Crop Comments: Making microbes meaner

My Canadian friend, Ann Clark — retired agronomy professor from Ontario’s Guelph University — emailed me a link (www.gmwatch.org/en/news/latest-news/18508) with the headline “Glyphosate and dicamba herbicides increase antibiotic resistance in bacteria”. The article accompanying this link appeared online on Oct. 12, 2018, with the following introductory sentence: “Antibiotic resistance development in bacteria increased by a factor of up to 100,000 times faster than occurs without the herbicide.”

Let’s mentally hop halfway around the planet to New Zealand. There “down-under” scientists have published a new study. That study has found that some of the world’s most widely used herbicides, glyphosate and dicamba, increase the rate of antibiotic resistance development in bacteria by as much as 100,000 times faster than what we expect in an herbicide-free environment. Both of these ag chemicals are used on crops that have been genetically engineered to tolerate them. The new study adds to volumes of proof that herbicides used on a mass industrial scale — but not as antibiotics — can still have profound effects on bacteria. Those effects include negative implications for medicine’s ability to treat infectious bacteria-caused diseases. University of Canterbury Professor Jack Heinemann, one of the study’s authors, said, “The combination of chemicals to which bacteria are exposed in the modern environment should be addressed alongside antibiotic use if we are to preserve antibiotics in the long-term.”

An important finding of the new study was that even in cases where the herbicides increased the toxicity of antibiotics, they also significantly increased the rate of antibiotic resistance. The authors say this fact could be contributing to the greater use of antibiotics in both agriculture and medicine. Previously these researchers found that exposures to the herbicide active ingredients glyphosate and/or dicamba typically increased antibiotic resistance of such human-targeting pathogens like Salmonella enterica and Escherichia coli. But increasingly these scientists have observed that the presence of these herbicides commonly increases the susceptibility of potential human pathogens like S. enterica and E. coli, depending on the antibiotic. Most people (including yours truly) tend to think that an outside chemical influence which enhances an antibiotic’s potency would be medically beneficial.

But Professor Heinemann looks at this scenario differently. His words, “We are inclined to think that when a drug or other chemical makes antibiotics more potent, that should be a good thing. But it also makes the antibiotic more effective at promoting resistance when the antibiotic is at lower concentrations, as we more often find in the environment. Such combinations can be like trying to put out the raging fire of antibiotic resistance with gasoline.”

The authors concluded that neither reducing the use of antibiotics nor the discovery of new ones may be adequate game plans for avoiding the post-antibiotic era, i.e., a much-dreaded new period in human history, in which antibiotics no longer function. Heinemann explains further, verbatim: “This is because bacteria may be exposed to other non-antibiotic chemicals that predispose them to evolve resistance to antibiotics more quickly. Herbicides are examples of some of the most common non-antibiotic chemicals in frequent global use. Thus antibiotic resistance may increase even if total antibiotic use is reduced, and new ones are invented, unless other environmental exposures are also controlled.” The new paper, “Agrichemicals and Antibiotics in Combination Increase Antibiotic Resistance Evolution” was published online in PeerJ on Oct. 12, 2018, https://peerj.com/articles/5801/ . This paper was written by Brigitta Kurenbach, Jack A. Heinemann, et al. I’m going to sum it up, beginning by quoting the first four sentences of the paper’s abstract:

“Antibiotic resistance in our pathogens is medicine’s climate change: caused by human activity, and resulting in more extreme outcomes. Resistance emerges in microbial populations when antibiotics act on phenotypic variance within the population. This can arise from either genotypic diversity (resulting from a mutation or horizontal gene transfer), or from differences in gene expression due to environmental variation, referred to as adaptive resistance. Adaptive changes can increase fitness allowing bacteria to survive at higher concentrations of antibiotics.” Let me explain a couple things: genotype for a given trait basically means what the individual’s chromosome package predicts for that trait; for example, how tall you or I become; how much milk a cow is expected to give; how much antibiotic resistance a bacterium is expected to develop. Phenotype combines genotype with environmental factors, thus quantifying how much milk the cow actually gives, etc. An analogy with meteorology might be helpful: climate is what you expect — weather in what you get.

Let’s put a face on this bacterial antibiotic resistance trait. As detailed in their paper, the New Zealand team experimented with the antibiotic ciprofloxacin. That’s the drug prescribed to me during, and following, major surgery in 2011. Kurenbach and Heinemann measured the frequency at which acquired ciprofloxacin (Cip) resistance increased during culture in the combination of Cip/dicamba/E. coli. The mutation rate of an E. coli monoculture was measured over the course of about 25 generations in a standard rich-growth medium. A control experiment was also run in which there was no dicamba, i.e., only Cip and E. coli (and the same medium). Punch line to the joke: the acquired resistance rate in the Cip/dicamba/E. coli culture was about 105 (or 100,000) times higher than the control (herbicide-free) culture.

There’s a formula for genetic change (GC) that I like to use when dabbling in population genetics. It’s from my textbook Breeding and Improvement of Farm Animals, by Rice. (McGraw-Hill, 1970). The formula says that mathematically GC depends on four variables. I’ll mention only one: selection intensity. Imagine being able to select for a dairy sire with a 100-pound predicted difference (PD) milk advantage; now increase that advantage to 200 pounds PD (or a lot more). Now let’s look at E. coli — or maybe a nice friendly Staph bacterium. These New Zealand scientists believe that when herbicides and antibiotics “rub shoulders” in nature, life quality improves greatly for mean microbes — and becomes much less secure for complex organisms — like this writer and his readers.

2018-12-11T16:10:01+00:00December 11, 2018|Eastern Edition, Western Edition|0 Comments

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