Assessment of virulence diversity of methicillin-resistant Staphylococcus aureus strains with a Drosophila melanogaster infection model
1 Department of Pathology & Laboratory Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, AB, T2N 4N1, Canada
2 Department of Microbiology, Immunology and Infectious Diseases, University of Calgary, Calgary, AB, Canada
3 Department of Medicine, University of Calgary, Calgary, AB, Canada
4 The Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, University of Calgary, Calgary, AB, Canada
5 Centre for Antimicrobial Resistance, Alberta Health Services/Calgary Laboratory Services/University of Calgary, Calgary, AB, Canada
6 Farncombe Family Digestive Health Research Institute, Departments of Medicine and Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada
7 Department of Medicine, University of Western Ontario, London, ON, Canada
8 Department of Microbiology & Infectious Disease, University of Western Ontario, London, ON, Canada
BMC Microbiology 2012, 12:274 doi:10.1186/1471-2180-12-274Published: 23 November 2012
Staphylococcus aureus strains with distinct genetic backgrounds have shown different virulence in animal models as well as associations with different clinical outcomes, such as causing infection in the hospital or the community. With S. aureus strains carrying diverse genetic backgrounds that have been demonstrated by gene typing and genomic sequences, it is difficult to compare these strains using mammalian models. Invertebrate host models provide a useful alternative approach for studying bacterial pathogenesis in mammals since they have conserved innate immune systems of biological defense. Here, we employed Drosophila melanogaster as a host model for studying the virulence of S. aureus strains.
Community-associated methicillin-resistant S. aureus (CA-MRSA) strains USA300, USA400 and CMRSA2 were more virulent than a hospital-associated (HA)-MRSA strain (CMRSA6) and a colonization strain (M92) in the D. melanogaster model. These results correlate with bacterial virulence in the Caenorhabditis elegans host model as well as human clinical data. Moreover, MRSA killing activities in the D. melanogaster model are associated with bacterial replication within the flies. Different MRSA strains induced similar host responses in D. melanogaster, but demonstrated differential expression of common bacterial virulence factors, which may account for the different killing activities in the model. In addition, hemolysin α, an important virulence factor produced by S. aureus in human infections is postulated to play a role in the fly killing.
Our results demonstrate that the D. melanogaster model is potentially useful for studying S. aureus pathogenicity. Different MRSA strains demonstrated diverse virulence in the D. melanogaster model, which may be the result of differing expression of bacterial virulence factors in vivo.