Quick Addition to Responses to Egnor

Various
ScienceBloggers have been thumping all over Egnor's case, which is a
well-deserved thumping.  



href="http://scienceblogs.com/afarensis/2007/03/18/sunday_paleopathology_blogging/?utm_source=sbhomepage&utm_medium=link&utm_content=sublink">The
Egnor Challenge: Tooth Decay and Human Origins (afarensis)

href="http://scienceblogs.com/goodmath/2007/03/pigheaded_egnorance_antibiotic.php?utm_source=sbhomepage&utm_medium=link&utm_content=sublink">Pigheaded
Egnorance, Antibiotic Resistance, and Tautologies (MarkCC)

href="http://scienceblogs.com/insolence/2007/03/the_egnor_challenge_day_2.php?utm_source=sbhomepage&utm_medium=link&utm_content=sublink">The
Egnor challenge, day 2 (Orac)

href="http://scienceblogs.com/pharyngula/2007/03/michael_egnor_paleyist_surgeon.php?utm_source=sbhomepage&utm_medium=link&utm_content=sublink">Michael
Egnor, Paleyist surgeon (PZ)



There are others, farther back.  The gist of it is that there
is
this dude at the Discorevy Institute who is trying to argue that
doctors do not need to understand evolution.  



I just want to take on a small piece of this.

As Mark quoted in the post linked above:

Our
battle against
bacterial resistance to antibiotics depends on the study of the
intricate molecular strategies bacteria use to fight antibiotics, and
our development of new antibiotics is a process of designing drugs to
counter the bacterial strategies. We use molecular biology,
microbiology, and pharmacology. We understand that bacteria aren't
killed by antibiotics that they're resistant to. We understand
tautologies. Darwin isn't a big help here.

The part I want to add is this: Egnor misses a big point.  He
does
not understand drug discovery and development.  Does he not
remember the Bactrim story?  Bactrim is a combination of two
antibiotics.  The combination was chosen specifically to make
it
harder for bacteria to evolve resistance.  It seemed to work
for a
while, although it could not, and did not, last forever.



Perhaps he should actually read up on the discovery of new
antibiotics before he goes off making unfounded statements.  A
full understanding of the basic science underlying antibiotics is
indeed necessary; that would include an understanding of evolution.
 



If it were otherwise, this paper would never have been written, much
less published in a top-tier journal:



Synergy
and contingency as driving forces for the evolution of multiple
secondary metabolite production by Streptomyces
species





Then there is href="http://www.the-scientist.com/article/display/15763/">this:

style="font-family: Helvetica,Arial,sans-serif;">For any new
antibiotic, resistant bacteria typically show up in four years, or
less. Penicillin resistance was reported clinically even before
large-scale use of the antibiotic began in 1942. The battle against
antibiotic-resistant bacteria demands new drugs and smarter, more
responsible ways to use existing ones. Some researchers, however, are
pursuing another type of weapon: drugs that sidestep natural selection.
Less virulent bacteria would decrease the need for antibiotics, some
reason, and drugs that drastically slow mutation rates might cut off
evolution's power source...



A drug that blocks MarA's activity, Levy reasons, would keep bacteria
in a free-floating state, both less dangerous and easier prey for the
immune system. Ideally, infections could be prevented in susceptible
patients without resorting to antibiotics that select for resistance.
Because the drug wouldn't actually kill the bacteria, mutations
blocking its function wouldn't be highly selected for...  

And href="http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0030176">this:

style="font-family: Helvetica,Arial,sans-serif;">The
emergence of drug-resistant bacteria poses a serious threat to human
health. In the case of several antibiotics, including those of the
quinolone and rifamycin classes, bacteria rapidly acquire resistance
through mutation of chromosomal genes during therapy. In this work, we
show that preventing induction of the SOS response by interfering with
the activity of the protease LexA renders pathogenic Escherichia
coli unable to evolve resistance in vivo to ciprofloxacin or
rifampicin, important quinolone and rifamycin antibiotics. We show in
vitro that LexA cleavage is induced during RecBC-mediated repair of
ciprofloxacin-mediated DNA damage and that this results in the
derepression of the SOS-regulated polymerases Pol II, Pol IV and Pol V,
which collaborate to induce resistance-conferring mutations. Our
findings indicate that the inhibition of mutation could serve as a
novel therapeutic strategy to combat the evolution of antibiotic
resistance.

Of course this could go on all day.  The fact is, an
understanding of evolution is essential to process of discovering new
antibiotics.