Autoimmunity to protective molecules (Re: What if......)

[Guest guest]

> This makes that title much more appropriate than intended: it

suggests that in autoimmunity, there's always a hidden germ involved,

stoking the fire...

Here's the main problem raised by that view. Why aren't there more

known symptom-causing autoreactivities in the classical infectious

diseases (especially chronic ones)? There is paroxysmal cold

hemoglobinuria, which is not rare in syphilis, known to be autoimmune,

and which often clears with syphilis treatment.

Myasthenia gravis, pemphigus, Graves', various cytopenias, SLE (to

some extent), and more have demonstrable AI pathogeneses. If varmints

underlie the AI, why are they all so undetectable? Is there some

common feature that makes them highly AI-genic and also poorly virulent?

I used to think there was a similar problem with explaining why so

many of these diseases that respond to abx anecdotally in our

community, all have the common features of being poorly responsive (vs

the classical bacterioses), often non-progressive (or nearly so) with

some stark exceptions like MS and ALS, and culture-negative and

otherwise hard to demonstrate as bacterioses. Etc. But actually

bacterial stress states are a possible explanation for the seemingly

unjustifiable coincidence of all these features. We know that stress

state bacteria are hard to kill and can be culture-negative, but they

also tend to be small (perhaps to increase their surface area : volume

ratio for better nutriment uptake). Morita states that many or most

starved cells in the environment are ultramicroscopic, ie around 200

nm across. This gives them a volume 125x smaller than that of a 1-um

cell and a surface area 25x smaller. If these were visible (via

immunostain) to a light microscope or a weak EM they would probably

look like " debris " to medical microbiologists who generally reject the

doctrine of bacterial pleomorphism. The only real sortie into this

realm is the high-quality EM of the Wirostko/ papers, but it's

hard to tell how they justify some of their identification of

bacterial bodies (others of the bodies they imaged are so bizarre and

novel as to be presumably exotrinsic, especially considering that they

could be passaged in mice). It would be great to add yersinial

arthritis to this, but as I mentioned it didn't work since I can't

find any high-quality EM out there in which the possible viability /

(ultramicro)cellularity / integrity of the yersinia-staining " debris "

might be discerned.