Evolution of antibiotic resistance impacts optimal temperature and growth rate in Escherichia coli and Staphylococcus epidermidis

Abstract

Aims Bacterial response to temperature changes can influence their pathogenicity to plants and humans. Changes in temperature can affect cellular and physiological responses in bacteria that can in turn affect the evolution and prevalence of antibiotic‐resistance genes. Yet, how antibiotic‐resistance genes influence microbial temperature response is poorly understood. Methods and Results We examined growth rates and physiological responses to temperature in two species—E. coli and Staph. epidermidis—after evolved resistance to 13 antibiotics. We found that evolved resistance results in species‐, strain‐ and antibiotic‐specific shifts in optimal temperature. When E. coli evolves resistance to nucleic acid and cell wall inhibitors, their optimal growth temperature decreases, and when Staph. epidermidis and E. coli evolve resistance to protein synthesis and their optimal temperature increases. Intriguingly, when Staph. epidermidis evolves resistance to Teicoplanin, fitness also increases in drug‐free environments, independent of temperature response. Conclusion Our results highlight how the complexity of antibiotic resistance is amplified when considering physiological responses to temperature. Significance Bacteria continuously respond to changing temperatures—whether through increased body temperature during fever, climate change or other factors. It is crucial to understand the interactions between antibiotic resistance and temperature.

Characterization of Extended Spectrum Beta-Lactamases (ESBL) Producing Escherichia coli Isolates from Surface Water Adjacent to Pharmaceutical Industries in Bangladesh: Antimicrobial Resistance and Virulence Pattern

“…Here, the temperature of the samples were in the range of 26.4℃ to 30℃, while the pH values were differed from 6.3 to 7.8 (slightly alkaline). According to the Department of Environment (DoE) standard in Bangladesh, the parameters were within the permissible limit for domestic, irrigation utilization and others [29,30]. The presence of bacterial community and their distribution could be significantly influenced by the temperature of the water habitat [31].…”

Interplay Between Antimicrobial Resistance and Global Environmental Change

“…E. coli cells grown at high temperatures for 2,000 generations in the absence of antibiotics contained mutations in rpoB that conferred rifampicin resistance by preventing binding of the antibiotic and also altered gene expression to enable heat-stress adaptation (123,125). The evolution of resistance in E. coli and Staphylococcus epidermidis to 13 antibiotics resulted in shifts of the optimal growth temperatures that depended on the drug, species, and strain and indicated complex interactions between resistance, temperature responses, and growth rates (101). Similar results were observed with E. coli cultures grown to tolerate increasing chloramphenicol concentrations at 37°C (65).…”