D'OH ! Fancy words...Originally Posted by chipc
D'OH ! Fancy words...
Dead Last > Did Not Finish > Did Not Start
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mea culpa (sorry, might be fancy too)
Just noting that in soaps the common detergent is sodium dodecyl sulfate (aka SDS or sodium lauryl sulfate) and as noted it is a surfactant. This property helps in removing grease such as that found in Homer's donut. Bacteria (as all living cells) are surrounded by a membrane composed of fat (grease) and protein. SDS basically loosens up the bacterial membrane (i.e. solubilization) by trying to remove the fat. This will damage many bacteria. While all living cells have a fat and protein membrane; they differ in how easily they will solubilize with detergents. Animals and organisms like giardia, I would guess, are much more resistant.
Just a biologist pretending to be a biochemist for few minutes
I've saved the entire thread as a pdf in my "hiking etc" folder on my computer. I know I'll be referring back to it again and again.
Thanks,
ecc
Traditional soaps were made from animal fat and were traditionally stearate (IIRC, I'm not a chemist). Modern "soaps" are frequently detergents.
In either case the primary purpose is as a wetting agent to allow fats and oils to be dissolved in water and swept away. Any pathogens that are killed along the way are an extra bonus.
Disinfectant "soaps" have been found to be no better than plain soaps in the home. I have no idea if they are any better in the woods.
The active ingredient in hand sanitizer is a high concentration of ethanol. Certainly effective against many pathogens--it is used in hospitals as a replacement for soap and water in many situations, but I don't specifically know if it is useful against crypto and giardia. (I carry hand sanitizer hiking and use it after visiting the woods and before meals.)
Doug
I shy away from antibacteria soap if I'm just looking to remove dirt. They kill all bacteria, including the ones that are good for you.
Routine use of such soaps also encourages the development of resistant strains of bacteria.
Doug
Evolution in action.
"Whatever doesn't kill you, makes you stronger." At least for the bacteria in that case.
There's no place like 127.0.0.1
I am curious as to how they do this. I have heard this and another statement, that waterborne organisms can build a resistance to chlorine, for years, but am not sure I'm buying it.
I am not trying to start a fight, I am just interested in the mechanics behind it, as it makes no sense to me. I equate the statement to saying a person can build a resistance to bullets or a Mack truck if they are exposed to them often enough. Or more accurately, that someone else can build a resistance to bullets if someone else gets shot.
Dead is still dead is my understanding, but I’m no biologist and don’t play one on TV. When you kill something it doesn't come back to life, unless it was never dead in the first place. What affects one group of organisms cannot affect the other unless some of the originals survive, and then they would have to mutate. It's not like the organisms can transmit data back to their comrade’s telling them this or that, they have no organizational link and thus cannot develop “resistance”.
What is happening is that we are the ones that are reducing our immunity to the organisms by using such destructive products. Our bodies stop producing the right kind and amount of antigens needed to combat the foreign invaders by letting the products, rather than our bodies, do the work. That is how we become more susceptible to disease, not that the organisms have developed a resistance to biocides.
.
Appearances are not everything, it just looks like they are.
I'm not a biologist either, but I do know one. My layman's explanation is that it isn't the individual organisms that get a resistance. It's most like evolution in action. When/if there is a (normal) mutation that allows bacteria to become resistant, it can now reproduce more quickly because the others are no longer competing.
So using the bullets analogy, if one of us just happened to mutate to where we had hide tough enough to stop bullets, the rest of us would be dead and that individual would have a much better chance of survival/procreation. And bacteria (like fruit flies and other lab test organisms) multiply much faster than us, their evolution is quicker.
At least that's how I understand it.
I never heard Chlorine, but that could be possible as well to an extent.
No, but people can build resistance/tolerance to things that could kill them otherwise. There are degrees. Note that the term is resistant, not imune. It takes a stronger dose to kill them.I am not trying to start a fight, I am just interested in the mechanics behind it, as it makes no sense to me. I equate the statement to saying a person can build a resistance to bullets or a Mack truck if they are exposed to them often enough.
Right. When you kill them they are dead. The problem comes with the ones that are not killed. Look at the case of antibiotic resistant bacteria. The problem comes when they are ALMOST killed. Those that survive are the ones that are more tolerant. It is an evolution thing, involving generations, not an individual microbe.Dead is still dead is my understanding, but I’m no biologist and don’t play one on TV. When you kill something it doesn't come back to life
It works both ways. Google on antibiotic resistant bacteria. You'll see that US FDA and CDC right up there on the list, so it isn't some namby-manby claiming this.What is happening is that we are the ones that are reducing our immunity .... That is how we become more susceptible to disease, not that the organisms have developed a resistance to biocides.
There's no place like 127.0.0.1
Pete's comment, "evolution in action" is right on the money.
In more detail:
Three cases: (This logic applies to a wide range of stressors, eg chemicals, radiation, natural or human selection (as in pulling weeds).) I also will refer to death, but anything which reduces, slows, or stops reproduction can have similar effects.
* 1. A stressor has no effect. Simple: no effect is no effect.
* 2. The slightest trace of a stressor is absolutely lethal. Dead is dead. Not much chance to adapt...
* 3. A stressor is partially lethal (perhaps due to a low concentration or inadequate contact time). There will be some genetic variation across a population of an organism, some will be more resistant than others. The resistant ones are more likely to live, the sensitive ones are more likely to die. Over time the population will contain a higher percentage of resistant organisms. And since variation is continually introduced into the gene pool by genetic copying errors, radiation damage, mutations, etc, the population as a whole can become more and more resistant. (Most such errors, radiation damages, and mutatations are harmful or lethal to the organism, but it only takes a few "good" ones...)
Examples:
1. A human scans bins of seeds for weed seeds and removes them. But he misses some of the weed seeds that look like the desired seeds. Thus over time, the weed seeds end up looking more like the desireable seeds. (Same for manual weeding of the growing plants, exept that the weed plants end up looking like the desired plants.)
2. Selective breeding. A human selects which individual organisms get to reproduce and kills those which are considered undesirable. Radiation or chemical insults may be used to increase the rate of genetic variation. Cross-breeding may also be used in introduce desireable genetic variation.
3. Antibiotic resistance. A human takes an antibiotic for some bacterial infection but stops when he "feels better". (A classic scenario...) At this point, most but not all of the bacteria are likely to have been killed. The most susceptable bacteria have died, those that remain are the resistant ones. Now free from the antibiotic, they multiply and you now have a population of resistant bacteria when you started with a population which only contained a few resistant bacteria. (This is why you should always take the full course of an antibiotic--you want to kill all of the bacteria before the population can become resistant.) Constant use of low levels of an antibiotic (such as is frequently used in the livestock industry) can have the same effect because the low dose may only kill some of the bacteria.
It is easier to adapt to some stressors than others. If a stressor attacks a specific vital molecule, perhaps a minor change in the molecule still does the biological job, but is not attacked by the stressor. (This appears to apply to the development of resistance to a number of drugs.) Stressors like chlorine and iodine (chemical ozidizers) are probably much broader in their effect and probably harder to adapt to. But these adaptation mechanisms are very powerful and will likely achieve some degree of resistance--higher concentrations may be required to kill the organisms.
Another effect of a stressor would be to alter the species makeup of an ecosystem--the population of more susceptable organisms decreases and the population of less susceptable organisms increases.
Frequent sub-lethal doses of any stressor could have either or both effects.
Not quite true: Some simpler (single celled etc) organisms can engage in conjugation. Two individuals (which, IIRC, can be of different species) connect and exchange gentic material. Thus a trait can cross species rather than having to be developed twice independently.What affects one group of organisms cannot affect the other unless some of the originals survive, and then they would have to mutate. It's not like the organisms can transmit data back to their comrade’s telling them this or that, they have no organizational link and thus cannot develop “resistance”.
This is a separate effect. Our immune systems appear to adapt in both general and specific ways to the stressors in our environments. So growing up in clean city houses (rather than playing in the dirt and being exposed to farm animals) is suspected to be a factor in the increase in allergies (generally over-sensitive immune systems). Prior exposure to some pathogens can result in specfic immunity to that pathogen or a specific strain of that pathogen (eg childhood diseases, flu). The same probably applies to a local's tolerance of the pathogens in the local drinking water which may not be shared by an unhappy traveler.What is happening is that we are the ones that are reducing our immunity to the organisms by using such destructive products. Our bodies stop producing the right kind and amount of antigens needed to combat the foreign invaders by letting the products, rather than our bodies, do the work. That is how we become more susceptible to disease, not that the organisms have developed a resistance to biocides.
Disclaimer: I am not a biochemist. This is just my (hopefully accurate) understanding of the topic.
Perhaps a little long-winded, but I hope this helps to answer your questions.
Doug
Last edited by DougPaul; 04-29-2006 at 09:27 AM.
Didn't see DougPaul's comment before posting mine. He's spot on; I just have elaborated on one area he's mentioned.
I don't know about chlorine, but it is true for antibiotic resistance. Yes it is evolution in action. Here's what happens in antibiotic resistance. (My apologies for the length of this post, but this is an area I am familiar with.)
You start with an infection by particular strain of bacteria. Assume that this strain can be killed by a common antibiotic, let's say streptomycin. Before you know you are infected, that one bacterium multiplies to a large population in your body, let's say a million. During this population explosion random mutations have occurred that result in one or two bacteria being a little less sensitive to streptomycin than the original infecting bacterium.
Now you know you are infected and you start antibiotic treatment. If you take the full-course treatment with a high enough dose of streptomycin, you probably will kill off all of the bacteria. However, let's say you stop the treatment early because the symptoms go away and you feel better. You may have killed off 99.9% of the bacteria, but the ones left are the those that have the mutations that make them slightly more resistant to strep. In essence you have selected for a more resistant mutant strain.
Then what happens. Your infection relapses only this time the bacterial population starts at a higher level of resistance due to those mutations. New mutations in this population can result in a bacterium with even higher resistance. This cycle can repeat until the only bacteria left are ones that have been selected for being resistant to streptomycin.
Three general points:
1) the killing agent (antibiotic or chlorine?) does not induce resistance to the specific agent; that is, "directed mutation" does not occur. You are selecting resistant variants already in the population.
2) if you are successful in wiping out the entire population with the antibiotic (or chemical or other catastrophe) then no resistant strains will appear in the population you originally targetted.
3) while antibiotics are quite effective at killing pathogenic bacteria, they also kill off beneficial bacterial strains in us. This is one of the reasons that it is now frowned upon to prescribe antibiotics without evidence that there is a bacterial infection. Its probably a simplification, but every time we take antibiotics we wipe out our bacterial population including the beneficial ones. When they repopulate our gut, it might be with more resistant strains that do it.
Last edited by chipc; 04-29-2006 at 09:44 AM.
Yep--after I finished the cleanup edit of mine I saw that we doubled. Both posts are consistent and complementary.
Great minds run in the same gutters...
Doug
As an aside, I have worked with genetic (evolutionary) methods for solving problems on a computer. They are very powerful at solving problems and can sometimes find a solution in a case were there is no traditional (numerical) method.
The keys are random variations (mutations) and a probabalistic selection function. The probabalistic selection function gives the better "organisms" a higher probability of surviving into the next generation to reproduce.
Doug
Don't mean to continue the tangent, but probably most sane people are out enjoying the day instead of looking at a blue sky through their office window.
Interesting approach - I have heard of some computational biologists who want to "evolve" (jargony use I know) a gene on a computer so that the protein the gene makes can have a new function. The limitation at this point is predicting what the overall effect of a mutation would be on the protein structure and how that would translate into a new activity. Until this happens, we are left with actually subjecting the DNA to random mutation and then assessing the physical properties of the protein. (Not as laborious as it sounds). Nonetheless, I think applying computational evolution to a gene is not that far off.
(I am looking for the icon with taped eyeglasses but I don't see it)
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