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Role of the host fibrinolytic system in invasive group A streptococcal disease
Dr Martina Sanderson-Smith, NHMRC CDA Research Fellow, School of Biological Sciences
A sore throat is a common, mild illness which affects thousands of people every year. Usually, the clever human immune system can rid the body of the bacterium, Group A streptococcus (GAS), which causes the infection, within days.
However, a sore throat is the moderate end of the damage this bacterium can cause to human health, with cases of the adverse complications of GAS becoming more common across the world. More worryingly, in developing countries and socioeconomically disadvantaged communities, infection rates are higher and increasing. In Indigenous communities in Australia’s Northern Territory, infection rates are five times higher compared to the rest of the country’s population. GAS is ranked as one of the top 10 human pathogens.
Invasive cases of Group A strep invade the bloodstream and deep tissue, and can lead to flesh eating disease, known as necrotising fasciitis; can infect the blood, causing bacteraemia; or cause toxic shock syndrome. Recurrent infections may lead to kidney disease and rheumatic heart disease, with one of the highest incidence rates in the world among Indigenous Australians.
Looking at ways to reduce the incidence, and better treat the nasty effects of Group A strep, is a significant research field that begins with a better understanding of how the bacterium takes hold in the human body.
Building this foundation of knowledge is the realm of Dr Martina Sanderson-Smith, who is investigating the “hijacking” of the body’s plasminogen activation system – which regulates blood coagulation, tissue remodelling and cell migration – by Group A strep in the first few hours of infection.
“A systemic or invasive infection happens so quickly – it can be a matter of hours from the time you first notice symptoms – and by that stage it becomes very difficult to treat with antibiotics. So if we can control or contain the infection at these very early stages then we should have a better chance of treating it,” Sanderson-Smith says.
Broadly, the GAS bacterium cleverly attaches an enzyme of the plasminogen activation system to its surface, and takes it under its control. The bacterium is then able to advance into tissue, or into the usually sterile blood stream.
“The plasminogen activation system has a role in the migration of immune cells to the site of the infection, but we don’t really know how group A strep hijacking the system affects the immune response. That’s really what I want to find out,” Sanderson-Smith says.
Results to come out of the early stages of the study show that multiple components of the plasminogen activation system are required for invasive disease, and targeting these host-specific factors may lead to new treatment options.
“So far it looks like we’re on the right track. This angle hasn’t really been looked at in the field before so I’m hoping that it will provide interesting new data.
“I’m not sure I’m ever going to come up with a new treatment for Group A strep infection – although that would be really nice – but the work that I do might contribute to better treatment and better disease outcomes for people in the longer term.”
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