Wow... it's been a long time since I was here... not sure how long I'll be back, but I'm going to give it a shot.
I've read through some recent posts....
Let's see if I can't increase the quality of posts and discussion in this forum. This should be interesting.
The classic story regarding the evolution of antibiotic resistance that is taught to students at more-or-less all levels is that the presence of
antibiotics - in growth medium, in an infected organism, etc. - kills off the susceptible bacteria, leaving resistant members to survive. More complex
versions of this story note that early resistant mutant phenotypes tend to somewhat sensitive to antibiotics, and as more and more generations appear,
the resistant phenotypes become more and more resistant, finally culminating in resistance to antibiotics at dosages that are utilized clinically.
Though quaint, plausible, and powerful with respect to explanatory scope, the story is simply not true.
It has been known for a good deal of time that most antibiotic resistance genes are acquired and passed to other bacteria via integrons, which are
mobile genetic elements that can capture and transfer genes, and subsequently integrate them into other genomes in a site-specific manner. For the
most part, antibiotic resistance in bacteria is a consequence of both inter- and intraspecies transfer of non-essential, self-replicating,
extrachromosomal collections of genes and other elements of DNA information known as plasmids. An excellent
detailing this information was published in the journal Cell back in March of 2007.The abstract from this article nicely
summarizes and supports what is written here (special emphasis added by mattison0922):
Molecular Mechanisms of Antibacterial Multidrug Resistance
Michael N. Alekshun and Stuart B. Levy
Treatment of infections is compromised worldwide by the emergence of bacteria that are resistant to multiple antibiotics. Although classically
attributed to chromosomal mutations, resistance is most commonly associated with extrachromosomal elements acquired from other bacteria in the
environment. These include different types of mobile DNA segments, such as plasmids, transposons, and integrons. However, intrinsic mechanisms not
commonly specified by mobile elements—such as efflux pumps that expel multiple kinds of antibiotics—are now recognized as major contributors
to multidrug resistance in bacteria. Once established, multidrug-resistant organisms persist and spread worldwide, causing clinical failures in the
treatment of infections and public health crises....
The means that microbes use to evade antibiotics certainly predate and outnumber the therapeutic interventions themselves. In a recent
collection of soil-dwelling Streptomyces (the producers of many clinical therapeutic agents), every organism was multidrug resistant. Most were
resistant to at least seven different antibiotics, and the phenotype of some included resistance to 15–21 different drugs...
This is actually summarized quite nicely in a story (Medical Tribune, 29 December 1988, pp.1, 23, no electronic resource known to be available) about
some unfortunate sailors who froze to death on an Arctic expedition back in 1845. The sailors were buried in the permafrost until 1986 when their
bodies were exhumed. Given that the sailors had been frozen solid in the permafrost, the bodies were extremely well preserved; in fact, researchers
were able to isolate and revive six strains of 19th century bacteria found within the contents of the sailors' intestines. These 19th century
bacteria - bacteria that were alive prior to the discovery of penicillin were found to be resistant to several modern-day antibiotics, including
has appeared that further corrupts the classic story of the
development antibiotic resistance via Darwinian evolution. The abstract is reproduced below:
Integrons are found in the genome of hundreds of environmental bacteria but are mainly known for their role in the capture and spread of
antibiotic resistance determinants among Gram-negative pathogens. We report a direct link between this system and the ubiquitous SOS response. We
found that LexA controlled expression of most integron integrases and consequently regulated cassette recombination. This regulatory coupling enhanced
the potential for cassette swapping and capture in cells under stress, while minimizing cassette rearrangements or loss in constant environments. This
finding exposes integrons as integrated adaptive systems and has implications for antibiotic treatment policies.
You got all that, right?
Perhaps not. I'll do the best I can do translate it: This particular article details the molecular mechanism behind the transfer of resistance genes
between bacteria. As the article details, it's the use of antibiotics themselves that actually triggers the synthesis of a specific bacterial enzyme
that identifies and preferentially captures the resistance genes, and subsequently facilitates their expression. Additionally, this enzyme promotes
the rearrangement of these resistance genes. The rearrangement of these genes alters the order of when the genes are expressed. New rearrangements
that are triggered by taking an antibiotics, and those bacteria that have 'correctly' rearranged their genes, creating a new resistance cassette,
will be able to survive and pass on resistance not only vertically, to subsequent generations, but also horizontally; bacteria can pass resistance
genes to their neighbors in a deliberate manner.
This is huge. The classic Darwinian story render the organism entirely a slave to the environment, unable to respond or adapt at the individual level.
Only a lucky few - a few that are resistant simply by chance - survive the selective pressure of antibiotic use, and are able to pass on their
Or as you've been more simply taught: Survival of the fittest.
This new research clearly indicates that this isnot
necessarily the case; indeed, it appears that - contrary to what I've been taught
more-or-less through my entire history in science - individual organisms, not just populations
are able to react to and adapt to the
Or at least individual microorganisms
are able to do this.
It cannot be stressed enough how significant of a break this is from the classic story of antibiotic resistance via Darwinian evolution. The idea that
the individual and not just the population of organisms can adapt to a changing environment at the DNA level is literally scientific heresy.
This is of course more evidence, another huge piece of evidence suggesting that The Theory of Evolution with respect Darwin's ideas is at least not
as well understood as was once believed, and at most completely, utterly, and totally false.