BACTERIA that are resistant to antibiotics are becoming disturbingly common in people. More worrying still is that the genes which confer this resistance are also showing up in bacteria found in other animals. When resistant bacteria hop between species, that can increase the rate of evolution and, over time (through the sharing of independently evolved traits) turn a mildly resistant bug that is merely a nuisance into a serious threat.
This has left researchers wondering how resistant bacteria get into animals in the first place. One possibility is that genes for antibiotic-resistance circulate naturally in wild populations. Many antibiotics are, after all, derived from the natural defence mechanisms of other micro-organisms, so it is not unreasonable to think that antiantibiotics, too, are widespread in nature. Another possibility is that human antibiotic use has promoted the circulation of resistance genes to other species.
Until recently, most of the studies that have looked at bacteria in such species have concentrated on domestic animals. But a team of biologists led by Trine Glad and Monica Sundset at the University of Tromso, in Norway, has now looked properly in the wild. In fact, they have gone just about as wild as it is possible to get, examining polar bears on the Arctic archipelago of Svalbard. They chose these bears because they neither interact with people nor prey on animals that spend any significant amount of time near human settlements. The team theorised that if the circulation of antibiotic-resistance genes was a natural phenomenon, they would find these genes even in this isolated population. If it was not natural, they reckoned the bears would carry few, if any, bacteria with such resistance.
To carry out their analysis, they needed samples of faeces. Simply travelling to the icy plains of Svalbard, however, and searching for polar-bear droppings was not practical, because such droppings might have become contaminated after they had left the animal that produced them. Instead, the team were forced to search for bears by helicopter and tranquillise each one they found with a dart. Once a bear went down, they landed and collected a sample directly from its rectum.
The team tested the bacteria that they found in samples from ten bears for the presence of blaTEM genes, which are known to encode resistance to a commonly used class of antibiotics that includes penicillins and cephalosporins. Cultures from the samples were grown on two sorts of media. One contained an antibiotic to which blaTEM confers resistance. The other, acting as a control, did not. The resulting colonies were then analysed to find out what strain of bug they had grown from.
Ms Glad and Dr Sundset report, in BMC Microbiology, that they were able to isolate only four strains of bacteria that carried blaTEM genes. In previous work with bulls, horses and domestic pets, an average of 13 strains of bacteria per species were found to be carrying blaTEM genes. In pigs, the number was 16. (In human hospital patients it is a staggering 40.)
The discovery that animals in pristine environments have few bacteria with resistance genes makes it likely that much of the antibiotic resistance found in these other species is a result of human influence, rather than natural gene-circulation.
Much, but perhaps not all. The bears are so isolated that Dr Sundset does not believe they could have picked up the resistant strains they do have from people. The only explanation she can offer is that there is indeed a low natural level of antibiotic resistance in the bears' bugs, a point that the team wants to look into next.
All things considered, this is good news for epidemiologists. High levels of antibiotic resistance in remote environments would imply the existence of vast natural reservoirs of the genes for such resistance. Instead, these data (albeit based on only ten animals) do suggest that only those animals which are in close contact with people act as reservoirs.