Scientists from the University of Groningen in the Netherlands, in collaboration with colleagues from the University of Montpellier in France and the University of Oldenburg in Germany, have made a significant discovery regarding the impact of fever on the development of antimicrobial resistance. Their findings could pave the way for innovative approaches to combat this global health threat.

In a series of laboratory experiments, the researchers investigated how a slight increase in temperature, from the normal human body temperature of 37 degrees Celsius to a feverish 40 degrees Celsius, influenced the mutation frequency in E. coli bacteria. 

They discovered that this temperature rise significantly changed the mutation rate, potentially facilitating the development of antibiotic resistance.

The study, published in the journal JAC-Antimicrobial Resistance, suggests that if these results can be replicated in human patients, controlling fever might become a new strategy to mitigate the emergence of antibiotic resistance.

This finding is particularly important given that antimicrobial resistance is recognized by the World Health Organization as one of the top global public health and development threats.

Dr. Timo van Eldijk, co-first author of the paper, explains that while it is known that temperature affects the mutation rate in bacteria, their research aimed to understand how the increase in temperature associated with fever influences this mutation rate towards antibiotic resistance. 

Previous studies had mostly focused on lowering ambient temperatures, but this research uniquely looked at moderate increases above normal body temperature.

In their experiments, Dr. Van Eldijk and Master's student Eleanor Sheridan cultured E. coli bacteria at both 37 and 40 degrees Celsius. They then exposed the bacteria to three different antibiotics: ciprofloxacin, rifampicin, and ampicillin.

The results were telling. For ciprofloxacin and rifampicin, the increased temperature led to a higher mutation rate towards resistance. However, for ampicillin, the mutation rate towards resistance actually decreased at the higher temperature.

To ensure the reliability of their findings, the researchers replicated the ampicillin experiment in two different laboratories, at the University of Groningen and the University of Montpellier, and obtained consistent results. 

They hypothesized that the efficacy of ampicillin might be temperature-dependent, and confirmed this through further experiments, demonstrating that ampicillin resistance is less likely to arise at 40 degrees Celsius.

Dr. Van Eldijk concludes, "Our study shows that a very mild change in temperature can drastically change the mutation rate towards resistance to antimicrobials. This is interesting, as other parameters such as the growth rate do not seem to change."

If these results can be confirmed in human patients, they could lead to new strategies for tackling antimicrobial resistance. By either lowering body temperature with fever-suppressing drugs or selecting antimicrobial drugs that are more effective at higher temperatures, healthcare providers might gain a powerful tool in the battle against antibiotic resistance. 

The research team suggests that an optimized combination of antibiotics and fever suppression strategies could become a new weapon in this critical fight.