Guest guest Posted August 8, 2006 Report Share Posted August 8, 2006 For several older papers on " intracellular protection " - all distinct from the 4-5 I have cited before - see refs 1-6 here: http://www.pubmedcentral.nih.gov/pagerender.fcgi? artid=302442 & pageindex=1 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 15, 2006 Report Share Posted August 15, 2006 Maybe I missed the point of your post -- I skimmed the article instead of looking at the refs, but it sure sounds like we all ought to be taking rifampin. Er, so why aren't we? - Kate On Aug 8, 2006, at 1:33 PM, wrote: > For several older papers on " intracellular protection " - all distinct > from the 4-5 I have cited before - see refs 1-6 here: > > http://www.pubmedcentral.nih.gov/pagerender.fcgi? > artid=302442 & pageindex=1 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 16, 2006 Report Share Posted August 16, 2006 > Maybe I missed the point of your post -- I skimmed the article > instead of looking at the refs, but it sure sounds like we all ought > to be taking rifampin. Er, so why aren't we? > > - Kate Actually, while its unfotunately inactive on spirochetes, my thinking so far is that rifampin is probably not something I'm going to pass up a trial of. (More later on this, probably much later.) I have not used it yet. (By the way, the usual belief is, it should not be used alone, nor in an on-and-off pattern - there may well be other important directives / contraindications as well, especially if one has a liver history.) I dont think the Mandell paper's conclusion is necessarily right, if I remember it correctly. What it says about that particular B-lactam having poor cellular penetration, may be true. But in many intracellular protection situations observed in vitro (in other papers), various bacteria (including staph) have survived even tho the cellular/extracellular ratio of the drug being used is well above one (tho not necessarily as high as rifampins C/E ratio). So, poor host cell penetration by the drug cant universally be the origin of protection within host cells. Either there is no univeral origin or the universal origin is something else. However, because intracellular protection is not absolute, in some infections the difference between a C/E ratio of one and a C/E ratio of ten might still (conceivably) be a significant determinant of what happens with a given therapy. So could certain other phenomena that also dont look to be the universal origin of intracellular protection - for example, the variation in power that some drugs undergo as a function of pH. Everything I'm discussing is pretty theoretical of course; in most cases we dont know if these intracellular protection phenomena extend beyond a day or so, as Barb underlined recently. One possible exception is the continuous culture-with-abx experiment on chlamydiae by I believe Hammerschlag et all, in which the chlamydia were cut to a few percent after a protracted period, but were far from eradicated. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 17, 2006 Report Share Posted August 17, 2006 Useless drug IMO. Shoemaker didn't win too many fans with his choice of rifampin and bactrim. I actually found rifampin to build resistance extremely quickly to your sinus bugs. tony > > > > Maybe I missed the point of your post -- I skimmed the article > > instead of looking at the refs, but it sure sounds like we all ought > > to be taking rifampin. Er, so why aren't we? > > > > - Kate > > Actually, while its unfotunately inactive on spirochetes, my thinking > so far is that rifampin is probably not something I'm going to pass up > a trial of. (More later on this, probably much later.) I have not used > it yet. > > (By the way, the usual belief is, it should not be used alone, nor in > an on-and-off pattern - there may well be other important directives / > contraindications as well, especially if one has a liver history.) > > I dont think the Mandell paper's conclusion is necessarily right, if I > remember it correctly. What it says about that particular B-lactam > having poor cellular penetration, may be true. But in many > intracellular protection situations observed in vitro (in other > papers), various bacteria (including staph) have survived even tho the > cellular/extracellular ratio of the drug being used is well above one > (tho not necessarily as high as rifampins C/E ratio). So, poor host > cell penetration by the drug cant universally be the origin of > protection within host cells. Either there is no univeral origin or the > universal origin is something else. > > However, because intracellular protection is not absolute, in some > infections the difference between a C/E ratio of one and a C/E ratio of > ten might still (conceivably) be a significant determinant of what > happens with a given therapy. So could certain other phenomena that > also dont look to be the universal origin of intracellular protection - > for example, the variation in power that some drugs undergo as a > function of pH. > > Everything I'm discussing is pretty theoretical of course; in most > cases we dont know if these intracellular protection phenomena extend > beyond a day or so, as Barb underlined recently. One possible exception > is the continuous culture-with-abx experiment on chlamydiae by I > believe Hammerschlag et all, in which the chlamydia were cut to a few > percent after a protracted period, but were far from eradicated. > Quote Link to comment Share on other sites More sharing options...
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