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DEVELOPING A TOOL FOR SITE-SPECIFIC GENE INACTIVATION IN CHLAMYDIAJohnson, Cayla Marie 01 December 2014 (has links)
Chlamydia trachomatis is an obligate intracellular bacterial pathogen that infects both humans and domestically important animals. Research in the field has until more recently been hindered by a lack of genetic tools. We have modified Sigma's TargeTronTM Gene Knockout System, which utilizes a mobile group II intron for site-specific insertion and gene inactivation, for use in C. trachomatis. As proof of principle, we used the system to inactivate incA, creating mutant strains DFCT3 and DFCT4 (independent clones both carrying incA::GII[bla]). IncA is a chlamydial inclusion membrane protein involved in homotypic fusion of inclusions when cells are infected with more than one bacterium. Genotypic and phenotypic analysis was performed to ensure successful intron insertion into incA and loss of IncA function. Further characterization of the incA::GII(bla) mutant examined its pathogenicity relative to the wild type strain and indicated that the mutant was attenuated for growth in a mouse infection model, but not in a cell culture infection model. Complementation of the incA mutant confirmed that the phenotype differences between the wild type strain and the mutant were due to inactivation of incA. As incA mutants arise spontaneously during human infections, future work will focus on the role of IncA in pathogenesis using the mutant strains derived from this study.
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Prévalence et indicateurs de risque d'infections cervicales à Chlamydia trachomatis lors de cytologies annuelles (Pap test) au CLSC St. Louis du Parc à MontréalMassé, Richard January 1989 (has links)
Note:
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Chlamydia trachomatis in university women an epidemological study /Hietpas, Kristine Kratzer. January 1980 (has links)
Thesis (M.S.)--University of Wisconsin-Madison. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 61-65).
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Modulation of interferon-gamma receptor expression during infection with Chlamydia psittaci 6bc and its influence on indoleamine 2,3-dioxygenaseShirey, Kari Ann. January 2006 (has links)
Thesis (Ph. D.)--Miami University, Dept. of Microbiology, 2006. / Title from second page of PDF document. Document formatted into pages; contains [3], vi, 176 p. : ill. Includes bibliographical references (p. 131-176).
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The use of magnetic resonance imaging to evaluate Chlamydia as an aetiological agent in Alzheimer's diseaseSzczerba, Stephen Michael 24 August 2009 (has links)
It has been suggested that infection with Chlamydia may play a role in the initiation/progression of Alzheimer’s disease (AD). To evaluate this hypothesis APP/PS transgenic mice (genetically manipulated to express AD pathology) and wild type (Wt) mice were infected with C. muridarum, and magnetic resonance imaging (MRI) and histopathology were used to assess pathological changes.
Congo red staining of tissue sections demonstrated no AD plaque pathology in Wt infected and non-infected mice, while clear pathology (neuritic plaques) was seen in transgenic mice, with a trend towards higher plaque counts in the brains in the infected transgenic mice.
When MRI was used to evaluate the effects of infection in vivo, hyperintensities in T2 times were observed in APP/PS infected mice compared to APP/PS control mice both at month 5 and month 20. Together these results suggest that infection with Chlamydia may accelerate the development of AD.
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The use of magnetic resonance imaging to evaluate Chlamydia as an aetiological agent in Alzheimer's diseaseSzczerba, Stephen Michael 24 August 2009 (has links)
It has been suggested that infection with Chlamydia may play a role in the initiation/progression of Alzheimer’s disease (AD). To evaluate this hypothesis APP/PS transgenic mice (genetically manipulated to express AD pathology) and wild type (Wt) mice were infected with C. muridarum, and magnetic resonance imaging (MRI) and histopathology were used to assess pathological changes.
Congo red staining of tissue sections demonstrated no AD plaque pathology in Wt infected and non-infected mice, while clear pathology (neuritic plaques) was seen in transgenic mice, with a trend towards higher plaque counts in the brains in the infected transgenic mice.
When MRI was used to evaluate the effects of infection in vivo, hyperintensities in T2 times were observed in APP/PS infected mice compared to APP/PS control mice both at month 5 and month 20. Together these results suggest that infection with Chlamydia may accelerate the development of AD.
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Studies in DNA immunization /Svanholm, Cecilia, January 1900 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 4 uppsatser.
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Funktionelle Proteomanalyse von Chlamydophila pneumoniaeWehrl, Wolfgang. January 2004 (has links)
Berlin, Freie Universiẗat, Diss., 2005. / Dateiformat: zip, Dateien im PDF-Format.
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Detección de Neisseria gonorrhoeae y Chlamydia trachomatis en hombres que tienen sexo con hombres (HSH) mediante la prueba de Amplificación Mediada por Transcripción de ácido ribonucleico, Epicentro, Lima 2013 - 2014Vásquez Vásquez, Francesca Rosalía de María January 2016 (has links)
Determina la frecuencia de N. gonorrhoeae y C. trachomatis anal en HSH usando Amplificación Mediada por Transcripción (TMA) en muestras de hisopado anal. El método de Amplificación Mediada por Transcripción (TMA) tiene la capacidad de detectar pequeñas cantidades de ARN ribosomal (ARNr) de N. gonorrhoeae y C. trachomatis. Este estudio es imperioso ya que existe una alta frecuencia de contagio de ITS en la población de estudio, para lo cual el uso de TMA en pacientes con infecciones asintomáticas permitiría una detección adecuada y oportuna evitando así la diseminación de estas enfermedades a otros sujetos. / Tesis
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Chlamydiae under stress : environmental conditions influence the production and localization of chlamydial antigensBrown, Wendy J. 28 June 2002 (has links)
Chlamydiae are obligate intracellular pathogens that cause several serious
conditions within the human host. Many of the symptoms associated with infection
are thought to stem from the development of aberrant, or persistent, chlamydiae.
Factors leading to chlamydial persistence include deprivation of amino acids, the
release of certain cellular factors, or the addition of inhibitors of bacterial cell wall
or DNA synthesis. Such changes within the chlamydial environment often lead to
modifications in cell morphology, gene expression, chlamydial development, and
antigen localization. In this report, I examine changes in antigen production and
localization in Chlamydia-infected cells cultured in the presence of environmental
stressors. There are three major areas of chlamydial biology examined: 1) how do
the chlamydiae divide in the absence of FtsZ, 2) what is the importance of the
predicted peptidoglycan hydrolase, PapQ; 3) what changes occur in antigen
production and localization during the development of chlamydial persistence. One
significant nonproteinacious factor apparently involved in chlamydial division is
the SEP (septum) antigen, which localizes to the midcell of dividing chlamydiae.
Non-dividing forms, such as persistent chlamydiae and EB, lack the septal
placement of SEP, further suggesting the involvement of SEP in RB division. The
production of the predicted hydrolase, PapQ, localizes to the cytosol of RB and, to
a limited extent, within the EB. PapQ begins to accumulate as early as 12 hours
after infection and during the time of RB-EB transition, an additional, smaller
PapQ product accumulates. Ampicillin and tetracycline treatment inhibits
accumulation of the smaller product suggesting that PapQ may be processed by a
late expressed protease. This may have significance in RB-EB transition. The
IncA-laden fibers protruding from the inclusion and into the host cytosol colocalize
with a variety of different antigens that are generally restricted to the chlamydial
outer membrane. Changes in culture conditions leads to changes in the amount and
type of antigens localizing within the fibers. Chlamydial persistence dramatically
influences the production and localization of several chlamydial antigens, creating
significant changes in chlamydial cell biology that may enhance survival within the
host. / Graduation date: 2003
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