Infectious Diseases and Immunology Division
Bacterial Pathogenesis Associate Professor Kadaba Sriprakash David McMillan , Michael Binks , Catherine Denham Josephine Shera, Mark Davies , Melina Georgousakis Karen Taylor, Thanh Tran
This laboratory investigates how Group A streptococcus (GAS) is able to overcome host defense and cause disease. Research is undertaken on characterising novel GAS vaccine antigens, and on the role and extent of horizontal gene transfers between different streptococcal species and how this can turn normally harmless commensal bacteria into potential disease causing bacteria
Biofilms are communities of bacteria that grow together for their mutual benefit. The bacteria in biofilms have different properties to individual free living bacteria. Group A streptococci also form biofilms, and this is probably their natural state during a throat infection. Researching how GAS behave in Biofilms gives a greater understanding of how they cause disease
Highlights Found that Group G streptococcus acquires group A streptococcal genes frequently among populations in whom GAS diseases are endemic Discovered that many different sub-types of GAS are circulating in Northern India, similar to observations seen in Indigenous Australians living in the Northern Territory of Australia
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Research towards effective vaccine against GAS infection Recent work confirmed the high diversity of circulating types in the northwest part of India, similar to isolates from Australia. However, the composition of the types may differ in these two countries, thus any vaccine based on the highly variable antigen would have to be specifically tailored for the region where it is targeted. The search for other vaccine antigens that will provide broad spectum protection continues. It has been suggested streptococcal adhesins such as SfbI can offer protection against GAS infection but the laboratory has now shown that although mucosal antibodies to this protein prevents GAS adherence, it does not elicit opsonic antibodies and does not prevent systemic bacterial growth and dissemination to internal organs after subcutaneous GAS challenge. Are commensal streptococci in bad company among pathogenic relatives? Human group G streptococci are largely commensal streptococci. Horizontal genetic transfers between this organism and pathogenic GAS have already been observed. Researchers in this laboratory recently confirmed the ongoing nature of phage-mediated lateral
acquisitions between these species, and that this occurs at an appreciable frequency. The significance of this finding for streptococcal epidemiology and in effective control of streptococcal diseases is far reaching, particularly in GAS-endemic regions. Fibronectin binding and GAS adherence GAS expresses a large number of fibronectin binding proteins which promote adherence to host cells. While fibronectin binding is important in adherence, the first event in the process of colonisation, it has now been shown that the extent of fibronectin binding is not a critical determinant of adherence. A collaborative study on phylogenetic analysis of two subtypes of PrtF2, another fibronectin binding adhesin, revealed that one subtype is more variable than the other. GAS and host innate immunity Some GAS strains express Streptococcal Inhibitor of Complement (SIC). SIC is a multifunctional protein with distinct structural domains. Molecular dissection of SIC to determine association between its structural and functional domains was undertaken in a collaborative study.
Queensland Institute of Medical Research