Intrigued, I of course had to hunt down the primary literature of these claims (tsk tsk, Professor Ayers!). Below is a compilation of my favorite excerpts; this is a beautifully put together review paper by Rashid et al 2009.
"Klebsiella microbes have been isolated from the large bowel biopsy specimens in more than 25% of patients with CD or UC , and relapses in patients with CD were found to be associated with Klebsiella intestinal infections . In a study using immunohistochemistry, however, it has been observed that the majority of patients with IBD had negative staining
specimens for E. coli, L. monocytogenes and K. pneumoniae taken from the bowel mucosa . These latter findings indicate that it is the microbial bulk in the intestinal lumen rather than at the sites of the pathological lesions, which is important in evoking both local mucosal and general antibacterial immune responses.
"Elevated levels of antiKlebsiella antibodies have been reported in patients with CD from six different centres in the UK (Table 2). Significantly elevated levels of antibodies against K. pneumoniae and Y. enterocolitica microbial agents were observed in patients with CD and UC when compared with healthy controls . Similar findings were later shown by other groups from Scotland, where IgA antibody levels against K. pneumoniae were found to be elevated in patients with AS and IBD [49,50].
"Klebsiella microbes possess a powerful debranching enzyme, pullulanase, which is a molecular complex consisting of 17 components and some of these exhibit molecular mimicry with several collagens. pulA cross-reacts with collagens I, III and IV ... Significantly elevated levels of antibodies against Klebsiella microbes as well as autoantibodies to collagens I, III and IV were observed in patients with AS and CD .
"The hypothesis proposed is that exposure to the cross-reactive antigens of pulA found in Klebsiella pullulanase leads to the production of autoantibodies that can have a pathological effect on the collagens found in the intestinal mucosa and eventually lead to the characteristic lesions of established CD (Fig. 2).
"In a study carried out by a group from Los Angeles, it was observed that the mean number of faecal Klebsiella microorganisms in individuals taking high-carbohydrate/ low-protein diet was 40 times higher than in those individuals receiving low-carbohydrate/high-protein diet . In a comparative study, it has been observed that the mean number of Klebsiella was 10 times higher for simple sugars per gram of substrate compared with the value obtained after incubation with 11 different amino acids .
"A clear link is observed between increased intake of starch and the bulk of intestinal microflora, among which Klebsiella microbes constitute an important part. High dietary starch intake leads to increased growth of these microbes in the bowel."But what about the provision of hydrogen gas to H. pylori by an intestinal Klebsiella bloom?
Crohn's patients have a heightened immuno-sensitivity to Klebsiella microflora (Rashid et al 2009).
Klebsiella yields a high molar ratio of hydrogen per starch (Chen et al 2005).
Hydrogen gas feeds H. pylori (Olson et al 2004).
Klebsiella feeds on starches, mono- and disaccharides (Rashid et al 2009).
Ergo: starve out the Klebsiella with a low starch/carbohydrate diet, and in doing so, starve out the H. pylori. Lowering your H. pylori levels, if this particular bacterium is a prominent contributor to your Crohn's, IBS or Colitis, may substantially alleviate a great deal of epithelial destruction, and suppress the inflammatory response. I like it. Go, science!
In other, more important news, last night was homemade sushi and Star Trek night. Tuna, crab, Tofutti BTCC, avocado, Insurrection. There are just too few relaxing evenings that even come close to challenging that.