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Sat Oct 31, 2009 10:16 pm  |
Hi everyone,
During my late teens, I used oral antibiotics to manage my acne. Now, at 29, I am struggling with acne again. I believe that the acne is hormone and stress related, as it becomes really inflamed right before my period but is generally manageable otherwise.
My question is, I think I built an immunity to a specific antibiotic years and years ago, but the antibiotic did wonders for my acne prior to reaching that point. I haven't used that antibiotic for at least 10 years now and was wondering if the body can/does "reverse" the immunity. Is this even possible or does it mean that my body will forever be immune to that antibiotic?
Thanks! Feedback is much appreciated! |
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Sat Oct 31, 2009 10:57 pm |
From this link:
http://www.scientificamerican.com/article.cfm?id=how-is-antibiotic-immunit
How is antibiotic immunity acquired?
Tony Mazzulli, an associate professor at the University of Toronto medical school and deputy chief microbiologist and infectious diseases specialist at Mount Sinai Hospital in Toronto, explains.
The concept of antibiotic immunity is a misnomer that can lead people to believe that they may become "immune" or "resistant" to an antibiotic if they take it too frequently or inappropriately. This notion stems from a misunderstanding in the general public of the concept of antibiotic resistance.
It is not people who become immune or resistant to an antibiotic. Rather it is the bacteria responsible for infections that become resistant. The purpose of an antibiotic is to kill--or at least inhibit the growth of--bacteria to quell an infection. Bacteria have been around for thousands of years and have had to survive in hostile environments. As a result, they are able to adapt and have a number of mechanisms for survival, one of which is the development of resistance to antibiotics.
Misuse or overuse of antibiotics selects for resistant bacteria. In a bacterial infection, billions of bacteria are present. Taking an antibiotic will kill or inhibit those bacteria that are susceptible to its effects and leave behind a subpopulation of bacteria that are resistant to the antibiotic. These remaining bacteria can survive and continue to grow. If they then spread from person to person, they may become the norm, and all future infections caused by these resistant bacteria will withstand the original antibiotic, rendering it useless for treatment. For many infections, patients often begin to feel better before all the bacteria have been eliminated. But it is important to complete a full course of antibiotics, even if one�s symptoms have improved, to ensure that as many bacteria as possible are destroyed.
Bacteria have a variety of mechanisms by which they become resistant to antibiotics, depending on the particular antibiotic (or class of antibiotic) and the type of bacteria involved. Because antibiotics work differently to attack an essential function of bacteria, it is necessary to consider both the phenotypic mechanism of resistance and the underlying genotypic mechanism of resistance.
From a physical or biochemical perspective, there are a number of factors that contribute to antiobiotic resistance. First, the cell wall of a bacterium can be altered so that an antibiotic cannot penetrate it. Second, some bacteria produce enzymes that can destroy antibiotics before they can work. Third, certain bacteria have developed mechanisms known as efflux pumps, which are able to "eject" antibiotics from the bacterial cell before they have a chance to exert any effect. Finally, the antibiotic target site within the bacteria can be altered. In this situation, when an antibiotic enters the bacterial cell it must bind to its intended target in order to have an effect on the bacteria. If the target within the bacteria has been changed to make this binding impossible, the bacteria will be resistant to the medicine�s effects.
Underlying the phenotypic mechanisms of antibiotic resistance are the genetics of antibiotic resistance. Bacteria, like other living organisms, possess DNA that codes for the proteins and enzymes it requires for survival. Changes to the DNA can result in alterations in the final proteins or enzymes, which in turn can lead to antibiotic resistance. A common genetic mechanism for the development of antibiotic resistance is the acquisition of tiny fragments of DNA known as plasmids or transposons. Transposons may code for a specific antibiotic-inactivating enzyme, which, when produced by the bacteria, destroys an incoming antibiotic before it has an opportunity to work. These tiny fragments may be passed directly from one bacterium to another by a process known as conjugation. Alternatively, small viruses may attack certain bacteria and inject DNA fragments by a process known as transduction.
HTH
DM |
_________________
I'LL SEE YOU ON THE DARKSIDE OF THE MOON.... |
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Sun Nov 01, 2009 11:03 pm |
Thanks for the reply, Dark Moon. Your resource was a very interesting one. I think I got the gist of the article but I'll be honest when I say that a lot of it went over my head a bit.
Since you posted the article, Dark Moon, maybe you can help me interpret the article a little?
According to this article, if the dna of the bacteria has managed to change/alter so that it is resistant to antibiotics, then could the bacteria not change/alter again so that antibiotics can have a positive effect on the infection? These are just my conclusions from reading the article and I could be making assumptions.
What do you think? |
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Sun Nov 01, 2009 11:16 pm |
I think what it is saying like all living things bacteria will evolve (change) to protect themselves and survive. Therefore it wouldn't make sense for them to revert to an earlier strain that could be killed off by the antibiotics. That would be evolving in reverse, making them susceptible to death, nature doesn't usually work that way, everything evolves to protect itself, keeping the species alive.
HTH
DM |
_________________
I'LL SEE YOU ON THE DARKSIDE OF THE MOON.... |
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Mon Nov 02, 2009 1:08 am |
Mutations in bacteria are essentially random events. When an individual bacteria randomly mutates in such a way as to make an anitbiotic ineffective, that particular one will take over rapidly because all the antibiotic susceptible ones will be wiped out, leaving a clear field for the mutants. (And given the huge numbers of bacteria involved, some of which will have every conceivable DNA mutation, you can see how inevitable it is that resistant strains develop and flourish.)
On the other hand, if a particular individual bacteria were to randomly mutate to become *susceptible* to antibiotics again, that bacteria would have no advantage over its resistant cousins and would thus just be one tiny little mutant in a vast sea of resistant bacteria. Until you took the antibiotic, of course, when the mutant would get utterly wiped out.
That's why, even if a susceptible strain were to arise by mutation, it wouldn't mean that resistant strains would cease to be a problem. |
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Late 50's, fair warm-toned skin, dryish except in T zone; regular user of CSRx Vitamin C, Avene Diacneal, Avene tinosorb sunscreen, Pro Light LED, and experiments on and off with many products. |
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Mon Nov 02, 2009 8:10 pm |
http://inkbluesky.wordpress.com/2009/10/20/evolution-shown-to-experiment-with-mutations-wetlands-and-volcano/
Not all random not all survival of the fittest!
evolution shown to experiment with mutations, wetlands and volcano
October 20, 2009 @ 6:06 pm › inkbluesky
Evolution details revealed through 21-year E. coli experiment
In 1988 an associate professor started growing cultures of Escherichia coli. Twenty-one years and 40,000 generations of bacteria later, Richard Lenski, who is now a professor of microbial ecology at Michigan State University, reveals new details about the differences between adaptive and random genetic changes during evolution.
Sequencing genomes of various generations of the bacteria, which had been frozen periodically over the years, Lenski and his team found that adaptive and random genomic changes don’t necessarily follow the same patterns. Rather than a plodding equilibrium, even in a consistent environment, the interplay between these two kinds of genomic changes “is complex and can be counterintuitive,” Lenski said in a prepared statement.
In some of the eraly stages of the experiment observations showed that adpatations followed what some would consider the classic and ievitable tendency of the bacteria to produce adptations that would ebenfit the survival of the bacteria. Yet as the experiment progressed – the 20,000 generation – some of the mutations did not seem to have any discernible advangtage of for the orgaisms. They were mutations that were neutral in terms of benefits to the bacteria or just random mutations. Is it really a wonder that nucletides would try out different products or be froced to by enviromental factors like variance in teperature, humidity and light. A commenter at the link seems to think since the experiment did not have a neat linear progression toward what we know in 20/20 hindsight is more complex and reached a dynamic stability the experiment failed to prove anything about how evolution works. On the contrary, evolution is the history of biological trial and error. It srtill is. Life in all its forms is beautiful, intriging and complex – all of the mechaims involved a far way from being fully explained. That bacteria, one of the less complex forms of life should try different kinds of macromolecular bonds is perfectly atutal. nature is in a way lazy. It is always lokking for an more enegitically favorable way of strurtucal support, energy storage, protection against destruction, nutrient transport, defense against environmental factors and destructive chemical bonds, regulation that maintains stability, movement, and storing the information that has helped it to survive. Human beings or the human brain does not involve itself at this level, they are issues resolved at the nucleotide and protein level. If the human brain in all its supposed perfection directed cellular function at the protein level, we could simply mentally repair cancer or heart disease. To regress, imagine those bacteria 4.6 billion years ago – about the age of when its thought some crude life began on earth. The bacteria in the experiment is a mere 20 years old. Imagine the sheer number of trials and errors that have taken places in 4.6 billion years of mutations – some to an organisms advantage, some neutral, some merely excess baggage. Just like those bacteria much of the human genome is excess baggage, is neutral, while and some is capable of and does in fact kill millions of us every year. Oncogenes are proof that if we had a perfect designer he or she designed a heart breaking defect into human DNA. One in a hundred human humans carry a mutation for heart disease. Again, given billions of years, our nucleotides are still trying to work out the best design. It doesn’t help that the environment we live in keeps changing so even if they suddenly got things perfect this year, next year they’d have to come up with more mutations to keep up. Nucleotides have no comprehension of perfection or divine insight, what they seem to strive for is surviving long enough to produce more nucleotides.
I was prepared to blame public education or private for that matter for anyone having the notion that evolution is guided by a kind of deluxe erector set of instructions in which the goal is to build ever more complex and beneficent beings, but I looked through a couple current high school level text books before i wrote this post and they do not meander off into any such quasi-philosophical views of evolution.
DM |
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I'LL SEE YOU ON THE DARKSIDE OF THE MOON.... |
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