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Discussion Starter · #1 ·
Hey all:A true newbie sort of question.I'm a bit confused about what C. diff and the rest of these bacterias I hear described here mean.What kinds of bacteria should they be looking for there not to be in your system? Also, what are the "good" bacteria that should be in the system? Thanks,rim
 

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Well, I'm not a newbie, and really ought to know, but I still don't have those bugs sorted out. A very good question, especially re: "good bacteria."Does anybody happen to have access to the journal Gastroenterology? Maybe you could post a bit of this article, which sounds very interesting although it is focused on IBD, not IBS:Therapeutic manipulation of the enteric microflora in inflammatory bowel diseases: Antibiotics, probiotics, and prebioticsGastroenterologyMay 2004 � Volume 126 � Number 6Abstract: Crohn�s disease, ulcerative colitis, and pouchitis are caused by overly aggressive immune responses to a subset of commensal (nonpathogenic) enteric bacteria in genetically predisposed individuals. Clinical and experimental studies suggest that the relative balance of aggressive and protective bacterial species is altered in these disorders. Antibiotics can selectively decrease tissue invasion and eliminate aggressive bacterial species or globally decrease luminal and mucosal bacterial concentrations, depending on their spectrum of activity. Alternatively, administration of beneficial bacterial species (probiotics), poorly absorbed dietary oligosaccharides (prebiotics), or combined probiotics and prebiotics (synbiotics) can restore a predominance of beneficial Lactobacillus and Bifidobacterium species. Current clinical trials do not fulfill evidence-based criteria for using these agents in inflammatory bowel diseases (IBD), but multiple nonrigorous studies and widespread clinical experience suggest that metronidazole and/or ciprofloxacin can treat Crohn�s colitis and ileocolitis (but not isolated ileal disease), perianal fistulae and pouchitis, whereas selected probiotic preparations prevent relapse of quiescent ulcerative colitis and relapsing pouchitis. These physiologic approaches offer considerable promise for treating IBD, but must be supported by rigorous controlled therapeutic trials that consider clinical disease before their widespread clinical acceptance. These agents likely will become an integral component of treating IBD in combination with traditional anti-inflammatory and immunosuppressive agents.Journal home page: Gastroenterology (W.B. Saunders)
 

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Well, I'm not a newbie, and really ought to know, but I still don't have those bugs sorted out. A very good question, especially re: "good bacteria."Does anybody happen to have access to the journal Gastroenterology? Maybe you could post a bit of this article, which sounds very interesting although it is focused on IBD, not IBS:Therapeutic manipulation of the enteric microflora in inflammatory bowel diseases: Antibiotics, probiotics, and prebioticsGastroenterologyMay 2004 � Volume 126 � Number 6Abstract: Crohn�s disease, ulcerative colitis, and pouchitis are caused by overly aggressive immune responses to a subset of commensal (nonpathogenic) enteric bacteria in genetically predisposed individuals. Clinical and experimental studies suggest that the relative balance of aggressive and protective bacterial species is altered in these disorders. Antibiotics can selectively decrease tissue invasion and eliminate aggressive bacterial species or globally decrease luminal and mucosal bacterial concentrations, depending on their spectrum of activity. Alternatively, administration of beneficial bacterial species (probiotics), poorly absorbed dietary oligosaccharides (prebiotics), or combined probiotics and prebiotics (synbiotics) can restore a predominance of beneficial Lactobacillus and Bifidobacterium species. Current clinical trials do not fulfill evidence-based criteria for using these agents in inflammatory bowel diseases (IBD), but multiple nonrigorous studies and widespread clinical experience suggest that metronidazole and/or ciprofloxacin can treat Crohn�s colitis and ileocolitis (but not isolated ileal disease), perianal fistulae and pouchitis, whereas selected probiotic preparations prevent relapse of quiescent ulcerative colitis and relapsing pouchitis. These physiologic approaches offer considerable promise for treating IBD, but must be supported by rigorous controlled therapeutic trials that consider clinical disease before their widespread clinical acceptance. These agents likely will become an integral component of treating IBD in combination with traditional anti-inflammatory and immunosuppressive agents.Journal home page: Gastroenterology (W.B. Saunders)
 

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Hey Rim-- Sorry for the length here, but it was a good q! Deserves some thought. At least 400 friendly species exist; L. acidophilus and B.bifidus are principal species that have been linked with successful rebuilding of friendly gut flora and which are available in supplement form. L. acidophilus and B. bifidus .For specific beneficial strains and their benefits: http://www.relfe.com/lactobacillus.html Probiotics inhibit pathogenic bacteria in the gut in multiple ways: � They secrete various substances, such as lactic and acetic acids, to decrease the pH of the gastrointestinal tract and vagina, rendering them less hospitable to pathogenic bacteria. � They also secrete bacteriocins, natural antibiotics that kill undesirable bacteria. For example, bacteria inhibited by L. acidophilus include: Bacillus subtilis, B. cereus, B. stearothermophilus, Candida albicans, Clostridium perfringens, Escheria coli, Klebsiella pneumoniae, L.bulgaricus, L. fermenti, L. helveticus, L. lactis, L. leichmannii, L. plantarum, Proteus vulgaricus, Pseudomonas aeruginosa, P. fluorescens, Salmonella typhosa, S. schottmuelleri, Shigella dysenteriae, S. paradysenteriae, S. paradysenteriae, Sarcina lutea, Serratia marcescens, Staphylococcus aureus, Streptococcus faecalis, S. lactis, Vibrio comma. fyi, other proven benefits of supplementing with probiotics:� Promotion of intestinal lactose digestion. � Positive influence on the intestinal microflora � Prevention of intestinal tract infections (bacteria or virus induced, Candida enteritis, Helicobacter pylori ulcus/neoplasia) � Regulation of gut motility � Improvement of the immune system � Regulation of intestinal inflammationA great article to read when you have time-- long article on probiotics--great info If you�re short on time: quick info on probiotics quick info 2 ******************************More specific info re: IBS & The BAD GUYS(if not kept in check�short list):Clostridium difficile http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15179608 Blastocystis hominis(like giardia, used to be considered non-pathogenic, now changing) http://www.ncbi.nlm.nih.gov/entrez/query.f...0&dopt=Abstract Cl. perfringens, Enterococcus, Streptomyces, Enterobacterial, Klebsiella, E. coli, Peptostreptococcus, Candida Albicans, genus of Streptococcus, of Staphylococcus, of Fusobacterium sp http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11565126 Campylobacter jejuni http://www.journals.uchicago.edu/JID/journ...067/010067.html Mycobacterium avium paratuberculosis (MAP) http://news.bbc.co.uk/1/hi/health/3130173.stm Klebsiella & Salmonella http://www.cdc.gov/foodnet/pub/CID/reesj.pdf **it seems it�s the ENDOTOXINS, & to some extent exotoxins, from the unchecked bad guys that cause the mucosal barrier of the intestinal wall to become inflamed--almost imperceptively for those of us with IBS.
 

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Hey Rim-- Sorry for the length here, but it was a good q! Deserves some thought. At least 400 friendly species exist; L. acidophilus and B.bifidus are principal species that have been linked with successful rebuilding of friendly gut flora and which are available in supplement form. L. acidophilus and B. bifidus .For specific beneficial strains and their benefits: http://www.relfe.com/lactobacillus.html Probiotics inhibit pathogenic bacteria in the gut in multiple ways: � They secrete various substances, such as lactic and acetic acids, to decrease the pH of the gastrointestinal tract and vagina, rendering them less hospitable to pathogenic bacteria. � They also secrete bacteriocins, natural antibiotics that kill undesirable bacteria. For example, bacteria inhibited by L. acidophilus include: Bacillus subtilis, B. cereus, B. stearothermophilus, Candida albicans, Clostridium perfringens, Escheria coli, Klebsiella pneumoniae, L.bulgaricus, L. fermenti, L. helveticus, L. lactis, L. leichmannii, L. plantarum, Proteus vulgaricus, Pseudomonas aeruginosa, P. fluorescens, Salmonella typhosa, S. schottmuelleri, Shigella dysenteriae, S. paradysenteriae, S. paradysenteriae, Sarcina lutea, Serratia marcescens, Staphylococcus aureus, Streptococcus faecalis, S. lactis, Vibrio comma. fyi, other proven benefits of supplementing with probiotics:� Promotion of intestinal lactose digestion. � Positive influence on the intestinal microflora � Prevention of intestinal tract infections (bacteria or virus induced, Candida enteritis, Helicobacter pylori ulcus/neoplasia) � Regulation of gut motility � Improvement of the immune system � Regulation of intestinal inflammationA great article to read when you have time-- long article on probiotics--great info If you�re short on time: quick info on probiotics quick info 2 ******************************More specific info re: IBS & The BAD GUYS(if not kept in check�short list):Clostridium difficile http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15179608 Blastocystis hominis(like giardia, used to be considered non-pathogenic, now changing) http://www.ncbi.nlm.nih.gov/entrez/query.f...0&dopt=Abstract Cl. perfringens, Enterococcus, Streptomyces, Enterobacterial, Klebsiella, E. coli, Peptostreptococcus, Candida Albicans, genus of Streptococcus, of Staphylococcus, of Fusobacterium sp http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11565126 Campylobacter jejuni http://www.journals.uchicago.edu/JID/journ...067/010067.html Mycobacterium avium paratuberculosis (MAP) http://news.bbc.co.uk/1/hi/health/3130173.stm Klebsiella & Salmonella http://www.cdc.gov/foodnet/pub/CID/reesj.pdf **it seems it�s the ENDOTOXINS, & to some extent exotoxins, from the unchecked bad guys that cause the mucosal barrier of the intestinal wall to become inflamed--almost imperceptively for those of us with IBS.
 

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There is NO inflammation of the colon wall in IBS!!!!"intestinal wall to become inflamed"This is misleading information. IBS does not inflame the colon wall and there is NO inflammation seen with colonoscopy.There is in a subgroup of IBSers, inflammed mast cells embedded in the colon wall they need an electron microscope to see, when they peel back the layers of the colon.Some IBSers have alter gut flora, but it is not believed to be the cause of IBS.Other problems in IBS have been found and have nothing to do with gut flora.Modern IBS research and consenses from the vast majority of experts studying IBS, regard IBS as a gut brain to brain and back dysfunction.
 

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There is NO inflammation of the colon wall in IBS!!!!"intestinal wall to become inflamed"This is misleading information. IBS does not inflame the colon wall and there is NO inflammation seen with colonoscopy.There is in a subgroup of IBSers, inflammed mast cells embedded in the colon wall they need an electron microscope to see, when they peel back the layers of the colon.Some IBSers have alter gut flora, but it is not believed to be the cause of IBS.Other problems in IBS have been found and have nothing to do with gut flora.Modern IBS research and consenses from the vast majority of experts studying IBS, regard IBS as a gut brain to brain and back dysfunction.
 

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Eric wrote:
quote: There is NO inflammation of the colon wall in IBS!!!!
Easy... I don't think that's what Talissa said. We're talking about microbes here that can cause symptoms of gut infection above and beyond the underlying irritable bowel syndrome. Talissa wrote:
quote: the ENDOTOXINS, & to some extent exotoxins, from the unchecked bad guys that cause the mucosal barrier of the intestinal wall to become inflamed--almost imperceptively for those of us with IBS
She will correct me if I'm wrong, but I took that to mean that IBSers' bowel function is already so screwed up most days that we can hardly tell when there is something else complicating it, be it enterotoxigenic E. coli or Campylobacter or a parasitic syndrome or whatever.
 

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Eric wrote:
quote: There is NO inflammation of the colon wall in IBS!!!!
Easy... I don't think that's what Talissa said. We're talking about microbes here that can cause symptoms of gut infection above and beyond the underlying irritable bowel syndrome. Talissa wrote:
quote: the ENDOTOXINS, & to some extent exotoxins, from the unchecked bad guys that cause the mucosal barrier of the intestinal wall to become inflamed--almost imperceptively for those of us with IBS
She will correct me if I'm wrong, but I took that to mean that IBSers' bowel function is already so screwed up most days that we can hardly tell when there is something else complicating it, be it enterotoxigenic E. coli or Campylobacter or a parasitic syndrome or whatever.
 

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Discussion Starter · #12 ·
Thanks to both of you!Am understandably concerned that perhaps the lab managed to miss the 'bad' bacteria or parasites when doing my culture, but concerned as to what can be done about it.
 

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Discussion Starter · #13 ·
Thanks to both of you!Am understandably concerned that perhaps the lab managed to miss the 'bad' bacteria or parasites when doing my culture, but concerned as to what can be done about it.
 

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Rim, you're welcome! The standard labs are notorious for missing the bad bugs--GSDL seems to have a better track record(but not perfect), plus they tell you which beneficial bacteria you're low on, which can leave you vulnerable...Hey Cranky Pants, you don't seem all that cranky! Actually, for post infectious IBS, sub-level inflammation HAS been found~Er's pal Drossman, THE irritable bowel syndrome �expert�? thinks so, at least for some of us-�Inflammation, Infection, and Irritable Bowel Syndrome: An Update�Yehuda Ringel, MD Douglas A. Drossman, MD http://www.medscape.com/viewarticle/434527 There�s also--�Inflammatory Mediators in Irritable Bowel Syndrome��Experimental (animal) data show that inflammation, even if mild, can lead to persistent changes in gastrointestinal nerve and smooth muscle function, resulting in dysmotility, hypersensitivity and gastrointestinal dysfunction (1, 4-6). In humans, the role of inflammation in the generation of IBS symptoms is less well studied, although there are important findings from people with 'post-infective IBS'. http://www.med.unc.edu/medicine/fgidc/infl...rymediators.htm ��Based on recent reports of low-grade mucosal inflammation in subpopulations of patients meeting current diagnostic criteria for irritable bowel syndrome,�� http://www.medscape.com/viewarticle/457728_print �We conclude that such patients may be susceptible to inflammatory stimuli, and that inflammation may play a role in the pathogenesis of PI-IBS.� http://www.ncbi.nlm.nih.gov/entrez/query.f...3&dopt=Abstract �Physiological changes which affect nearly all individuals following GI infections include shortening of whole gut transit and lowering of discomfort threshold for rectal distension, the severity of the abnormality being increased in those who meet the criteria for IBS. Associated with these changes there is also evidence of low grade inflammation and elevated enteroendocrine cells which resolves in most patients, but persists in those with persistent symptoms.� http://www.bsg.org.uk/pdf_word_docs/manage_treat.pdf �Inflammation may play a role in the pathogenesis of irritable bowel syndrome in some individuals, such as in those who develop symptoms following a dysenteric illness. Persisting inflammation, resulting from an imbalance of cytokines regulating the inflammatory response, is one possible mechanism.� http://www.ncbi.nlm.nih.gov/entrez/query.f...7&dopt=Abstract ***Apparently, the changes in inflammation along the intestinal wall, its brush border, are so minute, it takes a much more powerful microscope to be detected. And post infectious IBS populations are the only group so far that�s been studied for this sub-level inflammation. *************************I also have references for dysbiosis of microflora affecting the brain-gut axis, how stress lowers beneficial bacteria, etc, but no time!!! If himself persists, I'll post them in the future. Save you from more links right now!But who would've thought the bugs were so important??? Mind boggling.
 

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Rim, you're welcome! The standard labs are notorious for missing the bad bugs--GSDL seems to have a better track record(but not perfect), plus they tell you which beneficial bacteria you're low on, which can leave you vulnerable...Hey Cranky Pants, you don't seem all that cranky! Actually, for post infectious IBS, sub-level inflammation HAS been found~Er's pal Drossman, THE irritable bowel syndrome �expert�? thinks so, at least for some of us-�Inflammation, Infection, and Irritable Bowel Syndrome: An Update�Yehuda Ringel, MD Douglas A. Drossman, MD http://www.medscape.com/viewarticle/434527 There�s also--�Inflammatory Mediators in Irritable Bowel Syndrome��Experimental (animal) data show that inflammation, even if mild, can lead to persistent changes in gastrointestinal nerve and smooth muscle function, resulting in dysmotility, hypersensitivity and gastrointestinal dysfunction (1, 4-6). In humans, the role of inflammation in the generation of IBS symptoms is less well studied, although there are important findings from people with 'post-infective IBS'. http://www.med.unc.edu/medicine/fgidc/infl...rymediators.htm ��Based on recent reports of low-grade mucosal inflammation in subpopulations of patients meeting current diagnostic criteria for irritable bowel syndrome,�� http://www.medscape.com/viewarticle/457728_print �We conclude that such patients may be susceptible to inflammatory stimuli, and that inflammation may play a role in the pathogenesis of PI-IBS.� http://www.ncbi.nlm.nih.gov/entrez/query.f...3&dopt=Abstract �Physiological changes which affect nearly all individuals following GI infections include shortening of whole gut transit and lowering of discomfort threshold for rectal distension, the severity of the abnormality being increased in those who meet the criteria for IBS. Associated with these changes there is also evidence of low grade inflammation and elevated enteroendocrine cells which resolves in most patients, but persists in those with persistent symptoms.� http://www.bsg.org.uk/pdf_word_docs/manage_treat.pdf �Inflammation may play a role in the pathogenesis of irritable bowel syndrome in some individuals, such as in those who develop symptoms following a dysenteric illness. Persisting inflammation, resulting from an imbalance of cytokines regulating the inflammatory response, is one possible mechanism.� http://www.ncbi.nlm.nih.gov/entrez/query.f...7&dopt=Abstract ***Apparently, the changes in inflammation along the intestinal wall, its brush border, are so minute, it takes a much more powerful microscope to be detected. And post infectious IBS populations are the only group so far that�s been studied for this sub-level inflammation. *************************I also have references for dysbiosis of microflora affecting the brain-gut axis, how stress lowers beneficial bacteria, etc, but no time!!! If himself persists, I'll post them in the future. Save you from more links right now!But who would've thought the bugs were so important??? Mind boggling.
 

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Rim said:
quote: Am understandably concerned that perhaps the lab managed to miss the 'bad' bacteria or parasites when doing my culture, but concerned as to what can be done about it.
I sympathize, I have a similar concern at the moment as you may recall. From what I have been able to gather so far, it seems that "routine" (if that's what you had) stool culture will miss quite a few bad bugs. Some of them require a specific culture medium that the clinician must request. And checking for ova and parasites is a separate test as I understand it. My doc seems to feel that the best way to look for parasites is via biopsy, ugh. If you've been ailing and are not getting better, maybe it's time for your doc to consider repeat/additional tests to nail down a diagnosis?
 

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Rim said:
quote: Am understandably concerned that perhaps the lab managed to miss the 'bad' bacteria or parasites when doing my culture, but concerned as to what can be done about it.
I sympathize, I have a similar concern at the moment as you may recall. From what I have been able to gather so far, it seems that "routine" (if that's what you had) stool culture will miss quite a few bad bugs. Some of them require a specific culture medium that the clinician must request. And checking for ova and parasites is a separate test as I understand it. My doc seems to feel that the best way to look for parasites is via biopsy, ugh. If you've been ailing and are not getting better, maybe it's time for your doc to consider repeat/additional tests to nail down a diagnosis?
 

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Talissa--I'm overwhelmed!
I didn't realize you had post-infectious IBS in mind here. Will have to dig into some of your many citations later... but based on your excerpts I'm not sure these theories really contradict what Eric said. Inflammation provoked by infection may somehow damage the bowel and set the stage for IBS, but that doesn't make inflammation a feature of IBS. Am I missing something that can be easily summed up?And no, I'm actually not all that cranky, I just thought Crankypants was a funny handle for an IBS forum. I do get super-cranky in the presence of sarcasm and personal attacks, but otherwise I'm usually pretty genial.
 

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Talissa--I'm overwhelmed!
I didn't realize you had post-infectious IBS in mind here. Will have to dig into some of your many citations later... but based on your excerpts I'm not sure these theories really contradict what Eric said. Inflammation provoked by infection may somehow damage the bowel and set the stage for IBS, but that doesn't make inflammation a feature of IBS. Am I missing something that can be easily summed up?And no, I'm actually not all that cranky, I just thought Crankypants was a funny handle for an IBS forum. I do get super-cranky in the presence of sarcasm and personal attacks, but otherwise I'm usually pretty genial.
 

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Hi Cranky, again--real quick, can't talk(blabber
not theories-- studies, and those with post infectious IBS have sub-level inflammation. Those with standard IBS have not been studied yet to determine whether or not this sub-level inflammation(which is only possible to detect with special microscopic lenses)exists for them as well:�Inflammatory Mediators in Irritable Bowel Syndrome��Experimental (animal) data show that inflammation, even if mild, can lead to persistent changes in gastrointestinal nerve and smooth muscle function, resulting in dysmotility, hypersensitivity and gastrointestinal dysfunction (1, 4-6). In humans, the role of inflammation in the generation of IBS symptoms is less well studied, although there are important findings from people with 'post-infective IBS'. http://www.med.unc.edu/medicine/fgidc/infl...rymediators.htm And it's well known that those with IBS have dysbiosis(lots of references if needed), and the good bugs we're low on help keep the mucosal inflammation(immune system of gut)regulated(also lots of references.)Nice of you to say that Er & I agree, though! Comic relief, absolutely good for the soul.
 
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