# Citrobacter Freundii



## Reclamation Project (Jul 12, 2004)

Does anyone know what this is, how you get it, what effect it can have, and how you get rid?????Thanx


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## eric (Jul 8, 1999)

FYI http://vm.cfsan.fda.gov/~mow/chap20.html


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## eric (Jul 8, 1999)

FYI http://vm.cfsan.fda.gov/~mow/chap20.html


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## Reclamation Project (Jul 12, 2004)

Thanx Eric!


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## Reclamation Project (Jul 12, 2004)

Thanx Eric!


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## Talissa (Apr 10, 2004)

Hi RP,The following may be more info than you were asking for, but the more you know







Citrobacter freundii was just found in my stool sample test by great smokies diagnostic lab( see http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=5;t=000566 ), so I have several links that you may find interesting. From what Iï¿½ve read, this bacteria is genetically/chemically similar to salmonella and is implicated in diarrheal diseases. It has also been found to be one of the many bugs involved in urinary tract infections... It is resistant to several antibiotics, like tetracycline which I took for a year while in HS. It is also the bacteria in the mouth responsible for plaque formationï¿½ It is supposed to be killed by the following antibiotics: Ciprofloxin, Ceftiaxone, Gentamicin, & Sulfa/Trimethoprim. If considering Cipro/Levaquin/any fluouroquinolone pls read the cipro link in my signature as well as this open letter-- http://www.medicationsense.com/articles/ja...ngress_ltr.html . Do a search here on cipro & read other links provided. Be esp carefull not to take if a runner, wt lifter, have had previous head injury, any bipolar problems, or are low on magnesium. Never drink grapefruit juice or eat grapefruits while on a fluouroquinolone antibiotic, nor should you do any exercise at all, with the exception of very light stretching....Listed natural agents that can lower c. freundii, but not fully eradicate by themselves incl: plant tannins and oil of oregano. I personally am going the route of high probiotics intake and bee propolis, as well as a rotation of other natural antibacterialsï¿½.am going to try everything possible before resorting to antibiotics. If I do take antibiotics, will continue with the high probiotics and also take an antifungal with it to avoid a yeast overgrowthï¿½Anyways, hereï¿½s some discussions on c. freundii, as well as studies, etcï¿½ http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15538714 http://www.geocities.com/ctfutures2001/Cit...ter-frundii.htm http://www.diamondhead.net/c3.htm http://www.geocities.com/ctfutures2001/Antibiotics.htm http://aac.asm.org/cgi/content/full/46/11/3555 http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15493821 http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15375135 Another member here, Calid, was found to have c. freundii as well & has I believe successfully eradicated it with Cipro. Anmegrl has recently taken levaquin(sim to cipro) for c. freundii...


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## Talissa (Apr 10, 2004)

Hi RP,The following may be more info than you were asking for, but the more you know







Citrobacter freundii was just found in my stool sample test by great smokies diagnostic lab( see http://www.ibsgroup.org/ubb/ultimatebb.php...ic;f=5;t=000566 ), so I have several links that you may find interesting. From what Iï¿½ve read, this bacteria is genetically/chemically similar to salmonella and is implicated in diarrheal diseases. It has also been found to be one of the many bugs involved in urinary tract infections... It is resistant to several antibiotics, like tetracycline which I took for a year while in HS. It is also the bacteria in the mouth responsible for plaque formationï¿½ It is supposed to be killed by the following antibiotics: Ciprofloxin, Ceftiaxone, Gentamicin, & Sulfa/Trimethoprim. If considering Cipro/Levaquin/any fluouroquinolone pls read the cipro link in my signature as well as this open letter-- http://www.medicationsense.com/articles/ja...ngress_ltr.html . Do a search here on cipro & read other links provided. Be esp carefull not to take if a runner, wt lifter, have had previous head injury, any bipolar problems, or are low on magnesium. Never drink grapefruit juice or eat grapefruits while on a fluouroquinolone antibiotic, nor should you do any exercise at all, with the exception of very light stretching....Listed natural agents that can lower c. freundii, but not fully eradicate by themselves incl: plant tannins and oil of oregano. I personally am going the route of high probiotics intake and bee propolis, as well as a rotation of other natural antibacterialsï¿½.am going to try everything possible before resorting to antibiotics. If I do take antibiotics, will continue with the high probiotics and also take an antifungal with it to avoid a yeast overgrowthï¿½Anyways, hereï¿½s some discussions on c. freundii, as well as studies, etcï¿½ http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15538714 http://www.geocities.com/ctfutures2001/Cit...ter-frundii.htm http://www.diamondhead.net/c3.htm http://www.geocities.com/ctfutures2001/Antibiotics.htm http://aac.asm.org/cgi/content/full/46/11/3555 http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15493821 http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15375135 Another member here, Calid, was found to have c. freundii as well & has I believe successfully eradicated it with Cipro. Anmegrl has recently taken levaquin(sim to cipro) for c. freundii...


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## Talissa (Apr 10, 2004)

Btw, the standard labs that MDs use will not test for this organism or many others which can cause diarrhea/constipation...


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## Talissa (Apr 10, 2004)

Btw, the standard labs that MDs use will not test for this organism or many others which can cause diarrhea/constipation...


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## eric (Jul 8, 1999)

FYIReclamation Project *"These rod-shaped enteric (intestinal) bacteria have been suspected of causing acute and chronic gastrointestinal disease. The organisms may be recovered from natural environments such as forests and freshwater as well as from farm produce (vegetables) where they reside as normal microflora.* *They may be recovered from the stools of healthy individuals with no disease symptoms. The relative proportion of pathogenic to nonpathogenic strains is unknown."* I just had to renew my food handlers card yesterday and specifically went over food related bacteria.When they become pathogenic, *"Gastroenteritis is name of the disease occasionally and sporadically caused by these genera."* Gastroenteritis is not IBS, but certain people who get Gastroenteritis, can dvelop IBS later after the resolution of the infection. Usally" *Acute gastroenteritis is characterized by two or more of the symptoms of vomiting, nausea, fever, chills, abdominal pain, and watery (dehydrating) diarrhea occurring 12-24 hours after ingestion of contaminated food or water. * *Chronic diarrheal disease is characterized by dysenteric symptoms: foul-smelling, mucus-containing, diarrheic stool with flatulence and abdominal distention. The chronic disease may continue for months and require antibiotic treatment. "* These bacterial orginisms cause d, because the body works to try to dispel them. *"At least 500 different species of deadly bacteria have been found to inhabit a person's colon at any given time; "traveler's diarrhea" often results when this mix is changed through exposure to new pathogens. If this happens, the gut runs a program designed to expel as much of its contents as quickly as possible ï¿½ unpleasant for the vacationer, but much better than a fatal infection."* http://www.kiwiterapi.dk/whiplash/frames/gutthoughts.htm Vomiting and fever and chills are alarm symptoms to IBS. These symptoms require the physician to do additional workup. IBS is not a bacterial infection like gastroenteritis causes.To date no bacterial infectious process has been found for IBS like a disease process, only that bacterial and parasitic and perhaps now viral enteric infections can later lead to IBS after the intial reolution of the infection, that causes abnormalities in the cells of the digestive tract, which can later lead to the full blown IBS clinical presentation. This is called Post Infectious IBS or PI IBS.


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## eric (Jul 8, 1999)

FYIReclamation Project *"These rod-shaped enteric (intestinal) bacteria have been suspected of causing acute and chronic gastrointestinal disease. The organisms may be recovered from natural environments such as forests and freshwater as well as from farm produce (vegetables) where they reside as normal microflora.* *They may be recovered from the stools of healthy individuals with no disease symptoms. The relative proportion of pathogenic to nonpathogenic strains is unknown."* I just had to renew my food handlers card yesterday and specifically went over food related bacteria.When they become pathogenic, *"Gastroenteritis is name of the disease occasionally and sporadically caused by these genera."* Gastroenteritis is not IBS, but certain people who get Gastroenteritis, can dvelop IBS later after the resolution of the infection. Usally" *Acute gastroenteritis is characterized by two or more of the symptoms of vomiting, nausea, fever, chills, abdominal pain, and watery (dehydrating) diarrhea occurring 12-24 hours after ingestion of contaminated food or water. * *Chronic diarrheal disease is characterized by dysenteric symptoms: foul-smelling, mucus-containing, diarrheic stool with flatulence and abdominal distention. The chronic disease may continue for months and require antibiotic treatment. "* These bacterial orginisms cause d, because the body works to try to dispel them. *"At least 500 different species of deadly bacteria have been found to inhabit a person's colon at any given time; "traveler's diarrhea" often results when this mix is changed through exposure to new pathogens. If this happens, the gut runs a program designed to expel as much of its contents as quickly as possible ï¿½ unpleasant for the vacationer, but much better than a fatal infection."* http://www.kiwiterapi.dk/whiplash/frames/gutthoughts.htm Vomiting and fever and chills are alarm symptoms to IBS. These symptoms require the physician to do additional workup. IBS is not a bacterial infection like gastroenteritis causes.To date no bacterial infectious process has been found for IBS like a disease process, only that bacterial and parasitic and perhaps now viral enteric infections can later lead to IBS after the intial reolution of the infection, that causes abnormalities in the cells of the digestive tract, which can later lead to the full blown IBS clinical presentation. This is called Post Infectious IBS or PI IBS.


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## eric (Jul 8, 1999)

Citrobacter species, salmonella species, and shigella species are all bacterial species that can cause Gastroenteritis to name a few.They have studied this pretty extensively and are still doing sf those unfortunate people with Gastroenteritis caused by them, a few later develop IBS after the resolution of the intial infection. There are even certain predictors of those who do develop IBS after Gastroenteritis. Stress at the time of infection is one of them, the bodies stress ciruits are involved in fighting infection for one, this is also well known in IBS.Parasite infection that cause Enteric Gastroenteritis have also been shown to lead to PI IBS.There is also work in progress being done on the possiblity of Norwalk viruses, perhaps leading to PI IBS and then to IBS as well. The intial infections inflame the colon and when the inflammation resides, the person is left with celluar changes in the digestive tract which then can develop into IBS symptoms later. Most of the bacterial species like these Citrobacter species, salmonella species, and shigella species are commonly refered to and known to cause food poisoning.


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## eric (Jul 8, 1999)

Citrobacter species, salmonella species, and shigella species are all bacterial species that can cause Gastroenteritis to name a few.They have studied this pretty extensively and are still doing sf those unfortunate people with Gastroenteritis caused by them, a few later develop IBS after the resolution of the intial infection. There are even certain predictors of those who do develop IBS after Gastroenteritis. Stress at the time of infection is one of them, the bodies stress ciruits are involved in fighting infection for one, this is also well known in IBS.Parasite infection that cause Enteric Gastroenteritis have also been shown to lead to PI IBS.There is also work in progress being done on the possiblity of Norwalk viruses, perhaps leading to PI IBS and then to IBS as well. The intial infections inflame the colon and when the inflammation resides, the person is left with celluar changes in the digestive tract which then can develop into IBS symptoms later. Most of the bacterial species like these Citrobacter species, salmonella species, and shigella species are commonly refered to and known to cause food poisoning.


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## Talissa (Apr 10, 2004)

FYI"Fatty acids, that are microorganism's markers in blood and jejunum's, ileum's, and large intestine's bioptats of the *patients with irritable bowel syndrome were investigated * with gas chromatography. Markers of Cl. perfringens, Cl. difficile, Enterococcus, Streptomyces, Enterobacterial, Klebsiella, E. coli, Peptostreptococcus, Candida Albicans, genus of Streptococcus, of Staphylococcus, of Fusobacterium sp and others microorganisms were revealed. " http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11565126 Interesting how many of the above can be caused by antibiotics(resistant to), such as those antibiotics used on patients who later become post infectious IBS patients...For ex, I was told I had PI IBS. I now find out I have citrobacter freundii. The antibiotic I took before the PI IBS was diagnosed was flagyl. C. Freundii is resistant to flagyl/metronidazole.


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## Talissa (Apr 10, 2004)

FYI"Fatty acids, that are microorganism's markers in blood and jejunum's, ileum's, and large intestine's bioptats of the *patients with irritable bowel syndrome were investigated * with gas chromatography. Markers of Cl. perfringens, Cl. difficile, Enterococcus, Streptomyces, Enterobacterial, Klebsiella, E. coli, Peptostreptococcus, Candida Albicans, genus of Streptococcus, of Staphylococcus, of Fusobacterium sp and others microorganisms were revealed. " http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11565126 Interesting how many of the above can be caused by antibiotics(resistant to), such as those antibiotics used on patients who later become post infectious IBS patients...For ex, I was told I had PI IBS. I now find out I have citrobacter freundii. The antibiotic I took before the PI IBS was diagnosed was flagyl. C. Freundii is resistant to flagyl/metronidazole.


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## eric (Jul 8, 1999)

But you had PI IBS foru years ago.citrobacter freundii"They may be recovered from the stools of healthy individuals with no disease symptoms.does meant they have multiply to pathogens, and you would know if they did.So now you have an over population of citrobacter freundii and a case of Gastroenteritis? Do you have a fever, vomiting or chills?Or the same IBS symptoms. Wait you don't have pain, a must for IBS. Have you seen a regular doctor again about the recent citrobacter freundii infection?These are common causes of food poisoning. Perhaps it was something you recently ate?


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## eric (Jul 8, 1999)

But you had PI IBS foru years ago.citrobacter freundii"They may be recovered from the stools of healthy individuals with no disease symptoms.does meant they have multiply to pathogens, and you would know if they did.So now you have an over population of citrobacter freundii and a case of Gastroenteritis? Do you have a fever, vomiting or chills?Or the same IBS symptoms. Wait you don't have pain, a must for IBS. Have you seen a regular doctor again about the recent citrobacter freundii infection?These are common causes of food poisoning. Perhaps it was something you recently ate?


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## Jhouston (Nov 9, 2003)

Potential pathogens may be transient .....therefore, if one has symptoms then it would be a good idea to pay attention to the pp. If no symptoms it would probably just be passing through







Joann


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## Jhouston (Nov 9, 2003)

Potential pathogens may be transient .....therefore, if one has symptoms then it would be a good idea to pay attention to the pp. If no symptoms it would probably just be passing through







Joann


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## flux (Dec 13, 1998)

> quote:Citrobacter freundii was just found in my stool sample test by great smokies diagnostic lab


Just having this bacteria doesn't necessarily mean much.


> quote:Citrobacter species, salmonella species, and shigella species are all bacterial species that can cause Gastroenteritis to name a few


I wouldn't put Citrobacter in the same league as the other two. If you had Citrobacter, you may not even know it unless you had a Great Smokies test. The other two, you may not live long enough to get a Great Smokies test.


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## flux (Dec 13, 1998)

> quote:Citrobacter freundii was just found in my stool sample test by great smokies diagnostic lab


Just having this bacteria doesn't necessarily mean much.


> quote:Citrobacter species, salmonella species, and shigella species are all bacterial species that can cause Gastroenteritis to name a few


I wouldn't put Citrobacter in the same league as the other two. If you had Citrobacter, you may not even know it unless you had a Great Smokies test. The other two, you may not live long enough to get a Great Smokies test.


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## Reclamation Project (Jul 12, 2004)

Thanx for all the info you guys have posted.... I will try and go through and digest it now!


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## Reclamation Project (Jul 12, 2004)

Thanx for all the info you guys have posted.... I will try and go through and digest it now!


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## eric (Jul 8, 1999)

There was a rare outbreak of shigella in 2003 a public fountain on a hot summer in the next town north of where I live. A bunch of childred got very sick. "Fountain closed after users get shigellosis HUBBARD -- Health officials in Marion County have closed a fountain in the small community of Hubbard because of an outbreak of a fecal bacteria. Dr. Karen Landers, Marion County health officer, said that there are three confirmed cases of shigellosis, a highly infectious disease caused by a group of bacteria called shigella. There are eight more suspected cases. No one has been hospitalized. Everyone who has come down with symptoms reported being at the splash fountain at Rivenes Park between July 21 and Friday. Test results of water samples taken from the fountain are expected back Monday. The intestinal infection is usually caused by food or water contaminated by infected persons. Symptoms include fever, bloody diarrhea and abdominal cramps and usually occur one to four days after exposure. The infection is treatable with antibiotics." http://www.theolympian.com/home/news/20030...67539_ARC.shtml Salmonellosis http://www.niaid.nih.gov/factsheets/foodbornedis.htm#f What is Campylobacter jejuni? http://www.foodborneillness.com/ecoli1/cam...er-overview.htm "What are the symptoms of a Campylobacter infection?Diarrhea is the most consistent and prominent manifestation of campylobacter infection. It is often bloody.1 Typical symptoms of C. jejuni infection also include fever, nausea, and vomiting, abdominal pain, headache, and muscle pain. A majority of cases are mild and do not require hospitalization and may be self-limited. However, Campylobacter jejuni infection can be severe and life threatening. Death is more common when other diseases (e.g., cancer, liver disease, and immuno-deficiency diseases) are present.Children under the age of five and young adults aged 15-29 are the age groups most frequently affected. The incubation period (the time between exposure on onset of the first symptom) is typically two to five days, but onset may occur in as few as 2 days or as long as 10 days after ingestion.1 The illness usually lasts no more than one week; however, severe cases may persist for up to three weeks, and roughly 25% of individuals experience relapses of symptoms. http://www.foodborneillness.com/ecoli1/cam...er-symptoms.htm Foodborne Illness http://www.cdc.gov/ncidod/dbmd/diseaseinfo...nfections_g.htm


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## eric (Jul 8, 1999)

There was a rare outbreak of shigella in 2003 a public fountain on a hot summer in the next town north of where I live. A bunch of childred got very sick. "Fountain closed after users get shigellosis HUBBARD -- Health officials in Marion County have closed a fountain in the small community of Hubbard because of an outbreak of a fecal bacteria. Dr. Karen Landers, Marion County health officer, said that there are three confirmed cases of shigellosis, a highly infectious disease caused by a group of bacteria called shigella. There are eight more suspected cases. No one has been hospitalized. Everyone who has come down with symptoms reported being at the splash fountain at Rivenes Park between July 21 and Friday. Test results of water samples taken from the fountain are expected back Monday. The intestinal infection is usually caused by food or water contaminated by infected persons. Symptoms include fever, bloody diarrhea and abdominal cramps and usually occur one to four days after exposure. The infection is treatable with antibiotics." http://www.theolympian.com/home/news/20030...67539_ARC.shtml Salmonellosis http://www.niaid.nih.gov/factsheets/foodbornedis.htm#f What is Campylobacter jejuni? http://www.foodborneillness.com/ecoli1/cam...er-overview.htm "What are the symptoms of a Campylobacter infection?Diarrhea is the most consistent and prominent manifestation of campylobacter infection. It is often bloody.1 Typical symptoms of C. jejuni infection also include fever, nausea, and vomiting, abdominal pain, headache, and muscle pain. A majority of cases are mild and do not require hospitalization and may be self-limited. However, Campylobacter jejuni infection can be severe and life threatening. Death is more common when other diseases (e.g., cancer, liver disease, and immuno-deficiency diseases) are present.Children under the age of five and young adults aged 15-29 are the age groups most frequently affected. The incubation period (the time between exposure on onset of the first symptom) is typically two to five days, but onset may occur in as few as 2 days or as long as 10 days after ingestion.1 The illness usually lasts no more than one week; however, severe cases may persist for up to three weeks, and roughly 25% of individuals experience relapses of symptoms. http://www.foodborneillness.com/ecoli1/cam...er-symptoms.htm Foodborne Illness http://www.cdc.gov/ncidod/dbmd/diseaseinfo...nfections_g.htm


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## Talissa (Apr 10, 2004)

This was interesting~"Bacteriology can also culture for additional bacteria that are non-pathogens, potential pathogens, and pathogens. These include a-haemolytic Streptococcus, d-haemolytic Streptococcus, Citrobacter freundii, and Klebsiella pneumoniae.Through their ability to trigger bacterial translocation and molecular mimicry, these agents may be involved in various chronic or systemic illnesses seemingly unrelated to gastrointestinal function, such as arthritis and autoimmune disorders.For example, Klebsiella and Proteus are not routinely reported in conventional laboratories, but both have demonstrated antigenic cross reactivity to HLA antigens. Klebsiella has been associated with ankylosing spondylitis when cross reactivity occurs with the HLA-B27 antigen. Similarly, Proteus mirabilis has been associated with reactive arthritis and is known to cross-react with the HLA-DR4 antigen. (96,97)Other potential pathogens may cause clinical and subclinical malabsorption and increase bowel permeability to large molecules. Abnormalities of the immune or mechanical barriers can lead to enhanced uptake of inflammatory luminal macromolecules and pathogenic bacteria. Bacterial antigens are capable of inducing antibodies, which cross-react with host antibodies, forming systemic immune complexes. (98,99) This process has been linked with the etiology of chronic gut inflammation, systemic lupus erythematosus, and arthritis. "I have inflammation of the intestinal wall acc to the cdsa...very close to crossing over into IBD type inflammation, actually. Could be triggered by chronic c freundii infection?The above extract is from a 3 pg article/2 pages references detailing what the great smokies diagnostic lab's CDSA test covers. Really good article: http://www.findarticles.com/p/articles/mi_..._111496953/pg_2 If anyone is interested in GSDL's tests, you can read abt and order them here: http://www.crohns.net/Merchant2/merchant.m...Diagnostic_Test


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## Talissa (Apr 10, 2004)

This was interesting~"Bacteriology can also culture for additional bacteria that are non-pathogens, potential pathogens, and pathogens. These include a-haemolytic Streptococcus, d-haemolytic Streptococcus, Citrobacter freundii, and Klebsiella pneumoniae.Through their ability to trigger bacterial translocation and molecular mimicry, these agents may be involved in various chronic or systemic illnesses seemingly unrelated to gastrointestinal function, such as arthritis and autoimmune disorders.For example, Klebsiella and Proteus are not routinely reported in conventional laboratories, but both have demonstrated antigenic cross reactivity to HLA antigens. Klebsiella has been associated with ankylosing spondylitis when cross reactivity occurs with the HLA-B27 antigen. Similarly, Proteus mirabilis has been associated with reactive arthritis and is known to cross-react with the HLA-DR4 antigen. (96,97)Other potential pathogens may cause clinical and subclinical malabsorption and increase bowel permeability to large molecules. Abnormalities of the immune or mechanical barriers can lead to enhanced uptake of inflammatory luminal macromolecules and pathogenic bacteria. Bacterial antigens are capable of inducing antibodies, which cross-react with host antibodies, forming systemic immune complexes. (98,99) This process has been linked with the etiology of chronic gut inflammation, systemic lupus erythematosus, and arthritis. "I have inflammation of the intestinal wall acc to the cdsa...very close to crossing over into IBD type inflammation, actually. Could be triggered by chronic c freundii infection?The above extract is from a 3 pg article/2 pages references detailing what the great smokies diagnostic lab's CDSA test covers. Really good article: http://www.findarticles.com/p/articles/mi_..._111496953/pg_2 If anyone is interested in GSDL's tests, you can read abt and order them here: http://www.crohns.net/Merchant2/merchant.m...Diagnostic_Test


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## eric (Jul 8, 1999)

Did a real doctor tell you this? And scope you recently and see inflammation of the gut wall linng?"I have inflammation of the intestinal wall acc to the cdsa...very close to crossing over into IBD type inflammation"


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## eric (Jul 8, 1999)

Did a real doctor tell you this? And scope you recently and see inflammation of the gut wall linng?"I have inflammation of the intestinal wall acc to the cdsa...very close to crossing over into IBD type inflammation"


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## eric (Jul 8, 1999)

BecauseNational Digestive Diseases Information ClearinghouseIBS"The lining of the colon (epithelium), which is affected by the immune and nervous systems, regulates the passage of fluids in and out of the colon. In IBS, the epithelium appears to work properly."Were you scooped again recently?


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## eric (Jul 8, 1999)

BecauseNational Digestive Diseases Information ClearinghouseIBS"The lining of the colon (epithelium), which is affected by the immune and nervous systems, regulates the passage of fluids in and out of the colon. In IBS, the epithelium appears to work properly."Were you scooped again recently?


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## eric (Jul 8, 1999)

http://digestive.niddk.nih.gov/ddiseases/pubs/ibs/


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## eric (Jul 8, 1999)

http://digestive.niddk.nih.gov/ddiseases/pubs/ibs/


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## Talissa (Apr 10, 2004)

Hey Eric, Remember the calprotectin test for intestinal inflammation that you posted about a while back? That test along with measuring eosinophil protein X for inflammation are included in the new CDSA 2.0 by gsdl. Not invasive like a biopsy, so no risk of additional infection from the biopsy?A normal's calprotectin level is around 12 mcg/g, while someone with IBD is 50 or over. Mine was 47. A normal's level of EPX is 7 mcg/g, and mine was 42.3...I'd say I have inflammation. Some studies have found that IBS patients have cytokine dysregulation. For ex, too little of the anti-inflammatory IL-10, or too much pro-inflammatory IL-6. My hypothesis is that the ongoing inflammation is causing the D, due to close proximity to nerve trunks, and that I've got a genetic prediposition for the cytokine malfunction in the presence of the pp/c freundii overpopulation due to low bifidobacterium. I just don't know though if by getting rid of the cf, the inflammation/cytokine problem will be resolved. The gut is constantly defending ag pathogens...but then bifidobacteria, which I lack, is one other mechanism which regulates inflammation...so it may be a combo of ridding of the offending baceria & more importantly, re-populating the bifido...I'm just thinking out loud and am not saying this applies to all people diagnosed with IBS...Rather, I think I'm an example of what Dr Hunter says here:"John Hunter, MD, FCRPDirector or GastroenterologyAddenbrooke's HospitalCambridge, United Kingdom "'I.B.S. is organic. That is, all sufferers will eventually be found to have measurable, unique pathologic defects.'When that happy day arrives, the term 'IBS' will no longer be used and each patient will receive a more precise diagnosis." http://www.immunopharma.nl/html/profession...indigestion.asp


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## Talissa (Apr 10, 2004)

Hey Eric, Remember the calprotectin test for intestinal inflammation that you posted about a while back? That test along with measuring eosinophil protein X for inflammation are included in the new CDSA 2.0 by gsdl. Not invasive like a biopsy, so no risk of additional infection from the biopsy?A normal's calprotectin level is around 12 mcg/g, while someone with IBD is 50 or over. Mine was 47. A normal's level of EPX is 7 mcg/g, and mine was 42.3...I'd say I have inflammation. Some studies have found that IBS patients have cytokine dysregulation. For ex, too little of the anti-inflammatory IL-10, or too much pro-inflammatory IL-6. My hypothesis is that the ongoing inflammation is causing the D, due to close proximity to nerve trunks, and that I've got a genetic prediposition for the cytokine malfunction in the presence of the pp/c freundii overpopulation due to low bifidobacterium. I just don't know though if by getting rid of the cf, the inflammation/cytokine problem will be resolved. The gut is constantly defending ag pathogens...but then bifidobacteria, which I lack, is one other mechanism which regulates inflammation...so it may be a combo of ridding of the offending baceria & more importantly, re-populating the bifido...I'm just thinking out loud and am not saying this applies to all people diagnosed with IBS...Rather, I think I'm an example of what Dr Hunter says here:"John Hunter, MD, FCRPDirector or GastroenterologyAddenbrooke's HospitalCambridge, United Kingdom "'I.B.S. is organic. That is, all sufferers will eventually be found to have measurable, unique pathologic defects.'When that happy day arrives, the term 'IBS' will no longer be used and each patient will receive a more precise diagnosis." http://www.immunopharma.nl/html/profession...indigestion.asp


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## eric (Jul 8, 1999)

So you have not seen a doctor and are not going to be scoped again even though you may have Inflammatory bowel disease? IS that what your saying?"That test along with measuring eosinophil protein X for inflammation are included in the new CDSA 2.0 by gsdl. Not invasive like a biopsy, so no risk of additional infection from the biopsy?"A new scope would more accuratly diagnose and confirm the inflammation if you really have any, the above test would not be as accuate as the scope. It may even be misleading. Also the scope would find out where the infallmation is in the digesive linning and epithelium barrier, so the inflammation could be going on, if you have it, anywhere in the digestive tract and could be ulcerating. You may even prhaps be developing a commorbid disorder, an UC or IBD, regarless of IBS. Hence another important reason to see a doctor and be scoped again.Also if you have IBD, or an infection you might start to be experiencing new alarm symptoms, weight loss and fever and perhaps malabsorbition and the d might possibly change to more watery d, as the body trys to dispel the pathogens.From - Report on the 5th International Symposium onFunctional Gastrointestinal DisordersApril 4, 2003 to April 7, 2003 Milwaukee, Wisconsin By: Douglas A. Drossman, M.D., UNC Center for Functional GI and Motility Disorders at Chapel Hill, and William F. Norton, IFFGDBasic Principles -- Brain-Gut Moderators: Emeran Mayer MD; Robin Spiller MD. Panel: Robin Spiller MD; Jackie Wood PhD; George Chrousos MD; Yvette Tachï¿½ PhD; Lisa Goehler PhD; G.F. Gebhart PhD; Emeran Mayer MD. "In tissue mast cells accumulate around nerve endings of nerves that contain the neurotransmitter serotonin. The release of substances that can induce activity in excitable tissue (i.e., histamine, Interleukin-1 (IL-1), and bradykinin) by mast cells can affect receptor and neurotransmitter function in the enteric nervous system - the part of the autonomic nervous system that controls function of the gastrointestinal tract. In other words, when mast cells in the intestinal lining empty their contents in response to an infection, they activate nearby nerve endings. In a subgroup of patients, this can have significance in terms of resulting clinical consequences of diarrhea and abdominal discomfort" http://www.iffgd.org/symposium2003brain-gut.html *But from your own words you do not experience pain? * So there are problems with your theory. *I have also pointed out to you that a person can have inflammation without pain. You don't have pain you say, you also have said inflammation always causes pain. yet you disagree with the experts that inflammation does not always cause pain. So it would seem your contradicting yourself on inflammation and pain?* If however you feel you have inflamation you NEED to be scoped again for your own health sake and not just rely on the gsdl testings , especially if your symptoms have changed or you have new alarm symptoms.""John Hunter, MD, FCRPDirector or GastroenterologyAddenbrooke's HospitalCambridge, United Kingdom "'I.B.S. is organic. That is, all sufferers will eventually be found to have measurable, unique pathologic defects.'"This for the most part has already happened, alreay histologic abnormalities have been found, its just that " NOT ONE SPECIFIC" biological marker has been found in ALL IBSers. All the researchers I know of, talk to and read up on, would and do agree with the above. There are subtypes and subgroups of IBSers all leading to altered motility, viceral hypersensitivity and brain gut axis dysfunction. What is the clinical IBS.Your also quoting an older reference here, which is related to food intolernce and allergy, in a book written in 2002 on food allergy and intolerence." This reference use to be used by an older bb member, who pushed food intolernce and food allergy as a cause of IBS, without presenting a much bigger picture of IBS they already have and know about, and the sales person for that company.However, there is no proof of that and it has been studied extensively and still is, being studied. "In vitro particle size measurement for the purpose of screening hypersensitivity reactions to foods and chemicals is considered *"investigational."*"At present, very few studies have been published involving the use of this test in screening for hypersensitivity reactions to foods and chemicals. One independent study, published by Kaczmarski and colleagues in 1997, involved the Mediator Release Testï¿½ and 21 children with previously confirmed sensitivity to cow's milk." http://www.bcbst.com/MPManual/In_Vitro_Par...d_Chemicals.htm "Brostoff & Challacombe, Second Edition, 2002 Food Allergy and Food IntoleranceJohn Hunter, MD, FCRPDirector or GastroenterologyAddenbrooke's HospitalCambridge, United Kingdom 'I.B.S. is organic. That is, all sufferers will eventually be found to havemeasurable, unique pathologic defects.'When that happy day arrives, the term 'IBS' will no longer be used and eachpatient will receive a more precise diagnosis. Until then, it is sufficient to appreciate that Food Intolerance represents an important proportion of the conditions which together make up I.B.S."" http://www.immunopharma.nl/html/profession...n.asp#the-merck But as both of us have pointed out, already there are histologic abnormalities, that ARE NOT explained by food intolerence and food allergy. Foods are a TRIGGER."Dr Drossman's comments on foods for IBS Health.Shawn Eric,To say that people with IBS may get symptoms from food intolerances is an acceptable possibility, since the gut will over react to stressors of all types including food (high fat or large volumes of food in particular). Futhermore, there can be specific intolerances. So if you have a lactose intolerance for example, it can exacerbate, or even mimic IBS. Other examples of food substances causing diarrhea would be high consumers of caffeine or alcohol which can stimulate intestinal secretion or with the latter, pull water into the bowel (osmotic diarrhea). The same would be true for overdoing certain poorly absorbed sugars that can cause an osmotic type of diarrhea Sorbitol, found in sugarless gum and sugar substituted foods can also produce such an osmotic diarrhea. Even more naturally, people who consume a large amount of fruits, juices or other processed foods enriched with fructose, can get diarrhea because it is not as easily absorbed by the bowel and goes to the colon where it pulls in water. So if you have IBS, all of these food items would make it worse. *However, it is important to separate factors that worsen IBS (e.g., foods as above, stress, hormonal changes, etc.) from the cause or pathophysiology of IBS. Just like stress doesn't cause IBS, (though it can make it worse), foods must be understood as aggravating rather than etiological in nature. * The cause of IBS is yet to be determined. However, modern research understands IBS as a disorder of increased reactivity of the bowel, visceral hypersensitivity and dysfunction of the brain-gut axis. There are subgroups being defined as well, including post-infectious IBS which can lead to IBS symptoms. Other work using brain imaging shows that the pain regulation center of the brain (cingulate cortex) can be impaired, as well as good evidence for there being abnormalities in motility which can at least in part explain the diarrhea and constipation. So finding a specific "cause" of IBS has grown out of general interest in place of understanding physiological subgroups that may become amenable to more specific treatments. Hope that helps.Doug Drossman.Rome Criteria IBSFunctional GI Disorders Coordinating Committee


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## eric (Jul 8, 1999)

So you have not seen a doctor and are not going to be scoped again even though you may have Inflammatory bowel disease? IS that what your saying?"That test along with measuring eosinophil protein X for inflammation are included in the new CDSA 2.0 by gsdl. Not invasive like a biopsy, so no risk of additional infection from the biopsy?"A new scope would more accuratly diagnose and confirm the inflammation if you really have any, the above test would not be as accuate as the scope. It may even be misleading. Also the scope would find out where the infallmation is in the digesive linning and epithelium barrier, so the inflammation could be going on, if you have it, anywhere in the digestive tract and could be ulcerating. You may even prhaps be developing a commorbid disorder, an UC or IBD, regarless of IBS. Hence another important reason to see a doctor and be scoped again.Also if you have IBD, or an infection you might start to be experiencing new alarm symptoms, weight loss and fever and perhaps malabsorbition and the d might possibly change to more watery d, as the body trys to dispel the pathogens.From - Report on the 5th International Symposium onFunctional Gastrointestinal DisordersApril 4, 2003 to April 7, 2003 Milwaukee, Wisconsin By: Douglas A. Drossman, M.D., UNC Center for Functional GI and Motility Disorders at Chapel Hill, and William F. Norton, IFFGDBasic Principles -- Brain-Gut Moderators: Emeran Mayer MD; Robin Spiller MD. Panel: Robin Spiller MD; Jackie Wood PhD; George Chrousos MD; Yvette Tachï¿½ PhD; Lisa Goehler PhD; G.F. Gebhart PhD; Emeran Mayer MD. "In tissue mast cells accumulate around nerve endings of nerves that contain the neurotransmitter serotonin. The release of substances that can induce activity in excitable tissue (i.e., histamine, Interleukin-1 (IL-1), and bradykinin) by mast cells can affect receptor and neurotransmitter function in the enteric nervous system - the part of the autonomic nervous system that controls function of the gastrointestinal tract. In other words, when mast cells in the intestinal lining empty their contents in response to an infection, they activate nearby nerve endings. In a subgroup of patients, this can have significance in terms of resulting clinical consequences of diarrhea and abdominal discomfort" http://www.iffgd.org/symposium2003brain-gut.html *But from your own words you do not experience pain? * So there are problems with your theory. *I have also pointed out to you that a person can have inflammation without pain. You don't have pain you say, you also have said inflammation always causes pain. yet you disagree with the experts that inflammation does not always cause pain. So it would seem your contradicting yourself on inflammation and pain?* If however you feel you have inflamation you NEED to be scoped again for your own health sake and not just rely on the gsdl testings , especially if your symptoms have changed or you have new alarm symptoms.""John Hunter, MD, FCRPDirector or GastroenterologyAddenbrooke's HospitalCambridge, United Kingdom "'I.B.S. is organic. That is, all sufferers will eventually be found to have measurable, unique pathologic defects.'"This for the most part has already happened, alreay histologic abnormalities have been found, its just that " NOT ONE SPECIFIC" biological marker has been found in ALL IBSers. All the researchers I know of, talk to and read up on, would and do agree with the above. There are subtypes and subgroups of IBSers all leading to altered motility, viceral hypersensitivity and brain gut axis dysfunction. What is the clinical IBS.Your also quoting an older reference here, which is related to food intolernce and allergy, in a book written in 2002 on food allergy and intolerence." This reference use to be used by an older bb member, who pushed food intolernce and food allergy as a cause of IBS, without presenting a much bigger picture of IBS they already have and know about, and the sales person for that company.However, there is no proof of that and it has been studied extensively and still is, being studied. "In vitro particle size measurement for the purpose of screening hypersensitivity reactions to foods and chemicals is considered *"investigational."*"At present, very few studies have been published involving the use of this test in screening for hypersensitivity reactions to foods and chemicals. One independent study, published by Kaczmarski and colleagues in 1997, involved the Mediator Release Testï¿½ and 21 children with previously confirmed sensitivity to cow's milk." http://www.bcbst.com/MPManual/In_Vitro_Par...d_Chemicals.htm "Brostoff & Challacombe, Second Edition, 2002 Food Allergy and Food IntoleranceJohn Hunter, MD, FCRPDirector or GastroenterologyAddenbrooke's HospitalCambridge, United Kingdom 'I.B.S. is organic. That is, all sufferers will eventually be found to havemeasurable, unique pathologic defects.'When that happy day arrives, the term 'IBS' will no longer be used and eachpatient will receive a more precise diagnosis. Until then, it is sufficient to appreciate that Food Intolerance represents an important proportion of the conditions which together make up I.B.S."" http://www.immunopharma.nl/html/profession...n.asp#the-merck But as both of us have pointed out, already there are histologic abnormalities, that ARE NOT explained by food intolerence and food allergy. Foods are a TRIGGER."Dr Drossman's comments on foods for IBS Health.Shawn Eric,To say that people with IBS may get symptoms from food intolerances is an acceptable possibility, since the gut will over react to stressors of all types including food (high fat or large volumes of food in particular). Futhermore, there can be specific intolerances. So if you have a lactose intolerance for example, it can exacerbate, or even mimic IBS. Other examples of food substances causing diarrhea would be high consumers of caffeine or alcohol which can stimulate intestinal secretion or with the latter, pull water into the bowel (osmotic diarrhea). The same would be true for overdoing certain poorly absorbed sugars that can cause an osmotic type of diarrhea Sorbitol, found in sugarless gum and sugar substituted foods can also produce such an osmotic diarrhea. Even more naturally, people who consume a large amount of fruits, juices or other processed foods enriched with fructose, can get diarrhea because it is not as easily absorbed by the bowel and goes to the colon where it pulls in water. So if you have IBS, all of these food items would make it worse. *However, it is important to separate factors that worsen IBS (e.g., foods as above, stress, hormonal changes, etc.) from the cause or pathophysiology of IBS. Just like stress doesn't cause IBS, (though it can make it worse), foods must be understood as aggravating rather than etiological in nature. * The cause of IBS is yet to be determined. However, modern research understands IBS as a disorder of increased reactivity of the bowel, visceral hypersensitivity and dysfunction of the brain-gut axis. There are subgroups being defined as well, including post-infectious IBS which can lead to IBS symptoms. Other work using brain imaging shows that the pain regulation center of the brain (cingulate cortex) can be impaired, as well as good evidence for there being abnormalities in motility which can at least in part explain the diarrhea and constipation. So finding a specific "cause" of IBS has grown out of general interest in place of understanding physiological subgroups that may become amenable to more specific treatments. Hope that helps.Doug Drossman.Rome Criteria IBSFunctional GI Disorders Coordinating Committee


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## Jhouston (Nov 9, 2003)

Eric, am curious....what do you think about GSDL? On their site regarding calprotectin they show it as a marker and was tested against IBD patients and the IBD patients had high calprotectin. The whole point of using GSDL is to not risk invasive biopsy. Joann


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## Jhouston (Nov 9, 2003)

Eric, am curious....what do you think about GSDL? On their site regarding calprotectin they show it as a marker and was tested against IBD patients and the IBD patients had high calprotectin. The whole point of using GSDL is to not risk invasive biopsy. Joann


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## eric (Jul 8, 1999)

Drugs Today (Barc). 2001 Feb;37(2):85-96. Related Articles, Links Fecal calprotectin as an index of intestinal inflammation.Tibble JA, Bjarnason I.Department of Medicine, Guy's, King's, St. Thomas's Medical School, London, UK.The assessment of inflammatory activity in intestinal disease in man can be done using a variety of different techniques, from measurement of conventional noninvasive acute-phase inflammatory markers in plasma (C-reactive protein and the erythrocyte sedimentation rate) to the direct assessment of disease activity by intestinal biopsy. *However, most of these techniques have significant limitations when it comes to assessing functional components of the disease that relate to activity and prognosis. * Here we briefly review the value of a novel emerging intestinal function test, fecal calprotectin. Single stool assay of neutrophil-specific proteins (calprotectin, lactoferrin) give the same quantitative data on intestinal inflammation as the 4-day fecal excretion of indium-111-labeled white cells. *Elevated levels of fecal calprotectin have been demonstrated in patients with NSAID-induced enteropathy and have been used in the diagnosis of colorectal cancer. Fecal calprotectin is increased in over 95% of patients with inflammatory bowel disease (IBD) and correlates with clinical disease activity. * *It reliably differentiates between patients with IBD and irritable bowel syndrome (IBS). More importantly, at a given fecal calprotectin concentration in patients with quiescent IBD, the test has a specificity and sensitivity in excess of 85% in predicting clinical relapse of disease.* This suggests that relapse of IBD is closely related to the degree of intestinal inflammation and suggests that targeted treatment at an asymptomatic stage of the disease may be indicated. © 2001 Prous Science. All rights reserved.PMID: 12783101Ned Tijdschr Geneeskd. 2003 Nov 29;147(48):2360-5. Related Articles, Links [Calprotectin: a fecal marker for diagnosis and follow-up in patients with chronic inflammatory bowel disease][Article in Dutch]van den Bergh FA, Kolkman JJ, Russel MG, Vlaskamp RT, Vermes I.Medisch Spectrum Twente, Postbus 50.000, 7500 KA Enschede. f.vandenbergh###ziekenhuis-mst.nlChronic inflammatory bowel disease (IBD) is characterised clinically by periods of well being interspersed by exacerbations of disease activity. Differentiation between IBD and less severe disorders such as irritable bowel syndrome requires invasive and expensive diagnostic procedures." *There are not yet any laboratory parameters with sufficient discrimination in terms of sensitivity and specificity. Colonoscopy and histopathological examination remain the gold standards: in Crohn's disease this may be complex due to the variable localisation of the inflammatory process. "* http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=14677476 Ann Clin Biochem. 2004 May;41(Pt 3):230-2. Related Articles, Links Faecal calprotectin: a new marker for Crohn's disease?Wassell J, Dolwani S, Metzner M, Losty H, Hawthorne A.Department of Medical Biochemistry, Southmead Hospital, Westbury on Trym, Bristol BS10 5NB, UK. julie.wassell###north-bristol.swest.nhs.ukCONCLUSION: * A single calprotectin measurement may aid gastroenterologists in the differential diagnosis of Crohn's disease and IBS. Its use could decrease the number of invasive or radiological investigations undertaken in the latter group of patients.* Inflamm Bowel Dis. 2004 Sep;10(5):661-5. Related Articles, Links C-reactive protein as a marker for inflammatory bowel disease.Vermeire S, Van Assche G, Rutgeerts P.Department of Medicine, Division of Gastroenterology, University Hospital Gasthuisberg, Leuven, Belgium.The production of CRP occurs almost exclusively in the liver by the hepatocytes as part of the acute phase response upon stimulation by IL-6, TNF-alphaand IL-1-betaoriginating at the site of inflammation. *Its short half-life makes CRP a valuable marker to detect and follow up disease activity in Crohn's disease (CD). In contrast, ulcerative colitis has only a modest to absent CRP response despite active inflammation, and the reason for this is unknown. * http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15472532 I would say if you had a Faecal calprotectin test and the results were positive you should be scoped for Inflammatory Bowel Disease or cancer to check for where the inflammation is and what kind of inflammation! As well as blood testing."Colonoscopy and histopathological examination remain the gold standards:"


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## eric (Jul 8, 1999)

Drugs Today (Barc). 2001 Feb;37(2):85-96. Related Articles, Links Fecal calprotectin as an index of intestinal inflammation.Tibble JA, Bjarnason I.Department of Medicine, Guy's, King's, St. Thomas's Medical School, London, UK.The assessment of inflammatory activity in intestinal disease in man can be done using a variety of different techniques, from measurement of conventional noninvasive acute-phase inflammatory markers in plasma (C-reactive protein and the erythrocyte sedimentation rate) to the direct assessment of disease activity by intestinal biopsy. *However, most of these techniques have significant limitations when it comes to assessing functional components of the disease that relate to activity and prognosis. * Here we briefly review the value of a novel emerging intestinal function test, fecal calprotectin. Single stool assay of neutrophil-specific proteins (calprotectin, lactoferrin) give the same quantitative data on intestinal inflammation as the 4-day fecal excretion of indium-111-labeled white cells. *Elevated levels of fecal calprotectin have been demonstrated in patients with NSAID-induced enteropathy and have been used in the diagnosis of colorectal cancer. Fecal calprotectin is increased in over 95% of patients with inflammatory bowel disease (IBD) and correlates with clinical disease activity. * *It reliably differentiates between patients with IBD and irritable bowel syndrome (IBS). More importantly, at a given fecal calprotectin concentration in patients with quiescent IBD, the test has a specificity and sensitivity in excess of 85% in predicting clinical relapse of disease.* This suggests that relapse of IBD is closely related to the degree of intestinal inflammation and suggests that targeted treatment at an asymptomatic stage of the disease may be indicated. © 2001 Prous Science. All rights reserved.PMID: 12783101Ned Tijdschr Geneeskd. 2003 Nov 29;147(48):2360-5. Related Articles, Links [Calprotectin: a fecal marker for diagnosis and follow-up in patients with chronic inflammatory bowel disease][Article in Dutch]van den Bergh FA, Kolkman JJ, Russel MG, Vlaskamp RT, Vermes I.Medisch Spectrum Twente, Postbus 50.000, 7500 KA Enschede. f.vandenbergh###ziekenhuis-mst.nlChronic inflammatory bowel disease (IBD) is characterised clinically by periods of well being interspersed by exacerbations of disease activity. Differentiation between IBD and less severe disorders such as irritable bowel syndrome requires invasive and expensive diagnostic procedures." *There are not yet any laboratory parameters with sufficient discrimination in terms of sensitivity and specificity. Colonoscopy and histopathological examination remain the gold standards: in Crohn's disease this may be complex due to the variable localisation of the inflammatory process. "* http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=14677476 Ann Clin Biochem. 2004 May;41(Pt 3):230-2. Related Articles, Links Faecal calprotectin: a new marker for Crohn's disease?Wassell J, Dolwani S, Metzner M, Losty H, Hawthorne A.Department of Medical Biochemistry, Southmead Hospital, Westbury on Trym, Bristol BS10 5NB, UK. julie.wassell###north-bristol.swest.nhs.ukCONCLUSION: * A single calprotectin measurement may aid gastroenterologists in the differential diagnosis of Crohn's disease and IBS. Its use could decrease the number of invasive or radiological investigations undertaken in the latter group of patients.* Inflamm Bowel Dis. 2004 Sep;10(5):661-5. Related Articles, Links C-reactive protein as a marker for inflammatory bowel disease.Vermeire S, Van Assche G, Rutgeerts P.Department of Medicine, Division of Gastroenterology, University Hospital Gasthuisberg, Leuven, Belgium.The production of CRP occurs almost exclusively in the liver by the hepatocytes as part of the acute phase response upon stimulation by IL-6, TNF-alphaand IL-1-betaoriginating at the site of inflammation. *Its short half-life makes CRP a valuable marker to detect and follow up disease activity in Crohn's disease (CD). In contrast, ulcerative colitis has only a modest to absent CRP response despite active inflammation, and the reason for this is unknown. * http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15472532 I would say if you had a Faecal calprotectin test and the results were positive you should be scoped for Inflammatory Bowel Disease or cancer to check for where the inflammation is and what kind of inflammation! As well as blood testing."Colonoscopy and histopathological examination remain the gold standards:"


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## misummer nightmare (Feb 14, 2003)

HI everyone,I had the great smokies test done just over a year ago. THey found three pathogens: citrobacter freundii, candida albicans and aeromonas sobria (I realise all of these can be found in the gut in healthy individuals too but the test results suggested the levels of them in my gut were playing havoc). The problem was I had to go into hospital soon after as my heart was packing in and my weight plummeting dramatically and I have been spending the last year getting myself on track and my weight up so although the ibs is seriously disrupting my every day life and makes my struggle to fight the anorexia even harder I've had to focus on that rather than my gut. However i am now in a better position to start trying to sort that side of things out but am unsure as to whether the results still stand a year later, whether the remedies advised are still applicable. I am taking threelac for the candida but the remedies suggested for the other pathogens are uva ursi, plant tannins and oregano. I'd be really greatful for advice from Anyone who has experience with this with these products or knows whether the Great smokies results will still be relevant for me, I can't afford to have them done again. Thanks


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## misummer nightmare (Feb 14, 2003)

HI everyone,I had the great smokies test done just over a year ago. THey found three pathogens: citrobacter freundii, candida albicans and aeromonas sobria (I realise all of these can be found in the gut in healthy individuals too but the test results suggested the levels of them in my gut were playing havoc). The problem was I had to go into hospital soon after as my heart was packing in and my weight plummeting dramatically and I have been spending the last year getting myself on track and my weight up so although the ibs is seriously disrupting my every day life and makes my struggle to fight the anorexia even harder I've had to focus on that rather than my gut. However i am now in a better position to start trying to sort that side of things out but am unsure as to whether the results still stand a year later, whether the remedies advised are still applicable. I am taking threelac for the candida but the remedies suggested for the other pathogens are uva ursi, plant tannins and oregano. I'd be really greatful for advice from Anyone who has experience with this with these products or knows whether the Great smokies results will still be relevant for me, I can't afford to have them done again. Thanks


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## Reclamation Project (Jul 12, 2004)

Thanx for all the info everyone!Just one other thing..... I was rather shocked yesterday to hear my nutritionist recommend an antibiotic - so far she has recommended only natural/herbal products, and so after discussing Citrobacter with her I was really surprised for her to recommend the antibiotic route - the antibiotic she recommended was 'EMI Penem'..... has anyone heard of this?I am so reluctant to take antibiotics - the last time I did was about 6 years ago and I was very ill as a result, and my IBS really kicked in for the first time during this period


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## Reclamation Project (Jul 12, 2004)

Thanx for all the info everyone!Just one other thing..... I was rather shocked yesterday to hear my nutritionist recommend an antibiotic - so far she has recommended only natural/herbal products, and so after discussing Citrobacter with her I was really surprised for her to recommend the antibiotic route - the antibiotic she recommended was 'EMI Penem'..... has anyone heard of this?I am so reluctant to take antibiotics - the last time I did was about 6 years ago and I was very ill as a result, and my IBS really kicked in for the first time during this period


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## Talissa (Apr 10, 2004)

RP, That's why I'm very, very reluctant to go the antibiotic route...IMO, that's what got me to IBS. Hair of the dog? Am still going to look up that antibiotic. Let us know if you try it?Eric, The point was the tests showed I DON'T have IBD, but do have IBS with low grade inflammation. So no, if the calprotectin had been 50+, then I'd go in for another colonoscopy but have a biopsy with it this time. The test allowed me to skip that...







MW, good luck! So many of us are in the same boat. Think the key may be finding the right supp's as well as the right diet while taking them...T-


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## Talissa (Apr 10, 2004)

RP, That's why I'm very, very reluctant to go the antibiotic route...IMO, that's what got me to IBS. Hair of the dog? Am still going to look up that antibiotic. Let us know if you try it?Eric, The point was the tests showed I DON'T have IBD, but do have IBS with low grade inflammation. So no, if the calprotectin had been 50+, then I'd go in for another colonoscopy but have a biopsy with it this time. The test allowed me to skip that...







MW, good luck! So many of us are in the same boat. Think the key may be finding the right supp's as well as the right diet while taking them...T-


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## Talissa (Apr 10, 2004)

RP, Do you think it was imipenem? If so, acc to this study at ucsf, it was a VERY good call. Imipenem(as well as Amikacin) gets 100% of the c. freundii...where the following antibiotics all find some resistance to the cf~~Ampicillin;Cefazolin;Cefepime;Cefotaxime;Ceftazidime;Ceftriaxone;Ciprofloxacin; Colistin; Gentamicin;Nitrofurantoin; Piperacillin; Piperacillin/tazobactam; Tobramycin;Trimeth/sulfaThis report is from last year... http://www.ucsf.edu/idmp/antibiogram/pedi_citrobacter.htm


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## Talissa (Apr 10, 2004)

RP, Do you think it was imipenem? If so, acc to this study at ucsf, it was a VERY good call. Imipenem(as well as Amikacin) gets 100% of the c. freundii...where the following antibiotics all find some resistance to the cf~~Ampicillin;Cefazolin;Cefepime;Cefotaxime;Ceftazidime;Ceftriaxone;Ciprofloxacin; Colistin; Gentamicin;Nitrofurantoin; Piperacillin; Piperacillin/tazobactam; Tobramycin;Trimeth/sulfaThis report is from last year... http://www.ucsf.edu/idmp/antibiogram/pedi_citrobacter.htm


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## Reclamation Project (Jul 12, 2004)

Hey Talissa..... thank you for looking it up - yeah it may well be spelt 'imi...'...... my nutritionist is Swedish and we were talking about it on the phone so its very possible the spelling was incorrectI don't suppose you'd know anything about potential side effects would you? I am so hesitant to go on antibiotics but feel its important to get rid of the CF


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## Reclamation Project (Jul 12, 2004)

Hey Talissa..... thank you for looking it up - yeah it may well be spelt 'imi...'...... my nutritionist is Swedish and we were talking about it on the phone so its very possible the spelling was incorrectI don't suppose you'd know anything about potential side effects would you? I am so hesitant to go on antibiotics but feel its important to get rid of the CF


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## Talissa (Apr 10, 2004)

RP, yeh, I found out some side effects...after posting that yesterday, I looked up both imipenem & amikacin...both are ***injected***. Maybe in the UK you have it in oral form? Couldn't find it in my US medical databases.The side effects for amikacin weren't so bad--just things like common loss of hearing and the rare loss of eyesight! OyThese are the side effects for imipenem, which is combined in the US with cilastatin:"More commonConfusion; convulsions (seizures); dizziness; pain at place of injection; skin rash, hives, itching, fever, or wheezing; tremors. Less commonDizziness; increased sweating; nausea or vomiting; unusual tiredness or weakness. RareFever; severe abdominal or stomach cramps and pain; watery and severe diarrhea, which may also be bloody (these side effects may also occur up to several weeks after you stop receiving this medicine). Other side effects may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. However, check with your doctor if the following side effects continue or are bothersome:More commonDiarrhea; nausea and vomiting. Other side effects not listed above may also occur in some patients. If you notice any other effects, check with your doctor." http://www.mayoclinic.com/invoke.cfm?objec...560D20DB86307AE Just a barrel of fun.Think I'll stick with bee propolis and maybe also olive leaf extract, personally. It's too bad these effective synthetic anti's come with such huge risks...always a trade-off.Talissa


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## Talissa (Apr 10, 2004)

RP, yeh, I found out some side effects...after posting that yesterday, I looked up both imipenem & amikacin...both are ***injected***. Maybe in the UK you have it in oral form? Couldn't find it in my US medical databases.The side effects for amikacin weren't so bad--just things like common loss of hearing and the rare loss of eyesight! OyThese are the side effects for imipenem, which is combined in the US with cilastatin:"More commonConfusion; convulsions (seizures); dizziness; pain at place of injection; skin rash, hives, itching, fever, or wheezing; tremors. Less commonDizziness; increased sweating; nausea or vomiting; unusual tiredness or weakness. RareFever; severe abdominal or stomach cramps and pain; watery and severe diarrhea, which may also be bloody (these side effects may also occur up to several weeks after you stop receiving this medicine). Other side effects may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. However, check with your doctor if the following side effects continue or are bothersome:More commonDiarrhea; nausea and vomiting. Other side effects not listed above may also occur in some patients. If you notice any other effects, check with your doctor." http://www.mayoclinic.com/invoke.cfm?objec...560D20DB86307AE Just a barrel of fun.Think I'll stick with bee propolis and maybe also olive leaf extract, personally. It's too bad these effective synthetic anti's come with such huge risks...always a trade-off.Talissa


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## Reclamation Project (Jul 12, 2004)

Wow! Thanx Talissa!There's a flip-side to everything isn't there!!Don't know what to do!


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## Reclamation Project (Jul 12, 2004)

Wow! Thanx Talissa!There's a flip-side to everything isn't there!!Don't know what to do!


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