On Tue, Feb 12, 2013 at 10:22 AM, randy oliver <[log in to unmask]>wrote:
>
> >And the Vidau paper studies fipronil and thiacloprid. Fipronil is not a
> > neonicotinoid (but it is also systemic).
> >
>
> From memory, one insecticide increased nosema spore counts, the other
> decreased.
>
Actually:
"Interestingly, honeybee exposure to fipronil (Cox-Mantel test U = 38,41,
p<10-5) and thiacloprid (Cox-Mantel test U = 28,26, p = p<10-5) influenced
very highly significantly the amplitude and the time course of *N.
ceranae*-induced
honeybee mortality (*Fig.
3A*<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0021550#pone-0021550-g003>).
Indeed, honeybees infected with *N. ceranae* and then exposed to
insecticides died earlier than bees only infected. In addition, at the end
of the experiment (20 days p.i.), while mortality of only infected
honeybees reached a maximum of 47%, the mortalities observed in infected
honeybees exposed to fipronil and thiacloprid were not significantly
different from each other (Cox-Mantel test U = -10,4864, p = 0.132 65) and
reached a maximum of 82 and 71%, respectively (*Fig.
3A*<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0021550#pone-0021550-g003>).
Comparison of insecticide uptake in fipronil, thiacloprid, *N.
ceranae*-fipronil
and *N. ceranae*-thiacloprid groups revealed that total consumption of each
insecticide at 20 days p.i. was not different in non-infected and *N.
ceranae*-infected honeybees for both fipronil (W-W Runs test = 0.46, p =
0,648 08) and thiacloprid (W-W Runs test = 1.37, p = 0,170 90). Also, the
daily insecticide uptake was not different in non-infected and *N.
ceranae*-infected
honeybees for both fipronil (*Fig.
3B*<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0021550#pone-0021550-g003>)
and thiacloprid (*Fig.
3C*<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0021550#pone-0021550-g003>).
After exposure to insecticides, uninfected honeybees did not display any
signs of intoxication. By contrast, at this level of exposure, insecticides
triggered aggressiveness and tremors in infected honeybees during the first
days of exposure, and later exhibited ataxia."
You are correct, Randy, in that fibronil very slightly depressed spore
production rate of nosema, but that did not affect the toxicity of those
spores which was "very highly significantly" increased. The paper is
looking at chemistry of the immune system for the mechanism for that.
"Based on their oral LD50 values, fipronil (LD50: 4.17 ng/bee) and
thiacloprid (LD50: 17 µg/bee) are considered highly and slightly toxic,
respectively, to honeybees
[27]<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0021550#pone.0021550-Kievits1>.
We demonstrate, however, that a daily exposure 1/100th concentration of the
LD50 significantly affects the mortality rate of *N. ceranae*-infected
honeybees."
You have raised some "red flags" Randy about all three of these papers I
have referenced on synergism with nosema. But one thing is common to all
of them: the researchers who actually did them (and they were all
independent from the pesticide companies) unanimously say in their
discussion and conclusions that these results have serious implications
about the role of these pesticides in bee health and bee die-off. My take
is that these results also might explain why neonicotinoid residues could
be missed as being partially responsible (no residues at all in the brood
cohort that showed effects in the Pettis study, significant mortality
increase at 1/100 LD50 in the above study).
Stan
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