Resistance may arise through genetic mutation or by attaining a gene from an already resistant bacterium. Once resistant, subsequent reproduction means resistance genes will be passed onto the next generation of bacteria.

"It is not difficult to make microbes resistant to penicillin in the laboratory by exposing them to concentrations not sufficient to kill them."

Sir Alexander Fleming 1945, Nobel Lecture

Once resistance is acquired, bacteria then have a selective advantage and can reproduce quickly in the absence of competition as non-resistant bacteria are killed.

Antimicrobial resistance is developing faster than new medicines. The last new class of antimicrobial medicines was introduced in the late 1980s. This poses a global challenge as the number of drugs available to combat infections fails to keep pace.

There are several ways in which bacteria can dodge the antibiotic effects of drugs. For example, they may modify their own metabolic pathways to avoid the effects of a drug, or they can produce enzymes that break down the antimicrobial drug.

One such family of enzymes are the Extended-Spectrum beta-Lactamases (ESBLs) which confer resistance to penicillins and cephalosporins and are most widely associated with Escherichia coli and Klebsiella germs.

In addition, bacteria may also modify the site at which the antibiotic drug binds, thereby preventing it from attacking the bacteria. Penicillin resistance may arise in this way, and this is the mechanism that underpins MRSA (methicillin resistant Staphyloccocus aureus) resistance.

Finally, bacteria may pump out the antibiotic so there is less of it, therefore diminishing the efficacy of the drug. This method is involved in resistance to tetracyclines, a broad spectrum family of drugs used in human and animal health which works by getting inside bacteria and inhibiting protein synthesis.

Antimicrobial Resistance