Beware the Escape Artist!

MRSA, the marvelous Houdini of bacteria, has taken the stage yet again! 

For its debut stunt, staph aureus faced down the fearsome antibiotic, penicillin, and miraculously, it managed to evade this formidable foe! But how, you might ask? Staph aureus had an ace up its sleeve: penicillinase! This enzyme breaks the chemical bonds in penicillin, rendering it inept. So, scientists drew up a new challenge for the master illusionist. When bulky side chains were added to a penicillin molecule, turning it into methicillin, it befuddled penicillinase. But staph aureus still had a few more tricks up its sleeve.

Antibiotics such as methicillin and penicillin bind to proteins called PBPs or penicillin binding proteins. Staph aureus has four of these PBPs that happen to be critical in building new cell wall. When penicillin latches onto these proteins, it leaves them useless, causing cell wall upkeep and growth to plummet.

But staph aureus refused to be outsmarted. Not only has it pulled “methicillin-hydrolyzing beta lactamase,” a novel form of penicillinase that disrupts the bonds in methicillin, seemingly out of thin air, but it also has come up with a never-before-seen version of its second PBP! PBP2a is far less receptive to binding methicillin, so when methicillin stops the other PBPs in their tracks, PBP2a can pick up the slack and keep cell wall construction humming along!

It is simply astounding how staph aureus, the modest round bacterium behind many skin infections, has tamed the impossible and come to be the infamous methicillin resistant staph aureus (MRSA)!

Photo courtesy of NIAID. 

In fact, nearly one-third of us carry staph aureus in our nose or on our skin without harm. It is only able to cause more severe infections along the lines of pneumonia or even life-threatening sepsis, if it finagles its way inside, such as via a cut or surgical incision.

And as its name implies, MRSA can no longer be subdued with methicillin. But this just scratches the surface. The magician is resistant to a plethora of other antibiotics including penicillin, amoxicillin, oxacillin, and on and on! And it just keeps doing the impossible and finding ways to dodge any antibiotics we throw at it!

Recall me citing antibiotics as saving the day in last week’s post about pneumonia? Well, superbugs like MRSA have become our antibiotics’ kryptonite.

On the bright side, however, through much research, we have come to understand the tricks and sleight of hand behind antibiotic resistance.

Bacteria reproduce extraordinarily quickly, “doubling every 4 to 20 minutes” according to PNNL. This means that bacteria can evolve new genes with a breathtaking velocity. All it takes is a single mistake in copying the cell’s DNA, generating a slightly different protein. Just look to PBP2a. This penicillin-binding protein is a barely distinct form of PBP2, but it is different enough to keep from binding methicillin!

And once these resistant proteins have come to be, their blueprint DNA is often kept in small circles of DNA, called plasmids, that float around in a bacterial cell. These “DNA bubbles” can be copied and shared with other bacteria, spreading resistance in a flash.

Antibiotic resistance is an enormous issue for medicine and consequently a vast field of research in microbiology right now, especially since MRSA and other resistant bacteria can be spread through contact so effortlessly!

But MRSA does not only affect hospital patients; rather, it can sweep through a community through shared equipment and spaces such as gyms. In fact, the average age of a patient with community-associated MRSA is 23 years old.

Image by Arlington County. 

Harrowing isn’t it? Just remember to be diligent about washing your hands, covering open cuts and scrapes, and keeping your clothes clean. And while you are at it, check out some of the cool research going on with combating resistance and finding antibiotic alternatives!