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From:
James Fischer <[log in to unmask]>
Reply To:
Informed Discussion of Beekeeping Issues and Bee Biology <[log in to unmask]>
Date:
Fri, 5 Jul 2013 11:36:23 -0400
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Let's keep critique reasonable, shall we?  The comments offered seem far
less than a substantive critique. 
	
> The test and control colonies were kept in separate apiaries, 
> in small woodlots 150 meters apart, and thus exposed to 
> different forage and pesticides.  

Any beekeeper can refute that assertion.  How might a distance of a mere 150
meters between hives result in different exposure / forage?  The paper
clearly states "The probability of exposure to these chemicals [pesticides
applied in prior seasons] was the same for [control] and [test] hives".  Do
you want to challenge that statement on a statistical basis, or is this a
challenge to the basic veracity of the authors?

> The surrounding fields had been treated with a whole slew of 
> different pesticides.  No pesticide analysis was performed on 
> the combs or beebread, so we have no idea as to the actual 
> exposure of the larvae to various pesticides and plant allelochemicals.

See above.  The same refutation applies here.  The controls did not show the
unique measured impact, while the colonies treated with the 100ml feeding of
2 ppb Imidacloprid did show the measured impact.  The colonies can be
assumed to be foraging on the same blooms, and exposed to the same
pesticides, fungicides, and so on.

> The authors did not validate that the colonies exhibited similar 
> gene expression prior to the treatments, so we have no idea 
> whether they were similar to start with. 

The paper states "Six hives were divided into two groups: the control  group
(C1, C2, C3) and the experimental group (IE1, IE2, IE3), respectively."  Is
your accusation that a random selection/division of hives into two groups
JUST HAPPENED to select the only hives that expressed a unique set of gene
expressions from the get-go?   Just what would be the odds for that?  

> I have no idea as to how gene expression changes in 
> later instar larvae relative to younger instar.  

Then we should consult with someone who knows a little more genetics!  With
my limited knowledge, I can simply point out that, regardless of the age
differences in the larvae, the larvae from the control hives did NOT show
the impact, and the larvae from the test hives DID show the impact.  So, it
seems reasonable to say that REGARDLESS OF THE AGE OF LARVAE, the controls
tested as "normal" while the treated hives consistently showed "impact".  

> The authors ran no positive controls, such as the feeding 
> of any natural plant allelochemical, that might help us to
> judge how significant were the changes in gene expression.

The controls were freely foraging during the entire study, as were the
tested hives. Both sets of hives had unlimited access to "natural plant
alleochemicals".  The only difference here was the feeding of a very small
amount of feed to the tested hives, not even 10% of the typical intake of
nectar for a hive.  These were 100ml (3.3 oz) feeders!

The changes found included changes in 	expression of genes associated with
the Cytcochrome P450 process, a pretty a clear indicator that the changes
were directly caused by a toxin.  But the authors even took care to qualify
even these findings with "It remains to be shown if altered transcription of
these CYP/P450 genes is a specific detoxification-response and whether the
encoded enzymes are capable of metabolising imidacloprid." Sounds pretty
low-key and unassuming to me!

They also compared their findings to similar same genetic impact on other
insects, such as Drosophila, where there is more data, saying things like
"The overall altered transcription profile of the [test hive] data set
(Figure 1), echoes the observations reported for xenobiotic stress responses
in Drosophila".  To me, this is important, as there aren't too many
different ways for insects to metabolize sugars.

This paper is going to be far more difficult to shrug off than the other
"sublethal effects" papers, even for the most obstinate. 

But the only basis to suppose that any of these genetic impacts would have
negative impact on bee health would be extrapolated from what is known about
other insects.  To me, that is not an irresponsible extrapolation, given
that we have both P450 and sugar metabolization impact at the same time.
But any number can play at this, and the equipment required is widely
available and known-reliable.

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