The antibiotic Rifampicin inhibits an enzyme in bacteria cells with which read the genetic material in order to build a model for proteins (RNA polymerase). If this enzyme is changed, it cannot be attacked by antibiotics, but does not function as efficiently any more, and the microbes’ “fitness” deteriorates.
In the case of Pseudomonas-aeruginosa bacteria, the researchers discovered that these pathogens slowly but surely compensate for a fitness loss by means of a Rifampicin resistance. They can simply compensate for small handicaps by ensuring that other cellular functions become even more effective. The overall fitness level once again resembles the fitness of the non-resistant bacteria.
However, if the fitness loss is considerable as a consequence of the resistance to the antibiotics, they process no longer works. In this case the bacteria have to completely restore the function of the enzymes by detours. The scientists reported that this is up to 10,000 times more difficult (less probable). The study is designed to contribute to an understanding of the dynamic processes involved in a spreading of antimicrobial resistance, especially in a clinical environment.