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Be well, Mike D.

Oops! I've removed some material; my apologies to you both. M.

Hi Mike, [Monett]
I'm not interested in debate; I gave you some information, which you
have justifiably - from your point of view - questioned. I hope I have
presented enough additional material to reduce your doubt - and lack of
familiarity - in the field to curiosity. Pursue the subject rather
than my presentation, it's fascinating!

Take care, Malcolm

> > Check this out:
> > Cell Wall Deficient Forms: Stealth Pathogens / Lida H. Mattman.
> > 3rd ed. CRC Press 2001
> > In brief, there is no question; they exist.
>
> The title is a bit misleading. Any life form has to has some sort of
> barrier to keep its insides from floating away. The term "Stealth
> Pathogens" is just a marketing gimmick to get you to buy the book
> and find out what she is talking about. I tend to skip authors who
> use these tricks.

She is not writing to the popular audience, but rather to the research
community, which has exhibited - umm, reluctance; bordering on furious
denial - to embrace concepts ranging beyond Pasteur's "one disease, one
pathogenic bug of exactly one form" paradigm. Further, "stealth
pathogens" form a still somewhat loosely defined class of pathogenic
organisms to which she has brought considerable clarity. It is not
layman's slang nor sensationalistic journalism; the publisher, CRC
Press, should give you some clue to that fact. If the title seems
misleading to you I suggest that you read up in the area; CWD, or
cell-wall-deficient - ( or -divergent(preferred) or -defective) Is in
common use, along with "L form". Not a bit misleading.

Consider the L forms you mention, named by Emmy Kleineberger-Nobel
(yes, those Nobels) in loyalty to her association with the Lister institute;
Origin, development and significance of L forms in bacterial cultures.
J. GEN.MICROBIOL.., 3: 434-442, 1949. The Journal of General
Microbiology is not known for sensationalism or pandering to the
popular press. Nor do they indulge (usually) in ad hominen obfuscation.
(well, hey, nobody's perfect.)

from Mattman, op.cit.,
"ch.3 Comparing Mycoplasma, CWD Forms, and Rickettsia
"Introduction
"The one essential difference between Mycoplasma and CWD forms is that
Mycoplasma by definition are unable to make any cell wall components.
In contrast, CWD bacteria and fungi have potential for making wall
components and usually possess layers varying from vestigial to
substantial.
"Another characteristic which clearly sets Mycoplasma apart from
bacteria in any form is the G+C ratio of the Mycoplasma DNA, the mole
percent of guanine plus cytosine/adenine+thymine+guanine+cytosine.
Certain of the Mycoplasma have G+C ratios below those known for ahy
bacterium, i.e., in the range from 23 to 25%. Such species include M.
neurolyticum, and M. mycoides var. capri. In contrast, the G+C base
composition of bacteria may reach 70% for some Mycobacteria and does
not go lower than 28 to 30% for any bacterial genus. However, in general,
Mycoplasma resembles CWD so closely that differentiation is difficult."

She goes on to do so with grace and rigor. . . . .
I could continue with more quotation but I'm a lousy typist: RTFM,
please, and spare me the agony.

> There is nothing unusual about life forms that lack a true cell
> wall. Instead, they have a membrane to keep everything in.

They may have partial cell walls, " ... from vestigial to substantial,"
structurally competent if incomplete, and often of several layers.


> Mycoplasma is one example. Here's a partial description. The actual
> article is much longer.

Example of what? Neither the length of the article nor the solitary example chosen seem relevant to the discussion of L Forms/CWD in general, nor for that matter of
"Nanobacteria," the subjects you dismiss as being of doubtful validity;
the presence of a cell membrane is hardly in question. Is that a red herring?

> ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
> Background: Mycoplasmal organisms are the smallest known free-living
> life forms. They are nearly ubiquitous in both the plant and animal
> kingdoms as colonizers and pathogens. The following summary is modified from Baum's
> "Introduction to Mycoplasma Diseases" in Principles and Practice of
> Infectious Diseases (2000) (see Image 1).
>
> The general characteristics of Mycoplasma species include the
> following:
> Prokaryotic
> Size of 150-250 nm
> Lack of a cell wall
> Sterol-containing cell membrane
> Fastidious growth requirements
> Fried-egg or mulberry colonies on agar
>
> Mycoplasma species differ from viruses in the following ways:
> They grow on cell-free media in vitro
> They contain both RNA and DNA
> They have both intracellular and extracellular parasitism in vivo
>
> Mycoplasma species differ from bacteria (including L-forms) in the
> following ways:
> They have sterols in the cell membrane
> They share no DNA homology with known bacteria
> They have low guanine levels plus cytosine content
> Their genome has a low molecular weight
> They exhibit no reversion to walled forms
>
> Pathophysiology: Mycoplasma organisms cause infection primarily as
> extracellular parasites, attaching to the surface of ciliated and
> nonciliated epithelial cells. The attachment site, or receptor, is a
> complex carbohydrate structurally akin to antigen I of red blood
> cells. The antibody response to this receptor results in production
> of the anti-I antibody or cold agglutinin, which acts as an
> autoantibody.
> Mycoplasmal organisms commonly contaminate tissue cultures, in which
> they act as intracellular parasites and alter both cellular and
> viral molecular events. They are difficult to eliminate, and they
> raise questions regarding the validity of molecular biology results
> from tissue-culture experiments.
>
> http://www.emedicine.com/ped/topic1524.htm
>
> ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
>
> Note the last paragraph about contamination. This is suspected in
> tests done on so-called nanobacteria.

Perhaps this statement exemplifies the problem of interpretation; does
this contamination imply an exterior source, or simply the presence of
ubiquitous materials derived as an integral part of the sample? Are they
" ...primarily ...extracellular parasites," or do they " ...commonly contaminate
... as intracellular parasites and alter ... "
Theargument has been discussed from both points of view, and recourse to
Mattman might clear up the question(s) for you much better than I (or Dr. Baum)
could.
Further, the "contamination" sobriquet demeans the possible role of
such 'debris' to contaminant rather than pathogen with no examination
to support such a dismissal from disease etiology; in short, they simply
'get in the way' of conventional bacteriology - virology. Thus the
paragraph begs the question.

Take care, Malcolm

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