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07-17-2012, 11:31 PM   #1
kiny
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The many faces of Crohn’s Disease: Latest concepts in etiology

conflict of interest

*Thomas J. Borody has a pecuniary interest in both the Centre for Digestive Diseases and Giaconda Ltd., the licensor of MyocondaTM







07-18-2012, 03:04 AM   #2
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What a fascinating paper - the general premise that CD is an umbrella diagnosis representing a variety of aetiologies makes a lot of sense to me!

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07-18-2012, 03:21 AM   #3
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Very interesting, but one thing bugs me... where does fistula and stenosis stand when it comes to MAP, or the Crohn Syndrome? I like their theory, I just don't know where that part goes though...
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07-18-2012, 10:46 AM   #4
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Very interesting, but one thing bugs me... where does fistula and stenosis stand when it comes to MAP, or the Crohn Syndrome? I like their theory, I just don't know where that part goes though...
They're side effects of the inflammation and the mucosa that got broken down I would think. I only know how MAP works, don't know about E Coli and others. When MAP infects a tissue it causes a granuloma reaction and macrophages surround MAP because it's a pathogen, but because of our genetic predisposition (we have a weakened immune system) we have a hard time clearing the bacteria. MAP infected macrophages release a lot of TNF-alpha, I linked that study that showed it a while ago. So you get continuous inflammation.

There is another study that shows that not only does infliximab lower the inflammation, it has an effect that is almost never mentioned, infliximab is causing apoptosis of macrophages (not all TNF blockers do this btw) , infliximab is working as a type of anti-biotic because it's killing the macrophages MAP is hiding inside. Which could explain why infliximab is perceived as more potent for crohn than some other TNF blockers, because of it's ability to target MAP. There's a number of people who don't respond to infliximab at all btw, and others respond very well, a study suggested that people who have MAP might be the ones responding to infliximab.
07-28-2012, 08:33 AM   #5
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http://www.ncbi.nlm.nih.gov/pubmed/22508665

Multidrug resistance is common in Escherichia coli associated with ileal Crohn's disease.

Dogan B, Scherl E, Bosworth B, Yantiss R, Altier C, McDonough PL, Jiang ZD, Dupont HL, Garneau P, Harel J, Rishniw M, Simpson KW.
Source

Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York. [email protected].


BACKGROUND:


Escherichia coli is increasingly implicated in the pathogenesis of ileal Crohn's disease (ICD), offering a potential therapeutic target for disease management. Empirical antimicrobial targeting of ileal E. coli has advantages of economy and speed of implementation, but relies on uniform susceptibility of E. coli to routinely selected antimicrobials to avoid apparent treatment failure. Therefore, we examined the susceptibility of ileal E. coli to such antimicrobials.

METHODS:

E. coli from 32 patients with ICD and 28 with normal ileum (NI) were characterized by phylogroup, pathotype, antimicrobial susceptibility, and presence of antimicrobial resistance genes.

RESULTS:

In all, 17/32 ICD and 12/28 NI patients harbored ≥1 E. coli strain; 10/24 E. coli strains from ICD and 2/14 from NI were nonsusceptible to ≥1 antimicrobial in ≥3 categories (multidrug-resistant). Resistance to amoxicillin/clavulanic-acid, cefoxitin, chloramphenicol, ciprofloxacin, gentamicin, and rifaximin was restricted to ICD, with 10/24 strains from 8/17 patients resistant to ciprofloxacin or rifaximin (P < 0.01). Adherent-invasive E. coli (AIEC) were isolated from 8/32 ICD and 5/28 NI, and accounted for 54% and 43% of E. coli strains in these groups. In all, 8/13 AIEC strains from ICD (6/8 patients) versus 2/6 NI (2/5 patients) showed resistance to the macrophage-penetrating antimicrobials ciprofloxacin, clarithromycin, rifampicin, tetracycline, and trimethoprim/sulfamethoxazole. Resistance was associated with tetA, tetB, tetC, bla(TEM) , bla(oxa-1) , sulI, sulII, dhfrI, dhfrVII, ant(3″)-Ia, and catI genes and prior use of rifaximin (P < 0.01).

CONCLUSIONS:

ICD-associated E. coli frequently manifest resistance to commonly used antimicrobials. Clinical trials of antimicrobials against E. coli in ICD that are informed by susceptibility testing, rather than empirical selection, are more likely to demonstrate valid outcomes of such therapy.
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