Scientists just caught bacteria using a never-before-seen antibiotic-evasion trick : ScienceAlert

Scientists just caught bacteria using a never-before-seen antibiotic-evasion trick : ScienceAlert

Researchers have just caught bacteria evading antibiotic treatment with a never-before-seen trick.

The problematic talent of bacteria to develop resistance to antibiotics is a rapidly growing health hazard. This ability has ancient origin and allows drug-resistant bacterial infections such as MRSA and gonorrhea kill 1.3 million people worldwide every year.

These superbugs even find their way into wild animals, such as dolphins and bears.

Mutable microbes can they steal genes from each otherrapid transfer of antibiotic resistance tactics: strategies include directly inactivating antibiotics, preventing the accumulation of antibiotics in their systems, or changing the targets of antibiotics so that drugs are no longer effective.

Partly thanks to excessive use of antibioticssuperbugs have accumulated multiple resistance tactics, making them extremely difficult to treat.

“This new form of resistance cannot be detected under the conditions routinely used in pathology laboratories, making it difficult for clinicians to prescribe antibiotics that will effectively treat the infection, which can lead to very poor outcomes and even premature death.” explains Telethon Kids Institute Infectious Disease Researcher Timothy Barnett.

Telethon Kids Institute microbiologist Kalindu Rodrigo and colleagues discovered this new mechanism while investigating how Group A Streptococcus responds to antibiotics.

This bacterium usually causes sore throats and skin infections, but it can also lead to systemic infections such as scarlet fever. fever and toxic shock syndrome.

“Bacteria must make their own folic acid to grow and, in turn, cause disease. Some antibiotics work by blocking folate production to stop bacterial growth and treat infection,” explains Barnett.

“When we looked at an antibiotic commonly prescribed to treat group A streptococcal skin infections, we discovered a resistance mechanism where, for the first time ever, the bacteria showed the ability to take folate directly from their human host when they were blocked from making their own. “

So Streptococcus acquires already processed folic acids outside its cells; these molecules are abundant in our bodies.

The process completely bypasses the action of sulfamethoxazole, an antibiotic that inhibits folate synthesis within bacteria, rendering the drug ineffective.

Rodrigo and team identified at least one gene involved: thfT. It encodes part of the folate collection system, unlike ours, because we also can’t make folate and have to get it from our food.

Streptococcus bacteria with this gene therefore found a way to suck up folate and reverse sulfamethoxazole.

In the laboratory, Group A Streptococcus is subject to sulfamethoxazole antibiotics because there is no other available source of folate.

In this case, bacteria are resistant to antibiotics only when they cause an actual infection in our body. This means that there is still no simple way to detect antibiotic resistance in pathology laboratories.

This mechanism suggests that antibiotic resistance is much more diverse than researchers previously realized and highlights the need to establish more diverse treatments against bacteria.

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“Unfortunately, we suspect this is only the tip of the iceberg – we have identified this mechanism in Group A Strep, but it is likely to be a wider problem among other bacterial pathogens,” says Barnett.

Understanding these mechanisms is the first step to being able to test and counter them by prescribing other classes of antibiotics instead.

“It is vital that we stay one step ahead of the challenge of antimicrobial resistance and, as researchers, we should continue to investigate how resistance develops in pathogens and design rapid, accurate diagnostic methods and therapies,” urges Rodrigo.

This research was published in Nature Communications.

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