A tiny molecular strand might provide a solution to one of the most significant worldwide health issues. The emergence of bacteria resistant to antibiotics can have lethal consequences; however, researchers have recently made progress in understanding part of how these bacteria defend themselves.
Picture yourself suffering from a severe infection. Typically, a visit to the doctor results in a prescription for antibiotics, and after about a week, you’re usually back to your normal self. Sadly, that is no longer a guarantee. Conditions like pneumonia, tuberculosis, or blood poisoning are becoming increasingly tough to treat. The World Health Organization (WHO) warns that millions of lives could be at stake if we fail to address the antibiotic-resistant MRSA bacteria.
Bacteria often develop resistance to antibiotics by creating a biofilm made of proteins and sugars that serves as a barrier against medication. A recent study has begun to unravel this biofilm’s defense mechanism, according to Maria Andreasen, an Associate Professor at the Department of Biomedicine at Aarhus University and one of the study’s authors:
“We have successfully revealed the molecular structure of a key component in the bacterium known as S. aureus. This marks the first comprehensive look at how these specific molecules create their larger structure. Understanding these formations and the biofilm’s development can help us craft new treatment strategies and potentially stop the bacteria from creating biofilms in the first place.”
A life-threatening issue
Even though the research emphasizes molecular cell structures, it aims to tackle a broader and more impactful problem. A 2022 study indicated that 1.27 million individuals around the world died in 2019 due to infections caused by antibiotic-resistant bacteria.
This highlights the importance of the findings from the collaboration between Aarhus University and the University of Pittsburgh, according to Maria Andreasen.
“For the first time, we have mapped out the complete protein structure of the MRSA biofilm. Now, we can direct our research towards leveraging this knowledge to discover or create molecules that can inhibit biofilm formation. Achieving this would simplify the treatment of infections and help combat the rising issue of antibiotic resistance,” she explains.
If the research team, including members from the University of Pittsburgh in the USA, can dismantle or hinder the development of the protective biofilm, it could play a vital role in treating MRSA infections that are resistant to current therapies.
FACTS: What is MRSA?
MRSA stands for Methicillin-resistant Staphylococcus aureus. This bacterium has acquired resistance to many widely used antibiotics, such as methicillin and penicillin. Here are some essential facts about MRSA:
- Staphylococcus aureus: A common bacterium found in many people’s skin or noses without causing illness. However, if it enters the body through cuts, it can lead to infections like boils, wound infections, and in severe circumstances, pneumonia or sepsis.
- Resistance: MRSA is particularly concerning because it is resistant to most standard antibiotics, making infections harder to treat, sometimes necessitating stronger or more specialized antibiotic treatments.
- Healthcare settings: MRSA poses serious challenges in hospitals and nursing homes, where patients with weakened immune systems, open wounds, or invasive devices (like catheters) are at greater risk for infection. In these close-knit environments, the bacteria can spread rapidly.
- Health risks: Infections from MRSA can be extremely serious and potentially fatal, especially if not addressed quickly or if they spread to the bloodstream or critical organs.
What did the researchers discover?
The researchers at Aarhus University, in collaboration with the University of Pittsburgh, have elucidated the molecular structure of a significant part of the S. aureus biofilm, focusing specifically on the aggregated form of PSMα1, a type of functional amyloid. This component is fundamental in creating a protective biofilm that allows the bacterium to resist antibiotic treatment.
