Possible degradation in the effectiveness of antibiotics in the treatment of human diseases

rod hart rod at rhart.freeserve.uk
Sun Jul 18 16:18:04 EST 1999

Thank you for your reply, which is very explanatory.

Graham Shepherd wrote in message <7msaol$l7t$1 at gxsn.com>...

>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.

This process might well give a purposive appearance to the development of
resistance, leading to the inference
(possibly false) that random mutation was not the only
mechamism at work.

>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

This certainly is a feedback or reinforcement mechanism.
I have to admit that when I used the word 'feedback'
I had in mind the sort of process I have seen referred to
as 'direct feedback to the germline'  -  for example, the claim
by Steele that acquired immunoligical tolerance to
foreign antigens can be inherited via the male line.
But this is just one example from many cited in
'Genetic Engineering' by Mae-Wan Ho
(Chapter 8, The Fluid and Adaptable Genome).
I find the book thought-provoking, but lack the
learning to evaluate this chapter.

>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>

I think they are over-used. For example, if a patient goes to a doctor
with a lung infection and leaves with a prescription for an antibiotic,
the question must arise: how did the doctor know which antibiotic
to prescribe when he/she made no attempt to determine which
bacterium  (if any) was causing the problem?  Since this occurs
on a large scale, the effect of antibiotic guesswork must be considerable.

>Removal of the selective pressure may result in the incidence of retistance
being reduced, but I don't know if anyone has demonstrated that happening

Or maybe the resistance simply persists non-functionally
till it becomes a disadvantage.

Thanks again for your reply.

rod hart

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