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Undergraduate Research Project Management System

Panton-Valentine Leukocidin Expression in Community Associated Methicillin Resistant Staphyloccocus Aureus from Rural Alaska

Status Current
Seeking Researchers No
Start Date 09/01/2007
End Date 06/30/2008
Funding Source Alaska Heart Institute Fellowships
Funding Amount
Community Partner
Related Course
Last Updated 07/05/2008 01:25AM
Keywords

People

Faculty
  John Kennish

Student Researchers
  Mindy Graham

Abstract

Incidence of infection by Methicillin resistant Staphyloccocus aureus (MRSA) has historically been attributed to nosocomial sources, but there is currently an increasing trend towards community acquired infection not associated with hospital settings. Community-associated MRSA (CA-MRSA) is most often associated with skin and soft tissue infections rather than invasive disease. The majority of isolates causing skin infections in healthy peoplecarry a gene for a toxin called Panton-Valentine leukocidin (PVL). Presence of the PVL gene in the majority of community associated human skin infections has led to general acceptance for PVL as an important virulence factor. One recent study, however, has suggested that presence of the PVL gene has no effect on MRSA virulence and so this has become a point of contention in the understanding of the pathogenesis of these infections. The objective of this experiment is to verify if PVL is indeed a virulence factor in community associated-MRSA (CA-MRSA) by studying isolates collected from a skin infection outbreak in rural Alaska. This experiment will detect and quantify the expression of PVL by studying messenger ribonucleic acid (mRNA). PVL mRNA levels will be measured using reverse transcriptase real-time polymerase chain reaction (RT-PCR). I am hoping to determine whether or not CA-MRSA strains that carry the PVL gene are actually producing the PVL toxin. If findings show that the PVL gene is universally expressed, then it can be suggested that PVL plays a role in the pathogenicity of CA-MRSA skin infections. If PVL expression levels differ between isolates of the same outbreak, this might provide supporting evidence for an alternate mechanism of infection.

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