It wasn't so long ago that antibacterial products, from soaps to hand gels to wipes for your kitchen counter, became ubiquitous in our grocery stores and our daily lives. Not long afterwards, though, we started hearing reports that these products and their even more powerful cousins, antibiotic prescriptions, were actually doing more harm than good--by facilitating the evolution of bacterial resistance to antimicrobials. As it turns out, that may be just be one evolutionary side effect of exposing bacteria to strongly selective anthropogenic pressures. An even more fundamentally important one is the ability to evolve rapidly, quickly incorporating genetic changes in order to display a different phenotype--in this case, increased or more comprehensive robustness in the face of antimicrobial treatments. This means that our struggles to deal with antibiotic-resistant strains, such as the dreaded methicillin-resistant Stapholococcus aureus (MRSA), are only just the tip of the iceberg.
(Methicillin-resistant Stapholococcus aureus, otherwise known as MRSA)
The question of whether humans are increasing bacterial "evolvability" is addressed by two Australian researchers in a review article published in the latest issue of Trends in Ecology and Evolution. They define "evolvability" as "an increased potential for evolution," which can be driven by characteristics such as basal mutation rate, recombination rates, protection against the incorporation of foreign DNA into the genome, and propensity for lateral gene transfer (or acquiring genes from a source other than a "parent"). All of these traits "affect the rate at which genetic variation can be generated"--and some of this variation could very well confer resistance.
Interestingly, many antibiotics were originally isolated from soil bacteria, which probably developed these compounds for use in signalling or competition with neighbors. For cells to survive in these potentially toxic environments, they had to evolve resistance genes alongside those producing poison, and so the terrestrial environment is probably already teeming with genetic elements offering protection from various man-made drugs. Once our antibiotic runoff reaches these environments, bacteria without the genes die off, while those with them will survive, passing on the resistance not only to their "offspring" but also, potentially, to their neighbors. Cells with higher levels of evolvability will become resistant more quickly; in other words, exposure to antibiotics leads not only to the selection of resistance, but also of the ability to develop it. This process works so well that the number of antibiotic-resistant genetic elements has increased significantly over the years. Many such elements are located in wild animals or environments not directly exposed to antibiotics, strongly suggesting that resistance has spread along a bacterial supply chain that begins in anthropogenic environments and extends even into those otherwise considered "pristine."
The authors point out that evolvability is not always a useful characteristic for bacteria to possess. For instance, while some mutations can be advantageous, others can impair functionality or even remove it altogether; likewise, incorporation of DNA from an unrelated bacterium might result in the transcription of a useful protein, but it also could generate something that is ultimately toxic. Thus, we should expect evolvability to be high only in systems where it's a gamble that, more often than not, pays off. This describes the current state of affairs in both terrestrial and aquatic ecosystems, into which humans dump vast quantities of antibiotics each year--especially in the form of waste water. The exact amounts are difficult to measure, but are likely to be large if they are even a small portion of the millions of metric tons produced annually.
(Acinetobacter baumannii, a gram-negative bacterium that is sometimes known as "Iraqibacter" because of its prevalence among US soldiers wounded to Iraq.)
One particularly frightening aspect of the spread of resistance is how it can often involve whole suites of genes rather than just one. Acinetobacter baumannii, for instance, now possesses a "resistance island" containing 45 genes for antibiotic/antimicrobial resistance, as well as resistance to heavy metals such as mercury and arsenic. As a result, A. baumannii infections have become a much greater threat to human health over the last several decades; additionally, these bacteria have given rise to a number of new hybrids and variants that are also likely to cause trouble in the future. Indeed, higher levels of evolvability are likely not only to increase the threat from current pathogens, but also "stimulate the emergence of new disease agents" from organisms that used to be our friendly neighbors.
As mentioned earlier, however, evolvability should be found at relatively lower levels in systems where it leads to more harm than good--for instance, places where there is limited exposure to novel antibiotic products. It is unlikely that we will be able to easily remove current contamination, but we can limit the amount introduced in the future by minimizing unnecessary use of antimicrobials and by disposing of them in a more eco-friendly way. This won't stop bacteria from developing defenses against our drugs and disinfectants, but it might help reduce the speed with which they do so.
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Gillings, M.R., and Stokes, H.W. 2012. Are humans increasing bacterial evolvability? Trends in Ecology and Evolution, 27(6): online advance publication.
Thanks to the following websites for providing the images used in this post:
http://en.wikipedia.org/wiki/Acinetobacter_baumannii
In reality, bacteria are simply living in and exploiting the environment in which they find themselves. They are no more attempting to cause disease, than humans are when they cut down trees in a forest. In most cases, they can evade detection by the immune system by staying "below the radar" until a sufficient number is present. Once the population is large enough [detected via quorum sensing], the bacteria may change their behavior and begin producing toxic byproducts, thereby causing disease or infection in the host.
As indicated in the article, they can exchange genetic information through Horizontal Gene Transfer (HGT), however there is no barrier to exchanging that information between commensual [so-called "good" bacteria] and pathogens. In addition, as our commensual bacteria may become antibiotic resistant, then that information could be transferred to pathogens that enter our system [this doesn't even consider the effects of antibiotics on animals that may be food sources, etc.].
To compound the problem, resistance doesn't have to be directly passed to individuals, since antibiotic stress can result in bacteria forming biofilms which are fundamentally more resistant than individuals are. This can "buy them time" and render them nearly impossible to destroy with antibiotics [although compromising biofilms may render antibiotics more effective].
Interesting alternatives to antibiotics are being researched, such as drugs that may disrupt quorum sensing, effectively shutting down bacterial communication. This may be promising, because such a disruption doesn't appear to be subject to selection pressures, since it doesn't actually kill the bacteria.
http://scienceblog.com/848/drug-fights-bacteria-by-disrupting-quorum-sensing-and-biofilms/
In any case, it's an interesting topic.