Pathogenesis Take Home Activity

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School

University of South Florida *

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Course

3023

Subject

Biology

Date

Dec 6, 2023

Type

docx

Pages

1

Uploaded by hermionehpfan123

Name:___Sanika Kende ______ Lab Section:_901 _ Microbial Pathogenesis Activity: Part II Take-home writing assignment You will be working on this assignment individually to utilize the pathogen and review article from Part I of this activity, along with one additional source you have found. You can use this word doc as a template to complete parts A-C below, save, and print hard copy & upload electronic copy to Canvas. (15pt) Pathogen: _Clostridium difficile ________ A. Buonomo E., Petri W. A., The microbiota and immune response during Clostridium difficile infection, Anaerobe, Volume 41, (2016). pages 79-84, ISSN 1075-9964, https://doi.org/10.1016/j.anaerobe.2016.05.009 Rineh, A., Kelso, M. J., Vatansever, F., Tegos, G. P., & Hamblin, M. R. (2014). Clostridium difficile infection: molecular pathogenesis and novel therapeutics. Expert review of anti-infective therapy , 12 (1), 131–150. https://doi.org/10.1586/14787210.2014.866515 B. The additional article I have found and listed above is classified as a review article as it is reviewing the structure and mechanism of action of toxins A and B, rather than providing new research and disseminating the results. C. C. difficile is a gram-positive, anaerobe gastrointestinal bacterium that can cause many diseases such as diarrhea and colitis (Rineh et, al, 2014). The C. difficile pathogenicity locus, which is a 19.6- kb chromosomal region, contains the genes for toxins A and B, also known as TcdA and TcdB; these toxins make use of their cytotoxic activity by modifying cytoskeletal components (Buonomo et. al, 2016). This mechanism is carried out through the fact that the toxins are glucosyltransferases that “irreversibly inactivate small Rho GTPases,” which disrupts cytoskeletons and tight junctions and eventually leads to cell death in the host (Buonomo et. al, 2016). This mechanism allows for the pathogenicity of the toxins to spread.
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