James urquhart

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

The discovery, reported in the journal Science of the Total Environment, adds to growing evidence that bacteria living in soil, even in places devoid of human activity, can form reservoirs of antimicrobial resistance genes and promote their growth. spread, possibly again in the clinic.

Antibiotic resistance is one of the biggest health problems in the world. Their extensive use to treat humans and pets has allowed bacterial strains to develop defense mechanisms that render many drugs ineffective.

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

However, some strains overcome this by producing enzymes called extended spectrum beta-lactamases (ESBLs) which attack drugs.
The genes that code for these enzymes can evolve naturally or appear in response to exposure to antibiotics. They are prevalent in clinical settings and other human impacted environments such as agricultural soils.

However, they have also been found in places far away before, including deserts, remote caves, and the Arctic.

What makes the desert’s latest discovery unique is that an ESBL gene was found on a plasmid – a circular piece of DNA that is inside a bacterium separate from its genome. These can be easily shared between bacteria and are generally associated with the transmission of clinically relevant antibiotic resistance genes.
“The presence of the gene on a plasmid had never been reported in a desert environment before,” explains 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 probably has not evolved in this environment.”

Naidoo and his colleagues made the discovery after analyzing the genetic content of soil samples taken from the Namib Desert in April 2018.

Four of the six sampling sites contained a gene encoding an ESBL enzyme called TEM-116 on a plasmid present in the species of soil bacteria Rhodococcus ruber.
In addition, the plasmid also contained a metal resistance gene, allowing the bacteria to tolerate soils naturally rich in arsenic. Since the metal resistance gene helps bacteria survive, it increases the likelihood that the plasmid will spread to other bacteria and that the TEM-116 gene will persist in the desert.

But if the gene came from a clinical setting, how did it get in the wilderness?
Researchers believe birds could be responsible. After sporadic rains, millions of gray-backed larks descend to feed on the ground. This could lead to the transport of soil microorganisms from human environments to the desert, and vice versa, via their droppings.

To support this theory, the team found a bacteriophage – a virus that infects bacteria – on the plasmid, which is associated with fecal contamination. In addition, the bacteriophage itself could represent a new vehicle for the spread of TEM-116, explains Naidoo.

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

“If that were to happen, it would make treatment options very difficult. “

* James Urquhart is a science journalist based in Edinburgh, Scotland