Mike, if you haven't already seen this, I'm sure you'll be interested in this article. The article suggests an association between E coli and lymphocytic colitis.
The first link is to an abstract. The second link is to a PDF version of the entire article, and the third link is to an HTML version of the whole article, which is faster to download, but not as easy to read as the PDF version, (though this is probably a matter of personal opinion).
http://www.wjgnet.com/1007-9327/abstrac ... =7266&v=11
http://www.wjgnet.com/1007-9327/11/7266.pdf
http://209.85.173.104/search?q=cache:pl ... cd=8&gl=us
The plot thickens.
Tex
Is MC Caused By A Bacterial Infection?
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
Is MC Caused By A Bacterial Infection?
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Hi Tex,
This is REALLY interesting. You know, we have always suspected an infectious cause for at least some cases of MC, and it seems more likely all the time. I just can't get over the fact that some of us have had perfect bowel function on the antibiotic Cipro - in my case it was so striking that I could eat my intolerances with no problems at all. Hopefully, we'll know for sure in the not-too-distant future. Thanks for sharing.
Love,
Polly
This is REALLY interesting. You know, we have always suspected an infectious cause for at least some cases of MC, and it seems more likely all the time. I just can't get over the fact that some of us have had perfect bowel function on the antibiotic Cipro - in my case it was so striking that I could eat my intolerances with no problems at all. Hopefully, we'll know for sure in the not-too-distant future. Thanks for sharing.
Love,
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
Hi Polly,
I was hoping that would catch your eye. I found that article while searching for something else, so I guess I'd have to call that find a perfect example of serendipity. LOL.
I had the same experience on the two occasions when I took Cipro - it didn't matter what I ate, the D stopped. Of course, the reason I was eating gluten in the first place was because I didn't have the foggiest idea what was causing the D, back then.
I looked up how Cipro works, out of curiosity. I didn't have any epiphanic revelations after reading it, (though it is quite interesting), but maybe you can see something in there that might offer some more insight into the problem, and a possible solution. It turns out that it works by inhibiting bacterial nuclear DNA synthesis. IOW, it prevents a bacteria from uncoiling its DNA, so that it will die, due to the inability to feed itself, reproduce, or do just about any thing else essential to life. Quite interesting, but utilizing that information is beyond my area of expertise, (whatever that might hapen to be. LOL). Anyway, here's a link to that explanation. You have to read your way to the third page before you get to the punch line.
http://health.howstuffworks.com/cipro1.htm
The biggest problem I see that stands in the way of simply using cipro to combat this disease, is the indication that, (based on research), the repeated use of fluoroquinolone (norfloxacin and ciprofloxacin) appears to be the primary risk factor for creating ciprofloxacin-resistant strains of E coli. Therefore, a more sophisticated solution will probably be required. Here's a reference on that research:
http://www.pubmedcentral.nih.gov/articl ... tid=162571
Love,
Tex
I was hoping that would catch your eye. I found that article while searching for something else, so I guess I'd have to call that find a perfect example of serendipity. LOL.
I had the same experience on the two occasions when I took Cipro - it didn't matter what I ate, the D stopped. Of course, the reason I was eating gluten in the first place was because I didn't have the foggiest idea what was causing the D, back then.
I looked up how Cipro works, out of curiosity. I didn't have any epiphanic revelations after reading it, (though it is quite interesting), but maybe you can see something in there that might offer some more insight into the problem, and a possible solution. It turns out that it works by inhibiting bacterial nuclear DNA synthesis. IOW, it prevents a bacteria from uncoiling its DNA, so that it will die, due to the inability to feed itself, reproduce, or do just about any thing else essential to life. Quite interesting, but utilizing that information is beyond my area of expertise, (whatever that might hapen to be. LOL). Anyway, here's a link to that explanation. You have to read your way to the third page before you get to the punch line.
http://health.howstuffworks.com/cipro1.htm
The biggest problem I see that stands in the way of simply using cipro to combat this disease, is the indication that, (based on research), the repeated use of fluoroquinolone (norfloxacin and ciprofloxacin) appears to be the primary risk factor for creating ciprofloxacin-resistant strains of E coli. Therefore, a more sophisticated solution will probably be required. Here's a reference on that research:
http://www.pubmedcentral.nih.gov/articl ... tid=162571
Love,
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Thanks for the article, I think I remember reading that a year or more ago, but it's interesting to read after learning more about my particular findings.
My guess would be, for me at least, that motility is the biggest problem. This is why antibiotics worked great in the short term but they didn't in the long term. I found that while taking antibiotics I could pretty much eat everything that caused me problems before without issue, though I didn't try consuming gluten at the time. And as you've implied, continuing to take antibiotics long term is a sure fire way to get into a much worse state GI/bacteria wise.
My guess would be, for me at least, that motility is the biggest problem. This is why antibiotics worked great in the short term but they didn't in the long term. I found that while taking antibiotics I could pretty much eat everything that caused me problems before without issue, though I didn't try consuming gluten at the time. And as you've implied, continuing to take antibiotics long term is a sure fire way to get into a much worse state GI/bacteria wise.
This was an interesting article, Tex. It sure seems to imply a relationship between bacteria and LC. I notice that it's two years old and comes from Egypt (written in perfect English). I wonder what happens to studies like this? Wouldn't it be helpful in our diagnosis and possibly treatment, if the test mentioned in the quote below were included?
It sounds like they are doing another study:The demonstration of these bacilli in the colonic mucosa of our patients with lymphocytic colitis raises several questions. The first question is why they have not been seen before in colonic tissue sections of such cases? We think that these bacteria have not been previously demonstrated because Giemsa stain is not routinely applied for colonic mucosal biopsy specimens and bacteria are easily overlooked on H&E-stained sections.
The second question to be raised is whether these bacteria are pathogenic or merely commensals in the colonic mucosa. From our point of view, we suggest that these bacilli, which have been demonstrated histologically, are pathogenic rather than commensals, since they are closely related to the mucosal surface and within the lumen of crypts, and not within the tissue debris. Moreover, they are always associated with prominent colonic pathology. It is worthy of notion that we could not demonstrate such bacteria in all colonic biopsies obtained from the healthy controls.(emphasis is mine)
Since the study was published two years ago, one would think that the second study would have been completed by now, or would such a study take a long time?Further studies are now in process to investigate the pathogenicity of these organisms in case of lymphocytic colitis.
You never know what you can do until you have to do it.
Decided to do another pubmed search with regards to MC/LC/CC and bacteria. It came up with some interesting things. One study mentioned a case where an acid blocker caused LC, and once they stopped taking it the LC went away.
Another interesting one is similar to something I mentioned elsewhere that IBS is in the same family as MC:
http://www.ncbi.nlm.nih.gov/pubmed/1604 ... d_RVDocSum
Another interesting one is similar to something I mentioned elsewhere that IBS is in the same family as MC:
http://www.ncbi.nlm.nih.gov/pubmed/1604 ... d_RVDocSum
Whoa, and take a look at this one from 1993, I had wondered about how cholestyramine might have been helpful in some studies on MC. I had heard of cholestyramine helping to bind up toxins, but didn't realize that it would bind up the toxins produced by bacteria.
http://www.ncbi.nlm.nih.gov/pubmed/8438 ... d_RVDocSum
http://www.ncbi.nlm.nih.gov/pubmed/8438 ... d_RVDocSum
And here's more. I went through several of the drugs known to be potential drug causes of MC. The majority would also be potential causes for bacterial overgrowth.
Proton pump inhibitors(lansoprazole), H2receptor antagonists (ranitidine, cimetidine) - reduction of stomach acid would increase potential for bacterial overgrowth.
Acarbose, would mean there would be more undigested carbohydrates for the bacteria in the small bowel to grow.
http://en.wikipedia.org/wiki/Acarbose
Asprin and other NSAIDs would case damage to the gut, causing malabsorbtion and thus more food for the gut.
Proton pump inhibitors(lansoprazole), H2receptor antagonists (ranitidine, cimetidine) - reduction of stomach acid would increase potential for bacterial overgrowth.
Acarbose, would mean there would be more undigested carbohydrates for the bacteria in the small bowel to grow.
http://en.wikipedia.org/wiki/Acarbose
Asprin and other NSAIDs would case damage to the gut, causing malabsorbtion and thus more food for the gut.
Gloria,
It sometimes seems to take forever for research of this type to become mainstream medical information. A lot of doctors may be so busy that they feel that they just don't have time to devote to staying abreast of current developments. It often takes decades to change the way that many of them practice medicine.
Most of Dr. Fine's basic research was done over five years ago, but few GI docs are aware of it, and fewer still, accept it as factual.
It's possible that the continuing research mentioned in that article is not yet completed, but the most likely situation is that it has been completed, and is awaiting publication. It seems that many/most of the most prestigious publications have a waiting list, and articles are published in order of their deemed "importance". Since MC is still considered to be a rare disease, I would assume that it's not likely to be assigned any special priority in the ranking of articles waiting in the queue.
It's also possible that some pharmaceutical company may have waved a big grant under those researcher's noses, and diverted their attention to another project for a year or so.
Tex
It sometimes seems to take forever for research of this type to become mainstream medical information. A lot of doctors may be so busy that they feel that they just don't have time to devote to staying abreast of current developments. It often takes decades to change the way that many of them practice medicine.
Most of Dr. Fine's basic research was done over five years ago, but few GI docs are aware of it, and fewer still, accept it as factual.
It's possible that the continuing research mentioned in that article is not yet completed, but the most likely situation is that it has been completed, and is awaiting publication. It seems that many/most of the most prestigious publications have a waiting list, and articles are published in order of their deemed "importance". Since MC is still considered to be a rare disease, I would assume that it's not likely to be assigned any special priority in the ranking of articles waiting in the queue.
It's also possible that some pharmaceutical company may have waved a big grant under those researcher's noses, and diverted their attention to another project for a year or so.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Good info., Tex and Mike.
Mike, do you think that the bacterial infection first attacks the colon and then overflows into the small intestine?
I would agree that the bacteria are probably pathogenic strains that have become established or overgrown and are not "normal" gut bacteria. Mike, antibiotics can be added to your list of agents that cause the initial bacterial overgrowth. That's my case, I think. I took doxycline for 5 weeks before the MC hit. I'll bet it somehow promoted the growth of a pathogenic strain, which has been with me ever since. I am suspecting enterococci, since I read somewhere that Cipro had good activity against enterococci. But the article said E.coli were found, right? Maybe Cipro also has good activity against pathogenic E. coli. ? Hmmmmm. I'll try to do some more research.
Pathogenic E.coli can be killers (remember the contaminated ground beef and spinach?) Maybe our hunter-gatherer genes (which are basically good at fighting infection) somehow fight off the E. coli infection by sequestering the bugs in the lining of the colon indefinitely. So at least the bugs don't kill us, but neither does the body kill them.
Just thinking aloud - probably not making much sense. Maybe we need to be hearing more from the infectious disease docs - especially the ones working with the GI bugs.
Love,
Polly
Mike, do you think that the bacterial infection first attacks the colon and then overflows into the small intestine?
I would agree that the bacteria are probably pathogenic strains that have become established or overgrown and are not "normal" gut bacteria. Mike, antibiotics can be added to your list of agents that cause the initial bacterial overgrowth. That's my case, I think. I took doxycline for 5 weeks before the MC hit. I'll bet it somehow promoted the growth of a pathogenic strain, which has been with me ever since. I am suspecting enterococci, since I read somewhere that Cipro had good activity against enterococci. But the article said E.coli were found, right? Maybe Cipro also has good activity against pathogenic E. coli. ? Hmmmmm. I'll try to do some more research.
Pathogenic E.coli can be killers (remember the contaminated ground beef and spinach?) Maybe our hunter-gatherer genes (which are basically good at fighting infection) somehow fight off the E. coli infection by sequestering the bugs in the lining of the colon indefinitely. So at least the bugs don't kill us, but neither does the body kill them.
Just thinking aloud - probably not making much sense. Maybe we need to be hearing more from the infectious disease docs - especially the ones working with the GI bugs.
Love,
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
Polly,
From what I've read, Cipro is very effective against E coli, (UTI's are usually caused by E coli, aren't they? Cipro is claimed by some authorities to be 100% effective against them, when used to treat UTIs), but as noted, repeated use leads to cipro-resistant mutants.
That's a very interesting observation about the possible genetic significance of this issue. Maybe we are the lucky ones, and just don't realize it. Maybe we would be dead if our immune systems hadn't rescued us from an otherwise fatal E coli infection.
There's a fly in the ointment, though - E coli O157:H7, (the famous strain that has received so much national press in the last few years), normally causes hemolytic uremic syndrome. However, none of us presented with blood in the stool, at any time, (though some of us did have anemia).
I distinctly remember back when I first realized that I was the victim of a "mysterious" chronic condition, one of the possibilities that I considered was E coli, but I ruled it out, on the basis of the lack of blood in the stool.
So I wonder if we are talking about a different E coli strain here, and we just happen to be unlucky enough to be susceptible to a strain that most people can shrug off in a few days, or are we talking about E coli 0157:H7, and we are lucky that suppression of the hemolytic uremic syndrome is a key part of the package that our immune systems have developed in order to prevent the bacteria from achieving a potentially fatal status? Could it be that it's just one of the strains that everyone has in their colons, and for some reason, (presumably genetic), our immune systems just can't handle it?
IOW, are our immune systems wimps or heroes?
Love,
Tex
From what I've read, Cipro is very effective against E coli, (UTI's are usually caused by E coli, aren't they? Cipro is claimed by some authorities to be 100% effective against them, when used to treat UTIs), but as noted, repeated use leads to cipro-resistant mutants.
That's a very interesting observation about the possible genetic significance of this issue. Maybe we are the lucky ones, and just don't realize it. Maybe we would be dead if our immune systems hadn't rescued us from an otherwise fatal E coli infection.
There's a fly in the ointment, though - E coli O157:H7, (the famous strain that has received so much national press in the last few years), normally causes hemolytic uremic syndrome. However, none of us presented with blood in the stool, at any time, (though some of us did have anemia).
I distinctly remember back when I first realized that I was the victim of a "mysterious" chronic condition, one of the possibilities that I considered was E coli, but I ruled it out, on the basis of the lack of blood in the stool.
So I wonder if we are talking about a different E coli strain here, and we just happen to be unlucky enough to be susceptible to a strain that most people can shrug off in a few days, or are we talking about E coli 0157:H7, and we are lucky that suppression of the hemolytic uremic syndrome is a key part of the package that our immune systems have developed in order to prevent the bacteria from achieving a potentially fatal status? Could it be that it's just one of the strains that everyone has in their colons, and for some reason, (presumably genetic), our immune systems just can't handle it?
IOW, are our immune systems wimps or heroes?
Love,
Tex
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Carol Arnett
- Gentoo Penguin
- Posts: 423
- Joined: Fri Mar 17, 2006 12:07 pm
This is all really interesting to me, Tex, because when I was dx`d with LMC the GI doc removed a large impaction....from navel to appendix....then put me on Flagyl. That is the only medication I have ever been on for MC and have only had 2 episodes of D with only a duration of a couple of days since August, 2004. Before that I had taken Prilosec for 6 weeks and have always blamed it on that. Now, I wonder.
I only took the Flagyl for the normal time you would for any bacterial infection. At the time, I was too sick, and too ignorant about MC to ask any questiions. I have asked my regular doc but he just refers me to the GI, whom you can`t see or talk to unless you have an emergency or are having a routine colonoscopy. I seem to be able to eat anything or take any kind of meds, although I stay away from Prilosec, and don`t have any trouble. I have wondered if I am in remission or healed.
Interesting, to say the least. Love, Carol
I only took the Flagyl for the normal time you would for any bacterial infection. At the time, I was too sick, and too ignorant about MC to ask any questiions. I have asked my regular doc but he just refers me to the GI, whom you can`t see or talk to unless you have an emergency or are having a routine colonoscopy. I seem to be able to eat anything or take any kind of meds, although I stay away from Prilosec, and don`t have any trouble. I have wondered if I am in remission or healed.
Interesting, to say the least. Love, Carol
Carol Arnett
Hi Carol,
IMO, your gut has to be pretty much healed, in order for you to be in remission, so I would say that both apply to you.
You know, after reading your post, I was reminded that when I first went to the doctor about my uncontrollable D, he examined me, and when I asked him what he thought, he proclaimed that I had a tumor in my colon as big as a man's fist, (and he held his fist in front of my face to help get the point across. LOL). The GI doc that he sent me to, (the next afternoon), told me the same thing, and sent me to get prepped for a series of CT scans. I drank all the blue goop, and the scans were done about midnight, and while I was lying in the ER, waiting for the results, an intern came along, examined me, and almost apologetically, told me that he couldn't feel any tumor. (I'm sure that he was doubting his qualifications as a doctor since he couldn't even detect a tumor in my colon as big as a man's fist. LOL. I told him not worry, he was right, it wasn't there.
Anyway, apparently all the palpation exams, and the blue goop for the scans, had broken up the lump, and it had headed south for the season. He wrote me a prescription for Ciproflaxin, in case it was due to an infection, and the D went away for the two weeks that I took it. A few days later it returned, so when I went back to the GI doc for a followup, he gave me another script for two weeks of Cipro, with the same results. I had forgotten about that lump, until you mentioned your experience.
Interesting coincidence - or maybe it wasn't a coincidence.
Love,
Tex
IMO, your gut has to be pretty much healed, in order for you to be in remission, so I would say that both apply to you.
You know, after reading your post, I was reminded that when I first went to the doctor about my uncontrollable D, he examined me, and when I asked him what he thought, he proclaimed that I had a tumor in my colon as big as a man's fist, (and he held his fist in front of my face to help get the point across. LOL). The GI doc that he sent me to, (the next afternoon), told me the same thing, and sent me to get prepped for a series of CT scans. I drank all the blue goop, and the scans were done about midnight, and while I was lying in the ER, waiting for the results, an intern came along, examined me, and almost apologetically, told me that he couldn't feel any tumor. (I'm sure that he was doubting his qualifications as a doctor since he couldn't even detect a tumor in my colon as big as a man's fist. LOL. I told him not worry, he was right, it wasn't there.
Anyway, apparently all the palpation exams, and the blue goop for the scans, had broken up the lump, and it had headed south for the season. He wrote me a prescription for Ciproflaxin, in case it was due to an infection, and the D went away for the two weeks that I took it. A few days later it returned, so when I went back to the GI doc for a followup, he gave me another script for two weeks of Cipro, with the same results. I had forgotten about that lump, until you mentioned your experience.
Interesting coincidence - or maybe it wasn't a coincidence.
Love,
Tex
I took a combo of Flagyl and Levaquin for 1 week for diverticulitis. The D started immediately and continued for 5 weeks (never had continuous D before) and then Norman returned. I had taken Levaquin before without any problems, but the combo did me in. Six weeks later I took Cipro after foot surgery; no problem. Six weeks later, I had MC.
Until my Dx, I blamed the D on eating rare pork at a restaurant, but I've also wondered if I upset my bacteria balance with the combo. I wonder if they'll have any answers in our lifetime?
Until my Dx, I blamed the D on eating rare pork at a restaurant, but I've also wondered if I upset my bacteria balance with the combo. I wonder if they'll have any answers in our lifetime?
You never know what you can do until you have to do it.
Gloria,
The combination not only upset the balance, it almost surely "cleaned house". Levaquin is a broad-spectrum antibiotic that is often used when the target pathogen is unidentified, and Flagyl is used to treat anaerobic bacteria such as C difficile, and certain parasites, (among other things). Anyway, the point is, the combination probably pretty much wiped out all the flora and fauna residing in your gut, so that it had to start over and establish a new population of bacteria from scratch.
Despite the fact that Norman returned after five weeks, I'd bet a GF cookie that some pathogen got a toe-hold immediately following the initial antibiotic treatment, and triggered the MC. The remission after five weeks could have been spontaneous, as sometimes happens.
IMO, it is irresponsible for doctors to prescribe antibiotics for the GI tract, without offering advice on taking a suitable probiotic immediately afterwards, in order to encorage the re-population process to proceed in the right direction. Very, very few of them seem to offer that advice, presumably due to not either knowing any better, or simply not caring.
Tex
The combination not only upset the balance, it almost surely "cleaned house". Levaquin is a broad-spectrum antibiotic that is often used when the target pathogen is unidentified, and Flagyl is used to treat anaerobic bacteria such as C difficile, and certain parasites, (among other things). Anyway, the point is, the combination probably pretty much wiped out all the flora and fauna residing in your gut, so that it had to start over and establish a new population of bacteria from scratch.
Despite the fact that Norman returned after five weeks, I'd bet a GF cookie that some pathogen got a toe-hold immediately following the initial antibiotic treatment, and triggered the MC. The remission after five weeks could have been spontaneous, as sometimes happens.
IMO, it is irresponsible for doctors to prescribe antibiotics for the GI tract, without offering advice on taking a suitable probiotic immediately afterwards, in order to encorage the re-population process to proceed in the right direction. Very, very few of them seem to offer that advice, presumably due to not either knowing any better, or simply not caring.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.