Microban (resistance paper)

[ecoli]

For those of you who don't read my blog, I recently confronted Microban International Ltd, over their wide scale use of long lasting antimicrobials in products from pencils to flooring (and more).

 

At any rate, I wrote them an email about it, and got a response (which I share here).

 

They sent me a paper, and I need help trying to falsify it (I've turned it into a Google doc). I'm going to be reading it in detail over the course of the next couple days.

 

The purpose of this thread, is that I don't expect to have enough background in this area to tackle the paper on my own.

Anyone who wants to help, please read the paper and we can discuss it here. (I'll post specific questions when they come up, and I ask anyone else, who wants, should do this as well).

Thanks

[John Cuthber]

Did it occur to you that we might agree with them?

They certainly have a couple of valid points- their product is based on triclosan which is relatively non specific in its actions so, to become resistant, a bacterium would have to simultaneously change a number of its metabolic pathways. This is unlikely as shown by the rarity of triclosan resistance noted even after many years of its use in a wide variety of products.

Secondly their produc seeks to maintain a high enough concentration of the active material that it kills things. Dead things can't evolve resistance.

One of the major contributions to resistance to antibiotics is the unreliabillity of people. They take the pills for too short at time, so there is a better chance of the bugs surviving and being able to develop resistance.

 

Until you can answer these points (as well as any others they may make) I think you are not on the scientificly justfied side of this debate.

[foodchain]

I have a few questions as to how real world the studies are overall. In one reference a few homes were used as a study, I would say that can hardly account for the reality of the products use constantly all over the world. The phenome of a giving genome can be quite large. From the reality of gene regulation and signaling or splicing again regarding phenotype I could hardly see how this study can concretely prove no ability to gain resistance in a giving specie or population, more so if you simply lump mutation and selective pressures over time? I mean the later part of the question is off topic as you cant really test it, but resistance can be gained by bacteria in which you would then have to prove a mechanism I think of the antimicrobial as something that bacteria or microbes in general simply cannot evolve with.

[ecoli]

Did it occur to you that we might agree with them?

Of course... but we should still approach it with the intent to falsify. That's how science should work, anyway.

 

They certainly have a couple of valid points- their product is based on triclosan which is relatively non specific in its actions so, to become resistant, a bacterium would have to simultaneously change a number of its metabolic pathways. This is unlikely as shown by the rarity of triclosan resistance noted even after many years of its use in a wide variety of products.

Secondly their produc seeks to maintain a high enough concentration of the active material that it kills things. Dead things can't evolve resistance.

yes, but surely even triclosan isn't 100% lethal...

 

Until you can answer these points (as well as any others they may make) I think you are not on the scientificly justfied side of this debate.

I'm attempting to falsify their paper. It's not about being "scientifically justified." Meaning, I fully accept the fact that I could be wrong here.

[blike]

Awesome work ecoli! I'll read over the paper as well.

[John Cuthber]

It's just as viable as science if I seek to falsify your hypothesis (that this stuff is harmful).

"I have a few questions as to how real world the studies are overall. In one reference a few homes were used as a study, I would say that can hardly account for the reality of the products use constantly all over the world. "

If you don't think studies of a few houses are valid (which may be a fair point) then you can take comfort from the fact that this stuff has (as you say) been in use for ages without much evidence of resistance.

 

In the long run there's every chance that some bugs will become resistant to triclosan.

So what?

It's not used directly in medicine; there are other products that do the same job; resistance to triclosan will not make the bugs better able to harm people (probably the reverse). The only losers will be the manufacturers.

[foodchain]

It's just as viable as science if I seek to falsify your hypothesis (that this stuff is harmful).

"I have a few questions as to how real world the studies are overall. In one reference a few homes were used as a study, I would say that can hardly account for the reality of the products use constantly all over the world. "

If you don't think studies of a few houses are valid (which may be a fair point) then you can take comfort from the fact that this stuff has (as you say) been in use for ages without much evidence of resistance.

 

In the long run there's every chance that some bugs will become resistant to triclosan.

So what?

It's not used directly in medicine; there are other products that do the same job; resistance to triclosan will not make the bugs better able to harm people (probably the reverse). The only losers will be the manufacturers.

 

 

 

I guess I would or should word it as how do you gauge the impact of any particular variable in a fitness landscape for a giving taxa. Even prokaryotes have cellular memory mechanisms or epigenetic mechanism along with regulatory and signaling feature which lend support to a giving phenotype. The selection pressures or criteria for a giving phenotype I think needs to be equated as to find the mechanism in detail. If individuals have been found with resistance such should be in relation to say that individuals phenotype and how far that phenotype varies from the norm and why.

[CharonY]

Well, the white paper has essentially a simple negative statement: there is " no evidence of acquired bacterial resistance developing by triclosan."

 

Of course they simply disregard the problem of the increase of a resistant population (as opposed to non-resistant strains acquiring a new resistance). While the spread of AB resistance is often more of a concern than merely the propagation of resistant strains, the numeric increase or already resistant strains should not be totally disregarded.

But except this point, the only thing one can really do is to check whether the cited literature does in fact agree with that white paper. Chances are that they do, but maybe there also some side conclusions that are note detailed.

 

The next thing to do is to state a counter hypothesis (which has been only done implicitly). For example:

 

- triclosan use leads to spread of resistance against it

- triclosan use increases the titer of resistant strains

 

Then it is only a matter of doing the experiments, or more likely, search the literature to validate this. As it has been in use in all kinds of desinfectants, deodorants, toothpaste etc. there are scores of papers out there. Chances are, however, that there are not that many around which show that triclosan use really has an impact. At least just on top of my head I have not literature ready that demonstrates a a spread of desinfectant resistance (as opposed to defined AB resistance). Also I am not entirely sure about the mechanism of triclosan resistance, I only think that it was not a single gene contributing to the resistance and contrary to what is stated fabI overexpression was not the single source of resistance.

 

Due to lack of time I am not able to read all the papers available, however if anyone has any questions I'd be glad to fill in as much as I can.

[CharonY]

However, quite regardless of what is actually written in the paper I would probably ask something completely different:

are there any reports which highlight that the massive use of triclosan or any other desinfectant has any beneficial aspects in normal households?

The need of desinfectants in crititical areas as hospitals or labs are pretty obvious, but why incorporate it in anything else?

[ecoli]

according to microban's marketing division, at least, it's to kill those odor causing bacteria.

[Colleen]

Hi I am new here. I see this post is a few months old, but I was wondering if you could help me. I am doing a senior research project and I am proposing a study looking for bacterial resistance to triclosan in some common objects treated with triclosan (Microban). I know there is no real world evidence of resistance, but I am hoping to find something. My knowledge is limited and I am not entirely sure of the best way to set-up this study. Any tips would be greatly appreciated. Thanks!

[ecoli]

I've been giving some thought to this lately and have come to regret my original point.

 

Instead of worrying about creating microban resistance strains, what I should have stressed is the possibility of more virulent (new) bacteria evolving in the niche after the old, more passive, bacteria has been wiped out by microban.

 

The above is where the new research "anti" antibiotics is.

[CharonY]

Actually by chance I have gotten involved from a different direction into this area a bit. And at the moment I am actually more worried about the persistence and occurrence of triclosan in human bodies and accumulation in the environment rather than creation of resistant strains.

 

the possibility of more virulent (new) bacteria evolving in the niche after the old, more passive, bacteria has been

 

I would be careful with that notion. While it is true that the treated areas will be settled by more resistant strains, there is no reason to believe that they will be virulent at all. Also it is probably questionable whether it will have a medical impact as triclosan is not used as a treatment. In fact there is a paper which reports that triclosan resistant strains were more susceptible to antibiotics than sensitive ones.

 

However triclosan is often used not only in detergents but also in personal care products. While it is generally assumed that triclosan doe not have negative effects on health there is always the risk that once interacting with microorganisms for instance their metabolites could turn out to be more toxic. In addition endocrine disrupting functions are being discussed, though to date no hard evidence have been found (yet). On the other hand studies in countries were triclosan is excessively used (including the US) it not only been found in urine, but also in blood and human breast milk. Again, there is no conclusive evidence that it will really do harm for the moment, but given the fact that it is persistent (and thus accumulating e.g. in biosolids), that already infants get contaminated with it and that the dosage in which it is used is generally meaningless anyway, I do not see any good reason for continuous use.

There are quite a few papers addressing pros and cons. You may want to take a look.

[ecoli]

I would be careful with that notion. While it is true that the treated areas will be settled by more resistant strains, there is no reason to believe that they will be virulent at all.

Im actually talking about something a bit different. Lets say a child starts chewing on antimicrobial pencils and it kills some of the harmless mouth germs... (Even these harmless germs an be virulent if transported into a different part of the body - operating in a different niche) But by kiling the germs you know, it opens up the floor for germs you don't know (and potentially virulent ones).

 

I've been researching models of stable, but persistent infectious agents and, it seems, that the evolutionarily relationship between host and pathogen has had a stablizing effect on each other. Meaning, a nash equilibrium of limiting each other's harmful effects, but not changing strategies to avoid tipping te scales.

 

It's an interesting notion and would help explain why emergent pathogens are more virulent than pathogens we've "known" for a long time. Pathogens prefer a stable relationship, because developing new weaponry that helps transmission also causes more virulence (killing the host outright limits a pathogen's ability to spread over the long run).

 

The Host wants to get rid of pathogens, but its better to keep around mildly virulent pathogens rather than open up a niche for new pathogens that can cause even more virulence.

 

These are a problem being caused antibiotics but even modern notions of hygiene (which is arguably linked to things like asthma). I'm very interested in this area of research, specifically in modeling pathogen evolution in the context of complex ecological networks.

[CharonY]

I see what you are alluding at. If we are talking about actions of triclosan (or other antimicrobials) directly on the body microbiome, I can easily agree with you. An additional factor is of course also that the host builds up an immune defense against long-term settlers (regardless whether they are harmless or not) by virtue of being exposed to them. To be honest, though I do not believe that in the majority of products this will be an issue as the used concentrations tend to be too low to seriously disrupt the bacterial communities (with few exceptions). A shift may be occurring during long time exposure but I would not necessarily expect anything too dramatic.

At the moment I would still bet any detrimental effect of triclosan on human health due to accumulation for the moment. But I need to get more data to be sure.