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[EXCERPT: But antibiotics are under assault, for natural selection has equipped many of the bugs they were supposed to attack with resistance genes. As a result, old enemies such as tuberculosis, gonorrhoea and cholera are making an alarming comeback.]
Bugs and superbugs
April 2, 1998
From The Economist print edition
FOR a brief, vainglorious moment in the middle of this century, infectious disease looked vanquished. Vaccines had been developed for most childhood illnesses, and antibiotics were ridding the world of the rest. The vaccines, for the most part, still work. But antibiotics are under assault, for natural selection has equipped many of the bugs they were supposed to attack with resistance genes. As a result, old enemies such as tuberculosis, gonorrhoea and cholera are making an alarming comeback.
Nowadays, doctors are encouraged to use antibiotics sparingly. This, it is hoped, will prevent further resistance developing, and allow the existing resistance to fade. Until recently, this second hope seemed plausible. Wild bacteria do not normally carry antibiotic-resistance genes, suggesting that the evolution of resistance carries with it a cost of some sort, such as slower growth. If so, lifting the selection pressure (that is, removing antibiotics from the environment) should cause bacteria to revert to their earlier, vulnerable state.
Unfortunately, according to research just published in Proceedings of the National Academy of Sciences by Johanna Bjorkman, Diarmaid Hughes and Dan Andersson, biologists at Uppsala University and the Swedish Institute for Infectious Disease Control, this seems to be wrong. Strains resistant to antibiotics are initially less virulent than their susceptible counterparts, as you would expect, but the researchers found that virulence can be rapidly acquired without any loss of resistance. In other words, the evolutionary burden imposed by resistance may not be significant after all.
The researchers looked at antibiotic-resistant mutants of the bacterium Salmonella typhimurium and compared them with the normal, susceptible strain, to see how fast each one grew in mice. Growth, in this species at least, is a good measure of virulence: the nastier the strain, the faster it multiplies. They looked at seven strains in all-three with resistance to the antibiotic streptomycin, and two for each of rifampicin and nalidixic acid. Sure enough, they found that, at first, all of the resistant strains grew more slowly than the sensitive ones.
This soon changed, however. The researchers injected each resistant strain into mice-and found that within 30 generations, new mutations arose in the antibiotic-resistant strains that rendered them at least as fierce as the original, even though the mice were not being treated with the relevant antibiotics. And when they repeated the experiments in test tubes, the researchers found the same thing. In all, of 26 fast-growing mutants discovered in the tests, only four had lost antibiotic resistance as the price for accelerating their growth.
This result, if it holds for other species of bacteria, is worrying. It means that judicious use of antibiotics will help prevent the appearance of new antibiotic-resistant mutants, but it may not have any effect on the populations of antibiotic-resistant bacteria that already exist. Superbugs may be here to stay.
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