September 30, 2015 at 8:28 pm #154
It is unclear to me when CDiff becomes pathogenic. For example, it is well published (see attached articles) that infants under one year of age can be asymptomatic carriers of both toxigenic and nontoxigenic CDiff. Many infants become negative for CDiff after one year of age spontaneously and labs often refuse to test young babies. Is there any evidence that infants that don’t spontaneously become negative for CDiff have a higher risk of disease down the road – i.e. autism etc; you alluded to its association with celiac and I wonder if you have the original papers for that.
You also mentioned in your talk that adults can be carriers and sources of reinfection. What really defines a carrier from someone with CDiff or Clostridia related disease Is it just that in conventional medicine our definition of CDiff associated disease is limited to pseudomembranous colitis and we have ignored the neurologic disease/metabolic toxicity? Do we just need to redefine our definition of Clostridia related disease?
If you identify a carrier should you treat them?
Thanks and sorry for the multi question post
October 1, 2015 at 8:42 am #157
I don’t know of any evidence of infants with C Diff colonization later becoming autistic. This would be an interesting analysis though.
My comments regarding Celiac was more from the standpoint of potential mucosal damage seen with these conditions, as opposed to a direct link between celiac and C. Diff. – at least that was my intent.
I have recognized that in families, because of the potential for spore transfer, that it can be worthwhile to test other family members if possible. What I was eluding too is testing the Organic Acids or at least the Microbial Organic Acids test for 4-cresol and/or HPHPA evaluation. I don’t see that many C. difficile toxin A and B on stool testing, and have not been successful in obtaining an abundance of stool tests for A and B toxins along with Organic Acids Test for 4-cresol and HPHPA to cross-check. In those where both tests are done the A and B are negative. Therefore, there appear to be more people with C. diff 4-cresol production than the A and B toxin production.
Unfortunately, at this time, the recognition of 4-cresol linked to C. diff isn’t well known. I think redefining C. difficle disorders would be worthwhile knowing that C. diff and other clostridia bacteria can produce compounds that are toxic beyond just gut problems.
P.S. regarding treatment, I feel it is worthwhile trying to eliminate/reduce the C. diff if it is found, but the bulk of detection I see is from the OAT, not stool. However, antibiotics are not commonly needed, and certainly not in an asymptomatic individuals.
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