Antimicrobial Resistance Spread and the Role of Mobile Genetic Elements

Alexander Fleming discovered the first antimicrobial agent, penicillin (a β-lactam), in 1928 in the mold Penicillium notatum. Penicillin was initially found to be active against staphylococcal strains, which at that time were a major source of infectious diseases. Indeed, the mortality rate of individuals with severe Staphylococcus aureus infection in the early 1940’s was about 80% [1]. The discovery of penicillin gave clinicians an effective means to combat fatal microbial infections for the first time. Since that time, many different types of antimicrobial agents have been discovered, including aminoglycosides, macrolides and cephalosporins to name but a few. Further, current advances in biochemistry and engineering now mean that novel antimicrobial agents can be produced by 1) synthetically altering the structure of known antimicrobial agents, or by 2) high throughput screening strategies. However, even as new antibiotics are being discovered, bacteria are acquiring mechanisms to neutralise their effect.

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