Studies of soil microbes have shown that drought favors microbes that survive antibiotics. They also found that some resistance genes from soil-dwelling bacteria were found in samples of antibiotic-resistant pathogens taken from hospitalized patients. Because bacteria can easily exchange large chunks of genetic information (a process called horizontal gene transfer), increased resistance in soil-dwelling microbes could easily reach microbes that can easily infect humans, the study authors said.
“No place is immune,” said study lead author Diane Newman, a biologist at the California Institute of Technology. “This is a concern no matter where you live because when a pathogen emerges in one part of the world, it spreads quickly.”
resistant pathogens
Antibiotic resistance is already a major health problem, with the World Health Organization estimating that as of 2019, antibiotic-resistant pathogens directly cause 1.27 million deaths annually and contribute to an additional 4.95 million deaths. Antibiotics kill microorganisms, but drugs used in medical practice are also derived from microorganisms (or fungi, as in the case of the famous penicillin). Microorganisms synthesize antibiotics as part of their evolution with other microorganisms, with the aim of killing potential competitors and threats. One of the main battlegrounds in this evolutionary war is soil.
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Newman and the new study’s lead author, Caltech postdoctoral researcher Xiaoyu Xiang, found the first hint that drought may worsen antibiotic resistance in a set of five metagenomics databases that aggregate genetic information of soil microbes from different environments on continents around the world. Some of these databases included samples from the same locations before and after the drought.
In both cases, the researchers found that antibiotic synthesis genes were more prevalent after dry periods and less prevalent after the drought ended.
“This is found in farmland, grasslands, forests, wetlands, the United States, China and Switzerland,” Newman told Live Science.
To find out what was going on, Newman, Xiang, and their colleagues brought questions to the lab. They treated the sterile soil with phenazine, an antibiotic produced by a type of bacteria. They then added soil-dwelling bacteria and allowed half of the sample to dry for three days while the rest remained moist.
After this simulated drought, they found that, not surprisingly, as the water in the soil evaporated, the antibiotics in the soil became more concentrated. They also found that in response to this more concentrated antibiotic, antibiotic-sensitive bacteria in the soil suffered, while antibiotic-resistant bacteria multiplied.
These findings show that antibiotic resistance is driven by evolutionary pressures, Newman said. When drought concentrates antibiotics in other microorganisms to lethal levels, only the toughest and most resistant survive.
Now is not the time for governments to stop funding scientific research and drug discovery.
Diane Newman, California Institute of Technology biologist
To get a glimpse of this evolutionary battlefield at the genetic level, the researchers turned back to large metagenomics databases. They found that antibiotic resistance genes become more common during dry periods. This spread is coupled with an increase in antibiotic synthesis genes, supporting the idea that drought-stricken microbes develop antibiotic resistance in response to increased pressure from antibiotic attacks from neighboring countries.
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The researchers then took soil samples from the Caltech campus, added four different antibiotics, and dried half of the samples. Again, we found that more antibiotic-resistant microorganisms were present in the dried samples.
global crisis
The next question was whether these patterns could be seen on a global scale. The researchers used existing data on antibiotic-resistant pathogens and climate and weather data collected in hospitals around the world to quantify how dry each hospital was. They found that the drier the region, the more antibiotic-resistant pathogens hospitals reported. This finding held true even when the researchers controlled for the country’s socioeconomic status, which can affect pathogen testing.
The final genome scavenger hunt brought some more bad news. Many of the genes that confer antibiotic resistance in soil microorganisms have been found to be precisely duplicated in clinical pathogens known to evade antibiotics. These included common hospital pathogens Enterococcus faecium, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacteriaceae species, the researchers reported March 23 in the journal Nature Microbiology. Human pathogens and soil microbes are in constant contact as humans move through the environment, and drought-induced tolerance can easily be transferred from microbes in the soil to microbes on our bodies, Newman said.
“As we continue to get warmer and drier, dryness is expected to increase,” said Timothy Gurley, a microbial ecologist at Australia’s Macquarie University, in an editorial accompanying the study. That means climate change could accelerate the already serious problem of antibiotic-resistant pathogens, he wrote.
Newman said there are ways to wage an evolutionary battle between bacteria and ourselves. In addition to limiting climate change, more can be done to bring rapid diagnostic tests into clinics so that doctors can treat antibiotic-resistant bacteria more quickly. You may also choose a multi-antibiotic treatment to knock out resistant bacteria. Another important step is funding basic research in drug discovery, Newman said. Pharmaceutical companies have largely retreated from the search for new antibiotics due to lack of profitability, leaving governments and academic scientists to take the lead in basic research.
“Now is not the time for governments to stop funding scientific research and drug discovery,” Newman said.
Shan, X., Cao, K., Jeckel, H., Alcalde, RE, Trindade, IB, Kwiecinski, JV, and Newman, DK (2026). Drought increases antibiotic resistance throughout the soil. Natural microbiology. https://doi.org/10.1038/s41564-026-02274-x
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