Researchers have just caught bacteria bypassing antibiotic treatment with a novel trick.
Bacteria’s troublesome knack for developing antibiotic resistance is a rapidly growing health threat. This ability has ancient origins and enables drug-resistant bacterial infections like MRSA and gonorrhea to kill 1.3 million people worldwide each year.
These superbugs are even found in wild animals, such as dolphins and bears.
Sneaky microbes can steal genes from each other, quickly passing on antibiotic resistant tactics: Strategies include directly inactivating antibiotics, preventing antibiotic buildup in their system, or altering the targets of the antibiotic so that the drugs are no longer effective.
Thanks in part to the overuse of antibiotics, superbugs have accumulated multiple resistance tactics, making them extremely difficult to treat.
“This new form of resistance is undetectable under the conditions commonly used in pathology labs, making it very difficult for clinicians to prescribe antibiotics that will effectively treat the infection, which can lead to very poor outcomes and even death. premature,” says Telethon Kids Institute infectious disease researcher Timothy Barnett.
Telethon Kids Institute microbiologist Kalindu Rodrigo and his colleagues discovered this new mechanism by studying how group A Streptococcus responds to antibiotics.
This bacteria typically causes sore throats and skin infections, but it can also lead to systemic infections such as scarlet fever and toxic shock syndrome.
“Bacteria must make their own folate to grow and, in turn, cause disease. Some antibiotics work by blocking this folate production to stop the growth of bacteria and treat infection,” says Barnett.
“By examining an antibiotic commonly prescribed to treat group A streptococcal skin infections, we uncovered a resistance mechanism where, for the very first time, the bacterium demonstrated the ability to take up folate directly from its human host when she is prevented from producing theirs.”
So Streptococcus acquired already processed folate outside of its own cells; these molecules are abundant in our body.
The process completely bypasses the action of sulfamethoxazole, an antibiotic that inhibits folate synthesis in bacteria, thereby rendering the drug ineffective.
Rodrigo and the team have identified at least one gene involved: thfT. It encodes part of the folate harvesting system, much like ours, because we also can’t produce folate and have to get it from our diet.
Streptococcus bacteria with this gene have therefore found a way to suck up folate and subvert sulfamethoxazole.
In the lab, group A Streptococcus succumbs to sulfamethoxazole antibiotics because he has no other accessible source of folate.
In this case, the bacteria only resist antibiotics when they cause a real infection inside our body. This means that there is not yet an easy way to detect this antibiotic resistance in pathology laboratories.
This mechanism suggests that antibiotic resistance is much more varied than researchers previously thought and highlights the need for more diverse treatments against bacteria.
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“Unfortunately, we believe this is just the tip of the iceberg – we have identified this mechanism in Group A Strep, but it is likely to be a broader issue for other bacterial pathogens,” says Barnett.
Understanding these mechanisms is the first step in being able to test and counter them. by prescribing other classes of antibiotics instead.
“It is vital that we stay ahead of the challenges of antimicrobial resistance and as researchers we should continue to explore how resistance develops in pathogens and design diagnostic methods and treatments. fast and precise,” urges Rodrigo.
This research was published in Nature Communication.
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