Genes that make bacteria resist antibiotics hitchhike in the gut microbiomes of international travelers

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International travelers may be bringing more than souvenirs back with them. (Unsplash/Markus Winkler)

International travel can help spread genes that allow bacteria to become resistant to antibiotics, scientists reported Sunday in a study of nearly 200 Dutch adults who visited two continents.

The researchers sampled the participants' gut microbiomes after they traveled and identified 56 genes that convey antibiotic resistance, some of which hadn't been previously recognized. Still, many questions remain about the fate of these genes and their potential impact on people's health. The team published the findings Sunday in Genome Medicine.

"At this point, we're just assessing potential risk, and I think we can clearly say that risk exists," said Gautam Dantas, a professor of pathology and immunology, biomedical engineering and microbiology at the Washington University School of Medicine and co-author of the study. "One thing that's been clear — and I think the pandemic has really put this into focus — is that infectious diseases like to travel, and they travel through us."

Antibiotic resistance is a growing problem, with disease-causing bacteria evolving defenses against drugs much faster than new treatments can be developed. One way to track the emergence of genes that grant bacteria the ability to withstand antibiotics is to examine the population of microbes dwelling within the gut, Dantas says.

"Over the course of years, the microbiome appears to be relatively stable," he said. However, "If you go to a new location, as you change the food that you're eating and you're exposed to a brand new set of people and animals and habitats, that could be an easy way in which there are new bugs that are ingested."

To understand how travel might impact antibiotic resistance, Dantas and his team tracked 190 people who journeyed from the Netherlands to destinations in North Africa, Eastern Africa, South Asia and Southeastern Asia. The team extracted bacterial DNA from stool samples collected right before and after the trips, and found that people carried significantly more abundant and diverse genes associated with antimicrobial resistance post-travel.

The majority of these were known antimicrobial resistance genes. However, the researchers also expressed genes from the samples in lab-grown E. coli and monitored which ones protected the bacteria from being killed by antibiotics. This allowed the team to discover a handful of genes that hadn't been linked with antibiotic resistance before.

The genetic instructions that Dantas and his team identified would thwart antibiotics in a variety of different ways, including pumping drugs out of, or preventing them from entering, the cell and breaking down or chemically altering the drug. One of the genes the team observed is associated with resistance to colistin, a kind of antibiotic usually deployed as a last resort when more common treatments don't work. Also present were genes that make bacteria resistant to "whole swaths" of drugs, Dantas says. 

Another key question, he said, was, "What is the risk of these genes not only coming into these people but perhaps ... hopping around between other bugs in the microbiome?"

Concerningly, the team found that many of the antimicrobial resistance genes were also flanked by sequences called mobile genetic elements, which help unrelated bacteria swap genes. 

Dantas and his team found that antimicrobial resistance genes were most similar in people who'd traveled to the same region, suggesting that the travelers hadn't picked them up at the airport. The team found relatively more antimicrobial resistance genes among people who'd visited Southeastern Asia compared with other regions, but the number of participants was too small to draw any conclusions about the abundance of these genes in the region more broadly, Dantas says.

It's unclear whether the antimicrobial resistance genes that a person acquires abroad would become integrated into their own microbiome or simply pass through their system, Dantas says. 

"There's ample support now from our study that when you go to a new location, you pick up resistance genes that are endemic to that region," he said. "Now we need to do the next step, to ask, 'Are they going to be sticking around or not?'"

Dantas adds that he and his team didn't explore whether any of these genes actually harmed the health of the travelers; the researchers didn't ask participants if they felt sick after returning home or screen them for infections. Another open question is the extent to which people deposit antimicrobial resistance genes from their own microbiomes in the places they visit. 

Still, Dantas says, the findings illustrate how international travel may elevate the levels of antibiotic resistance across the globe. 

"This is not a story about [saying], 'Don't do international travel at all!' Nor is this a study to paint particular regions of the world as 'dangerous regions,'" he said. "We're a globalized world, and we're going to travel."

Rather, he says, the results both indicate that scientists must investigate what happens to these genes after they voyage to new countries and provide new information for global public health surveillance programs.

"We have just increased the database of known resistance genes, so the next time someone does a study of this type they have that many more genes to count, that many more genes to identify," Dantas said.

The study, "Destination shapes antibiotic resistance gene acquisitions, abundance increases, and diversity changes in Dutch travelers," published June 6 in Genome Medicine, was authored by Alaric W. D'Souza, Manish Boolchandani, Sanket Patel and Gautam Dantas, Washington University School of Medicine; Gianluca Galazzo and John Penders, Maastricht University Medical Center; Jarne M. van Hattem and Menno D. de Jong, Amsterdam University Medical Center; Constance Schultsz, Amsterdam University Medical Center and Amsterdam Institute for Global Health and Development; Maris S. Arcilla and Damian C. Melles, Erasmus University Medical Centre; and COMBAT Consortium. 

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