Antimicrobial Usage & Spread of Resistance -Reply -Reply

Matthew or Dawnita Nilles nilles at mis.net
Thu Jan 23 18:38:17 EST 1997

In article <s2e71c94.073 at war.wyeth.com>, PROJANS at war.wyeth.com (Steven
Projan) wrote:

> And just to remind Matthew Nilles to read the data - Levy's worked
> required "Prolonged" continuous exposure, in the lab, over many more
> generations of bacterial growth than are inivolved during a patient's
> treatment.  Another point about mar - Levy found that salicylic acid
> (found in aspirin) also selects for mar mutants!!!!  Should we stop
> using aspirin (and other NSAIDS) because it may select for antibiotic
> resistance???  If you are out there Dr. Levy what do you think?

To remind Steve Projan to read the literature more closely.  Cohen and
Levy isolated the original Mar mutations in 1983.  They characterized
their resistance phenotype as occuring in 2-steps the first step mutations
resulted in cross-resistance to multiple antibiotics, these strains were
then exposed to a prolonged regimen of low-level antibiotic.  This
treatment resulted in very high levels of resistance to multiple
antibiotics.  The high-level resistance was transitory and required
continued exposure to maintain.  The MarA mutation was isolated as a Tn5
insertion that abolished the low-level resistance phenotype.  Subsequent
work on the system has focused on the low-level resistance and the nature
of the high-level resistance is yet unknown.  Also, Judah Rosner showed
that salicylate (NOT FOUND IN ASPIRIN), acetylsalicylate (ASPIRIN), and
acetaminophen induced drug resistance in E. coli.  Subsequent work by
Levy's lab, Rosner's lab., and Paul Miller's lab. all showed that the
phenolic induced resistance and the Mar resistance are related but not
entirely the same phenomena.  In the course of my Ph.D research in Kevin
Bertrand's lab. I showed that MarA directly induces expression of the
AcrAB operon in E. coli and showed that salicylate and MarA induced
resistance to most compounds is dependent on AcrAB function (similar
results were produced by the H. Nikaido and J. Hearst labs).  So perhaps
it would be wise to use NSAIDS sparingly when undergoing antibiotic

> We all should be aware that it is, indeed, the use of antibiotics
> that selects for resistant strains - select for them and they will
> come. 

Why won't the same thing happen in vivo?

> However, no one has come forward with data that the
> prescription of antibiotics for what may be viral infections has any
> real impact on the acquisition and spread of antibiotic resistance.  

Where is the DATA that use of antibiotics to treat viral infections is

> Obnoxius as ever,

Is it really necessary to be obnoxious?

Matt Nilles

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