Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.601682
Title: Investigating the virulence factors of Staphylococcus aureus
Author: Rudkin, Justine K.
Awarding Body: University of Bath
Current Institution: University of Bath
Date of Award: 2012
Availability of Full Text:
Access from EThOS:
Abstract:
Staphylococcus aureus is an important human pathogen and is a common cause of hospital -associated infections. It has the ability to cause a wide range of diseases, facilitated by a plethora of virulence factors. Resistance to antibiotics has played an important role in the recent evolution of this bacterium, allowing it to persist in the face of antibiotic treatment. The ever- increasing levels of resistance to multiple classes of antibiotics, has earned MRSA the name "superbug". However this antibiotic resistance comes at a biological cost. The aim of this thesis were to examine the negative effect of the methicillin resistance encoding type II SCCmec element on cytotoxicity and investigate the lack of an effect caused by the type IV SCCmec element We found that; The type II SCCmec element is implicated in the reduced cytotoxicity of type Il HA-MRSA. Expression of the mecA gene from the SCCmec element is directly responsible for this effect. High levels of mecA expression are required to produce the loss of cytotoxicity . Loss of cytotoxicity is caused by a lack of Agr quorum system activity. The cell wall of highly resistant type Il HA-MRSAs prevent quorum system signalling. Reduced cytotoxin expression in type IJ HA-MRSAs leads to reduced virulence in a murine model of sepsis. The relatively low level of mecA expression from the type IV element explains the maintenance of cytotoxicity in type IV CA-MRSAs. By increasing the level of mecA expression in type IV CA-MRSA we can reduce cytotoxin production. By addition of sub-inhibitory concentrations of oxacillin to the growth environment of type IV CA-MRSAs we can reduce cytotoxicity and reduce infection related morbidity in an invertebrate model of infection.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.601682  DOI: Not available
Share: