New research has found that as the superbug resists antibiotics, it becomes less virulent
LIFE IS full of trade-offs, and it seems the hospital-acquired “superbug” MRSA is no exception. A new study led by Irish scientists has discovered that when the bacterium acquires resistance to antibiotics, it becomes less virulent, at least in a lab model.
The finding could help shed light on why patients who have compromised immune systems are particularly vulnerable to healthcare-associated MRSA infections.
MRSA develops when a bacterium called Staphylococcus aureus (SA) acquires resistance to a number of antibiotics and becomes methicillin-resistant Staphylococcus aureus (MRSA).
The new study, just published in the open-access journal PLoS Pathogens, looked at SA and MRSA infections associated with medical devices that are surgically implanted in a laboratory model, explains lead author Dr Jim O’Gara from UCD’s Conway Institute.
“Bacteria are naturally present on the skin, where they often don’t cause any problem. But if they stick onto medical devices that are put into the body they can get access through the skin’s barrier and then they can potentially establish an infection,” he says.
“They will form biofilms, which are communities of bacteria attached to the medical device, and those biofilms are almost indestructible. In that case you have to take the device out and put in a new one, which is not always a trivial thing for the patient.”
O’Gara and a colleague at Beaumont Hospital noticed several years ago that SA and MRSA biofilms looked different.
“Our early research in this area revealed a hugely surprising result – that MRSA and SA use different ways of forming biofilms,” says O’Gara.
Their discovery was that SA bacterial cells use sugars to stick to each other and to surfaces as biofilms, while MRSA instead use proteins to form biofilms.
With funding from the Health Research Board, his group brought the project further and looked at the effects of turning SA into MRSA in the lab. They used a preclinical model that introduced infection by allowing the bacteria to form biofilms on implanted medical devices.
Again, the results far exceeded their expectations: when SA became resistant to the antibiotic methicillin (and so became MRSA), its ability to cause illness was toned down.
“What the data show is that if you take SA and you make it resistant to methicillin, you change the way it forms biofilms, but you also make it less virulent in a preclinical model,” says Dr O’Gara, whose group at UCD worked on the project with colleagues at the University of Bath, Harvard Medical School and the University of Nebraska.
“It’s like the bacteria are making a decision to divert their energy towards becoming resistant to the drugs, and they are not going to expend energy producing as many toxins or enzymes.”
In essence, the findings suggest that hospital-acquired MRSA may have have adapted to the hospital environment by sacrificing virulence for antibiotic resistance, according to O’Gara.
“This trade-off works for the pathogen because patients in hospital, particularly in an intensive care setting, can be very immuno-compromised and the pathogen does not need to be very virulent,” he says. “On the other hand, the bacterium does need to be very antibiotic resistant, due to the necessarily high levels of antibiotic usage in intensive care units.”
O’Gara is now looking into how the discovery could be used to help make MRSA less nasty for patients who get infected. “It may open up new ways to find anti-virulence drugs,” he says.
