Advances in Probiotics

Fructose intolerance is now known to be due to the upsurge in activity of particular bacteria in the intestine which rapidly metabolise fructose and produce toxins that produce the symptoms. There are some questions over inulin which is a branched-chain molecule made up of fructose molecules. Does inulin, which should, by rights, be more slowly metabolised than single units of fructose, produce the same effects as fructose. Also, if inulin is consumed with a probiotic which utilises fructose and inulin, does it offset that effect by suppressing the bad bacteria? Any comments?

A woman who was successfully treated for Helicobacter pylori (the stomach ulcer bug) with antibiotics, reported that she suffered bloating (a common side-effect of antibiotic treatment). She states that she effectively controls it by taking Entralive.

Kelly GS.

Labels: arabinogalactan, immune system., probiotics

Interesting feedback from a family with an autistic son. The son has epileptic fits associated with his autistic/aspergers symptoms. A new synbiotic, Entralive LoAlaG, was seen to alleviate the child's autistic tendancies and at the same time to reduce fitting. The father reports that if he doesn't take the product he fits in 12+/-1 hours. As many as 26% of autistic children suffer from epilepsy.
Autism has been shown to be associated with high levels of certain Clostridia in the colon of the sufferer. Often the Clostridium concerned is Cl. tetani; often it is, as yet unnamed, Clostridia which are different to those in normal individuals. Cl. tetani, which causes tetanus, does so by producing a neurotoxin which affects nerve function and is thought to induce the autistic symptoms. One pointer to the fact that an abherent intestinal microflora is involved is the fact that autistic children usually suffer from bowel problems.
Entralive contains cultures that were selected by researchers from CSIRO, Division of Dairy Research in Melbourne to be able to most effectively inhibit the multiplication of Clostridia and other pathogenic bacteria.

Labels: Autism, Clostridia, intestine., probiotics

Implantation of Bacteroides assisted by Methanobrevibacter smithii.

(This was sent to me by Kevin and it could have significant implications for attempts to implant Bacteroides, which normally makes up 30-50% of the bacteria in the bowel and which seems to have a controlling role. It has been shown to be able to displace Clostridium dificile, a major cause of post-antibiotic diarrhoea.)

Please see:http://www.nature.com/news/2006/060522/full/060522-19.htmlA recent study in mice has highlighted the importance of methanogenic bacteria in the intestines for efficient digestion of food. The mouse model system used is rather artificial, but could have implications for obesity.Samuel Buck of Washington University in St Louis, Missouri presented the results at the American Society for Microbiology meeting in Orlando, and will publish them shortly in the Proceedings of the National Academy of Sciences.Paraphrasing from the article:"The researchers took mice that had been grown in a sterile environment, with no microbes in their guts, and injected them with a very common strain of human intestinal bacteria, called Bacteroides thetaiotaomicron. Some of the mice also received a dose of of Methanobrevibacter smithii, which is effectively a waste-removal bug. M. smithii acts by clearing waste products and hydrogen produced by other bacteria, and so helps other gut bacteria digest some of the fibrous components of food that we cannot, and turn them into material that our bodies can use. Without these bugs, waste accumulates and blocks the activity of other gut bacteria.About 100 times more microorganisms took up residence in the colon of mice injected with both B. theta and M. smithii than in those injected with B. theta alone. This suggests that the presence of waste-removing M. smithii was somehow helping other bacteria to thrive. The researchers found that mice with a hefty dose of M. smithii in their guts are fatter than those that don't have the bacteria".

Autism can be considered to be an infection.
In Clin Infect Dis. 2002 Sep 1;35(Suppl 1):S6-S16, Finegold et al report the correlation between the presence of intestinal spore-forming bacteria and late-onset autism.
"Some cases of late-onset (regressive) autism may involve abnormal flora because oral vancomycin, which is poorly absorbed, may lead to significant improvement in these children. Fecal flora of children with regressive autism was compared with that of control children, and clostridial counts were higher. The number of clostridial species found in the stools of children with autism was greater than in the stools of control children. Children with autism had 9 species of Clostridium not found in controls, whereas controls yielded only 3 species not found in children with autism. In all, there were 25 different clostridial species found. In gastric and duodenal specimens, the most striking finding was total absence of non-spore-forming anaerobes and microaerophilic bacteria from control children and significant numbers of such bacteria from children with autism. These studies demonstrate significant alterations in the upper and lower intestinal flora of children with late-onset autism and may provide insights into the nature of this disorder."
This theme is further developed in a paper entitled "Real-time PCR quantitation of clostridia in feces of autistic children.Appl Environ Microbiol. 2004 Nov;70(11):6459-65 by Song Y, Liu C and Finegold SM. They conclude the following:-
"Based on the hypothesis that intestinal clostridia play a role in late-onset autism, we have been characterizing clostridia from stools of autistic and control children. We applied the TaqMan real-time PCR procedure to detect and quantitate three Clostridium clusters and one Clostridium species, C. bolteae, in stool specimens. Group- and species-specific primers targeting the 16S rRNA genes were designed, and specificity of the primers was confirmed with DNA from related bacterial strains. In this procedure, a linear relationship exists between the threshold cycle (CT) fluorescence value and the number of bacterial cells (CFU). The assay showed high sensitivity: as few as 2 cells of members of cluster I, 6 cells of cluster XI, 4 cells of cluster XIVab, and 0.6 cell of C. bolteae could be detected per PCR. Analysis of the real-time PCR data indicated that the cell count differences between autistic and control children for C. bolteae and the following Clostridium groups were statistically significant: mean counts of C. bolteae and clusters I and XI in autistic children were 46-fold (P = 0.01), 9.0-fold (P = 0.014), and 3.5-fold (P = 0.004) greater than those in control children, respectively, but not for cluster XIVab (2.6 x 10(8) CFU/g in autistic children and 4.8 x 10(8) CFU/g in controls; respectively). More subjects need to be studied. The assay is a rapid and reliable method, and it should have great potential for quantitation of other bacteria in the intestinal tract."
Another paper by Parracho HM, Bingham MO, Gibson GR, McCartney AL entitled "Differences between the gut microflora of children with autistic spectrum disorders and that of healthy children." has been published in J Med Microbiol. 2005 Oct;54(Pt 10):987-91.
The abstract reads "Children with autistic spectrum disorders (ASDs) tend to suffer from severe gastrointestinal problems. Such symptoms may be due to a disruption of the indigenous gut flora promoting the overgrowth of potentially pathogenic micro-organisms. The faecal flora of patients with ASDs was studied and compared with those of two control groups (healthy siblings and unrelated healthy children). Faecal bacterial populations were assessed through the use of a culture-independent technique, fluorescence in situ hybridization, using oligonucleotide probes targeting predominant components of the gut flora. The faecal flora of ASD patients contained a higher incidence of the Clostridium histolyticum group (Clostridium clusters I and II) of bacteria than that of healthy children. However, the non-autistic sibling group had an intermediate level of the C. histolyticum group, which was not significantly different from either of the other subject groups. Members of the C. histolyticum group are recognized toxin-producers and may contribute towards gut dysfunction, with their metabolic products also exerting systemic effects. Strategies to reduce clostridial population levels harboured by ASD patients or to improve their gut microflora profile through dietary modulation may help to alleviate gut disorders common in such patients."
Read more at http://www.neurotransmitter.net/autismclostridia.html or by putting "clostridia +autism" into Google.

Some interesting work is being done in the area of leaky gut syndrome. It is beginning to be acknowledged now in bona fide research circles that bacterial translocation may be associated with the development of auto-immune diseases. Although medical science is only just beginning to catch up with the naturopaths in this regard (never thought I'd say something like that!) it is becoming clear that such problems are not all due to Candida overgrowth up the small intestine. It now seems far more likely that many of these food sensitivity and autoimmune conditions are due to overgrowth with good old E. coli. Certainly, the previously quoted cross-reaction between the lac7 gene of E. coli and the antibodies associated with lupus supports this case.
See below for one piece of the puzzle.
http://www.childrenshospitalla.org/body.cfm?id=75&action=detail&ref=131
Michelle M. Pietzak, MD
Assistant Professor
Research Interest
Bacterial Translocation of the Gastrointestinal Tract
Phone
(323) 669-2181
Fax
(323) 664-0718
Email
mpietzak@chla.usc.edu

Escherichia coli K1 Interactions with Intestinal Epithelium

Dr. Pietzak's research focuses primarily on the mechanisms by which E. coli is able to translocate across the intestinal epithelium. This pathogen is then able to disseminate systemically, causing sepsis and meningitis. E. coli is a leading cause of severe bacterial infections in premature infants, neonates, immunocompromised hosts, and children with central lines and primary intestinal diseases. Enteric pathogens may also serve as a trigger to the development of autoimmune gastrointestinal diseases, such as celiac disease and Crohn's disease, in genetically susceptible individuals. E. coli strain RS218 is the clinical isolate from the cerebrospinal fluid of an infant with E. coli meningitis. Dr. Pietzak's research focuses on investigating the mechanisms by which RS218 is able to penetrate the intestinal epithelial barrier. Enteric bacteria may contribute to the development of inflammatory bowel diseases by directly damaging the intestinal mucosa or by the translocation of whole bacteria or bacterial products. Via translocation, specific microbial components (such as E. coli OmpC) can gain access to the lamina propria and potentially activate or regulate adaptive immune responses involved in intestinal inflammation. Adherent and invasive E. coli strains have recently been reported to be associated with both Crohn's disease and ulcerative colitis. In addition, antibodies to numerous E. coli antigens, such as OmpC and S-fimbriae, have been found with increased frequency in patients with inflammatory bowel disease and immune-deficient states. Translocation of bacteria across the intestinal epithelial barrier first involves binding and invasion of the enterocyte. E. coli K1, a common enteric organism, is able to translocate the gut barrier and disseminate, causing meningitis in susceptible hosts. Dr. Pietzak has identified two virulence factors in E. coli K1, which are important in E. coli-small bowel enterocyte interactions: the S-fimbriae operon for binding and gene ibeA for invasion. Deletion of the S-fimbria operon abrogates the ability of E. coli K1 to bind, invade and translocate intestinal epithelium in vitro and in neonatal rats in vivo. Deletion of ibeA renders E. coli K1 less effective at invasion in vitro, and leads to less dissemination, sepsis and meningitis in the neonatal rat. Complementation with ibeA restores the invasive phenotype. Furthermore, the E. coli K1 parent strain induces a particular type of small bowel damage located at the villous tips where bacteria are in direct contact. The mechanism of this damage is the subject of ongoing research, which will utilize various techniques to study apoptosis of the intestinal epithelial cell in response to E. coli K1, both in vitro and in vivo. The contributions of S-fimbriae and ibeA to this particular type of small bowel injury will be examined. Further investigations regarding the importance of S-fimbriae and gene ibeA in E. coli K1 bacterial translocation may lead to novel therapeutics in both the treatment and prevention of inflammatory bowel disease.

Neurological disorders: Are they infections?
In one study, 90 percent of the brains of Alzheimer's victims contained the pneumonia bacteria, Chlamidia pneumoniae while only 5 percent of non-Alzheimer's brains contained the same bacteria. Read more at....
http://www.usnews.com/usnews/health/briefs/alzheimers_neurological/hb041102.htm

In the case of MS, there is evidence for an association of the disease with chronic bacterial and viral infections. Chmielewska-Badora et al. [10] found that 38.5% of MS patients showed evidence of Borrelia antigens in their blood, whereas other neurological patients carried these antigens in blood at a lower prevalence (19%). Chlamydia pneumoniae has also been found in a subgroup of MS patients [11]. By examining cerebral spinal fluid (CSF) these authors found that 10% of MS patients and 18% of patients with probable MS had Chlamydia infections but none of 56 control patients with other neurological disease were positive [11]. Read more at......
http://www.fibromyalgiasupport.com/library/showarticle.cfm/ID/4243/e/1/T/CFIDS_FM/

...evidence that the bacteria (C. pneumoniae) could be involved in the disease (MS) came from the Subramaniam Sriram’s team at the Vanderbilt University Multiple Sclerosis Center in Nashville, Tenn. He previously reported that 97 percent of MS patients had evidence of C. pneumoniae infection in the central nervous system, compared with only 16 percent in patients with other neurological diseases.
More importantly, Chlamydia antigens precipitated out of the oligoclonal bands. “That’s an amazing result – nobody had been able to do that before and the existence of these bands has been known about for more than 60 years,” Dr. Lenz said.
Now Dr. Lenz and his colleagues have taken the work a stage further. By searching through the chlamydial genome, they found a region coding for a protein fragment that closely resembled the MBP 68-86 region of the myelin protein known to be the main target in EAE. Both peptides were found to activate the T cells that stimulate the encephalitis response, and affected rats showed similar signs of disease. Read more at...
http://www.med.wayne.edu/Scribe/scribe01-02/winter02/a-bacterial%20genomics%20reveals%20ms%20trigger.htm

It has been noted that certain neurological diseases have accompanying gastrointestinal manifestations, particularly constipation and diarrhea. This suggests the possibility that an intestinal microorganism may be the cause of both aspects of the disease. In turn, this implies that appropriate antimicrobial therapy might lead to improvement in both gastrointestinal and the neurological aspects. This has been demonstrated in late onset autism (response has been demonstrated with the administration of oral vancomycin and metronidazole), and there are isolated anecdotal reports of improvement in patients with Alzheimer’s disease, schizophrenia, and Parkinson’s disease. Additional diseases that might have similar pathogenesis include attention deficit hyperactivity disorder (ADHD), depression, bipolar disorder, Whipple’s disease, Tourette’s syndrome, Asperger’s syndrome, and Rhett’s syndrome. Disrupted gut microbial flora can also lead to antimicrobial-associated diarrhea and play a role in irritable bowel syndrome and inflammatory bowel disease (ulcerative colitis and Crohn’s disease).
Read more at....
http://www.vard.org/tts/avail/00-075.htm

Could probiotic preparations containing immune-stimulating species such as L. acidophilus LAFTI strain L10 and B. lactis LAFTI strain B94, which also have the ability to suppress intestinal populations of pathogenic bacteria, be a useful adjunct in the treatment of neurological disorders?

Are probiotic yoghurts potent enough to do any good?
The de facto standard for the level of probiotic cells in probiotic yogurts at the end of shelf-life is generally accepted to be in Australia 10^6 (one million) cfu (colony forming units)/g. At the beginning of shelf life, an AB (acidophilus/bifidus) yogurt that meets that standard needs to have around 10^7 cfu/g. The Lactobacillus acidophilus count will then meet the standard at the best before date but the bifido in all likelyhood will not. Bifidobacterium lactis strains will have dropped to around 10^5 cfu/g and if they use human strains such as B. infantis it will have dropped a log or two more, which makes the latter pretty useless.