Mechanisms of antibiotic resistance

The discovery of antibiotics is one of the most important advancements in clinical medicine and public health. It has laid the foundation for a number of other advancements including the ability to perform surgeries more safely and reduction of infant and maternal mortality rates.

Many antibiotics are derived from other bacteria or fungi. For example, penicillin, secreted by the fungus Penicillium, can kill bacteria.

This is because microbes use antibiotics to fight off other microbes. But the use of antibiotics, and, more broadly, antimicrobials, which includes medications that target not only bacteria, but also viruses and fungi, has exploded in recent years.

Antimicrobials have been used on an industrial scale, partially because of overprescription in humans, but more so because of routine use in farm animals!

In fact, a good number of antimicrobials are excreted from humans and animals unchanged, and these get flushed into waste water, which allows pathogens to be perpetually exposed to antimicrobials. In response to this enormous selective pressure, many pathogens have become highly resistant to antimicrobials.

Now when it comes to bacteria, generally speaking, there are four mechanisms for how they become resistant to antimicrobials.

The first mechanism is antibiotic inactivation or modification, which is where bacteria develop specific enzymes that destroy and inactivate antimicrobials.

One example is beta lactamase, which is a bacterial enzyme that destroys antimicrobials that contain a beta lactam ring, like penicillins and cephalosporins. As a result, bacteria that produce beta lactamases are immune to the action of many beta lactam antibiotics.

The second mechanism is the alteration of a target, or binding site. An antibiotic that cannot bind anywhere is rendered useless.