Here’s a test.

What do ibuprofen, naproxen, diclofenac, gemfibrozil, and propranolol have in common?  No, not that you never heard of them.  The first three are non-steroidal anti-inflammatories (NSAIDs).  Gemfribrozil is a drug that lowers our lipid levels.  And, propranolol is a β (beta)- blocker.

Give up?

These compounds have been found to create world-wide problems.  How?  These compounds accelerate the conjugation of plasmid-borne antibiotic resistance.

Yes, I’ll explain what I just said.

First, you know that we have been worried about antibiotic resistance for a very long time.  After all, we haven’t developed a new antibiotic since forever- and our arsenal is getting attenuated as the microbes that cause diseases develop resistance to our drugs.  Which means many of us succumb to diseases that were easily treated in the past.

And, one of the primary methods microbes rapidly transfer resistance to one another is when a microbe that already resists the administration of a given drug transfers a plasmid  from one to another microbe.

So, what is a plasmid?  (It’s also known as a replicon.)  These are chunks of DNA (the genetic material in our cells) that are not part and parcel of our chromosomes.  “Floating” independently in a cell, they can replicate themselves (duplicate independently from cellular replication). These contain far fewer DNA segments than chromosomes, and they typically contain genes that are necessary for a simple task (in this case, antibiotic resistance- and most of the microbes that have developed antibiotic resistance did so via plasmids).   The plasmids often form circular, double-stranded structures that not only replicate- but can be transmitted from one microbe to another.

The transfer of plasmids from one cell to another progresses by transformation.  [Transformation  is defined as the genetic alteration of a cell resulting from the direct uptake and incorporation of exogenous genetic material, transported across its cellular membrane(s).]  Transformation usually occurs when the recipient microbe is starved, under stress, or – d-uh- when antibiotics are present trying to eradicate it.  (Some artificial plasmids [ones we researchers produce] are used to effect cloning- providing recombinant DNA sequences within the host organisms. This is how we produced a bunch of the specialized microbes capable of removing pollutants over the years.)

Now, back to those chemicals mentioned above.

Drs. J. Wang, J. Lu, S. Zhang, J. Li, L. Mao, Z. Yuan, P.L. Bond, and J. Guo are all professors at the University of Queensland (Australia). Their experiments involved placing each of the chemicals in growth media with two different types of microbes- only one of which is already resistant to antibiotics. (See the picture above.) The microbes were incubated together for 8 hours, and then tested to see if they developed new antibiotic resistance.  (There also were control mixtures that lacked any of the inducing chemicals above, with the same microbial species involved.)

Please note:  Their article has not yet been peer-reviewed, and is only available as a preprint here.

Those microbes that were subject to the inducing chemicals developed new antibiotic resistance; those lacking the chemicals did not develop any resistance.  That was true even if the offending chemicals were present at ultra-low concentrations of 0.005 milligrams/L (5 µg/L, 5 micrograms per liter).    And, the resistance was confirmed by DNA analysis.

This really is bad news, because those low levels of these compounds are often found in sewage- which means bacteria can impart bacterial resistance to one another almost ubiquitously.

Plus, we have no idea what other compounds may wreak havoc with our antibiotic arsenals.