella enterica, and Shigella sonnei infection on altering the metabolic homeostasis of the host. Drosophila melanogaster flies were orally infected with Escherichia coli, Salmonella enterica, or Shigella sonnei, a method that mimics the natural route used by enteric pathogens to gain access to the gastrointestinal tract in humans. The results of our study revealed that both Escherichia coli and Shigella sonnei pathogens were capable of colonizing the host gut, resulting in a reduction in the life span of the infected host. Escherichia coli and Shigella sonnei infected flies also exhibited altered metabolic profiles including lipid droplets deprivation from their fat body (normal lipid storage organ in flies), irregular accumulation of lipid droplets in their gut, and significant elevation of systemic glucose and triglyceride levels. These metabolic alterations could be mechanistically attributed to the differential down-regulation in the expression of metabolic peptide hormones (Allatostatin A, Diuretic hormone 31, and Tachykinin) detected in the gut of Escherichia coli and Shigella sonnei infected flies. Salmonella enterica; however, was unable to colonize the gut of the host; and therefore, Salmonella enterica infected flies exhibited a relatively normal metabolic status as that of non infected flies. Gaining a proper mechanistic understanding of infection-induced metabolic alterations helps in modulating the pathogenesis of gastrointestinal tract diseases in a host and opens up for promising therapeutic approaches for infection induced metabolic disorders

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Mawlood, Ahang. "The Role of Escherichia coli and Klebsiella pneumoniae in Urinary Tract Infections in Erbil City." In 1st Scientific Conference of College of Health Sciences. Hawler Medical University, 2021. http://dx.doi.org/10.15218/hsc1.

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"Extended-spectrum Beta-lactamase mediated resistance in Escherichia coli isolates from patients with Urinary tract infections in Erbil." In Second Scientific Conference on Women's Health. Hawler Medical University, 2021. http://dx.doi.org/10.15218/whc.02.11.

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Lin, Yu, Zhilu Xu, Wenli Huang, Xiangqian Dong, Yang Sun, Fengrui Zhang, Caroline Chevarin, et al. "IDDF2022-ABS-0230 Impact of urbanization on prevalence of adherent-invasive escherichia coli in crohn’s disease patients: cause for pathogenesis?" In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 2–4 September 2022. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2022. http://dx.doi.org/10.1136/gutjnl-2022-iddf.5.

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Gao, Yali, Philip M. Sherman, Yu Sun, and Dongqing Li. "Multiplexed High-Throughput Electrokinetically-Controlled Immunoassay on a Chip for the Detection of Specific Bacterial Antibodies in Human Serum." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-42512.

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This work presents a multiplexed electrokinetically-controlled heterogeneous immunoassay that can process ten samples in parallel. The immunoassay microchip was soft-lithographically fabricated using poly(dimethylsiloxane) and glass. Controlling parameters of the electrokinetically-driven flow in the microfluidic network was determined by numerically simulating transport processes. Multiple passively adsorbed antigens captured antibodies present in samples, which then bound with TRITC-labeled detection antibodies to generate fluorescent signals. Antibodies against Escherichia coli O157:H7 and Helicobacter pylori were studied as model analytes. After conditions for antigen-coating were optimized, a 24-minute assay detected E. coli O157:H7 antibody in the concentration range of 0.02–10 μg/mL, and H. pylori antibody in the range of 0.1–50 μg/mL. In testing human serum samples, non-specific binding of serum components was effectively suppressed by using 10% (w/v) bovine serum albumin. An accuracy of 100% was achieved in detecting either E. coli O157:H7 antibody or H. pylori antibody from human serum samples. Simultaneous screening of both antibodies was also successfully demonstrated. The immunoassay chip shows an excellent potential for efficiently detecting multiple pathogenic infections in clinical environments.

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"Surveillance of Urine Cultures and Evaluation Gram Negative Uropathogens; Five Year Data from Erbil." In 4th International Conference on Biological & Health Sciences (CIC-BIOHS’2022). Cihan University, 2022. http://dx.doi.org/10.24086/biohs2022/paper.592.

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Urinary tract infections (UTIs) are most common infectious disease and a public health problem that imposes a large economic burden. The aim of this study is to gather surveillance data of urine cultures and determine the prevalence of uropathogens in urine samples of patients referred to outpatient clinics in Erbil region and to evaluate the antimicrobial susceptibility of the gram negative uropathogens. All urine cultures result of patients referred to Erbil hospitals in the last 5 years (2015-2020) are retrospectively examined in this study. Microorganisms are identified by standard bacterial methods and their susceptibilities are assessed by VITEK 2 automated system. The results of urine culture of 3380 suspected UTI cases are examined and out of 3097 positive cultures observed, a total of 1961 (63.3%) isolates are gram-negative and 1136 (36.7%) are gram-positive pathogens. The most common urinary pathogen determined in this study is Escherichia coli. The highest resistances of gram-negative urinary pathogens are against the ampicillin, trimethoprim/sulfamethoxazole and ceftriaxone. It is thought that the data obtained from this study will be useful in the planning of empirical treatment of urinary tract infections and in the development of rational antibiotic use policies.

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"PREVALENCE OF BACTERIAL AND PARASITIC URINARY TRACT INFECTION AMONG ASYMPTOMATIC FEMALES IN RURAL COMMUNITIES OF OGBOMOSO." In International Conference on Public Health and Humanitarian Action. International Federation of Medical Students' Associations - Jordan, 2022. http://dx.doi.org/10.56950/eklu3082.

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Urinary tract infection is one of the most important infection causing serious diseases in tropical and sub- tropical countries of Africa. Several factors have been associated with the high prevalence of urinary tract infections in Nigeria. This study was carried out to determine the urinary tract infection status among two hundred and forty (240) asymptomatic females over a period of six weeks (March to April 2022) among 240 females between the 20-50 years of age at Iluju and Saamo village, Ogbomoso, Oyo state, Nigeria. Two hundred and forty urine samples were collected from the females. The mid- stream urine samples collected were examined microscopically for the presence of parasites, after which they were cultured, biochemical findings and antimicrobial susceptibility tests were also carried out. Out of the 240 samples, only 1(0.4%) was found positive for parasitic infection. 34(14.2%) were found to harbour Escherichia coli, 18(7.5%) were positive for Proteus mirabilis, 8(3.3%) were infected by Klebsiella pneumonia, 45(18.8%) had Staphylococcus aureus. Prevalence was found to be higher in women of reproductive age 21-25years (78%) than women above 40years (10.5%). The antimicrobial suspectibility profile indicates that the fluoroquinlonones were the most active antibacterial agents followed by the aminoglycosides. Trimethorim, oxacillim, amoxicillin showed very poor activity. This may be due to long term use of these drugs. The socio- economic status as well as the hygiene practice of the women influence the prevalence of urinary tract infections. Most of the women 134(55.8%) were aware about Urinary tract infection and 106 (44.2%) were unaware. Thus, the high infection rate among asymptomatic females in these villages were due to poor hygiene, lack of good toilet facilities and poor socio- economic status. Keywords: Bacterial, Parasitic, Rural, Ogbomoso, Females, hygiene

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Abibu, Wasiu Ayodele, Abdul Wasiu Sakariyau, Gafar Bamigbade, Amos Kolawole Oyebisi, and Isqeel Ogunsola. "Consumer Perception of Ready-To-Eat Fruits Sold in Ogun and Lagos, Nigeria During the Covid-19 Pandemic." In International Students Science Congress. Izmir International Guest Student Association, 2021. http://dx.doi.org/10.52460/issc.2021.013.

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Covid-19 pandemic is a global health issue that adversely affected every sector of the world’s economy. Fruits are known to be a source of vitamins providing the body with necessary defense against infections (inclusive of Coronaviruses). Nigerians prefer to buy ready-to-eat (RTE) fruits than whole fruits due to their high prices. Consumer perception of RTE fruits sold in Ogun and Lagos, Nigeria during the Covid-19 pandemic months in 2020 and within January and March 2021 via an online survey were compared. Ogun and Lagos states were selected because they represent major entry routes for land and air travel into Nigeria respectively. 500 respondents were obtained with 49.7% each as male and female respectively in Ogun state while Lagos had 49.5% and 50.5% of the male and female gender. In addition, the predominant age group that responded to the questionnaire falls within 21 – 30 with 49.7% in Ogun state and 54.1% in Lagos state. 96.1% of the respondents in Ogun state had a tertiary education while 99% was recorded to possess tertiary education in Lagos state. 34% respondents took RTE fruits 2- 3 times a week, 31.2% less than once a week while only 2.8% took RTE fruits 4 – 5 times a week. From the survey, 84% of the respondents were aware that fruits possess needed vitamins to fight infections while only 87.4% of the respondent were aware of fruit borne poisoning and have knowledge of fruit borne pathogens like Staphylococcus aureus, Escherichia coli, Klebsiellaspp, Pseudomonas aeruginosa, Penicilliumspp, Aspergillusnigerand Rhizopusstolonifer. This study shows that fruit consumers neglected health consciousness in the purchase of RTE fruits in Ogun and Lagos in the first 3 months of 2021 compared to 2020. This negligence may result in a spike of another Covid-19 wave in Ogun and Lagos if the necessary food and health regulatory authorities fail to act timely. Also, the application of an effective hazard analysis and critical control point (HACCP) application reduces the chance of contamination of ready- to- eat fruits.

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Khair, Nedaa Kamalalden. "Activity of Antibiotic Producing Bacteria Isolated from Rhizosphere Soil Region of Different Medicinal Plants." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0093.

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The rhizosphere soil of medicinal plants is rich in microorganisms that develop antibiotics as natural mechanism of protection against other microbes that live in their vicinity. The present study aims to explore the production of antibacterial agents from rhizosphere soil bacteria of 11 medicinal plants and determine their activity against Gram-negative (Pseudomonas aeruginosa, Escherichia coli) and Gram-positive (Bacillus cereus, Staphylococcus aureus) bacteria. Soil samples were collected and used to isolate antibiotic producing bacteria (APB). Those isolates (108) were first tested using Cross-streak method against test bacteria. Then, isolates that showed a positive antibacterial effect (12) were tested by antibiotic susceptibility test (AST) of their cell free supernatant (CFS) and their extracellular and intracellular secondary metabolites extraction which gave positive results. Staphylococcus aureus found to be the most sensitive test bacteria with inhibitory zones ranging from 13.5 - 19 mm. Moreover, combinatorial effect of isolates CFS with two organic acids (3% Acetic acid and 0.4 mg/ml Acetylsalicylic acid), two commercial antibiotics (0.016 mg/ml Augmentin and 0.128 mg/ml Doxycycline), and two pure antibiotics (10 mcg/disk Penicillin and 25mcg/disk Carbenicillin) was in vitro evaluated using AST. The combinations of CFS-carbenicillin showed a marked synergistic activity against all test bacteria. The presence of possible antibacterial agents as acetic acid, lactic acid and citric acid in CFS of APB was confirmed by HPLC analysis. Ultimately, in vitro antibacterial study for rhizosphere soil bacteria in this work suggests the possibility of using these bacterial metabolites in clinical infections caused by selected test bacteria, especially when they combine with antibiotics or organic acids.

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Reports on the topic "Escherichia coli infections Pathogenesis"

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Shpigel, Nahum Y., Ynte Schukken, and Ilan Rosenshine. Identification of genes involved in virulence of Escherichia coli mastitis by signature tagged mutagenesis. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7699853.bard.

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Mastitis, an inflammatory response of the mammary tissue to invading pathogenic bacteria, is the largest health problem in the dairy industry and is responsible for multibillion dollar economic losses. E. coli are a leading cause of acute mastitis in dairy animals worldwide and certainly in Israel and North America. The species E. coli comprises a highly heterogeneous group of pathogens, some of which are commensal residents of the gut, infecting the mammary gland after contamination of the teat skin from the environment. As compared to other gut microflora, mammary pathogenic E. coli (MPEC) may have undergone evolutionary adaptations that improve their fitness for colonization of the unique and varied environmental niches found within the mammary gland. These niches include competing microbes already present or accompanying the new colonizer, soluble and cellular antimicrobials in milk, and the innate immune response elicited by mammary cells and recruited immune cells. However, to date, no specific virulence factors have been identified in E. coli isolates associated with mastitis. The original overall research objective of this application was to develop a genome-wide, transposon-tagged mutant collection of MPEC strain P4 and to use this technology to identify E. coli genes that are specifically involved in mammary virulence and pathogenicity. In the course of the project we decided to take an alternative genome-wide approach and to use whole genomes bioinformatics analysis. Using genome sequencing and analysis of six MPEC strains, our studies have shown that type VI secretion system (T6SS) gene clusters were present in all these strains. Furthermore, using unbiased screening of MPEC strains for reduced colonization, fitness and virulence in the murine mastitis model, we have identified in MPEC P4-NR a new pathogenicity island (PAI-1) encoding the core components of T6SS and its hallmark effectors Hcp, VgrG and Rhs. Next, we have shown that specific deletions of T6SS genes reduced colonization, fitness and virulence in lactating mouse mammary glands. Our long-term goal is to understand the molecular mechanisms of host-pathogen interactions in the mammary gland and to relate these mechanisms to disease processes and pathogenesis. We have been able to achieve our research objectives to identify E. coli genes that are specifically involved in mammary virulence and pathogenicity. The project elucidated a new basic concept in host pathogen interaction of MPEC, which for the best of our knowledge was never described or investigated before. This research will help us to shed new light on principles behind the infection strategy of MPEC. The new targets now enable prevalence and epidemiology studies of T6SS in field strains of MPEC which might unveil new geographic, management and ecological risk factors. These will contribute to development of new approaches to treat and prevent mastitis by MPEC and perhaps other mammary pathogens. The use of antibiotics in farm animals and specifically to treat mastitis is gradually precluded and thus new treatment and prevention strategies are needed. Effective mastitis vaccines are currently not available, structural components and effectors of T6SS might be new targets for the development of novel vaccines and therapeutics.

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Gutnick, David, and David L. Coplin. Role of Exopolysaccharides in the Survival and Pathogenesis of the Fire Blight Bacterium, Erwinia amylovora. United States Department of Agriculture, September 1994. http://dx.doi.org/10.32747/1994.7568788.bard.

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Fireblight, a disease of apples and pears, is caused by Erwinia amylovora. Mutants of E. amylovora that do not produce the extreacellular polysaccharide (EPS), amylovoran, are avirulent. A similar EPS, stewartan, is produced by E. stewartii, which caused Stewart's wilt of corn, and which has also been implicated in the virulence of this strain. Both stewartan and amylovoran are type 1 capsular polysaccharides, typified by the colanic acid slime produced by Escherichia coli. Extracellular polysaccharide slime and capsules are important for the virulence of bacterial pathogens of plants and animals and to enhance their survival and dissemination outside of the host. The goals of this project were to examine the importance of polysaccharide structure on the pathogenicity and survival properties of three pathogenic bacteria: Erwinia amylovora, Erwinia stewartii and Escherichia coli. The project was a collaboration between the laboratories of Dr. Gutnick (PI, E. coli genetics and biochemistry), Dr. Coplin (co-PI, E. stewartii genetics) and Dr. Geider (unfunded collaborator, E. amylovora genetics and EPS analysis). Structural analysis of the EPSs, sequence analysis of the biosynthetic gene clusters and site-directed mutagenesis of individual cps and ams genes revealed that the three gene clusters shared common features for polysaccharide polymerization, translocation, and precursor synthesis as well as in the modes of transcriptional regulation. Early EPS production resulted in decreased virulence, indicating that EPS, although required for pathogenicity, is anot always advantageous and pathogens must regulate its production carefully.

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