Mooshie peas writes

Bottom line though is that BT expressed is no more likely fo cause
resistance development problems than intemittent application of BT.

Hard to answer.

The persistent and uniform use of any pesticide tends to lead to some
level of resistance. The speed resistance arrives is rather variable and
varies from locally almost immediate (eg dimfop) to hugely delayed (eg
hormone weedkillers). Others allow decades of use before resistance is a
problem (eg OP's).

I suspect it depends on how easily the organism can bypass the pathways
blocked by the pesticide.

In the case of dimfop, a single change on a single gene seems to be
enough. For OP's tolerance seems to develop by multiple gene changes,
each of which confers a small tolerance, so resistance development is
slow. In the case of hormones the auxin systems are so fundamental and
old that it takes many rather large changes for true resistance to
develop and we only see a partial tolerance.

I would suggest from the evidence we have (ie no complete control
failures) that Bt resistance is most likely to follow the second or
third routes. Alternative GM insecticide molecules would, however, be
advantageous, IMHO.

--
Oz
This post is worth absolutely nothing and is probably fallacious.
Note: soon (maybe already) only posts via despammed.com will be accepted.

Mooshie peas writes
Of course, but it is a well known mechanism of resistance development,
sub-lethal doses that leave the partially susceptible mutants still
alive. Antibiotic treatments are a case in point. The importance of
finishing the full course prescribed, and not stopping when you feel
better.

1) A reminder that bacteria are much simpler than insects, and with a
higher breeding rate.

2) No farmer applies pesticides in the above mentioned manner anyway.
It varies from typically one to three applications per season.


--
Oz
This post is worth absolutely nothing and is probably fallacious.
Note: soon (maybe already) only posts via despammed.com will be accepted.

On Tue, 12 Aug 2003 07:37:17 -0700, Walter Epp
posted:

"Moosh:}" wrote:
On Thu, 07 Aug 2003 07:20:22 -0700, Walter Epp
posted:

"Moosh:]" wrote:
On 29 Jul 2003 08:52:24 GMT, Brian Sandle
posted:
As we discussed with DDT, anything used for too long breeds resistant
creatures.

So? The point is that the use of BT in the plant and on the plant is
hardly different. When the insects are not present, they can't be
developing resistance.

Where is there a place without insects?

The relevant insects are those that damage the crop. If they don't,
they won't be ingesting BT.

but they can pass resistance genes to those who didn't
ingest but can fly in and have a resistant feast.

Only if they breed with the resistant ones and have resistant
offspring, but this happens all the time.

Welcome to the real world, where things are not black and white,
where we don't have either 0 or trillions of insects but varying
degrees inbetween, where not all insects are dumb enough to
keep eating bt until they've got a fatal dose but different ones
eat different amounts and so trigger varying amounts of
selective pressure.

And this happens with applied BT, only better coz the BT slowly
reduces due to washing off and so on. So if you want to be accurate,
applied BT can be worse than expressed BT wrt resistance development.

Applied Bt is the most accurate way to minimize selective pressure.
The crude approach of continual and high exposure makes for high
selection pressure for resistance.

No, you apply everytime you have pest damage. That application wanes.
If no pest damage, then there is no contact wih the expressed BT.
The bottom line is it makes no difference in the end. Just get used to
the fact that pesticides will lose their effect sooner or later, and
new ones must be developed. The old ones may be returned to at a later
date, and different strategies can be used to minimise resistance
formation. Resistance 0ccurs whenever a pest is partially killed by a
pesticide. This can happen with applied or expresssed BT at more or
less the same rate.

When the pesticide is interrupted then resistance to it is no
longer an advantage.

And the pest destroys your crop, and you go bankrupt.

Not necessarily, if the natural predators have not been wiped
out by overuse of pesticides and the plants natural defenses
have not been weakened by toxic and/or cultural damage to
the soil ecology.

BT is very specific, so your fear of pest predator damage is
unfounded. Why are you postulating that the natural defences of the
plant will be weakened? What are you trying to say about the soil
ecology?

Mycorrhizal fungi can effectively connect their plant hosts with as
much as 1,000 times more soil area than the roots themselves.
A single gram of soil may contain several miles of fungal hyphae. As they
pump water and mineral nutrients to the roots, the fungi form a
protective armor against disease bacteria around the roots, and sometimes
innoculate the soil with antibiotics that kill disease bacteria.
Root zone fungi and bacteria exude glues (polysaccharides) that bind soil
particles together, resulting in better retention and movement of air and
water. Mycorrhizal fungi break down nitrogen into forms that can be used
by plants. Mats of fungi in the soil store nutrients that otherwise would
be likely to dissolve and leach away.

Roughly speaking.

Roundup/Glyphosate is toxic to many beneficial mycorrhizal fungi,
inhibiting growth at levels as low as 1ppm, and increases susceptibility
of crop plants to a number of diseases.

In vitro, I believe. Glyphosate will not reach the majority of the
roots of fungal hyphae in real soils. It is too strongly bound to
surface soil particles. Now the wetting agents may be a different
matter. Dish liquid/hair shampoo is what caused the problems with
amphibia.

The mycorrhizal hyphal network is easily disrupted by mechanical
disturbance. Disking a field, for example, can greatly reduce the ability
of the soil to make new plants mycorrhizal, even though no fungal material
is actually removed by disking.

Exactly why "no till" using Roundup is so much better in so many
places..

Then DDT will work again, or Bt. But if it is there all
the time resistance to it remains an advantage for pests.

Sorry, "there all the time" means nothing if the pests are not there.
It might as well be withdrawn if the pests are absent.
No contact, no advantage for the resistant mutations.

When home gardners use it, or non-GM soy farmers &c, it is only present as
needed, then disappears.

And why does it matter if it's there or not, if the pests aren't
predating the crop?

There are always a few about, from the mandatory refuges, or other crops
near by.

But how does this matter? The chances of a resistance mutation are so
much lower.

Check out what's already happened:
Independent on Sunday (London) March 30, 2003
INSECTS THRIVE ON GM 'PEST-KILLING' CROPS
BY GEOFFREY LEAN ENVIRONMENT EDITOR

Genetically modified crops specially engineered to kill pests in fact
nourish them, startling new research has revealed.

Biotech companies have added genes from a naturally occurring poison,
Bacillus thuringiensis (Bt), which is widely used as a pesticide by
organic farmers.
Drawbacks have already emerged, with pests becoming resistant to the
toxin. Environmentalists say that resistance develops all the faster
because the insects are constantly exposed to it in the plants, rather
than being subject to occasional spraying.

Occasional spraying will result in many occasions where dose is
sublethal. Ideal circumstances for resistance development.

If the spraying is only occasional the selection pressure is low.

Rubbish. If you kill half the pests occasionally, allowing the
resistance gene to multiply and strentgen, you are going to get much
more resistance problem. Keep up the 'cide constantly, and you kill
many more pests.

If the exposure is continual and high the selection pressure for
resistance is high.

The exposure is only continual when the pest are doing damage, so you
would be applying continually anyway. There is very little difference.

On Wed, 13 Aug 2003 11:09:54 GMT, Mooshie peas
wrote:

On Fri, 08 Aug 2003 17:30:28 +0200, Torsten Brinch
posted:

On Fri, 08 Aug 2003 05:48:09 GMT, "Moosh:}"
wrote:
On Fri, 8 Aug 2003 06:18:46 +0100, Oz
posted:

Someone wrote:
They fed resistant larvae of the diamondback moth - an increasingly
troublesome pest in the southern US and in the tropics - on normal
cabbage leaves and ones that had been treated with a Bt toxin. The larvae
eating the treated leaves grew much faster and bigger - with a 56 per
cent higher growth rate.
..
Plants attacked by pests will elevate their toxin levels as a response.
If the untreated plants were under attack (or their neighbours were)
then they would increase their toxin level.
..
It amazed me that such a tiny amount of one protein could produce such
growth differences. Your explanation of growth inhibition from a
predated crop certainly fits.

It doesn't fit or explain anything at all, since the same cabbage leaf
material was fed in all treatment groups in the experiment. The
researchers grew a single cabbage crop, cut discs from its leaves, and
fed the discs to different groups of larvae kept in petri dishes, with
or without Bt toxin fortification.

You obviously have the advantage of reading the full paper. Care to
share? So how do you explain the marked growth increase from this
tiny amount of one protein?

You mean the 56% increase? It is beyond me where the authors get that
particular figure from. On the face of it the data shows a growth rate
increase of only about 30 %, and I would be wary to accept even that.

The main observation in the experiment IMO is that feeding BT
fortified substrate (10ppm) to larvae, re-selected to yield high Bt
resistance (LC50~200 ppm), increased their mean pupae weight
significantly - about 20% - relative to feeding them non-BT fortified
substrate -- while leaving their time to pupation unchanged or perhaps
a bit shorter.

Has the experiment been replicated?

I don't know, Jack. You can ask the authors if they are working on
that or something similar, email: h dot cerda at ic dot ac dot uk

If not, perhaps we should wait until the attempt has been made?

Funny you did not get that thought while you and Oz were happily
explaining the findings. Boy, you couldn't even wait until you'd
read the article :-)

On Wed, 13 Aug 2003 11:07:51 GMT, Mooshie peas
wrote:

On Fri, 08 Aug 2003 17:30:23 +0200, Torsten Brinch
posted:

On Fri, 08 Aug 2003 04:20:48 GMT, "Moosh:}"
wrote:

On Thu, 07 Aug 2003 07:20:22 -0700, Walter Epp
posted:
[Quoting Independent on Sunday (London) March 30, 2003:]
.. Environmentalists say that resistance develops all the faster
because the insects are constantly exposed to it in the plants, rather
than being subject to occasional spraying.

Occasional spraying will result in many occasions where dose is
sublethal. Ideal circumstances for resistance development.

However, reminding ourselves of the perils of assumption-based
reasoning, let us hear what the experienced farmers over at
sci.agriculture has to say about that.

Of course, but it is a well known mechanism of resistance development,
sub-lethal doses that leave the partially susceptible mutants still
alive. Antibiotic treatments are a case in point. The importance of
finishing the full course prescribed, and not stopping when you feel
better.

Also, we should not forget to ask the agricultural scientist over at
sci.agriculture whether resistance building is typically found
where spraying has been done occasionally -- or whether resistance is
more typically found where spraying has been done extensively,
frequently or constantly.

Torsten Brinch writes

Also, we should not forget to ask the agricultural scientist over at
sci.agriculture whether resistance building is typically found
where spraying has been done occasionally -- or whether resistance is
more typically found where spraying has been done extensively,
frequently or constantly.

Pests are typically too mobile for small plots not to be genetically
similar to the wider environment. The spread of dimfop resistant
blackgrass from a few sites to most of the blackgrass areas in the UK
took (from memory) about five years. The precise pattern of resistance
found in a field, though, seems to be related to the most recent
applications, which is not unexpected.

--
Oz
This post is worth absolutely nothing and is probably fallacious.
Note: soon (maybe already) only posts via despammed.com will be accepted.

On Wed, 13 Aug 2003 13:58:38 +0100, Oz
posted:

Mooshie peas writes

Bottom line though is that BT expressed is no more likely fo cause
resistance development problems than intemittent application of BT.

Hard to answer.

The persistent and uniform use of any pesticide tends to lead to some
level of resistance. The speed resistance arrives is rather variable and
varies from locally almost immediate (eg dimfop) to hugely delayed (eg
hormone weedkillers). Others allow decades of use before resistance is a
problem (eg OP's).

I suspect it depends on how easily the organism can bypass the pathways
blocked by the pesticide.

In the case of dimfop, a single change on a single gene seems to be
enough. For OP's tolerance seems to develop by multiple gene changes,
each of which confers a small tolerance, so resistance development is
slow. In the case of hormones the auxin systems are so fundamental and
old that it takes many rather large changes for true resistance to
develop and we only see a partial tolerance.

I would suggest from the evidence we have (ie no complete control
failures) that Bt resistance is most likely to follow the second or
third routes. Alternative GM insecticide molecules would, however, be
advantageous, IMHO.

--
Oz
This post is worth absolutely nothing and is probably fallacious.

You're too modest. Thanks

On Wed, 13 Aug 2003 14:00:59 +0100, Oz
posted:

Mooshie peas writes
Of course, but it is a well known mechanism of resistance development,
sub-lethal doses that leave the partially susceptible mutants still
alive. Antibiotic treatments are a case in point. The importance of
finishing the full course prescribed, and not stopping when you feel
better.

1) A reminder that bacteria are much simpler than insects, and with a
higher breeding rate.

Of course. But their biochemistry is quite similar, save for the speed
of generation change.

2) No farmer applies pesticides in the above mentioned manner anyway.
It varies from typically one to three applications per season.

Of course, again, economics plays a strong role. Antibiotics are taken
on the assumption that reinfection will not occur, whereas pests are
constantly returning.

Mooshie peas wrote:
On Fri, 8 Aug 2003 17:15:49 +0100, Oz
posted:

Torsten Brinch writes
On Fri, 08 Aug 2003 04:20:48 GMT, "Moosh:}"
wrote:

On Thu, 07 Aug 2003 07:20:22 -0700, Walter Epp
posted:
[Quoting Independent on Sunday (London) March 30, 2003:]
.. Environmentalists say that resistance develops all the faster
because the insects are constantly exposed to it in the plants, rather
than being subject to occasional spraying.

Occasional spraying will result in many occasions where dose is
sublethal. Ideal circumstances for resistance development.

Only if too little is applied. So with organic Bt a heavy dose is applied
when needed. It degrades quite quickly so new generations of insects are
not exposed to it.

With GM Bt crops the dose much more gradually decreasses as the crop
ripens.


However, reminding ourselves of the perils of assumption-based
reasoning, let us hear what the experienced farmers over at
sci.agriculture has to say about that.

There are two arguments:

1) Apply full dose and kill 99.999% except the 0.001% that have a
resistance gene and next season you will have a 100% resistant
population. If (as is common) you have a pest with a very high
reproductive rate then you are stuffed in a year or two.

This is what happened for dimfop resistant blackgrass.
This might be typical of single gene resistance (not tolerance).

This will happen whether or not the gene is less efficient than the
'natural' gene.

2) Apply a reduced rate, kill 99% of the pest, leave 1% of which 1:1000
have a resistance gene. Hope the resistance gives less efficient pest,
outbred by 'natural' genes, leaving a final pest population still with
about 0.001% resistance. So no change.

Most field weeds are more tolerant of pesticides than their wild
relatives, but often not by much.

Pesticides acting on single genes are MUCH more likely to become
completely useless due to single point mutation.

Pesticides with multiple-point action are pretty unlikely to develop
resistance.

Obviously simultaneously using several pesticides with different action
mimics multiple-point resistance.

If a pesticide targets a key site, that is hard for the pest to alter
because it is critical (perhaps used in many subsystems or is very
basic), then tolerance rather than resistance seems to be the normal
mode of action (eg hormone weedkillers, IPU). I haven't seen it stated,
but I suspect the progeny are less competitive.

Certainly resistant blackgrass seems to be highly susceptible to mildew,
for example.

Bottom line though is that BT expressed is no more likely fo cause
resistance development problems than intemittent application of BT.

No it is, because it always there selecting a bit. Why do you think the NZ
Royal Commission recommended education about refuges before releasing GM
crops?

Mooshie peas writes
On Wed, 13 Aug 2003 14:00:59 +0100, Oz
posted:

Mooshie peas writes
Of course, but it is a well known mechanism of resistance development,
sub-lethal doses that leave the partially susceptible mutants still
alive. Antibiotic treatments are a case in point. The importance of
finishing the full course prescribed, and not stopping when you feel
better.

1) A reminder that bacteria are much simpler than insects, and with a
higher breeding rate.

Of course. But their biochemistry is quite similar, save for the speed
of generation change.

The plant genome is immense by comparison.

2) No farmer applies pesticides in the above mentioned manner anyway.
It varies from typically one to three applications per season.

Of course, again, economics plays a strong role. Antibiotics are taken
on the assumption that reinfection will not occur, whereas pests are
constantly returning.

Indeed. The aim is to prevent significant damage, not to eradicate the
pest for the season (except perhaps weeds).

--
Oz
This post is worth absolutely nothing and is probably fallacious.
Note: soon (maybe already) only posts via despammed.com will be accepted.

On Wed, 13 Aug 2003 23:24:57 +0200, Torsten Brinch
posted:

On Wed, 13 Aug 2003 11:09:54 GMT, Mooshie peas
wrote:

On Fri, 08 Aug 2003 17:30:28 +0200, Torsten Brinch
posted:

On Fri, 08 Aug 2003 05:48:09 GMT, "Moosh:}"
wrote:
On Fri, 8 Aug 2003 06:18:46 +0100, Oz
posted:

Someone wrote:
They fed resistant larvae of the diamondback moth - an increasingly
troublesome pest in the southern US and in the tropics - on normal
cabbage leaves and ones that had been treated with a Bt toxin. The larvae
eating the treated leaves grew much faster and bigger - with a 56 per
cent higher growth rate.
..
Plants attacked by pests will elevate their toxin levels as a response.
If the untreated plants were under attack (or their neighbours were)
then they would increase their toxin level.
..
It amazed me that such a tiny amount of one protein could produce such
growth differences. Your explanation of growth inhibition from a
predated crop certainly fits.

It doesn't fit or explain anything at all, since the same cabbage leaf
material was fed in all treatment groups in the experiment. The
researchers grew a single cabbage crop, cut discs from its leaves, and
fed the discs to different groups of larvae kept in petri dishes, with
or without Bt toxin fortification.

You obviously have the advantage of reading the full paper. Care to
share? So how do you explain the marked growth increase from this
tiny amount of one protein?

You mean the 56% increase? It is beyond me where the authors get that
particular figure from. On the face of it the data shows a growth rate
increase of only about 30 %, and I would be wary to accept even that.

The main observation in the experiment IMO is that feeding BT
fortified substrate (10ppm) to larvae, re-selected to yield high Bt
resistance (LC50~200 ppm), increased their mean pupae weight
significantly - about 20% - relative to feeding them non-BT fortified
substrate -- while leaving their time to pupation unchanged or perhaps
a bit shorter.

Has the experiment been replicated?

I don't know, Jack. You can ask the authors if they are working on
that or something similar, email: h dot cerda at ic dot ac dot uk

So how are you placing so much weight on this paper as to dismiss out
of hand Oz's hypothesis? Without replication, this paper should be put
on the "rubbish" spike "pending".

BTW, have you heard of spam bots that can translate "dot" to "." and
"at" to "@" and close up the spaces?

If not, perhaps we should wait until the attempt has been made?

Funny you did not get that thought while you and Oz were happily
explaining the findings.

You presume too much. The paper is out of my financial means (and I
presume Oz is not willing to spend the required sum on the full paper)
And we were merely "hypothesising" and wondering from the brief
details we had seen.
Even you can't explain the findings, having apparently read it.

Boy, you couldn't even wait until you'd
read the article :-)

To discuss the findings that were mentioned on this group?
Are you chronically constipated by any chance?

On Wed, 13 Aug 2003 23:24:58 +0200, Torsten Brinch
posted:

On Wed, 13 Aug 2003 11:07:51 GMT, Mooshie peas
wrote:

On Fri, 08 Aug 2003 17:30:23 +0200, Torsten Brinch
posted:

On Fri, 08 Aug 2003 04:20:48 GMT, "Moosh:}"
wrote:

On Thu, 07 Aug 2003 07:20:22 -0700, Walter Epp
posted:
[Quoting Independent on Sunday (London) March 30, 2003:]
.. Environmentalists say that resistance develops all the faster
because the insects are constantly exposed to it in the plants, rather
than being subject to occasional spraying.

Occasional spraying will result in many occasions where dose is
sublethal. Ideal circumstances for resistance development.

However, reminding ourselves of the perils of assumption-based
reasoning, let us hear what the experienced farmers over at
sci.agriculture has to say about that.

Of course, but it is a well known mechanism of resistance development,
sub-lethal doses that leave the partially susceptible mutants still
alive. Antibiotic treatments are a case in point. The importance of
finishing the full course prescribed, and not stopping when you feel
better.

Also, we should not forget to ask the agricultural scientist over at
sci.agriculture whether resistance building is typically found
where spraying has been done occasionally -- or whether resistance is
more typically found where spraying has been done extensively,
frequently or constantly.

Typically found wherever there is pesticide in contact with pests, I
think you'll find.

On Tue, 19 Aug 2003 14:02:42 GMT, Mooshie peas
wrote:

On Wed, 13 Aug 2003 23:24:57 +0200, Torsten Brinch
posted:

On Wed, 13 Aug 2003 11:09:54 GMT, Mooshie peas
wrote:

On Fri, 08 Aug 2003 17:30:28 +0200, Torsten Brinch
The main observation in the experiment IMO is that feeding BT
fortified substrate (10ppm) to larvae, re-selected to yield high Bt
resistance (LC50~200 ppm), increased their mean pupae weight
significantly - about 20% - relative to feeding them non-BT fortified
substrate -- while leaving their time to pupation unchanged or perhaps
a bit shorter.

Has the experiment been replicated?

I don't know, Jack. You can ask the authors if they are working on
that or something similar, email: h dot cerda at ic dot ac dot uk

So how are you placing so much weight on this paper as to dismiss out
of hand Oz's hypothesis? snip

I already explained why I think Oz's hypothesis as to what caused the
observed difference is untenable. Look back the thread.

On 17 Aug 2003 12:53:23 GMT, Brian Sandle
posted:

Mooshie peas wrote:
On Fri, 8 Aug 2003 17:15:49 +0100, Oz
posted:

Torsten Brinch writes
On Fri, 08 Aug 2003 04:20:48 GMT, "Moosh:}"
wrote:

On Thu, 07 Aug 2003 07:20:22 -0700, Walter Epp
posted:
[Quoting Independent on Sunday (London) March 30, 2003:]
.. Environmentalists say that resistance develops all the faster
because the insects are constantly exposed to it in the plants, rather
than being subject to occasional spraying.

Occasional spraying will result in many occasions where dose is
sublethal. Ideal circumstances for resistance development.

Only if too little is applied.

And when too little is present. And this will be after EVERY
application, as an application necessarily wanes.

So with organic Bt a heavy dose is applied
when needed.

That would be constantly during a pest presence? You're dreaming.
Only BT expression can do this.

It degrades quite quickly so new generations of insects are
not exposed to it.

How long does it take to become a sublethal presence? How long does a
sub-lethal level occur with intermittent application. How do you
ensure that every pest that takes a bite from the crop gets a lethal
dose. I put it to you that that's impossible without the even
expression of the 'cide within the crop, continuously.

With GM Bt crops the dose much more gradually decreasses as the crop
ripens.

But the pests are not feeding then?

However, reminding ourselves of the perils of assumption-based
reasoning, let us hear what the experienced farmers over at
sci.agriculture has to say about that.

There are two arguments:

1) Apply full dose and kill 99.999% except the 0.001% that have a
resistance gene and next season you will have a 100% resistant
population. If (as is common) you have a pest with a very high
reproductive rate then you are stuffed in a year or two.

This is what happened for dimfop resistant blackgrass.
This might be typical of single gene resistance (not tolerance).

This will happen whether or not the gene is less efficient than the
'natural' gene.

2) Apply a reduced rate, kill 99% of the pest, leave 1% of which 1:1000
have a resistance gene. Hope the resistance gives less efficient pest,
outbred by 'natural' genes, leaving a final pest population still with
about 0.001% resistance. So no change.

Most field weeds are more tolerant of pesticides than their wild
relatives, but often not by much.

Pesticides acting on single genes are MUCH more likely to become
completely useless due to single point mutation.

Pesticides with multiple-point action are pretty unlikely to develop
resistance.

Obviously simultaneously using several pesticides with different action
mimics multiple-point resistance.

If a pesticide targets a key site, that is hard for the pest to alter
because it is critical (perhaps used in many subsystems or is very
basic), then tolerance rather than resistance seems to be the normal
mode of action (eg hormone weedkillers, IPU). I haven't seen it stated,
but I suspect the progeny are less competitive.

Certainly resistant blackgrass seems to be highly susceptible to mildew,
for example.

Bottom line though is that BT expressed is no more likely fo cause
resistance development problems than intemittent application of BT.

No it is, because it always there selecting a bit.

It can only select when pests are feeding, and when some pests are
surviving it. Intermittent allows this after every application.
Expression ensures a lethal dose at every bite (theoretically)

Why do you think the NZ
Royal Commission recommended education about refuges before releasing GM
crops?

The NZ RC has a bad taste in it's mouth after that lady professor lied
to them with phony evidence.

Aren't the refuges for pest predators? Why would you want refuges for
the pests?

On Sun, 17 Aug 2003 17:54:49 +0100, Oz
posted:

Mooshie peas writes
On Wed, 13 Aug 2003 14:00:59 +0100, Oz
posted:

Mooshie peas writes
Of course, but it is a well known mechanism of resistance development,
sub-lethal doses that leave the partially susceptible mutants still
alive. Antibiotic treatments are a case in point. The importance of
finishing the full course prescribed, and not stopping when you feel
better.

1) A reminder that bacteria are much simpler than insects, and with a
higher breeding rate.

Of course. But their biochemistry is quite similar, save for the speed
of generation change.

The plant genome is immense by comparison.

Yep, but the biochemistry is surprisingly similar.

2) No farmer applies pesticides in the above mentioned manner anyway.
It varies from typically one to three applications per season.

Of course, again, economics plays a strong role. Antibiotics are taken
on the assumption that reinfection will not occur, whereas pests are
constantly returning.

Indeed. The aim is to prevent significant damage, not to eradicate the
pest for the season (except perhaps weeds).

Sure, the aim is to get as much crop for as little expense as
possible. With farsightedness, a smaller profit might be accepted for
a likely increased profit over the next decade. The aim with pests
might be to eradicate them forever but being pragmatic....