Bacteria eat antibiotics, and warn each other of threats


Microbes with a penchant for penicillin pose a challenge for researchers. Paul Biegler reports.


E.coli can be engineered to eat penicillin.
E.coli can be engineered to eat penicillin.
Manfred Rohde, Helmholtz-Zentrum für Infektionsforschung (HZI)/Getty Images

In the world of bacteria, joining the resistance movement, far from being subversive, is rapidly becoming the norm.

So much so, one report estimates that the galloping number of infections resistant to any form of antibiotic could cut short the lives of 300 million people and cost the global economy USD 100 trillion by 2050.

And now for the bad news.

Bacteria are carrying another ace up their single-celled sleeves: they have a penchant for dining out on antibiotics. Yes, eating them.

That might seem to be the coup de grâce for the hapless antibiotic, but a new study led by Gautam Dantas from the Washington University in St Louis, Missouri, US, has worked out how some bacterial strains do it, a finding that could turn the tables on the smarty-pants bugs.

Most antibiotics are made by bacteria in the soil, essentially weaponising them to beat off rival bugs in the war for resources such as food. But antibiotics don’t accumulate in the dirt, so where do they go?

It’s been known for a while that some antibiotics, by virtue of being excellent sources of carbon and nitrogen, simply become fodder for bacteria. What is less clear is how the microbes gobble them up.

To find out, the study, published in Nature Chemical Biology, isolated a number of soil bacteria, including one called Pseudomonas, and put them on a strict diet of the antibiotic penicillin. The bacteria’s response was, more or less, “bring it on”, with colonies expanding on the agar plate pretty much in proportion to how much penicillin they were fed.

But how did they do it?

Using genome sequencing, the researchers found that bacteria were able to supercharge the genes making enzymes that chomp through nutrients, including beta-lactamase, the enzyme that confers resistance to some antibiotics, when faced with a penicillin meal. Going further, they engineered a version of the bacterium Escherichia coli, the misery-inducing cause of traveller's diarrhoea and urinary infection, with a cluster of those very genes. It conferred a similar ability on the E. coli to use pencillin as food.

How is any of that good?

One surprising answer comes from the waste water produced by pharmaceutical factories. It can heavily contaminate nearby soil and water with antibiotics, in one case up to 1000 times the amount needed to kill bacteria, something that spawns the emergence of resistant bugs.

Engineered bacteria, the authors write, could be released into those environments to mop up the antibiotics. Duly cautious, they forewarn of the risk that letting anthropogenic bugs loose could also, unhelpfully, transfer resistance to other bacteria.

The game-changer, however, could be the ability to use this new intelligence to unravel bacterial defences and turn the tide against them.

“Antibiotic degradation may ... paradoxically contribute to the development of the next generation of novel antibiotics,” the authors conclude.

Of course, any organism that likes to eat could hardly be averse to a chat – and some bacteria, according to another paper published in the Journal of Biological Chemistry, are no exception.

The study, led by Nydia Morales-Soto from the University of Notre Dame, Indiana, US, also concerned itself with the bacterium Pseudomonas, in this case the species P. aeruginosa.

It’s a dastardly bug that causes a host of illnesses, including pneumonia and blood poisoning, often in hospitalised people with weakened immune systems. It is also frequently resistant to antibiotics.

The researchers found that bacteria exposed to the antibiotic tobramcyin communicate with brethren bugs by sending out chemical distress signals. The swarms of moving microbes then adopt defensive behaviours that shield them from the effects of the antibiotic.

Again, the future pay-off may come from insights into antibiotic resistance. Co-author Joshua Shrout says, “[T]his work opens a new window into understanding P. aeruginosa behaviour and potentially how this bacterium promotes tolerance to antibiotics.”

Contribs paulbiegler 2.jpg?ixlib=rails 2.1
Paul Biegler is a philosopher, physician and Adjunct Research Fellow in Bioethics at Monash University. He received the 2012 Australasian Association of Philosophy Media Prize and his book The Ethical Treatment of Depression (MIT Press 2011) won the Australian Museum Eureka Prize for Research in Ethics.
  1. https://www.scientificamerican.com/article/antibiotic-resistance-will-kill-300-million-people-by-2050/
  2. https://www.nature.com/articles/s41589-018-0052-1
  3. https://www.sciencedirect.com/science/article/pii/S0304389407009909
  4. http://www.jbc.org/content/early/2018/03/27/jbc.RA118.002605.abstract
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