Guest guest Posted January 29, 2006 Report Share Posted January 29, 2006 This free paper gives a nice overview of how Mitchison developed the hypothesis of nonreplicating Mtb subsets in human TB, and thus explained why multi-month therapy was necessary to prevent clinical relapse. It is most valuble for its description of how Mitchisons hypothesis was verified. Lesions from humans treated with multi-drug therapy were cultured. Culture of open lesions rapidly grew Mtb with some acquired resistance to the treatment drugs. Culture of closed lesions (where hypoxia causes Mtb dormancy) produced Mtb only after months of incubation, and said Mtb had no resistance, demonstrating that they belonged to a subset of the bacterial population which had faced little mortality during treatment. The best explanation for this (well-supported by work in vitro) is phenotypic resistance due to a nonreplicating status. http://gasp.med.harvard.edu/micro200/Rubin/TB%20persistence% 20review.pdf Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 30, 2006 Report Share Posted January 30, 2006 I like the quotation at the top from the YALE guy. - Kate D. On Sunday, January 29, 2006, at 07:49 PM, wrote: > http://gasp.med.harvard.edu/micro200/Rubin/TB%20persistence% > 20review.pdf Quote Link to comment Share on other sites More sharing options...
Guest guest Posted January 30, 2006 Report Share Posted January 30, 2006 I think it's pretty well known that in CF (cystic fibrosis) that low dose Zith keeps the bacteria in a non- replicating colony. I've often wondered if some of the improvements on low dose abx is exactly that - meaning the offending chronic bacteria is a species that CAN be held in check by low dose. Barb > > This free paper gives a nice overview of how Mitchison developed the > hypothesis of nonreplicating Mtb subsets in human TB, and thus > explained why multi-month therapy was necessary to prevent clinical > relapse. It is most valuble for its description of how Mitchisons > hypothesis was verified. > > Lesions from humans treated with multi-drug therapy were cultured. > Culture of open lesions rapidly grew Mtb with some acquired resistance > to the treatment drugs. Culture of closed lesions (where hypoxia > causes Mtb dormancy) produced Mtb only after months of incubation, and > said Mtb had no resistance, demonstrating that they belonged to a > subset of the bacterial population which had faced little mortality > during treatment. The best explanation for this (well-supported by > work in vitro) is phenotypic resistance due to a nonreplicating status. > > http://gasp.med.harvard.edu/micro200/Rubin/TB%20persistence% > 20review.pdf > Quote Link to comment Share on other sites More sharing options...
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