In March 2013, the Centers for Disease Control sounded the alarm. Healthcare facilities around the U.S. reported a dramatic rise in drug-resistant bacteria. The culprit fueling this increase was CRE (carbapenem-resistant Enterobacteriaceae). This microbe normally resides in the human gut, where it is harmless—but if it travels to other parts of the body, it causes a nasty infection called sepsis.
Usually, sepsis can be treated with antibiotics, but more and more Enterobacteriaceae antibiotic-resistant strains are turning up. Reports that other bacteria have also acquired resistance to carbapenem antibiotics add to the alarm. Physicians reserve carbapenem antibiotics as a last resort when treating bacterial infections. If resistance to this antibiotic becomes widespread, a healthcare crisis will ensue.
Many evolutionary biologists point to the rise of “superbugs” as prima facie evidence for biological evolution. They claim that the overuse and misuse of antibiotics has caused antibiotic-resistant bacteria to evolve right before our eyes. The emergence of antibiotic resistance is an example of “evolution in action”; thus, evolution must be a fact.
When evolutionary biologists point to the emergence of antibiotic resistance in human pathogens, they often give the impression that this capability arose when humans began using antibiotics about a century ago. Accordingly, random mutations of the pathogen’s genetic material eventually created drug resistance. Once resistance emerged by chance, natural selection took over, driving an increase in the number of antibiotic-resistant strains in the population.
But a recent study demonstrates that human activity did not spur evolution into creating superbugs. Instead the genes for antibiotic resistance may date back to the Precambrian era. Researchers from Spain recently produced proteins that they believe existed on Earth 3 billion years ago. These proteins would have imparted antibiotic resistance to bacteria.1
Operating within the evolutionary framework, the scientists built an evolutionary tree using the different versions of an enzyme called β-lactamase. This biomolecule breaks down β–lactam antibiotics and is found among a wide range of bacteria. From this evolutionary tree, the scientists determined what the structure of β-lactamase looked like 3 billion years ago and then produced it in their labs. When they incorporated the gene for the ancient enzyme into the genomes of bacteria, the microbes became resistant to β–lactam antibiotics. They argue that their work supports the view held by an increasing number of scientists: bacterial resistance to antibiotics is an ancient phenomenon.
How could this be?
The antibiotics used today derive from materials produced by fungi. These organisms secrete antibiotics into the environment to inhibit the growth of bacteria in their immediate surroundings. By eliminating their competition, the fungi gain sole access to nutrients and other resources. But bacteria are not passive victims—they possess elaborate biochemical mechanisms to counteract antibiotics, including enzymes like β-lactamase.
The genes responsible for antibiotic resistance are often housed on small, circular pieces of DNA called plasmids. These molecules can be exchanged between bacteria through a mechanism known as conjugation. Bacteria can also swap large pieces of DNA through other processes, collectively termed horizontal gene transfer (HGT).
Through HGT, human pathogens—which would not normally be exposed to fungi and, therefore, lack antibiotic resistance genes—can acquire resistance. In fact, a recent study by scientists from Washington University (St. Louis, MO) demonstrates that the antibiotic resistance genes in human pathogens (for several classes of antibiotics, including β–lactams, aminoglycosides, amphenicols, sulfonamides, and tetracyclines) are identical to those isolated from soil bacteria. This result indicates that these two communities of microbes exchange genes with high frequency. 2
The Washington University scientists point out that this gene exchange sets up a vicious cycle. When antibiotic-resistant genes are transferred from soil bacteria to human pathogens, such “misuse” of antibiotics will select for resistant strains. These drug-resistant human pathogens can, in turn, transfer resistance genes to soil bacteria. Drug resistance is selected among soil microbes because of the high levels of antibiotics in the environment that come from the manure of cattle that are fed antibiotics.
Humanity has a real problem on its hands. But the realization that antibiotic resistance genes predate human use of antibiotics is key insight that will help us avert a healthcare crisis.
The emergence of drug-resistant human pathogens is due to the activity of natural selection operating on preexisting genetic information, not the de novo creation of drug-resistant genes via iterative random mutations operated on by natural selection. In other words, the emergence of antibiotic-resistant bacteria is not an example of “evolution in action” and remains consistent with a creation perspective.
Does the Evolution of Bacteria Validate the Evolutionary Paradigm? Even though I am a creationist and intelligent design adherent, I do believe ample evidence exists to conclude that bacteria evolve. Does this mean that evolution is a fact? For an answer to this question, check out the following links:
“Does the Evolution of Caffeine-Eating Bacteria Stimulate the Case for Biological Evolution?”
“Long-Term Evolution Experiment: Evidence for the Evolutionary Paradigm? Part 1 (of 2)”
“A Brief Update on the Long-Term Evolution Experiment”
- Valeria A. Risso et al., “Hyperstability and Substrate Promiscuity in Laboratory Resurrections of Precambrian β-Lactamases,” Journal of the American Chemical Society 135 (February 2013): 2889–902.
- Kevin J. Forsberg et al., “The Shared Antibiotic Resistome of Soil Bacteria and Human Pathogens,” 337 (August 2012): 1107–11.