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mechanisms of resistance in SCVs, nuts and bolts

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I always have to blabber about something before getting up the

momentum to actually study it :) but no harm done.

Heres some info... looks like Proctor feels the low metabolism of

SCVs produces much of their resistance - but I am not sure he has

any idea why they become so much more resistant yet when adhered to

certain surfaces.

The way it works, is that the uptake of many drugs by bacteria is

energy dependant. Ie the drugs are taken up not principally by

diffusion but rather thru active transport proteins that consume

energy. (Obviously bacteria didnt evolve these transporters in order

to take up abx - but particular abx happen to be in what I am

assuming is a large spectrum of different chemical species which a

given particular transporter will take up.)

Therefore, when we say that the cidal concentration of ceftriaxone

for Gross Lil Enemy X is .002 ug/mL, refering to the concentration

found in the extrabacterial environment, I guess the concentration

in the cell might actually be 5x that high due to active transport.

I dont think I realized that.

To really get round this whole biz, one needs to audit what is

happening not just with uptake, but any efflux or degradation of the

molecule by the cell. Those activities too should be slowed down in

a hypometabolic cell, but maybe not enough. Then the questions are

- do these phenomena apply to the tx-refractoriness of bacteria we

hold responsible for so much chronic suffering

- do they apply to people who got sick fast (lot of apparant

contradictions there)

- is there anything to do about it all

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Oh yeah, forgot to throw in this stuff, electrical and pH gradiants

seem to be important (delta-psi and delta-pH)... heres a blurb on

those:

methanogens.pdx.edu/boone/courses/BI481/BI481Lec02.html

Heres a paper saying staph dont mind gentamicin at pH 5.0 and talking

about some ways this can be addressed... perhaps this has something to

do with the inactivity of zith at acid pH? Fortunately I think I can

understand the chem involved nowadays once I really squint at it:

http://www.pubmedcentral.gov/articlerender.fcgi?artid=347195

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Have you looked into vitamin K2?

infections

/message/2532

infections

/message/2546

I never got far enough into this to figure out if only a subset of

SCVs would be reversed by vitamin K2, or if all of them would be.

Also, I think you mentioned that SCVs can invade cells. I wonder

if vitamin K2 can enter our cells in large enough amounts to act

on the SCVs.

Matt

>

> - is there anything to do about it all

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