Guest guest Posted July 4, 2005 Report Share Posted July 4, 2005 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 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 4, 2005 Report Share Posted July 4, 2005 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 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 4, 2005 Report Share Posted July 4, 2005 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 Quote Link to comment Share on other sites More sharing options...
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