Scientists just caught bacteria using a never-before-seen antibiotic-evasion trick: ScienceAlert
Researchers have just used an unprecedented trick to catch bacteria avoiding antibiotic treatment.
The problematic ability of bacteria to develop resistance to antibiotics is a a rapidly growing threat to health. This ability has ancient origin and enables drug-resistant bacterial infections such as MRSA and gonorrhea kill 1.3 million people in the world every year.
Motile microbes can they steal each other’s genesrapid transfer of antibiotic resistance tactics: strategies include directly deactivating antibiotics, preventing antibiotics from accumulating in their systems, or changing the targets of antibiotics so that drugs are no longer effective.
Thanks in part excessive use of antibioticssuperbugs have accumulated multiple resistance tactics, making them extremely difficult to treat.
“This new form of resistance cannot be detected under conditions routinely used in pathology laboratories, making it very difficult for clinicians to prescribe antibiotics that will effectively treat the infection, potentially leading to very poor outcomes and even premature death,” explains Telethon Kids Institute Infectious Disease Researcher Timothy Barnett.
Telethon Kids Institute microbiologist Kalinda 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 can also lead to systemic infections such as scarlet fever fever and toxic shock syndrome.
“Bacteria need to produce their own folate in order to grow and, in turn, cause disease. Some antibiotics work by blocking this 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 found a resistance mechanism where, for the first time in history, the bacterium showed the ability to take folate directly from its human host when its own production was blocked.”
So Streptococcus takes up already processed folate outside its own 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 a folate collection system, similar to our own, since we also cannot manufacture folate and must obtain it from food.
Streptococcus bacteria with this gene therefore found a way to suck up folate and subvert sulfamethoxazole.
In the laboratory, group A Streptococcus subject to sulfamethoxazole antibiotics because there is no other source of folate available.
In this case, bacteria are resistant to antibiotics only when they cause an actual infection inside our body. This means that there is still no simple way to detect this antibiotic resistance in pathology laboratories.
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“Unfortunately, we suspect this is only the tip of the iceberg – we have identified this mechanism in Group A Streptococcus, but it is likely to be a wider problem in other bacterial pathogens,” he says Barnett.
Understanding these mechanisms is the first step towards being able to test and counter them by prescribing other classes of antibiotics instead.
“It is important to 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 therapy,” drives Rodrigo.
This research was published in Nature Communications.