Researchers discover never-before-seen mechanism bacteria use to resist antibiotic treatment
The discovery was made through a fatal bacteria named Group A Streptococcus.
Australian researchers have recently discovered a previously unknown mechanism used by bacteria to resist antibiotic treatment. According to a press release published by Telethon Kids Institute, it’s predicted that this antimicrobial resistance (AMR) will kill ten million people annually by 2050.
To prevent this, Dr. Timothy Barnett — head of the Strep A Pathogenesis and Diagnostics team at the Wesfarmers Centre of Vaccines and Infectious Diseases, based at Telethon Kids Institute in Perth — and his team launched a brand-new mechanism through which bacteria can absorb nutrients from their human hosts while evading antibiotic therapy.
The study team looked into Group A Streptococcus, a potentially fatal bacteria frequently found on the skin and in the throat.
“When looking at an antibiotic commonly prescribed to treat Group A Strep skin infections, we found a mechanism of resistance where, for the first time ever, the bacteria demonstrated the ability to take folates directly from its human host when blocked from producing their own. This makes the antibiotic ineffective, and the infection would likely worsen when the patient should be getting better,” said Dr. Bartnett.
“This new form of resistance is undetectable under conditions routinely used in pathology laboratories, making it very hard for clinicians to prescribe antibiotics that will effectively treat the infection, potentially leading to very poor outcomes and even premature death,” he also added.
“AMR is a silent pandemic”
“AMR is a silent pandemic of much greater risk to society than COVID-19 – in addition to ten million deaths per year by 2050, the World Health Organization estimates AMR will cost the global economy $100 trillion if we can’t find a way to combat antibiotic failure,” Dr. Barnett also explained.
“In order to preserve the long-term efficacy of antibiotics, we need to further identify and understand new mechanisms of antibiotic resistance, which will aid in the discovery of new antibiotics and allow us to monitor AMR as it arises.”
What exactly is AMR?
AMR is the ability of a microorganism to resist the effects of antibiotics. It is a special kind of drug resistance. Antibiotic resistance evolves on random mutation through natural selection but can also be achieved within a population by application of evolutionary stress.
Once such a gene is formed, bacteria can transfer this genetic information on a horizontal axis between individuals by plasmid exchange. If a bacterium carries a variety of resistance genes, it is called “multi-resistant” or, informally, “superbug.” The term antimicrobial resistance is sometimes used explicitly to include organisms other than bacteria.
The study was published in Nature on November 30.
Study abstract:
Described antimicrobial resistance mechanisms enable bacteria to avoid the direct effects of antibiotics and can be monitored by in vitro susceptibility testing and genetic methods. Here we describe a mechanism of sulfamethoxazole resistance that requires a host metabolite for activity. Using a combination of in vitro evolution and metabolic rescue experiments, we identify an energy-coupling factor (ECF) transporter S component gene (thfT) that enables Group A Streptococcus to acquire extracellular reduced folate compounds. ThfT likely expands the substrate specificity of an endogenous ECF transporter to acquire reduced folate compounds directly from the host, thereby bypassing the inhibition of folate biosynthesis by sulfamethoxazole. As such, ThfT is a functional equivalent of eukaryotic folate uptake pathways that confers very high levels of resistance to sulfamethoxazole, yet remains undetectable when Group A Streptococcus is grown in the absence of reduced folates. Our study highlights the need to understand how antibiotic susceptibility of pathogens might function during infections to identify additional mechanisms of resistance and reduce ineffective antibiotic use and treatment failures, which in turn further contribute to the spread of antimicrobial resistance genes amongst bacterial pathogens.
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