Dr. McGavin is an Associate Professor in the Department of Microbiology and Immunology at Western University, and is a member of the Centre for Human Immunology. Previous appointments were at University of Manitoba (1992-1996), and University of Toronto Sunnybrook Health Science Centre (1997-2009) B.Sc. (1985) and Ph.D (1989); University of Guelph, Departments of Applied Microbiology (1985) and Microbiology (1989) Postdoctoral Fellow (1989-1992); University of Alabama at Birmingham, Department of Biochemistry Premiers Research Excellence award; 1999-2002 Medical Research Council Scholarship Award; 1994-1999

Research in the McGavin laboratory is focused on understanding how Staphylococcus species colonize and infect human hosts. With an emphasis on S. aureus, we use a broad range of genetic and biochemical tools and techniques to study mechanisms of colonization and tissue invasion. Approximately 15-25% of the human population is persistently and asymptomatically colonized by S. aureus. The preferred site of colonization is the anterior nares (nose), and other common sites include the axillae and perineum. Although S. aureus benefits from establishing an asymptomatic commensal relationship with humans, it is also a leading cause of infectious morbidity and mortality, ranging from minor skin and soft tissue infections, to severe life threatening infective endocarditis, osteomyelitis, necrotizing pneumonia, and toxic shock. The status of S. aureus as a leading cause of hospital associated infections is compounded by hospital associated methicillin resistant S. aureus (MRSA), which are resistant to multiple antimicrobial agents, and in the past decade, hyper-virulent community associated MRSA (CA-MRSA) have become endemic in the community. Current research supported by NSERC aims to understand how S. aureus and skin commensal S. epidermidis respond to conditions that would be encountered on colonization of human skin.

Arsic B, Zhu Y, Heinrichs DE, McGavin MJ. 2012. Induction of the staphylococcal proteolytic cascade by antimicrobial fatty acids in community acquired methicillin resistant Staphylococcus aureus. PLOS One 7:e45952 McGavin M.J., Arsic, B., and Nickerson, N.N. 2012. Evolutionary blueprint for host- and niche-adaptation in Staphylococcus aureus clonal complex CC30. Front Cell Infect Microbiol 2:48 DeLeo FR, Kennedy AD, Chen L, Bubeck Wardenburg J, Kobayashi SD, Mathema B, Braughton KR, Whitney AR, Villaruz AE, Martens CA, Porcella SF, McGavin, MJ, Otto M, Musser JM, Kreiswirth BN. 2011. Molecular differentiation of historic phage-type 80/81 and contemporary epidemic Staphylococcus aureus. Proc Natl Acad Sci USA 108(44):18091-18096 Yeung M, Balma-Mena A, Shear N, Simor A, Pope E, Walsh S, McGavin MJ. 2011Microbes Infect. 2011 Identification of major clonal complexes and toxin producing strains among Staphylococcus aureus associated with atopic dermatitis. Microbes Infect 13(2):189-97 Nickerson N., Ip J., Passos, D., and McGavin, MJ. 2010 Comparison of Staphopain A (ScpA) and Staphopain B (ScpB) precursor activation mechanisms reveals unique secretion kinetics of proSspB (Staphopain B), and a different interaction with its cognate staphostatin, SspC. Mol. Microbiol. 75(1):161-177