An antibiotic resistance gene from a clinical environment has found its way into soil bacteria in one of the most unlikeliest places – the Namib desert in Namibia.

The discovery, reported in the journal Science of the Total Environment, adds to growing evidence that soil-dwelling bacteria, even in places devoid of human activity, can form reservoirs of antimicrobial resistance genes and aid their spread, possibly back into the clinic.

Antibiotic resistance is one of the world’s biggest health concerns. Their extensive use to treat humans and domesticated animals has allowed bacterial strains to evolve defence mechanisms that make many drugs ineffective.

Beta-lactam antibiotics are one of the most common type, which includes penicillin and its derivatives. They work by preventing certain pathogenic bacteria such as E. coli from growing cell walls, which kills them.

However, some strains overcome this by producing enzymes called extended spectrum beta lactamases (ESBLs) which attack the drugs.

Genes that encode these enzymes may evolve naturally or appear in response to antibiotic exposure. They are widespread in clinical settings and other human-impacted environments such as agricultural soils.

However, they have also been found in faraway places before, including deserts, isolated caves and the Arctic.

What makes the latest desert discovery unique is that a ESBL gene was found on a plasmid – a circular bit of DNA that sits inside a bacterium separate from its genome. These can be easily shared between bacteria and are commonly associated with transmitting clinically relevant antibiotic resistance genes.

“The presence of the gene on a plasmid has not been reported in a desert environment before,” says Yashini Naidoo who led the work at the University of Pretoria, South Africa.

“Being on a plasmid implies that the gene has been acquired and not likely to have evolved in this environment.”

Naidoo and her colleagues made the discovery after analysing the genetic content of soil samples taken from the Namib desert in April 2018.

Four out of six sample sites contained an ESBL enzyme-encoding gene called TEM-116 on a plasmid that was present in the soil-dwelling bacteria species Rhodococcus ruber.

What’s more, the plasmid also contained a metal resistance gene, enabling the bacteria to tolerate soils with naturally high levels of arsenic. Since the metal resistance gene helps the bacteria survive, it increases the likelihood of the plasmid spreading to other bacteria and for the TEM-116 gene to persist in the desert.

But if the gene came from a clinical setting, how did it get into the desert?

The researchers think birds could be responsible. After sporadic rainfall, millions of gray-backed sparrow-larks descend to feed on the ground. This could result in transporting soil microorganisms from human environments to the desert, and vice versa, via their droppings.

Supporting this theory, the team found a bacteriophage – a virus that infects bacteria – on the plasmid, which is associated with fecal contamination. Moreover, the bacteriophage itself could represent a new vehicle for spreading TEM-116, says Naidoo.

“Since TEM-116 is circulating between the clinic and the environment, the persistence of this gene in the environment may mean that its highly likely it could reappear in the clinic during antibiotic therapy in this current form,” explains Naidoo.

“If this should happen, it would make treatment options very difficult.”