Re: ultrasctructure of osteomyelitis - biofilms?

[Guest guest]

Well, many of us with OM have believed bio-films are a big part of our problem for quite a while. That's why I usually post anything I come across on the subject. Beyond thinking biofilms are involved in OM (and probably most infections) I really haven't known what to do about them. Biofilms seem to be pretty impossible to eradicate. This is why I think that many people's illnesses are originating in sinuses (or bone) that are easily affected by biofilms, even though there are no overt signs of it. Those places are great breeding grounds for the biofilms. For example, it doesn't matter how many sinus surgeries people have, those biofilms are going to come back. As far as eradicating them. There is some evidence that vitamin C breaks down biofilms, and I've wondered aloud more than once if this might explain why some people seem to be doing well with the salt/C

combo, as that simple combo addresses a multitude of our issues with a very straight forward and bare bones approach. If you can find some other possible approaches to breaking down these biofilms, I will be more than happy to test them out for you. :-) penny <usenethod@...> wrote: At least one

paper I read has suggested that the "indolent" course and abx-refractory nature of osteomyelitis may well be due to intracellular location of the organisms.So I searched "osteomyelitis ultrastructure" assuming there would be TEM evidence of an intracellular locus.Apparantly not. I can't find anything like that. Instead there seems to be evidence that biofilms are found:Free text: http://jcm.asm.org/cgi/content/abstract/22/6/924Science, Vol 228, Issue 4702, 990-993Copyright © 1985 Adherent bacterial colonization in the pathogenesis of osteomyelitis Direct scanning electron microscopy of material obtained during surgical debridement of osteomyelitic bone showed that the infecting bacteria grew in coherent microcolonies in an adherent biofilm so extensive it often obscured the infected bone surfaces. Transmission

electron microscopy showed this biofilm to have a fibrous matrix, to contain some host cells, and to contain many bacteria around which matrix fibers were often concentrated. Many bacterial morphotypes were present in these biofilms, and each bacterium was surrounded by exopolysaccharide polymers, which are known to mediate formation of microcolonies and adhesion of bacteria to surfaces in natural ecosystems and in infections related biomaterials. The adherent mode of growth may reduce the susceptibility of these organisms to host clearance mechanisms and antibiotic therapy and thus may be a fundamental factor in acute and chronic osteomyelitis. How did I not hear about biofilms possibly being involved? Where are the confirmations? Neither paper seems to have been cited very much. Well, this recent paper, which I can't access, seems rather confident about the role of biofilms:August 2005, 437: Biofilm

Theory Can Guide the Treatment of Device-Related Orthopaedic Infections. Clinical Orthopaedics & Related Research. 437:7-11, August 2005.Costerton, J PHD Abstract: Direct observations of the surfaces of orthopaedic prostheses that have failed and of bone affected by osteomyelitis with and without the presence of a prosthesis have shown that the bacteria that cause these infections live in well-developed biofilms. The cells within these matrix-enclosed surface-associated communities are protected from host defenses and antibiotics, and clinical experience has shown that they must be removed physically before the infection can be resolved. The biofilm etiology of these diseases demands new diagnostic methods because biofilm cells typically do not grow on agar plates when recovered by scraping or swabbing. I will recommend new molecular and immunologic diagnostic methods that have been useful in

other biofilm infections. These diseases progress through quiescent periods that alternate with acute exacerbations, and clinicians must realize that antibiotic therapy can control the acute phases but cannot resolve the basic biofilm nidus of the infection. Now that it has been realized that these orthopaedic infections are caused by relatively common biofilm-forming bacterial pathogens, new technologies that deliver very high concentrations of antibiotics locally and "on demand" and novel molecular "mimics" that block the signals that control biofilm formation need to be examined.So if in fact biofilms are at the heart of osteomyelitis (including non-prosthetic osteomyelitis), the question becomes why and how do they form, and, how and why the resistance to drugs (low growth rate, stress responses, etc). These things have been studied by K , K Poole, and others, but I haven't paid the greatest attention to

biofilm stuff in the past.This paper is interesting for saying that the generation time of Sa in experimental osteomyelitis is ~20h. Presumably this rate was measured sometime during the early phase of the disease. http://jcm.asm.org/cgi/reprint/27/11/2403.pdfThe paper cites nutrient restriction including iron restriction as a probable partial cause. But where are the effects of this iron restriction when people have fulminant Sa sepsis?