Antibiotic Resistance Finding: Attempt two, page 1
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Topic started on 1-6-2009 @ 08:37 PM by mattison0922
Okay, let's try this again:

The story typically taught to students regarding antibiotic resistance goes something like this: The presence of antibiotics in bacterial growth medium, soil, host organism, or other environment selects for variants that are, fortuitously and randomly, resistant the particular antibiotic present. It is generally noted that early resistant strains are minimally resistant to the antibiotic, with subsequent generations becoming more and more resistant, until the resistance level reaches clinically relevant concentrations.

I'm going to reproduce the next statement from my original post, and I think be within the terms and conditions of this site; it's a great line.

Though quaint, plausible, and powerful with respect to explanatory scope, the story is simply not true.

Indeed it has been known for a good deal of time - and I teach it this way to my students: Antibiotic Resistance are, in general, NOT acquired via this classic story. Many, if not most, antibiotic resistance genes are acquired and passed via mobile genetic elements whose cellular role appears to be exactly that - capture, transfer, and integration of genes - often in a site-specific manner.

In general, antibiotic resistance results not from Darwinian evolution, but rather from both intra- and interspecies transfer of extrachromosomal, self-replicating, collections of generally non-essential genes and a variety of regulatory nucleic acid sequences called plasmids. An excellent summary of what I've written above was published in the Journal Cell, back in march of 2007. It is quoting this article at length, with special emphasis by mattison0922:

Molecular Mechanisms of Antibacterial Multidrug Resistance Cell 128(6):1037-1050 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 information is nicely supported in a story (Medical Tribune, 29 December 1988, pp.1, 23, no electronic resource known to be available) that details the plight of some unfortunate sailors who froze to death on an Arctic expedition back in 1845. These sailors were buried under the permafrost until 1986 when their bodies were exhumed. The sailors had been frozen solid in the permafrost, and their bodies were extremely well preserved; so well preserved that researchers were able to isolate and revive six strains of 19th century bacteria obtained from 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 penicillin.

Another article was recently published that further undermines the Darwinian story of the evolution of antibiotic resistance. 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 understood that, didn't you?

Perhaps not, I'll translate it for you here and now: This article details the molecular mechanism behind the transfer of resistance genes between bacteria. As described in the article, the use of antibiotics actually triggers the synthesis of a specific enzyme that not only identifies, but also preferentially captures the resistance genes and facilitates their expression. This enzyme also promotes the rearrangement of these resistance genes. This alters the order of when the genes are expressed. New rearrangements 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 this resistance not only vertically, but also horizontally - to their peers; bacteria can pass resistance genes to their neighbors in a deliberate manner.

This is extremely significant; the classic Darwinian story describes the organism as entirely a slave to the environment, unable to respond or adapt at the individuallevel. Only a lucky few - those that are resistant by chance - survive the selective pressure of antibiotic use, and are able to pass on their genes.

Or as you've been more simply taught: Survival of the fittest.

This new research clearly indicates that this is not necessarily the case, and in fact, contrary to what I've been taught more-or-less through my entire history in science - individual organisms - not just populations are able to not only react to, but also to adapt to the environment.

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.

Finally, in response to astyanax's comment on my original post:



I'm pleased to be the first to welcome you back, mattison. You've been sorely missed; we get a different class of creationist in here nowadays.

If there are organisms that synthesize and secrete antibiotics in nature, as indeed there are, why is it surprising that bacteria should have evolved defences against them?

Thanks for the welcome, I'm not sure who long I'll be around... added a couple of pups to the litter since the last time, and am trying to do a bit more serious writing in addition to my internet stuff.

In response to the second part of your statement, it's not surprising that organisms have evolved defenses to antibiotics, what is surprising, and what goes against what is most commonly taught is the mechanism by which organisms become resistant.

The classic Darwinian story describes this as a random chance with respect to which organisms survive. Organisms are blessed with genes that allow them survive go on to reproduce, those that die... well they don't. However, this new data suggests that individuals do have an adaptive response, one that may or may not result in antibiotic resistance.... that's the big change, the fact that antibiotic resistance is a response, not a pre-existing condition.

Does that make sense?


reply posted on 1-6-2009 @ 08:58 PM by rogerstigers
reply to post by mattison0922


Yeah, this all makes sense. I discussed this earlierr today with NRA4ever333 here. Specfically I pointed out an interesting article about epigenetics which says in a nutshell that DNA is not the only thing that controls what traits are expressed. This plus the role of "junk" DNA, which I believe to be merely compressed (zipped) instruction sets, raises a lot of questions about the function of DNA in adaptive mutations.


I don't hold anything against Darwin. He did the best that he could with what he had, just as Newton and Corpurnicus(sp?) did. I believe evolution is real, but it is a mechanism for adapting, not necessarilly the driving force behind it.


reply posted on 1-6-2009 @ 10:07 PM by liveandlearn
I am a mere Infection Control nurse who must deal with resistance organisms daily but I struggle to wrap my brain around what you have written.

So if I may, on a more simplified, level explain what I believe to be the case, at least in part, and hope that you can say yes or no to me and explain so that I can understand.

All we here about and a concern for me is that resistant organisms are mostly acquired in the hospital. Not true, as there is what is commonly known as a community acquired MRSA (methicillin resistant staph aureus) as well as many gram negative organisms not as widely known.

I am here to place the fault elsewhere, at least in part based on my on observations and what I can understand of your post, and that is squarely on doctors who very often and in most circumstances give multiple antibiotics to patients. I mean 3 or 4 different classes of antibiotics. Not only do they give multiple antibiotics they give them at the most common dosage instead of giving them on a weight based dose. It is a 'one size fits all' from the 200 lb 5 ft tall woman to the 200 lb 6'2" tall man. Children are given doses based on weight and while there are weight based recommendations for adults they are not adhered to by most physicians.

In my facility we do bariactric surgeries. This is a bypass surgery for obese patients. We were having a lot of infections so I had to do some research. I found that a study done on these subjects during surgeries at different times with the appropriate weight based antibiotic in the end showed 35 % approximately never reached a minimum initiatory concentration of antibiotic in their tissue for gram negative or gram positive bacteria.

I took a look at patients having surgery in my facility and the antibiotic received vs the appropriate antibiotic for their weight and 89 percent of obese patients, patients over 190 lbs, received an inappropriate dose of antibiotic ( I think this should be base on BMI instead of weight). That amounted to 59 percent of all patients.

If sufficient antibiotic isn't given the patient then the remaining organisms are free to mutate and develop resistance.

If surgeons and hospital physicians who are required and even inundated with this information do not keep up, how much more likely is the family practitioner to keep up.

We have a growing obese population yet they are given the same dose as someone of normal weight.

Can you tell me, based on what you have posted, the validity, or not, of what I have suggested.


reply posted on 1-6-2009 @ 10:16 PM by mattison0922
Originally posted by rogerstigers
reply to post by mattison0922


Yeah, this all makes sense. I discussed this earlierr today with NRA4ever333 here. Specfically I pointed out an interesting article about epigenetics which says in a nutshell that DNA is not the only thing that controls what traits are expressed. This plus the role of "junk" DNA, which I believe to be merely compressed (zipped) instruction sets, raises a lot of questions about the function of DNA in adaptive mutations.


There are multiple levels of information in DNA, 6 potential reading frame, epigenetic codes, nucleosome codes, etc. I actuallyblogged about function in junk DNA fairly recently, you may want to check it out.

I don't hold anything against Darwin. He did the best that he could with what he had, just as Newton and Corpurnicus(sp?) did. I believe evolution is real, but it is a mechanism for adapting, not necessarilly the driving force behind it.


I don't believe I knocked Darwin, just pointed out the the Darwinian explanation provided typically for antibiotic resistance is gradually unraveling; this is one such example.


reply posted on 1-6-2009 @ 10:28 PM by mattison0922
Originally posted by liveandlearn
All we here about and a concern for me is that resistant organisms are mostly acquired in the hospital. Not true, as there is what is commonly known as a community acquired MRSA (methicillin resistant staph aureus) as well as many gram negative organisms not as widely known.

Hospitals are the most common sources of antibiotic resistant bacteria; this is simply a function of the fact that hospitals are generally the places where the largest concentrations of antibiotics are used per capita.

I am here to place the fault elsewhere, at least in part based on my on observations and what I can understand of your post, and that is squarely on doctors who very often and in most circumstances give multiple antibiotics to patients. I mean 3 or 4 different classes of antibiotics. Not only do they give multiple antibiotics they give them at the most common dosage instead of giving them on a weight based dose. It is a 'one size fits all' from the 200 lb 5 ft tall woman to the 200 lb 6'2" tall man. Children are given doses based on weight and while there are weight based recommendations for adults they are not adhered to by most physicians.

What you describe here is in fact a problem. Physicians tend to overprescribe antibiotics. Most bacterial infections will resolve themselves, and don't require antibiotics. We've grown impatient in the modern world, and want to be cured as quickly as possible. Physicians do want to retain patients, and if patients want antibiotics, they can generally find someone to prescribe them. I've always assumed that physicians do account for a patient's weight; perhaps they don't.

In my facility we do bariactric surgeries. This is a bypass surgery for obese patients. We were having a lot of infections so I had to do some research. I found that a study done on these subjects during surgeries at different times with the appropriate weight based antibiotic in the end showed 35 % approximately never reached a minimum initiatory concentration of antibiotic in their tissue for gram negative or gram positive bacteria.

That's certainly less than ideal.

If sufficient antibiotic isn't given the patient then the remaining organisms are free to mutate and develop resistance.

In theory, yes. In general what happens is that a person who doesn't have a sufficient dose does breed resistant strains, however resistant strains have historically been outcompeted by sensitive strains. In other words, it used to be that you could defeat antibiotic resistant bacteria by ceasing antibiotic usage. Normal flora historically outcompete resistant flora.

However we are starting to see more and more community acquired cases of antibiotic resistant, which indicates that trend is coming to an end.

If surgeons and hospital physicians who are required and even inundated with this information do not keep up, how much more likely is the family practitioner to keep up.

Not very.

Can you tell me, based on what you have posted, the validity, or not, of what I have suggested.

What you've written appears to be valid, but is really only part of the problem. If we could every physician in the world to comply, we've got antibacterial toys, antibacterial wipes, antibiotics are used prophylactically in the agriculture industries; their use is wide spread, and each little bit contributes to the overall problem of resistance.


reply posted on 1-6-2009 @ 11:19 PM by liveandlearn
reply to post by mattison0922




Hospitals are the most common sources of antibiotic resistant bacteria; this is simply a function of the fact that hospitals are generally the places where the largest concentrations of antibiotics are used per capita.


This is true but the implication is that it is the nurse, not the doctor, who is mostly at fault. While nurses can carry it on their unwashed hands, I think it is mostly due to the prescribing habits of physicians.



In theory, yes. In general what happens is that a person who doesn't have a sufficient dose does breed resistant strains, however resistant strains have historically been outcompeted by sensitive strains. In other words, it used to be that you could defeat antibiotic resistant bacteria by ceasing antibiotic usage. Normal flora historically outcompete resistant flora.


Well, in hospitals across the nation we now consider once MRSA always MRSA. This is mostly true in patients with multiple comorbidities but with essentially healthy patients of normal weight many do overcome with normal bacteria.



However we are starting to see more and more community acquired cases of antibiotic resistant, which indicates that trend is coming to an end.


And this relates to my posit that family practitioners
are giving inappropriate antibiotics as well as patients not completing their medication.


What you've written appears to be valid, but is really only part of the problem. If we could every physician in the world to comply, we've got antibacterial toys, antibacterial wipes, antibiotics are used prophylactically in the agriculture industries; their use is wide spread, and each little bit contributes to the overall problem of resistance.


There have been many papers questioning all the antibacterial items you mention and their contribution to the problem.

As for Streptomyces, I had to google it because I was only familiar with streptococcus. I found that the predominate Streptomyces was Actinobacter which is indeed becoming a highly resistant organism. One of our sister hospitals had an outbreak and found that the index patient was a pilot who bailed out in Iraq and it is thought that the organism came from the soil there which would imply that it's resistance occurred naturally over time. I think that is what you were saying in your OP; correct me if I am wrong.


reply posted on 2-6-2009 @ 09:33 AM by mattison0922
Originally posted by liveandlearn
reply to post by mattison0922




This is true but the implication is that it is the nurse, not the doctor, who is mostly at fault. While nurses can carry it on their unwashed hands, I think it is mostly due to the prescribing habits of physicians.

I don't believe I implied this; I certainly didn't intend to imply this. To tell you the truth, the blame here is something that is peripheral to my discussion. Personally, I'm interested in the molecular mechanism behind the origins of antibiotic resistance, not who is responsible for overuse of antibiotics.



Well, in hospitals across the nation we now consider once MRSA always MRSA. This is mostly true in patients with multiple comorbidities but with essentially healthy patients of normal weight many do overcome with normal bacteria.

Yes, there has been a definite trend in an increase in overall 'fitness' of antibiotic resistant microbes. Historically, resistant strains tended to be 'less fit' than sensitive strains in the absence of antibiotics. I loosely mentioned this when I discussed the fact that normal flora have historically supplanted resistant strains.

It's interesting that you say once MRSA, always MRSA... in general if those genes aren't required, they won't be retained... In other words, the easiest way to rid yourself of MRSA is to simply stop taking antibiotics.

I wonder if the bacteria has undergone some integration event wherein these resistance genes are now carried on the main bacterial chromosome.

Maybe I'll add that to my list of stuff to look up.



And this relates to my posit that family practitioners
are giving inappropriate antibiotics as well as patients not completing their medication.

This is probably a part of it. Again, I'm less concerned with this aspect, but will add what I can.


As for Streptomyces, I had to google it because I was only familiar with streptococcus.

Completely different. Streptomyces are soil microbes. Streptomyces spp. are notable because they possess complex secondary metabolisms; this secondary metabolism produces a variety of chemicals, from which about 2/3 of our natural antibiotics are derived.

Streptomyces produce antibiotics, and thus, are necessarily resistant to the antibiotics they produce.


reply posted on 2-6-2009 @ 07:26 PM by liveandlearn
reply to post by mattison0922




I don't believe I implied this; I certainly didn't intend to imply this.


No, in no way did you imply this. It is the media and physicians who discuss it as well as how consumers read the information.



Completely different. Streptomyces are soil microbes. Streptomyces spp. are notable because they possess complex secondary metabolisms; this secondary metabolism produces a variety of chemicals, from which about 2/3 of our natural antibiotics are derived.

Streptomyces produce antibiotics, and thus, are necessarily resistant to the antibiotics they produce.


I am well aware that most drugs, antibiotics must have a lock for the key to fit and there would be no lock if there were not a key in nature. I did not know that streptomyces were a group of organisms.

You may not have gotten the discussion you wanted at the level you wanted but you have enlightened one person here on ATS. Thank you.



reply posted on 2-6-2009 @ 07:36 PM by soficrow
reply to post by mattison0922


YEAH mattison. Well done. S&F

Good to see you posting again.

And thanks. I have been floundering trying to figure out how to argue against 'survival of the fittest.'


reply posted on 3-6-2009 @ 05:30 AM by Astyanax
reply to post by mattison0922

The classic Darwinian story describes this as a random chance with respect to which organisms survive. Organisms are blessed with genes that allow them survive go on to reproduce, those that die... well they don't. However, this new data suggests that individuals do have an adaptive response, one that may or may not result in antibiotic resistance.... that's the big change, the fact that antibiotic resistance is a response, not a pre-existing condition.

Does that make sense?

I follow your reasoning. But bacteria evolve too. Can you see any insuperable obstacle to their evolving a mechanism for extracting from other, related bacteria, chemicals useful in their own defence? I freely admit to being a non-biologist; perhaps I do not have the subject knowledge to see why this could be impossible? Given the weirdness and variety of life, I should think it quite likely.

***

reply to post by rogerstigers

I pointed out an interesting article about epigenetics which says in a nutshell that DNA is not the only thing that controls what traits are expressed... raises a lot of questions about the function of DNA in adaptive mutations.

I don't hold anything against Darwin. He did the best that he could with what he had...

I think you have been slightly misinformed. Darwin knew nothing of DNA. He didn't even know about genes - Mendel's work didn't come to the attention of the world until after Darwin published his theories. Those theories propose no biological mechanism of inheritance, speaking only of the heritability of a trait or 'character'.

Darwin would have been as comfortable with epigenetic effects, 'junk' DNA turning out not to be junk, etc., as he would have been with straightforward Mendelian inheritance tables. And his theory is equally comfortable with them.

I believe evolution is real, but it is a mechanism for adapting, not necessarilly the driving force behind it.

Here you are correct. Evolution is not the driving force behind adaptation to an environment. The driving force is the environment itself, and the mechanism it powers is that of natural selection. Adaptation is the short-term result of this. Evolution is the long-term result.


reply posted on 3-6-2009 @ 11:08 AM by Astyanax
reply to post by mattison0922

Thank you for the clarification. I really don't see that the studies you cite in the OP imply what you say they do. Why does the fact that bacteria have an adaptive response of this kind suggest that evolution is directed? How does it differ from other adaptive traits of a phenotype, such as - say - a squid's camouflage response to its surroundings?

These little beggars aren't evolving antibiotic resistance; they're acquiring it from theirr fellows.


reply posted on 3-6-2009 @ 09:59 PM by soficrow
reply to post by mattison0922


Hi again,

F means flagged; s means starred.

Checked your blog - we may not be as far apart on H1N1 as you seem to assume. ...good blog btw.

Check out my two H1N1 threads - could use some knowledgeable commentary.

H1N1 Flu: A Tale of Evolution, Economics, Power Politics and International Law.

How Could an Event in 1997 Cause a Pandemic in 2009? What Happened?

Thanks. Later.


reply posted on 4-6-2009 @ 09:04 PM by mattison0922
reply to post by Astyanax

Thank you for the clarification. I really don't see that the studies you cite in the OP imply what you say they do.


Okay…. Firstly, in my OP, I forgot to post the link to the article that actually prompted me to post this. I’ve corrected this, and that article can be viewed here.

Let me see if I can break it down more simply. I’ll post the original abstract here, and go through it piece by piece:

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.


This is the first sentence of the abstract… basically it says these things called integrons - which are mobile genetic elements capable of capturing and transferring genes are found in lots of bacteria, and are largely responsible for acquisition of antibiotic resistance. That is mobile genetic elements – transfer of genetic information between bacteria - is largely responsible for antibiotic resistance.

This statement in and of itself stands in opposition to the story of Darwinian evolution of antibiotic resistance.


We report a direct link between this system and the ubiquitous SOS response.

This sentence is critical; the SOS response is a DNA repair system, basically, it enables DNA replication to proceed when there are errors, gaps, mistakes, or other impassable lesions in the DNA to be replicated. Two proteins are critical in the SOS response: LexA, a repressor protein, and RecA, a protein the relieves LexA suppression. This article pretty clearly demonstrated that the SOS response was directly involved in generating antibiotic resistance; preventing induction of the SOS response inhibited the ability of the bacteria to evolve antibiotic resistance.

That clearly suggests that the SOS repair system is somehow involved with generating the mutations that induce antibiotic resistance. In other words, mutation, in this instance is mediated – in a deliberate manner – by the SOS system. The SOS system accomplishes this by upregulating the expression of error-prone DNA polymerases.

In other words, the SOS repair system activates genes that actually deliberately result in mutation.
In other words, the mutation is directed.

We found that LexA controlled expression of most integron integrases and consequently regulated cassette recombination.

LexA the repressor involved with SOS response regulates expression of the proteins that are responsible for the deliberate mutation of DNA; in this case, the particular activity is repression of recombination and mutation at single base positions.

This regulatory coupling enhanced the potential for cassette swapping and capture in cells under stress, while minimizing cassette rearrangements or loss in constant environments.


Basically, coupling the SOS repair response to the activity of DNA recombination increased ability of the bacteria to acquire resistance cassettes when required, and helped them both retain the cassettes when they were not required.

This finding exposes integrons as integrated adaptive systems and has implications for antibiotic treatment policies.

This says that mobile genetic elements, and the transfer of genetic information are highly regulated and directed processes, and that development of antibiotic resistance is largely an active process, not a passive response to environmental changes.

How does it differ from other adaptive traits of a phenotype, such as - say - a squid's camouflage response to its surroundings?

It differs significantly because the release of a squid’s ink is a pre-programmed response; it exists in the squid from the time of birth to the time of death (presumably). There are no changes at the DNA sequence level that induce release of ink. With these bacteria, were talking about the acquisition of new genetic information; the difference is like night and day.

These little beggars aren't evolving antibiotic resistance; they're acquiring it from theirr fellows.

Exactly, in stark contrast to the classic Darwinian story.



reply posted on 4-6-2009 @ 09:42 PM by soficrow
Originally posted by mattison0922
reply to post by Astyanax

These little beggars aren't evolving antibiotic resistance; they're acquiring it from theirr fellows.


Exactly, in stark contrast to the classic Darwinian story.


So it's not 'survival of the fittest' - it's survival of the most cooperative and approachable...

Interesting.


reply posted on 5-6-2009 @ 02:00 AM by Astyanax
Originally posted by mattison0922
Mobile genetic elements capable of capturing and transferring genes are found in lots of bacteria, and are largely responsible for acquisition of antibiotic resistance.

Yes. Why could such elements not have evolved through natural selection?

This statement in and of itself stands in opposition to the story of Darwinian evolution of antibiotic resistance.

I don't see that it does; it merely adds a new chapter to the story.

The SOS repair system is somehow involved with generating the mutations that induce antibiotic resistance. In other words, mutation, in this instance is mediated – in a deliberate manner – by the SOS system.

Which is an evolved system.

And the SOS response is triggered by environmental factors just like any mutation in a gamete. It's all chemicals at this level, isn't it?

In other words, the mutation is directed.

By an evolved mechanism.

The release of a squid’s ink is a pre-programmed response; it exists in the squid from the time of birth to the time of death (presumably). There are no changes at the DNA sequence level that induce release of ink. With these bacteria, were talking about the acquisition of new genetic information; the difference is like night and day.

I think not; it is merely the difference between a prokaryote and a eukaryote. As you know, eukaryotes swap DNA with each other in order to acquire disease resistance; it's called sexual reproduction. But eukaryotes have specialized cells with which to do it, so they don't have to monkey with their own DNA. Prokaryotes, having only one cell, must evolve some other mechanism to swap genes in order to beat Müller's ratchet. This is it. Another step forward for evolutionary biology and certainly no threat to Darwin.

A deleterious mutation coupled with an advantageous one can be undone in organisms with sexual reproduction. Horizontal gene transfer in bacteria allows a similar situation. Source


* * *


Originally posted by soficrow
So it's not 'survival of the fittest' - it's survival of the most cooperative and approachable.

This betrays a misunderstanding of the phrase.

First, an aptitude for cooperation, at least between related individuals, is an aspect of fitness in all social species. Darwinian fitness isn't the kind you acquire in a gym.

Second, what mattison0922 has found does not imply what you say it does. The most cooperative bacteria - individuals, not species - may well be losers, along with the least cooperative, while some happy medium of cooperation and competition turns out to be the ideal of fitness.

[edit on 5/6/09 by Astyanax]


reply posted on 5-6-2009 @ 11:25 AM by mattison0922
Originally posted by Astyanax
Yes. Why could such elements not have evolved through natural selection?

Who said they couldn't? What I said is that mobile genetic elements are not part of the story of the evolution of antibiotic resistance according to Darwin. They aren't.

I don't see that it does; it merely adds a new chapter to the story.

It may add a new chapter to the story of evolution, but irrespective of that stands in opposition to the Darwinian story as described in the original post.

Which is an evolved system.

Perhaps, but so what? The origins of the SOS system have nothing to do with the larger point. The larger point is that the mutation that drives antibiotic resistance is directed - it's an active response to the enviroment, which - whether you like it or not is not part of the classic evolutionary story; indeed the notion of directed mutation is practically scientific heresy. It's not just another element to the story; it's a revolutionary idea in genetics.

And the SOS response is triggered by environmental factors just like any mutation in a gamete. It's all chemicals at this level, isn't it?

No. The SOS response isn't present in organisms that produce gametes. It's a prokaryotic system exclusively. The SOS system is described as DNA repair; it's not necessarily triggered by environmental factors, it's triggered by DNA damage, and cellular stress, which are not necessarily environmental in origin.


By an evolved mechanism.

The origin of the mechanism is peripheral. This thread is about the mechanism of mutation, not the origin of complex biological systems.


I think not; it is merely the difference between a prokaryote and a eukaryote. As you know, eukaryotes swap DNA with each other in order to acquire disease resistance; it's called sexual reproduction.

Wrong. Sexual reproduction is not about disease resistance. There are complex recombinatory proteins that contribute to disease resistance (which is also a form of directed mutation).

But eukaryotes have specialized cells with which to do it, so they don't have to monkey with their own DNA.

Wrong. Sure they do. There are all kinds of site specific recombinases, there are transposons, pseudogenes, all of which have a role in creating new genetic diversity in an already existing organism.

Prokaryotes, having only one cell, must evolve some other mechanism to swap genes in order to beat Müller's ratchet. This is it. Another step forward for evolutionary biology and certainly no threat to Darwin.

If you'll read through, this is not about swapping genes, it's about generating mutations in a directed manner in response to environmental stress.


reply posted on 6-6-2009 @ 01:19 AM by Astyanax
Originally posted by mattison0922
The story of the evolution of antibiotic resistance according to Darwin.

There's no such story. Darwin didn't know anything about antibiotics, or drug resistance in bacteria. All that stuff happened long after his time.

It... stands in opposition to the Darwinian story...

Sorry, mattison, you haven't satisfactorily demonstrated this - in fact, you haven't demonstrated this at all. All you have shown is that the modern synthesis as originally modelled back in the 1970s, at a time when biologists understood little more than that genes were somehow related to bits of DNA, did not account for all the facts of gene transfer. But that synthesis has long been modified to accommodate other mechanisms of gene transfer and exchange without doing any violence whatever to Darwin's theory. If you disagree, show us how I'm wrong.

The... mutation that drives antibiotic resistance is directed - it's an active response to the enviroment, which - whether you like it or not is not part of the classic evolutionary story.

My emphasis. You have not shown that it is directed, merely that a somewhat sophisticated autonomous response is in play. And this kind of mechanism is very much part of the modern evolutionary story - which is rather the point, isn't it?

the notion of directed mutation is practically scientific heresy.

This is not directed mutation. It's an environmentally triggered response like any other. You're making it out to be more than it is.


Astyanax: And the SOS response is triggered by environmental factors just like any mutation in a gamete. It's all chemicals at this level, isn't it?

No. The SOS response isn't present in organisms that produce gametes. It's a prokaryotic system exclusively. The SOS system is described as DNA repair; it's not necessarily triggered by environmental factors, it's triggered by DNA damage, and cellular stress, which are not necessarily environmental in origin.

Of course the SOS system isn't present in sexually reproducing organisms! My quoted statement assumes that. It isn't there because they don't need it: sex makes it unnecessary. DNA doesn't need repair unless it is damaged, and all such damage must be triggered by factors in the environment, unless you are going to argue for uncaused events in a causal universe. Cellular stress for a prokaryote is the same thing, precisely, as environmental stress; actually, is always is, even in eukaryotes - where are the stress factors coming from? - but it is more egregiously so in a single-celled animal.

Sexual reproduction is not about disease resistance.

I doubt you are unaware of the Red Queen hypothesis, so I find it difficult to understand why you feel you can dismiss it out of hand.

(From above source: in species where asexual reproduction is possible (as in many plants and invertebrates), coevolutionary interactions with parasites may select for sexual reproduction in hosts as a way to reduce the risk of infection in offspring.

See also the Wikipedia entry on the origins of sexual reproduction

Astyanax: But eukaryotes have specialized cells with which to do it, so they don't have to monkey with their own DNA.

Sure they do. There are all kinds of site specific recombinases, there are transposons, pseudogenes, all of which have a role in creating new genetic diversity in an already existing organism.

No disagreement there. All the same, eukaryotes don't need an SOS-type response to swap genes; they have sex instead. Slower-acting but much more fun, as I'm sure you will agree.

This is not about swapping genes, it's about generating mutations in a directed manner in response to environmental stress.

By swapping genetic material. By swapping genes.

No, I don't think there's any challenge here to Darwin whatsoever.

[edit on 6/6/09 by Astyanax]
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