ultrasctructure of osteomyelitis - biofilms?

[Guest guest]

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/22/6/924

Science, Vol 228, Issue 4702, 990-993

Copyright © 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.pdf

The 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?