A New Super-Strain of Drug-Resistant Bacteria Is on the March in the Midwest

A new super-strain of an already drug-resistant and very common bacterium is on the march in the Midwest.

This version of P. aeruginosa, currently responsible for about one in every 10 hospital-acquired infections in the US, is armed with a whole new mechanism for defeating not just antibiotics generally, but the last-ditch drugs administered when all others have failed.

What's more, it's been spreading mostly in the shadows, leaving public health officials to play catch-up, but so far with very little idea of just how much catching up is actually needed.

When we say a bacterium is "drug resistant" it's often not to imply that no drugs are effective against it. Rather, it may well just be resistant to the usual drugs, while so-called last resort drug therapies remain available, whether it's a matter of volume—at some point it may be necessary to hook the body up to basically a river of antibiotics via a surgically-placed "port"—or of antibiotic type. The latter case involves drugs like the very old antibiotic vancomycin, which is a nephrotoxin, e.g. poisonous to the kidneys, but can be effective against a MSRA infection when other drugs have failed.

Another "agent of last resort" is a compound called colistin. Colistin isn't an antibiotic in itself, but it's administered with a more conventional antibiotic called imipenem. This antibiotic has the downfall of being easily broken down by common enzymes in the body, but its non-antibiotic partner colistin suppresses those enzymes, allowing the antibiotic to survive and do its work.

That work is often directed against the aforementioned bacteria P. aeruginosa, which contains a gene coding for the production of the anti-imipenem enzyme. So, to fight it, colistin may be required. It all works out, right? Maybe not anymore, according to research published this week in the journal Antimicrobial Agents and Chemotherapy describing the newly discovered, super-resistant form of P. aeruginosa.

The super-resistant version of P. aeruginosa, first isolated in 2012 in the foot wound of an elderly diabetic patient, has a uniquely powerful mechanism for beating down antibiotic treatments—an enzyme called verona integron-encoded metallo beta-lactamse (VIM). This enzyme acts against the beta-lactam ring found in the common antiobiotics of the classes carbapenems, cephalosporins, and penicillins; the ring is a critical piece of these drugs' basic structures and with it destroyed, they're rendered useless. "VIM enzymes confer resistance to imipenem and all other beta-lactams," said the paper's lead author Federico Perez in a statement from the American Society for Microbiology. "They are not inhibited by metallo beta-lactamase inhibitors," e.g. colistin.

The situation right now appears smaller than it likely is. From 2012 to 2013, the researchers found the new version of P. aeruginosa in six additional patients surveyed in Ohio, one of which died of the infection. Most of those patients are linked by residences in long-term care facilities and admissions to local community hospitals. One patient, however, hailed from Qatar, and had been transferred to a medical center in Ohio.

P. aeruginosa lives absolutely everywhere—in particular, skin flora, soil, water, and most man-made surfaces. Popular vectors for transmission include medication instruments and hot tubs. P. aeruginosa is also quite adept at breaking down oil in oil spills and, in the microgravity of space, takes on bizarre and highly creepy superpowers. Take some comfort in the fact that its usual victims tend to be already have weak immune systems, such as the elderly or those already hospitalized, at least so far.

The genetic sequencing involved in the new study revealed one other ominous peculiarity: P. aeruginosa has been swapping code with salmonella, another very common form of bacteria making great strides in antibiotic resistance.

"This is the first description of genetic exchange of a large mobile element—the Salmonella Genome Island—and resistance genes between P. aerugenosa and Salmonella," said Perez. "This movement of genetic material creates concern that metallo beta-lactamases will disseminate rapidly in these enteric pathogens that are also very invasive. We are also concerned about the possibility of enhanced virulence."