Researchers have found a new way to sidestep antibiotics.
A rapidly growing health threat is the emergence of antibiotic resistance. 1.3 million people are killed annually by drug-resistant infections like MRSA and gonorrhea, thanks to this ability.
Animals such as dolphins and bears are being colonized by these bugs.
The shifty microbes can steal genes from each other, quickly passing on antibiotic-resistant tactics, such as changing the antibiotics' targets so that they are no longer effective.
Superbugs have been accumulating multiple resistant tactics due to antibiotic use.
The new form of resistance makes it hard for clinicians to prescribe antibiotics that will effectively treat the infections, which can lead to poor outcomes and even premature death.
The new mechanism was discovered by Kalindu and colleagues.
It can cause sore throats and skin infections, but it can also lead to systemic infections such as scarlet fever.
Folates need to be made bybacteria to grow and cause diseases. Barnett explains that some antibiotics block the production of folate to stop the growth ofbacteria.
When looking at an antibiotic commonly prescribed to treat Group A Strep skin infections, we found a mechanism of resistance where thebacteria demonstrated the ability to take folates directly from its human host when blocked from producing their own.
Folate is abundant in our bodies and Streptococcus has been getting it from outside its own cells.
The drug was rendered useless because the process completely bypassed the action of sulfamethoxazole.
The team was able to identify at least one genes involved. Folate can't be produced and must be obtained from our food, so it's part of the system.
Streptococcusbacteria have found a way to subvert sulfamethoxazole.
Group A Streptococcus is susceptible to antibiotics because it doesn't have another source of folate.
Thebacteria are resistant to the antibiotics when they cause an actual infections inside of us. There is no easy way to detect antibiotic resistance.
The mechanism suggests that antibiotic resistance is more varied than previously thought.
We have identified this mechanism in Group A Strep, but it's likely it will be a broader issue across otherbacterial pathogens.
Understanding these mechanisms is the first step towards being able to test for and counter them.
As a researcher, we should continue to explore how resistance develops in pathogens and design rapid accurate diagnostic methods.
The research was published in a journal.
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