rod hart wrote in message <7ms49p$5rq$1 at news8.svr.pol.co.uk>...
>>Graham Shepherd wrote in message <7mnqvg$120$1 at gxsn.com>...
>>Of course, overuse of these antibiotics will probably lead to the same
>problem that we have with bacterial infections - eventual resistance>
>>>The development of resistance seems marked.
>One example among many would be MRSA
>(methicillin resistant Staphlococcus aureus),
>which shows highly developed reistance
>to Vancomycin.
>>What I do not know is how resistance comes about.
>Is it by random mutation, with resistant mutations
>being favoured?
>>Is it a result of feedback, the bacteria in a given case
>responding to changes in their environment brought
>about by the presence of antibiotics
>(I have not read the book Lamarck's Signature)
>>Or is it occurring by both of these mechanisms?
>>I apologise if this strays too far from the original post.
>>>rod hart
>>>>>>
Fundamentally, resistance to antibiotics is genetically determined. The
actual mode of resistance varies. There may be more than one mode of
resistance to a given antibiotic, and resistance to one antibiotic may also
confer resistance to other related antibiotics. Classically, (ie this could
be out of date!) resistance arises as the result of a mutational event.
Survival of the mutation is enhanced only when it confers evolutionary
advantage - ie when it's beneficial. In the absence of the antibiotic there
is nothing to promote the mutant organism's growth at the expense of
non-resitant organisms. It may be that there is a metabolic penalty
associated with the resistance (eg energy is used to synthesise an enzyme)
which in the absence of selective pressure leads to the mutation dying out
(or rather being outgrown by non-mutants).
The genes for resistance are not just carried on the bacterial chromosome -
some are found in plasmids - extra bits of DNA which can effectively
propagate themselves and which can be transferred between bacteria - which
can be of different species. This means that resistance once it arises can
spread widely. Plasmids can carry multiple factors - eg resistance to more
than one antibiotic - which can result in an organism becoming resistant to
several unrelated antibiotics at once.
All this basically applies to resistance which is determined by a single
gene. There can be multiple factors involved in resistance, so that an
organism may acquire resistance to a given agent incrementally - one
mutation produces a low level of resistance, survival is enhanced by the
presence of the antibiotic selecting for it, further mutations occur and
when one with a higher level of resistance arises it survives better; so
there's what looks like a feedback mechanism, but it's still natural
selection. (If you consider the presence of antibiotics in the environment
natural). This is why it's important that antibiotics are not overused, and
that when they are used they are used properly - is at high enough dose
levels to clear infection and reduce the risk of resitance arising. Removal
of the selective pressure may result in the incidence of restistance being
reduced, but I don't know if anyone has demonstrated that happening
experimentally.
GS
GS
