Sep 28, 2007
Slowburn Treatment for Chronic Disease
For years, the notion that bacteria could cause ulcers was brushed aside, until the work of Robin Warren, who “rediscovered” the gut microbe Helicobacter pylori, was finally accepted. More recently, periodontal disease, a bacterial infection of the gums, has been implicated in heart disease, it’s the toxins released by the bacteria that are to blame. And in a recent discussion with one leading researcher about the genetics of obesity, he told me that he considered it more likely that a bacterial infection was more likely to be to blame for some cases of obesity than genetics and conversely there may be bacteria that make some people thin.
Interestingly, Amy Proal of the Bacteriality blog contacted me to tell me that she believes doctors and the medical community are slow to warm to these very new ideas that bacteria might be to blame for chronic disease and obesity.
“The evidence is overwhelming if you connect the dots,” Proal, a Biology graduate and chronic fatigue syndrome (CFS) sufferer told me, “Particularly interesting is the work of researcher Trevor Marshall who is using molecular modelling software to reveal many of the ways bacteria can interact with our innate immune system.
Marshall is known for his eponymous Protocol, which uses low doses of antibiotics to apparently treat chronic health problems including CFS, fibromyalgia, and rheumatoid arthritis and a growing list of other problems.
Key to the Protocol is the concept of “L-form bacteria. Bacteria that develop from classical bacteria, lose their cell walls, and then secrete themselves within white blood cells and biofilms, undetected. It’s that word “undetected” that should set alarm bells ringing, how do we know they’re there if they are undetected. This whole new biological arena exists only in Marshall’s computer simulations as far as I know.
The Marshall Protocol is said to target these so-called L-form bacteria and there are apparently thousands of patients with a variety of chronic illnesses undergoing this form of treatment and reportedly seeing serious improvement and even resolution of their symptoms. Of course, there aren’t any control patients being given a placebo (under double blind control, as far as I am aware), which makes it all seem a little too good to be true…
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@David There is a large body of research on l-forms. Did you see Amy’s article on l-forms? Have a look at the references at the bottom.
http://bacteriality.com/2007/08/15/l-forms/
By the way, for the record the Marshall Pathogenesis implicates other bacterial forms in disease including biofilm bacteria. Biofilm bacteria produce Capnine, which downregulates Vitamin D Receptor activity. Recent research has shown that other pathogens including M. tuberculosis, EBV, etc. downregulate VDR transcriptional activity as well But I digress.
@Paul Some of those links gave up errors. At least one is to a paper by Marshall, the other to Emmy Nobel’s work from the 1930s. Others are reviews. Is there a current independent research group demonstrating strong evidence of the L-form? It seems that the existence or otherwise of these “organisms” is still open to debate.
There are a fair number of studies on l-forms. Try searching PubMed for “l-form.” As you’ll be able to see, there are a variety of groups “confirming the existence” of these forms. Then have a look at the Domingue article (mentioned below) and the photos he took of the forms.
One researcher who is currently working with the L-form is Nadya Markova, who was interviewed by Amy on Bacteriality:
http://bacteriality.com/2007/09/09/markova-interview/
Another researcher who retired within the last ten years is Gerald Domingue, who was also profiled by Amy:
http://bacteriality.com/2007/08/22/domingue/
Why hasn’t there been more recent work on l-forms? I’m not sure exactly. I do know that culturing these “wee beasties” is difficult and that many researchers still adhere to Koch’s Postulates, which Amy has also discussed on good ol’ Bacteriality.
Sorry about the dead links. I have to update the links on that page.
Okay. Thanks for that Paul
David,
These responses have been interesting. You might find the following easily-found website quotes from Scientific American articles interesting. I’ve cut out a lot but you can find these quotations in context in the articles linked:
http://www.scientificamerican.com/article.cfm?id=recruiting-a-dangerous-foe&sc=rss
May 21, 2008
Recruiting a Dangerous Foe to Fight Cancer and HIV
“… Listeria monocytogenes bacterium is the infectious agent responsible for the food borne illness Listeriosis.”
“… L. monocytogenes replicates in a host cell’s cytoplasm (its gelatinous fluid filling) and can move from one cell to another.”
… “Listeria lives within cells, instead of floating around the bloodstream.”
http://www.scientificamerican.com/article.cfm?id=a-pathogens-wily-ways
November 6, 2000
A Pathogen’s Wily WaysA Pathogen’s Wily Ways
… “the world’s top three infectious killers, … convert the cell into a microbial manufacturing plant. After multiplying, the microbes break out of the cell and go on to invade other cells, repeating the process. Details of these events have eluded investigators because such intracellular pathogens are difficult to study.”
… “scientists have finally learned how one microbe, the food-borne bacterium Listeria monocytogenes (which can lead to meningitis and death), accomplishes this feat. The new findings could shed light on how other deadly pathogens operate.”
“Listeria bacteria, it turns out, have a remarkable mechanism for establishing infection. First they prompt immune system scavenger cells called macrophages to ingest them such that they wind up enclosed in bubbles called vacuoles inside the cells. The Listeria then make a toxin known as listeriolysin O, which is used to rupture the vacuole, gaining entry into the cell’s interior. It subsequently coopts the cell machinery in order to replicate.”
David, the last reference I am going to give here is to the Wikipedia article on Listeria at:
http://en.wikipedia.org/wiki/Listeria
It covers much the same territory (and many other aspects) and gives numerous references.
Here is a relevant section:
/***
Mechanism of infection
The majority of Listeria bacteria are targeted by the immune system before they are able to cause infection. Those that escape the immune system’s initial response, however, spread though intracellular mechanisms and are therefore guarded against circulating immune factors (AMI).[2]
To invade, Listeria induces macrophage phagocytic uptake by displaying D-galactose in their teichoic acids that are then bound by the macrophage’s polysaccharide receptors . Other important adhesins are the internalins. [3] Once phagocytosed, the bacteria is encapsulated by the host cell’s acidic phagolysosome organelle. [1] Listeria, however, escapes the phagolysosome by lysing the vacuole’s entire membrane with secreted hemolysin, [4] now characterized as the exotoxin listeriolysin O.[1] The bacteria then replicate inside the host cell’s cytoplasm. [2]
Listeria must then navigate to the cell’s periphery to spread the infection to other cells. Outside of the body, Listeria has flagellar-driven motility, sometimes described as a “tumbling motility.” However, at 37°C, flagella cease to develop and the bacteria instead usurps the host cell’s cytoskeleton to move. [2] Listeria, inventively, polymerizes an actin tail or “comet” [4], using host-produced actin filaments [5] with the promotion of virulence factor ActA[2]. The comet forms in a polar manner [6] and aids the bacteria’s migration to the host cell’s outer membrane. Gelsolin, an actin filament severing protein, localizes at the tail of Listeria and accelerates the bacterium’s motility.[6] Once at the cell surface, the actin-propelled Listeria pushes against the cell’s membrane to form protrusions called filopods[1] or “rockets”. The protrusions are guided by the cell’s leading edge [7] to contact adjacent cells which subsequently engulf the Listeria rocket and the process is repeated, perpetuating the infection.[2] Once phagocytosed, the Listeria is never again extracellular: it is an intracytoplasmic parasite [4] like Shigella flexneri and Rickettsia.[2]
***/
The implication that struck me the hardest is that Listeria not only lives intracellularly inside human macrophages, but actually seems to “try” hard to get eaten! It seems this comfy existence inside our own cells, hijacking our cells’ machinery, is not unusual, but something of the norm.
I hope I’m not violating copyright laws to give these quotes without permission. The links will take you to the originals. When I said you could find many references on the web to L-form bacteria, I was referring to quotes like these. There are others.