Soil Provides Library of Antibiotic Resistance
The “evolution of antibiotic resistance” is a staple in the creation-evolution debates, providing evolutionists with a living illustration of evolution taking place right before our eyes. What if all the information for antibiotic resistance, however, already exists in a library from which bacteria can find it?
That seems to be the implication of a study by D’Carlo et al. in Science.1 A Canadian biochemical research team decided to survey the techniques of antibiotic resistance already present in soil bacteria. They were astonished. Every antimicrobial medicine, including some only recently developed, had a defensive weapon ready for it:
This study provides an analysis of the antibiotic resistance potential of soil microorganisms. The frequency of high-level resistance seen in the study to antibiotics that have for decades served as gold-standard treatments, as well as those only recently approved for human use, is remarkable. No class of antibiotic was spared with respect to bacterial target or natural or synthetic origin. Although this study does not provide evidence for the direct transfer of resistance elements from the soil resistome to pathogenic bacteria, it identifies a previously underappreciated density and concentration of environmental antibiotic resistance.
The authors could not determine whether “The presence of antibiotics in the environment has promoted the acquisition or independent evolution of highly specific resistance elements in the absence of innate antibiotic production,” and are not sure whether today’s resistant pathogens acquired their resistance from soil organisms. They could not rule it out, however: “The soil could thus serve as an underrecognized reservoir for resistance that has already emerged or has the potential to emerge in clinically important bacteria.” A frightening implication is that no matter what agents we throw at them, bacteria may be able to check out a defense from this “environmental resistome.”
Alexander Tomasz commented on this study in the same issue of Science.2 He said that, “Actually, the majority of the most effective antibiotic-resistance mechanisms in human pathogens are acquired,” or gained not by evolution but by lateral gene transfer. The acquired resistance, he says, is superior to that gained by mutations:
The superiority of such acquired mechanisms is illustrated by the contrast between Staphylococcus aureus strains that have decreased susceptibility to vancomycin through mutations (so-called VISA strains) as compared to VRSA strains, S. aureus that acquired a complete vancomycin-resistance gene complex via the transposon Tn1546. The VISA strains have low-level resistance (the minimal inhibitory concentration of vancomycin is 6 to 12 g/ml), are often associated with reduced oxacillin resistance, and show abnormal cell wall synthesis; the multiple transcriptional changes documented by DNA microarray analysis reflect the complexity of this mechanism. In contrast, in VRSA strains, the Tn1546-based mechanism produces high-level vancomycin resistance (with a minimal inhibitory concentration of more than 500 g/ml) that does not interfere with oxacillin resistance, and cell wall synthesis proceeds with a depsipeptide cell wall precursor specific to these strains.
Though the transfer mechanism is not known, “Clearly, mobilization of a resistance mechanism must involve ‘packaging’ into a plasmid, phage, or some transposable element,” he believes. Tomasz called the sheer variety of resistance mechanisms catalogued by D’Carlo et al. “remarkable”. It appears that microorganisms might not only make antibiotic weapons in profusion, but also make a plethora of defenses against them.
1D’Costa et al., “Sampling the Antibiotic Resistome,” Science, 20 January 2006: Vol. 311. no. 5759, pp. 374 – 377, DOI: 10.1126/science.1120800.
2Alexander Tomasz, “Weapons of Microbial Drug Resistance Abound in Soil Flora,” Science, 20 January 2006: Vol. 311. no. 5759, pp. 342 – 343, DOI: 10.1126/science.1123982.
Neither of these papers ruled out that the resistance mechanisms have always been present in the gene pool. If so, then the claim that bacteria “evolve” resistance to antibiotics is negated. Bacteria may simply find access to an existing library of information, a “resistome” that, coupled with a packaging and delivery mechanism (plasmids and transposons), confers the resistance that previously appeared to evolve out of thin air.
Notice that the resistance conferred by mutations harms the organism. The case cited by Tomasz reduced the fitness of the organism by weakening its cell wall. Mutationally-gained resistance is like the illustration Lee Spetner gave: cutting off a man’s arms makes him resistant to handcuffs. In a population of prisoners being handcuffed, this person would be the fittest, but only in a specific environment and at the cost of overall fitness. In the wild, he would be at a disadvantage. Scott Minnich also illustrated this type of bacterial resistance in the film Icons of Evolution with cultures of bacteria exposed to antibiotics. The kind of resistance conferred by specialized enzymes able to disable the agent, however, require specific genetic information that appears designed.
Too little is known at this point, but these articles uncover the possibility that genetic information that confers antibiotic resistance is already present in the environmental resistome. If so, this undermines a commonly-used evidence for evolution.