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halsgluten
11-01-2006, 07:36 PM
OR

Unrelenting(Unremitting) anti-gliadin antibodies levels?

Under How much gluten = GF? Anne mentioned:

I recentlly had an Enterolab test that showed rising antibody levels after being on a GF diet for over 2 years. My blood tests were negative. ...


From recent readgin I learn that common infections from some (most?) strains of rotavirus or adenovirus elevate anti-gliadin antibodies. A person could be expected to test with higher anti-gliadin antibodies for some time after such infections.

Note, since anti-gliadin antibodies cross-react with other tissues, other gluten sensitive symptoms (ataxia, migraines, rashes, arthritis, etc.) could be aggravated by such infections.

A present hypothesis is that frequent rotavirus or adenovirus infections have the effect of repeated high doses of gluten and thus accelerate early childhood development of Celiac Disease. (see link at bottom) If true, this suggests to me that higher rates of Celiac Disease should occur in communities with high rates of children in daycare.

I also ask whether a person can become “asymptomatic” chronic carriers of rotavirus or adenovirus just as some become asymptomatic carriers of chlamydia or typhus. This is a S.W.A.G., but such a person could have chronically elevated anti-gliadin antibodies or even refractory gluten-sensitive symptoms on the gluten free diet. I suggest a literature search with a report back here. (I’m presently consumed with studying the significances of methane breath-test results.)

I could also ask if disposition towards Celiac Disease also causes weakness against rotavirus or adenovirus infections increased or behavior that increases exposure to viruses (e.g., putting your infants in daycare).

Hal

rotavirus = fever, v*miting, watery diarrhea
adenovirus = lung infection, eye infection, OR diarrhea
S.W.A.G. = Some Wild A**ed (engineer’s) Guess

Rotavirus articles on Celiac.com:
http://www.celiac.com/st_prod.html?p_prodid=1380

annelb
11-01-2006, 11:42 PM
OR


I also ask whether a person can become “asymptomatic” chronic carriers of rotavirus or adenovirus just as some become asymptomatic carriers of chlamydia or typhus.
[

Looks as though a person can be a carrier of rotavirus. Asymptomatic Rotavirus Infections in Day Care Centers http://jcm.asm.org/cgi/reprint/22/1/116.pdf
Anne

Zonulin
11-02-2006, 12:09 AM
I could also ask if disposition towards Celiac Disease also causes weakness against rotavirus or adenovirus infections increased or behavior that increases exposure to viruses - Hal

Seems like all of medicine is some type of genetic trait and/or enviromental exposure which in turn triggers another problem, ad infinum. Vulnerability begets vulnerability. I got 11 hits on PubMed for "rotavirus +celiac," which tells me there's a definite connection there. This interests me because my son began having projectile vomiting and diarrhea from the time he was just a few months old, and this continued a couple times a year until he was about 5. He was so badly dehydrated after a number of these occasions that he had to be hospitalized. We were always told it was "some sort of virus." Don't know if this "virus" was responsible for his eventual elevated Antigliadin IgG antibodies, H. pylori, lack of acetylcholine, elevated levels of mercury and lead, a reaction to 25 different foods, or a "compromised" immune system...? It's a chicken/egg scenario.

I will make it a priority of sorts to sift through those 11 articles...

Karen
We're all in our places/With bright shining faeces...

Zonulin
11-02-2006, 01:14 PM
Okay - here's what I found from those articles (the ones which could be accessed)...

Stene et al. (Oct 06) found that a rotavirus "may increase celiac in those who are genetically predisposed" (HLA DQ2). Zanon et al. (Sep 06) was able to link infection and autoimmunity (celiac) by noting that celiacs who eat gluten have anti-transglutaminase IgA antibodies that "recognize" the viral protein VP-7, which causes an increase in intestinal permeability.

Mehta et al. at the DuPont Institute in Delaware found that rotaviruses can cause "mucosal injury," and that "celiac disease continues to be a puzzle." And then there's this:
: J Hyg (Lond). 1981 Oct;87(2):313-9. Links
Virus diarrhoea associated with pale fatty faeces.Thomas ME, Luton P, Mortimer JY.
Steatorrhoea was a significant feature in an outbreak of rotavirus gastroenteritis which affected adults and infants in hospital. Fat globules or fatty acid crystals were obvious by light microscopy (LM) in faeces from 14 of 25 patients examined. Ten of the fatty stools and two of the remainder were very pale. By electron microscopy (EM) a rotavirus was seen in 11 of the 14 fatty faeces and in only two of 11 specimens without visible fat. In a further study of pale or fatty faeces 20 such specimens sent for laboratory examination from patients not involved in the hospital outbreak were compared microbiologically with a similar number which were neither pale nor fatty. Viruses were found by EM in 11 (55%) of the pale or fatty stools; eight rotaviruses, two astroviruses and an uncultivable adenovirus were seen; one further patient had acute jaundice. In contrast, no viruses were seen by EM in the twenty specimens which were normally pigmented and without evident fat. Steatorrhoea was significantly associated with rotavirus infection of the alimentary tract which usually presented as a fatty enteritis. We conclude that rotaviruses certainly, and other viruses possibly, can impede both the digestion of fat and the pigmentation of the faeces. Inspection and LM of faeces are easy. In acute enteritis a fatty or pale stool is an indication for virological examination.

PMID: 6270209 [PubMed - indexed for MEDLINE]

Seems to me that Enterolab tests for malabsorption by determining the fat in stool samples. And didn't a number of Braintalkers (before the Braintalk crash) mention their childrens' stools were "pale?" :confused:

Karen
We're all in our places/With pale fatty faeces

halsgluten
11-03-2006, 10:31 AM
But Thomas, et. al., were studying acute rotavirus cases.

I want to know if repeated pale fatty stools could indicate chronic rotavirus infection (or just too much transfats).

Hal

(good one, Karen) :)

halsgluten
11-03-2006, 10:40 AM
Zonulin Question

Karin, since you take the name Zonulin, can you answer me these?

Are Vibrio cholerae* bacteria candidates for Small Intestine Bacterial Overgrowth? (SIBO)

Are Vibrio cholerae bacteria methane-generating?**

Hal

* Zonula occludens toxin producers
** Lactulose Breath Test

Zonulin
11-03-2006, 01:46 PM
Are Vibrio cholerae* bacteria candidates for Small Intestine Bacterial Overgrowth? (SIBO)

Are Vibrio cholerae bacteria methane-generating?**

Hey Hal -

Why do you always ask these easy questions? :rolleyes: I did some googling to figure out that Vibrio cholerae is the bacterium of Cholera (both Classic and El Tor) and that it causes "metabolic disturbance of the epithelial cells of the small bowel" and "penetrates the mucus layer" of the aforesaid small bowel. That certainly sounds like it could provide an optimum environment for small intestine bacterial overgrowth. In fact, it sounds a lot like the bacterium H. pylori, which lives in the stomach lining, causes a great deal of damage, and ultimately causes stomach cancer (you cannot get stomach cancer without H. pylori). Of course you've seen this link? http://www.cehs.siu.edu/fix/medmicro/vibri.htm Does a family member have Vibrio cholerae? It is everywhere - on the beaches in California, etc.

I cannot figure out whether Vibrio cholerae is a methylotroph (a bacteria that obtains energy by metabolizing methane: family Methylomonadaceae) or methanogenic (generates methane during metabolism: family Methanobacteriaceae). There are a lot of PDF files out there which take forever to load with our dial-up system...I suspect it generates methane, so a lactulose test might catch it...

I'll do some more sleuthing later. :(

Karen

Zonulin
11-04-2006, 01:46 PM
Oh I get it - you're interested in the Vibrio cholorae because it's been used as sort of a control in gastro-related experiments. That's why it's mentioned in PubMed articles such as this one: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10801176&dopt=Citation. This link, a 6-page PDF file, http://jcs.biologists.org/cgi/reprint/113/24/4435.pdf reports that they used the Vibrio cholerae bacterium because it is a "pathogen confined to the gastrointestinal tract" and presumably cannot break through the spaces made by having too much Zonulin ("tight junction dysfunction").

Karen

halsgluten
11-06-2006, 07:38 PM
I cannot figure out whether Vibrio cholerae ...
Karen

(Hey, KimS, intestinal biofilms)

I’m interested because only because Vibrio cholerae are associated with Zonlulin and because bacterial overgrowth is associated with IBS. OK, Vibro are neither methane producers or eaters. But...

I’m reading up because I’m on an antibiotic course following a methane positive and hydrogen negative Lactulose breath test, and wondering what might be in the overgrowth. (I can’t say how it is going so far, since I seem to have caught a mild influenza in the middle of the course.)

Thank you for the leads. I was able to find the following definitions. It is interesting that Methanobactcriaceae have to live in mixed bacterial colonies to survive in intestines. Some also feed on sulfites/sulfates.

I’ll have a report later on. Input is appreciated.

Hal


Methane Producing Bacteria - They, also known as methanogens represent a highly specialised physiological group. Members of the family Methanobactcriaceae form methane by the reduction of carbon dioxide. They are very strict obligate anaerobes. In order to produce methane they utilise electrons generated in the oxidation of hydrogen or simple organic compounds, such as acetate and methanol

They are unable to use carbohydrates, proteins or other complex organic substrates. Methanogens often form consortia in association with other microbes*. Microbes associated with methanogens maintain the low oxygen tensions and provide the carbon dioxide and fatty acids required by the methanogens. Such associations are extremely important in the rumen of herbivore animals as cow; A major source of atmospheric methane is the rumen of these animals.

Methanobacteriaceae
meth′ă-nō-bak-tēr′ē-ā′sē-ē
Archaea bacteria containing gram-negative and gram-positive, motile or nonmotile, strictly anaerobic rods and cocci, which obtain energy either by the reduction of carbon dioxide to form methane or by the fermentation of compounds such as acetate and methanol with the production of methane and carbon dioxide; they are found in anaerobic habitats such as sediments of natural waters, soil, anaerobic sewage digestors, and the gastrointestinal tract of animals.

jcc
11-06-2006, 08:39 PM
My daughter's problems all began after an illness that appeared to be rotavirus. At least her doctor thought her symptoms seemed like rotavirus, but he never tested for it because he said it just needs to run its course. Of course, looking back, I wished he would have tested so we'd know.

Don't you suppose rotavirus just causes gut damage and those predisposed to gluten sensitivity and /or celiac disease will then experience it. In other words, it is just one of many triggers? And I suppose, in some, if the gut heals...the gluten sensitivity may go away?

I do believe some cases of gluten sensitivity may be secondary to any number of things that may cause gut damage, but since so many things can cause gut damage... it seems the risk of revisiting the problem would continue throughout ones life. NSAIDS damage the gut, too, and may be a cause of "induced" gluten sensitivity.

Hal, did you ever read this? Yet another possibility of secondary gluten/casein sensitivity~

"We've had many patients who were extremely sensitive to dairy and wheat.... and did marvelously after the CF/GF diet. Many of these same patients completely lost their sensitivity to casein and gluten after the antioxidant supplementation..... and now can eat a normal diet without a problem. (Aug 21, 2003) " [NOT Celiac Disease...jcc.. please read in entirety.]
Oxidative Stress by William Walsh (http://www.alternativementalhealth.com/articles/walshMP.htm#Ox)


Cara

Zonulin
11-07-2006, 12:23 PM
Check this out (from www.gsbs.utmb.edu/microbook/ch024.htm ):

Other Vibrio Infections
Other vibrios may be clinically significant also. These include non-O group 1 V cholerae. Vibrio parahaemolyticus, a halophilic (salt-loving) vibrio associated with enteritis is acquired by ingestion of raw or improperly cooked seafoods. Another halophilic vibrio, which ferments lactose and for this reason was called the L + vibrio, has recently been identified as V vulnificus. It has been associated with wound infections as well as fatal septicemias. Other groups of vibrios, previously referred to as group F and EF-6, have recently been classified into species: V fluvialis, V hollisae, V furnissia, and V damsela. Vibrio mimicus is a recently described sucrose-negative species. Vibrio fetus, a group of anaerobic to microaerophilic spirally curved rods associated with venereally transmitted infertility and abortion in domestic animals, is now called Campylobacter jejuni and is considered to belong in the family Spirillaceae rather than in the family Vibrionaceae. Campylobacter jejuni has been associated with dysentery-like gastroenteritis, duodenal and gastric ulcers, as well as with other types of infection, including bacteremic and central nervous system infections in humans (see Ch. 23). Another vibrio-like organism, Helicobacter pylori (formerly known as C pylori) causes gastritis and predisposes to duodenal ulcers and gastric cancer. Although some similarities in habitat and other properties occur, members of the family Vibrionaceae are separated taxonomically from members of the family Enterobacteriaceae. The oxidase test (vibrios are usually oxidase positive) is particularly useful. Other vibrios exist, and some of these may be responsible for diseases in fish and other lower animals. As vibrios are widely distributed in the environment, particularly in estuarine waters and in seafoods, reports of their isolation from patients with diarrheal disease do not necessarily always imply an etiologic relationship.No more clam chowdah for ME! ;)

Karen

halsgluten
11-08-2006, 11:49 PM
"We've had many patients who were extremely sensitive to dairy and wheat.... and did marvelously after the CF/GF diet. Many of these same patients completely lost their sensitivity to casein and gluten after the antioxidant supplementation..... and now can eat a normal diet without a problem. (Aug 21, 2003) " [NOT Celiac Disease...jcc.. please read in entirety.]
Oxidative Stress by William Walsh (http://www.alternativementalhealth.com/articles/walshMP.htm#Ox)
Cara

But, anyone with untreated food sensitivity will have inflammation. Inflammation >>>increases<<< your antioxidant needs! So, even if you are eating normally healthy levels of antioxidant you are deficient with respect to your relative needs. All supplementation (without the GFD) does is mask the symptoms that result form the inflammation soaking up your antioxidants – you are still sensitive and the damages is still going on, just more quietly. The supplements should stop working some day.

Gluten sensitivity is progressive, but its progress can likely come in stages. If you are sensitive after a rotavirus infection, your were likely sensitive before, only less obviously. Rotavirus is both a heavy dose of “gluten” and a punch to your immune system.

Hal