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#1 · (Edited)
Here is a link to one of the small cell studies, and abstracts for the other two: http://beebehavior.com/small_cell_comb_varroa_mites.php

I wanted to discuss these because they are often mentioned in discussions about the use of small cell comb. This IS NOT a thread about the use of small cell comb in hives and pros and cons thereof. This thread is to discuss [small cell] studies only. The forum rules still apply.

For my own part, I don't want to be seen as someone who ignores scientific evidence and instead runs with disproved crackpot theories. So there are these three studies which seem to say that small cell comb is ineffective at controlling varroa mites and may in fact exacerbate the problem. But there is so much anecdotal evidence that says it works or at least has an effect.

To me, these studies are flawed. They take a complex issue, varroa parasitism, and distill it to simple variables, cell size and mite counts. But the issue of the varroa mite does not come down simply to mite counts and cell size. Ultimately there are many more issues involved. I don't know of anyone who's been doing this for any length of time who thinks that cell size is the only or even just the main issue. Dee Lusby said it was a third cell size, a third genetics and a third management. One thing I really want to know is were the combs they used treated before hand. Even more important than that is how well they survived even with the mite load they had. I do no mite drop testing whatsoever, my only metric is survival. If they survive, they get to move on to more nuanced levels of investigation.

Whether or not it can be proven that small cell comb helps with varroa, I have been keeping bees for years with no treatments whatsoever and with only small cell comb and whatever powers the bees have to keep the varroa to manageable levels. I'm interested in other's views of these studies in light of what they have seen and experienced.
 
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#39 · (Edited)
I thought quite a while about how to set up a small cell vs large cell study. There are complexities that are hard to manage. Here are some thoughts on a way to do the job with a very high level of confidence.

1. Set up a total of 240 colonies split into 6 different apiaries. 120 colonies would be on small cell and 120 on large cell. All of the colonies in an apiary should be one cell size to minimize effects caused by varroa moving via drifting bees from overwhelmed colonies to nearby colonies. (reasoning, 240 colonies is enough to be statistically significant)
2. Get queens from three different sources, 80 Italians from a commercial queen breeder, 80 Carniolans from a commercial queen breeder, 80 queens from known long term survivor stock that is on small cell. Divide the queens so that an entire yard is all the same type. (reasoning, this will allow genetic variables to be calculated)
3. Setting up the colonies will be a pain, you MUST have a source of small cell bees to get them to draw out small cell foundation. Establish packages in all 240 colonies using commercial package bees for the large cell and using small cell bees for the small cell colonies. (reasoning, this will get consistent brood comb built to measure the effects)
4. Run the colonies for a minimum of 3 years capturing weekly mite counts. This infers a modified bottom board that allows mite counts. Do not treat with any miticides at all. (reasoning, the varroa cycle is arguably 3 years so you have to keep records for 3 years. The only way to ensure valid results is to use no treatments.)
5. As colonies die out, replace them with walk away splits so that the genetics in a given yard remain pretty much the same. (reasoning, if there are genetic effects, you have to maintain consistent genetics to differentiate from cell size effects)
6. Maintain detailed colony records on all 240 colonies so that anova can be calculated on relevant variables. This includes recording buildup, swarming, queen replacement, honey production, etc. (reasoning, There are 3 variables to resolve, cell size, genetics, and mite virulence. With enough colonies in the test and with detailed records on all of them, some simple math will show which are operative in long term survival)


There would be quite a bit more detail involved, but this should be a start.

Side note, Dennis Murrell used to post here quite a bit as BWrangler.

DarJones
 
#42 ·
QUOTE=Fusion_
1. Set up a total of 240 colonies split into 6 different apiaries. All of the colonies in an apiary should be one cell size

How do you account for dfferences in yards? One yard can do poorly while 2 miles down the road another of equal strength initially can do great.

5 As colonies die out, replace them with walk away splits

But that's a managment plan that will effect the varroa populations. If they die out, should they even be replaced?
 
#44 ·
But that's a managment plan that will effect the varroa populations. If they die out, should they even be replaced?
Mr. Palmer makes a good point. However, I would think not replacing means you're testing the stock and less the method. Replacements should be noted of course.
 
#43 ·
DarJones, I'd sign off on that. But it's probably bigger than necessary and it's easily involved enough to be somebody's Ph. D. project. It would be a full time job for two or more people. I kinda like Barry's idea. How feasible would it be for each of two dozen or more beekeepers to set aside ten hives to follow the exact same procedure qualified under the categories you suggest? The queens could be provided from common sources. The results could be agglomerated and I believe they would be more valid because they're being collected from a broader variety of locations.

A thought occurred to me a little while ago. The biggest thing this whole discussion proves is that the anecdotal evidence given is contradictory in every possible direction, including within the stories of some individuals.
 
#45 ·
I know it isn't "done that way", but I've always thought a research team from a university ought to send one student out to a SCer and simply study, take data, observe, etc. and verify that the beekeeper is successful not treating. Then, based on that data, decided what a study should look like and have at it, with existing hives.
 
#51 ·
I know it isn't "done that way", but I've always thought a research team from a university ought to send one student out to a SCer
You do recall that the UGA study was conducted with the active participation of Bill Owens (aka Billybob)? You remember him, don't you?
And I swore I wouldn't get sucked into this again......
 
#46 ·
The authors withheld the real findings, and substituted plausible ones, because they would conflict with another major project. -WLC
If you have evidence to back up your accusation, I recommend you post it to support this claim. Otherwise, I'd like to see this statement retracted. Such an accusation is extremely inflammatory and downright libelous to anyone involved in peer-reviewed research (as the authors of the papers are).
 
#47 · (Edited)
"If you have evidence to back up your accusation, I recommend you post it to support this claim. Otherwise, I'd like to see this statement retracted."

Kieck:

It happens all the time.

The authors consulted with Gillespie about QW33 who would have told them that it contained the famous R2 insertion site and that polyadenylation was a hallmark of retrotransposition.

So, they certainly did withhold the information because of another project. The Beeologic/Monsanto project.

A project that was launched because of the discovery of immunity by retrotransposition/RNAi in the Honeybee.

Unless of course, you think that they're simply incompetent and have no business doing genomics research.

I could live with that.

That site is a hotspot for Honeybee molecular immunity, and it is also a critical marker for those interested in proving the efficacy of treatment free beekeeping and the use of small cell/natural comb.

Or, would you prefer to relegate these folks to counting mites and dead colonies instead?
 
#48 ·
The authors consulted with Gillespie about QW33 who would have told them that it contained the famous R2 insertion site and that polyadenylation was a hallmark of retrotransposition. -WLC
But that's not a finding of the research conducted in these papers. It could possibly be a note in the discussion at the end of one or more of the papers, but it's not a finding.

You claimed they withheld the real results of their results (the results of the data collected in the field) and replaced those results with "more plausible" results. You've accused them of falsifying data, in essence, or of deliberately modifying their data to fit with a hypothesis that they prefer.

A project that was launched because of the discovery of immunity by retrotransposition/RNAi in the Honeybee. -WLC
Such things may actually run concurrent with the findings of these papers. Immunity this way would be to viruses vectored by Varroa mites. These studies found that smaller cell sizes do not reduce mites numbers in hives. Very simple finding. An explanation for why so-called small-cell hives might continue to survive despite mite numbers being just as high as in so-called large-cell hives might rely on just such transpositional immunity. That still doesn't change the numbers of these studies and goes beyond the scope of the projects in these papers.
 
#50 ·
I have to toss a monkey wrench into WLC's tub. You obviously have a hobbyhorse to ride re RNA transposition. Unfortunately, it meets reality head on in the varroa mite. If RNA transposition were part of the equation with honeybees, then rationally you would have colonies that could acquire immunity to the viral assault. That would leave the mites to deal with. If unchecked, the mite load in the colony would spiral out of control until there were more mites than bees. Then it would climb higher still until each bee was inundated in mites. Just when do you think the bees start to die? If RNA transposition were a cure all, then feral colonies would now be immune to just about everything. Why aren't they immune to AFB? EFB? Sacbrood? BPV? IAPV? add as many others as you like.

At one time, Penicillin was considered a wonder drug. Just take a little and it would cure what ails you. Today we know that the efficacy of penicillin is limited and that all subsequently developed antibiotics are similarly limited. You can bet that RNA transposition will also be limited.

Enough OT.

DarJones
 
#52 · (Edited)
You need a proxy for mite virulence.

Something that you can measure simply or in greater depth using the same marker.

I'll avoid getting into the backstory, but measuring the proxy will avoid false positives, that you can get when using standard methods for measuring virus loads (AKA-virulence)and pathogens, by using a single primer pair that measures the status of the Honeybee's molecular immunity.

It can answer the fundamental question of how small cell (and treatment free beekeeping) can positively affect the Honeybee's immunity.

There are already more than enough studies that miss the mark.

It's time to aim for the heart of the matter with a 'robust' and flexible methodology.
 
#53 ·
Yes, the part you quoted was done, but what I went on to say was not, AFAIK. Did Berry spend a couple of years observing Bill's bees before the study? Did she verify how the bees were dealing with Varroa? If she found the varroa level in his hives to be no different than her LC bees, why do a study on mite loads? Commonsense would say there is something else at work and the study should have been done on another aspect. I know of no published statements by her that say "going into this study, the mite counts in Bill's hives were such and such over a two year period.

I drew you in and didn't even try! :banana:

:)
 
#54 ·
Did Berry spend a couple of years observing Bill's bees before the study?
Why would she? She trusted (and I'm sure still does) Bill's reporting. While I don't think Bill was doing any varroa testing, I expect that he presumed that his mite populations were low. Much of the impetus for the study was a result of Bill's experience. Bill had considerably more than two years with sc. There was never any doubt that the results were a disappointment to both Jennifer and Bill. But they were obligated to report them honestly. Last I heard, following the study, Bill was going to use up whatever remaining sc foundation he had and then go traditional.
The entire idea of following the colonies for x number of years is purposeless. They set out to determine if, as was commonly reported, small cell reduces varroa mite loads. Under the conditions they had...it did not. Six months, ten years, it doesn't matter. The trial was designed to eliminate as many variables as possible. It did a pretty good job. No real world testing can eliminate everything. The longer a trial goes on, the more variables enter in. The small cell folks complained about all kinds of ‘faulty trial’ conditions. Then the Florida group with Jerry Hayes and Amanda Ellis eliminated many of those. Then the Seeley group eliminated more.
The research folks spent valuable time, energy and money studying the small cell proponents’ main argument. Small cell failed that test. Now those same small cell folks want these researchers to perform countless, extended trials for every imaginable combination of variables that they can dream up. It ain’t gonna happen. The honey bee research community is strapped for funding…..always has been…and now even more so. They aren’t going to invest more in pure speculation.
If anyone has a pet theory and can finance or conduct their own trial, then that is what they need to do.
 
#55 ·
The small cell folks complained about all kinds of ‘faulty trial’ conditions. Then the Florida group with Jerry Hayes and Amanda Ellis eliminated many of those. Then the Seeley group eliminated more.
Is it time to actually discuss the studies yet? That does seem to be the topic of the thread.

Is it your contention that the Seeley study is the most refined of the studies, and that the results/claims are robust and defendable? Have you read the study?

deknow
 
#63 ·
...id like to discuss the seeley paper....its the most recent, tom has an excellent reputation for doing good work. Wlc, thanks for the link..I didnt know it was freely available.
Deknow
 
#64 ·
Very interesting indeed, and I would like to discuss it as well.

1.I didn't understand the part about cutting out the drone cells. It was my understanding that the mites prefer the drones (is this true?) and so the drones are sacrificial.
2. As he noted, the small cell seemed to do poorly. Can this alone explain the difference? Hives under stress are naturally more susceptible to mites, right?
2. A followup study would be interesting to see a test of foundationless vs standard frame, with no drone removal.
 
#66 ·
Haven't finished reading it, but so far I have a couple of things that give rise.

One on wax comb, the other on plastic.
Study done for such a short period.
The whole measuring bees part I don't get. How long after bees emerged were they measured? Why measure bees? A more accurate measurement of bee to cell ratio would be to measure the bee before it emerges.
 
#67 ·
Dee proposed long ago that one, if not the main effect, of large cell is the pseudo drone effect. Which is that the Varroa mistake the worker cells for drone cells and therefore infest both drones and workers.

I have stated here on beesource before ( http://www.beesource.com/forums/sho...es-small-cell-really-work&p=486705#post486705 ) that perhaps the cause of higher counts during the spring with small cell in the experiments that have been done, is because there are a lot of drones reared in the spring and the mites on small cell are more efficient at reproducing during that period because of the abundance of drone cells. As the drone cells fall off more later, those get infested even more and probably result in drone mortality at that point, but that may actually mean the Varroa are less successful because they are killing their host, and since they aren't infecting the workers (which they are not mistaking for drones) they are not less successful later in the year so that the Varroa population curve may spike in early spring and drop off by fall. I do not cull drone comb at all, and I have a LOT of drone comb because I do foundationless and never throw out drone combs and yet in the fall I have trouble finding Varroa. I think it was a huge mistake for Seeley to remove all the drone comb and drone cells. It removes one of the primary and likely theories on how small cell works. But counting mites also leads to erroneous conclusions unless you track the population over a couple of years minimum. But I think counting mites is a mistake. Counting survivors when not treating would be a more useful test.
 
#68 ·
... perhaps the cause of higher counts during the spring with small cell in the experiments that have been done, is because there are a lot of drones reared in the spring and the mites on small cell are more efficient at reproducing during that period because of the abundance of drone cells.
As I mentioned before, I see this in my hives. I have crawlers in the spring, but later in the year, they disappear.
 
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