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Previously published data from our group (McMahon et al., 2007) and others (Gilbert & McBain, 2003) have demonstrated that when bacteria are exposed to environmental stresses, such as altered pH, heat shock and increased salinity, they are able to alter their antibiotic susceptibility by becoming either more susceptible or, conversely, more resistant to antibiotic agents. For example, when we stressed Staphylococcus aureus organisms with increased but sublethal salt or pH levels, we observed up to a fourfold increase in MICs of gentamicin and erythromycin against these organisms (McMahon et al., 2007). c-Radiation has the ability to kill bacteria, mainly through DNA damage (Cerutti, 1976), depending on the dose absorbed by target bacterial cells. Such radiation, therefore, has the potential to induce mutations, ranging from mild, or ‘silent’, mutations through to catastrophic mutations that lead to terminal events within the bacterial cell. In nature, mutagenesis is hypothesized to play roles in adaptation and subsequent propagation via chromosomal rearrangement, alteration in target sites on cells and deregulation of enzyme synthesis. What has not been examined, to date, is the effect of sublethal doses of c-radiation on clinical pathogens carried in or on patients undergoing radiotherapy, particularly in relation to the effect it has on the bacteria’s susceptibility to antibiotics.

journal of medical microbiology/journal of medical microbiology

Exposure to sublethal clinical radiotherapeutic doses of ionizing γ-radiation gives rise to mutants of Gram-negative and Gram-positive clinical pathogens with increased antibiotic resistance