# Question about mites adapting to non-"hard" treatments



## Erik T (May 22, 2007)

Thymol and formic acid kill mites in a different fashion than pesticides. 

Pesticides try to distrupt some basic function of a mite thereby killing it. Some of the mites that were stronger in the functional area that the pesticide targeted will survive. These survivors multiply and eventually all the mites will be tough enough to standup to the pesticide.

Thymol and formic acid cause severe damage at a cellular level to the mites. They have a more general action and do not target specific functions of the mite. Since the damage affects the entire mite organism, it is unlikely for them to develop resistance. 

The lower kill rates in thymol and formic acid treatments is probably due to them not effectively penetrating capped brood cells.


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## BjornBee (Feb 7, 2003)

When you do use a treatment that is 100% effective, and re infestation (as with mites) is almost 100% guaranteed, then your bees will never, ever, develop the ability to handle mites on their own.

Treating only those colonies that need treatment, not using hard chemicals, selecting from your best stock, and other factors, will one day see the bees handle the mites on their own. Why anyone would want to kill 100% of the mites and weaken the bees natural ability to deal with mites is beyond me. That makes as much sense as choosing a treatment that needs weekly application, even if it does claim to kill mites 100%. That does not make it easier for the bees or the beekeeper in the long run.


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## Jim Fischer (Jan 5, 2001)

> When you do use a treatment that is 100% effective, and re infestation 
> (as with mites) is almost 100% guaranteed, then your bees will never, 
> ever, develop the ability to handle mites on their own.

This received enlightenment has been going around for a while, so
I'll ask the question I continue to ask - where is an example of
this happening "in nature" or via breeding *EVER BEFORE*? 

We have a parasite here, and I'm a little confused as to why
no animal has ever become "resistant" to things like leeches,
bedbugs, mosquitoes, you name it.

Can anyone name any example of any animal developing some sort
of "natural resistance" or "ability to deal with" a parasite?

Yes, I know the claims made about bees, I mean a proven example
(which would have to be another example) from the past. 

Anyone?


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## Jim Fischer (Jan 5, 2001)

> The lower kill rates in thymol and formic acid treatments is probably 
> due to them not effectively penetrating capped brood cells.

The lower numbers are due to the refusal of beekeepers to buy and
use a simple $3.00 plastic push-in queen cage to limit brood area
before treatment.


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## Keith Benson (Feb 17, 2003)

Jim Fischer said:


> Can anyone name any example of any animal developing some sort
> of "natural resistance" or "ability to deal with" a parasite?


There is considerable evidence that being heterozygous for sickle cell confers resistance to plasmodium.

The benefit is such that it outweighs the cost of occasionally having offspring that her homozygous at that locus and therefore clinical with SCA. Cost here being defined as reproductive success or lack thereof. IOW, in the end you will have, on average, more kids reach reproductive age.

If you are the kind of person that doesn't think that humans are animals and are somehow special in that regard, here is another:

Hofer rainbow trout and _Myxobolus cerebralis_

http://wildlife.state.co.us/Research/Aquatic/WhirlingDisease/WDResistantTroutBroodstock.htm

Like mollusks?

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11769280&dopt=AbstractPlus&holding=f1000%2Cf1000m%2Cisrctn

http://cat.inist.fr/?aModele=afficheN&cpsidt=2433780

Sheep?

http://209.85.165.104/search?q=cach...tance+to+a+parasite&hl=en&ct=clnk&cd=40&gl=us

http://www.howlingoak.com/sheep_page/Parasite_resistance.htm

Skeeters?

http://www.med.nyu.edu/communications/news/pr_07.html

Mice?
http://iai.asm.org/cgi/content/abstract/74/1/549

General theory:

http://www.journals.uchicago.edu/cg....1086/374202&erFrom=-3438048089698077369Guest

In a large population of anything, there are going to be some hosts that are more sensitive to infestation/infection by certain parasites than others. This degree of variability will depends on a lot of factors and while it is possible that a particular parasite might be able to "get" every last member of a population, there is more to epidemiology of parasites than simply host susceptibility. 

In some cases the host behaves differently and reduces it's exposure, in others the host "tastes" less inviting than other members of it's species. It might have an accentuated immune response, it might have eosinophils that make higher levels of chemical weapons, it might simply lack some receptor that the parasite keys into, or have a receptor protein that the parasite has a 20% reduced binding affinity for (but it may in certain instances be enough). ETC. ETC. ETC. There are many ways resistance can be conferred to a host, and if there is a benefit that is realized by increased reproductive potential, then one can expect those traits to eventually become well represented in the population over time.

There are myriad ways all this can come to pass and no one has a lock on all of them by a long shot. Forcing the issue, i.e. trying to breed for resistance will depend on having some number of individuals in the population you are working with, with the traits you want (unless you are forcing mutation, and that is another kettle of fish). If they don't, you are up the creek without a paddle, or swimming in the shallow end of the gene pool depending on which metaphor you prefer.

Resistance is rarely the all out "sensitive or immune" deal that many want it to be. It is usually more of a partial effect. Most "resistant" hosts can still be overwhelmed if presented with enough of a parasite load or are compromised in some other way. You might be inherently twice as resistant to TB relative to say me, but if you are exposed to twice as many organisms twice as often, eat a crappy diet and are in otherwise poor health, it may do little for you in the real world.

The whole thing is fascinating and complicated. It almost get a kick out of it when I see guys with 6 hives trying to breed for resistance and develop a "sphere of genetic influence" and such. Correct me if I am wrong, but since bees can't fly into the ground, it would really a hemisphere of influence right? 

Keith

Since it dovetails here is something on developing resistance to bacterial infections (and lets face it, bacteria are just little parasites)

Careful on this one, it is not for the evolution-sensitive:
http://notexactlyrocketscience.word...ance-to-male-killing-bacteria-in-record-time/


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## NeilV (Nov 18, 2006)

*What d'ya think about this?*

Thanks to ErikT. That makes sense, and explains what's going on with these types of treatments. I think I get it now.

Just to keep things stirred up, I think I'll disagree with some of what Bjorn and Jim Fischer have to say, even though they know much more than I do.

First, Bjorn, it does not make sense to me that using a treatment with a 100% kill rate would slow down a process of the bees developing increased immunity to mites more than using a treatment with a 95% kill rate. The way that bees could develop resistance -- in theory anyway -- is that some bees would have some characteristic(s) that help combat mites and increase survivability. Bees without that characteristic would be less likely to survive at all. What would be left would be the bees with the favorable characteristic. Over time, the bee population would have increased survivability to the mites. 

However, if a beekeeper steps in every year and kills 95% of the mites, that natural selection won't happen. The bees that are not adapted to the mites would still live and reproduce if you get rid of 95% of the mites. It would not matter if the kill rate of the treatement was 95% or 100%. Any treatment that keeps the non-adapted hives going will disrupt the natural selection process. 

If a beekeeper's going to treat at all, it would be better to kill as many mites as possible. The mites that are there would be a drag on the productivity of the hive. Even if there would likely be a prompt reinfestation, I say its best to kill as many of the mites as possible, if you are going to treat.

Also, I don't breed queens. Even if you are right, it would make no difference to me. If I'm going to treat, I would rather kill 100% of the mites.

As to JF's post, as I understand it, your point is that it is unlikely that bees will have an adaptation that makes them immune to parasites. However, in the case of v. mites, this is an invasive species that is supposed to be living on A. Cerannae (sp?). Parasites are not supposed to kill their hosts, at least not on a regular basis, as committing suicide on a regular basis is a bad strategy. I think that both bees and mites could have adaptations that make the mite-bee relationship less fatal to bees. For example, bees could be more hygenic, while mites could have fewer babies. 

However, that would only happen if the beekeeper does not treat at all, letting nature take its course. I have seen a study in a Bee Culture which reported that this outcome was observed when somebody in some Scandinavian country let the bees and mites do what came naturally. By year 2, there were staggering losses, but then things improved dramatically by year 5. However, they just reported the results without identifying a mechanism. I also read somwhere a report which argued that this process may already have happened on a large scale regarding T-mites.

To really stir things up, I would propose another personal speculation involving the always fun and energetic topic of small cell foundation. (After I write this, I think I'll go kick the neighbor's fence and make their dog bark for entertainment.) As I understand it, there is an ongoing study at UGA which has, so far, concluded that small cell use does not lower total mite counts. However, SC users report that they simply do not have the same problems with mites as people on large cell. 

In the interest of full disclosure, although new to this, I am also on small cell and I bought my nucs from a small cell bee breder (Don K aka fat/beeman). The last time I did 24 hour mite count drops I found exactly one dead mite per each hive The hives did not grow as well as I hoped, but that's another story. I have not treated at all form varroa. (I am considering using thymol and some large cell next year if I expand to more hives, which is why I was thinking about this topic in the first place.)

How could everybody be right about this? One possibility is that the UGA study is incomplete and/or flawed in some way. I think MB has some objections to the study.

However, another possibility is that the small cell itself is not the cause (or sole cause) of the decrease in mites. What if small cell people are instead just breeding more mite tolerant/resistant queens, since they are not using chemicals that interfere with the evolution of the mite-bee relationship. I know that these folks do tend to get queens from survivor/feral stock, which could at least tend to help the process along. Then, when mites are not a problem without other treatments, the sc folks incorrectly assume that the small cell itself is the cause. (In other words, maybe this is a situation where correlation does not equal causation.)

I'm not saying this is true or I know what I'm talking about. Heck, I will readily admit that I do not have enough experience to know what I'm talking about. However, to me, it is an interesting idea that could be added to the list of "there oughta be a study."


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## Jim Fischer (Jan 5, 2001)

Keith, you are being deliberately disingenuous here.

I asked for a "success story", where a host BECAME or
was BRED to become resistant to a parasite to which
it had not been resistant before. What I'm looking for 
here is a reasonable model for the bee/varroa case.

_*Every single one*_ of the citations you offer are either:

a) highly speculative, offering the same vague hopes of 
speculative success currently offered by bee researchers.

b) offering the simple use of known resistance that *
already exists* in a population, but has been "bred out"
of the mainstream breeds by breeders more interested 
in other factors.

Also, NONE of these citations cover the case of a parasite
that is an EXTERNAL parasite of the host, let alone one that
is of (roughly) equal complexity to the host. All your examples
are of very simple creatures infesting the insides of much more
complex creatures. Intestinal bugs are a little different from
something like a leech that sucks your blood.

Why aren't there any humans that leeches "don't like",
and can avoid being parasitized by them? What about
mammals and fleas? Ticks? Where is the development
of some form of "natural resistance"? Where are the
bulletproof deer? The vampire-proof necks of humans?

To address and debunk each of your citations in turn:

> There is considerable evidence that being heterozygous 
> for sickle cell confers resistance to plasmodium.

Uh, I don't think anyone would view Sickle-cell as a good
thing, no matter what the claims are as to the "advantages"
of the disease, or even being heterozygous.

> Hofer rainbow trout and _Myxobolus cerebralis
_
* Pure speculation.*
"..._a management technique that *may* be successful..."_

> http://wildlife.state.co.us/Research...Broodstock.htm
> Like mollusks?

* Speculation again:*
"... _persistent efforts have been made to understand the *basis* 
for compatibility and incompatibility in molluscan schistosomiasis_..."

"_A *possible* molecular basis for the susceptibility/resistance dichotomy_..."

> http://www.ncbi.nlm.nih.gov/sites/en...1000m%2Cisrctn

"_this *strongly suggests* that 1 or several unidentified humoral 
factors are responsible for the non-development of the sporocysts 
from the challenge infection..._"

> http://cat.inist.fr/?aModele=afficheN&cpsidt=2433780
> Sheep?

"_in total, more than 28,000 lambs.... were *measured
for* host resistance..." 
_
So, the resistance already existed in sheep, and had been
"bred out" by breeders ignorant of the advantage of a
more diverse gene pool, or unconcerned with the 
specific issue of including and promoting the known
resistance.

Note that no one has ever found any Apis mellifera bees 
"resistant" to varroa, not surprising given that varroa only 
recently moved to Apis mellifera, and Apis mellifera had 
no similar parasite. Also note that attempts to hand-wave 
things like "hygienic behavior" so that it looked like 
"resistance" have pretty much failed.

> Skeeters?

Mosquitoes *DON'T GET MALARIA*!
They merely transmit it.
Malaria does not bother them one bit.

> http://www.med.nyu.edu/communications/news/pr_07.html
> Mice?

* Speculation still:*
"_*Innate* *immune responses* mediating resistance to this 
parasite *are not completely understood*."_

"Innate" means that they would have been there before, n'est pas?

But thanks for playing.


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## NeilV (Nov 18, 2006)

*Response and Question for Jim Fischer*

Why the focus on "external parasites" vs. "internal parasites." 

Probably the most important distinction would be that the external parasites you identify reproduce off/out of the host. Many internal parasites reproduce in the host. Reproducting off of the host would give the host less opportunity to develop resistance. There is, for example, nothing that my body can do to kill misquito larvae that are in the pond outside. However, when the whole life cycle takes place on/in the host, there would be more opportunites to interfere with reproduction and combat the parasite. I think this must be part of your point -- how do you adapt to something that just show up and sucks your blood? 

However, varoa don't fall into the category of critters that just show up and suck the host's blood. The mites reproduce in the hive. That gives bees plenty of opportunities to have characteristics that lead to adaptability to the mites. Possibilities include hygenic behavior, different pheremones or smell that are less appealing or attractive to the mites when looking for brood to infect, or possibly even small cell size. 

The question I pose to you is much like the question about thymol that I posed to start this thread: If there is not any relevant variation in bee populations, why would varoa mites kill some hives but not others? Is there some characteristic of the hive or is it just dumb luck that some hives live?. Why do populations of untreated hives drop after being exposed to varoa and then recover? 

The failure of scientists to identify the actual mechanism for adaptation does not mean the absence of the mechanism for adaptation. I think that is particularly true when there are, relatively speaking, so few researchers and so little $ devoted to answering these questions. 

BTW, is it "varoa" or "varroa"?

ndvan


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## BjornBee (Feb 7, 2003)

JM,
>>>>Why aren't there any humans that leeches "don't like",
and can avoid being parasitized by them? What about
mammals and fleas? Ticks? Where is the development
of some form of "natural resistance"? Where are the
bulletproof deer? The vampire-proof necks of humans?

I'm not going to answer these absurd requests.

First, I guess we are quite vague on what resistance is. What is resistance? Are we talking about bees ability to handle mites and keep them in check? Or are we talking about bees that can handle the damage that the mites can transmit.

I look at resistance in many forms as Keith has said. I have read that the human body does immune itself against the common cold. I have read that once you have a cold, you will never get the same cold twice. But with over 550 or more different strains of the cold virus, you just end up getting another cold sooner or later from a different strain.



Certainly, humans can handle a wide range of viral and bacterial issues. We are exposed to many agents on a regular basis. Now, what happens to a human when your immune system crashes (AIDS)? You become very vulnerable to once low risk diseases. Where perhaps the flu or pneumonia can be handles by healthy individuals, without a strong immune systems, these non-deadly issues now become life threatening.

I see bees the same way. If through grooming, selection of various traits, and keeping healthy colonies, and mite levels kept from reaching some overload point...then bees are able to cope with the viruses and other associated problems.

Some viruses are found in almost every bee sample. But why does one hive crash, and the next hive thrive with the same virus being present? Why does one hive constantly have counts of 2 or 3, and the hive next to it have numbers of something like 50 or 60? There is obviously something different between the hives. I have seen hives like this for several years. Many times, these counts can be averaged higher or lower with simply changing the queen. Why?

I am not sure what your definition of "resistant" bees is Jim. Bees with no mites? Bees with no tested viruses?

I don't think anybody has resistant bees if your definition includes bees with no mites or viral issues. But I do see a difference in one strain, or one hive as compared to the next. This gives me hope that there are differences between hives that make selection and further propagating from the survivors as worthwhile. Is it solely from one hive controlling mites? Or one hive with a better immune system? I think they are related.

We don't control the next black plague by becoming immune to the disease. We lessen the chances of outbreak by lessening the flea population, understanding whats makes the disease outbreak, using hygienic issues (cleanliness, personal health and hygiene), etc. Are we immune to the black plaque or some other flea transmitted desease? I don't think so. But its been awhile since anyone in my family has died from it. I can't suggest resistance. But this may be the closest thing to it.

So why not the same with bees? Are they resistant to mites or the real issues that kill bees...virus, bacterial and suppressed immune systems, etc. Not really. But as with humans and the plague, are there not traits, and management strategies that would control the devastation just the same? I think so.


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## Jim Fischer (Jan 5, 2001)

> how do you adapt to something that just show up and sucks your blood?

*Bing bing bing!*

We have a winner!

Yes, you got the point exactly.

> The failure of scientists to identify the actual mechanism for adaptation
> does not mean the absence of the mechanism for adaptation.

Uh, ok, but it would have to be both "random mutation" and a significant
change for the bees. Akin to the appearance of a bee with a very
hard ("stainless steel") exoskeleton. Please accept that there is no such
bee now. Please understand that the same bee would be "sting proof"
as well as "varroa proof". Kinda like a bullet-proof deer.


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## NeilV (Nov 18, 2006)

Yeah Jim, but what about the rest of my questions? 

ndvan


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## Dr. Pedro Rodriguez (Feb 5, 2002)

*honey bee parasites and the bees ability to survive*

Hello folks. 
This is one of the most interesting debates that I have seen in this forum. The reason for that is precisely that healthy honey bees can cope with their ailments or have demonstrated to be able to do so or else we would not have any bees at all. I have worked with honey bees for a very long time. I have seen a sizable amount of conditions involving sickenss in bees. Fortunately, prior to Varroa and tracheal mites, we were fortunate to have only a couple of illnesses to worry about, American Foul Brod and Nosema. Those of us who have been around prior to the coming of the mites know that bees were able to cope with AFB and Nosema. The bees were able to cope with the diseases most of the time except when added factors, mainly beekeeper added and weather influenced. We had AFB when I was a teenager beekeeper and definitely we did not know a thing about antibiotics because they did not exist. We managed to keep our bees and did a good job of it. In my household we did by recognizing each individual sick colony and destroying it. Mark my words. I was sick at heart every time that my father put a torch to a colony! But the lesson was clear. The only way to prevent having AFB was to have strong rules about sanitation. The bees did the rest. 
Today, there are way too many influencing factors than when I was a youg beekeeper but illnesses have slowly crept into the beekeeping scene. Add to that, viruses, parasites,
environmental changes, GMO´s and pesticides and other hard chemcials. It is a wonder that we have any bees that can cope with so many infuential factors acting simultaneously. This is the reason why I say that conditions like CCD are the result of the sum of all these factors acting together. 
Why do some colonies survive and others do not? The answer is not easy to be identified but it is likely that colonies that survive are those which do oot have to cope with all of these factors working together. Example. Colonies that are isolated at a site, never moved away, fewer virus carrying mites, high hygienic behavior traits, open bottoms through which mites may fall,
and added ventilation, treatments to reduce mite populations (thus reduced viral transmission) less deformed workers readily contributing to the welfare of their existence. 
I do not know about "resistance mechanisms" in honey bees. However I do know from all these years working with honey bees that sick honey bees abandon their ability to perform their colony functions. On the contrary healthy honey bees are able to survive natural catastrophies and although weakend bounce back next season. 
I have carefully explained in writings detailed description how I "think" that my FGMO/thymol concept works. Rather than listing all of them at this point (it would take too long) I respectfully suggest that my essays be read. The principle is easy to understand because it is based on physical and biologic charateristics of the mites and the host bees. 
I humbly suggest that my readers examine the message "with a grain of salt" and defer killing the messenger to a later date if you feel that the FGMO/thymol message is not a worthy utility for beekeeping.
Have a blessed day in the company of The Lord.
Dr. Rodriguez


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## Michael Bush (Aug 2, 2002)

The mites that cause mange on dogs are an interesting example of an external parasite and an immune response that fights them off. Most dogs have the immune system to deal with them. A few do not. Did they all used to have that ability? Did only a few have that ability and they survived?

Since most external parasites usually don't kill their host, there is no reason for natural selection in this matter. Since Varroa do, there would be natural selection (assuming you aren't treating for them).

People aren't killed by leeches so why would there be any natural selection?


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## Keith Benson (Feb 17, 2003)

Jim Fischer said:


> > how do you adapt to something that just show up and sucks your blood?
> 
> *Bing bing bing!*
> 
> We have a winner!


No we don't. 

There are a number of strategies found in mammals against arthropod blood sucking parasites. Many are behavioral - but they work to the degree they need to. Ever watch an elephant carefully coat itself in mud? I do, at least several times a week. Many animals use this strategy. Ever watch lemurs use their grooming combs to remove ectoparasites from one another? It works. In fact social grooming a a big thing with many primates. Even simple scratching provides some aid. It is not perfect, but mother nature rarely goes for perfect. She is more of a "good enough" kind of gal. 

A number of animals alter their habits so as to be out and about at the times when there is the least parasite pressure.

In addition to conspecific grooming there are many instances of interspecies beneficial grooming to remove or reduce the incidence of external parasites.

Changes in cutaneous leukocytes can also create a resistance to ectoparasitism (look up basophil and guinea pig and tick)



> > The failure of scientists to identify the actual mechanism for adaptation
> > does not mean the absence of the mechanism for adaptation.
> 
> Uh, ok, but it would have to be both "random mutation" and a significant
> change for the bees.


Nah, not at all. The change might be rather subtle. One could propose many (A lower threshold to initiate grooming behaviors. An increased sensitivity to the odors given off by stressed larvae etc.) An while it is interesting and should be described if we are to exploit it's full potential, it can exist outside of an explaination as to it's mechanism of action. I can't explain gravity, and in the end neither can you, but we both make use of it.

Resistance to a parasite is developed over time incrementally, There isn't the sudden deposition of iron and carbon in an exoskeleton. It will be a collection of a number of things, some present now, some the result of fortuitous mutation in the future. Most will be subtle and the thing most easily measured will be the sum of a lot of little things, not the actual things themselves, at least initially. And changes will happen in both host and parasite. Things like traveling and distance to other susceptible colonies or individuals will play a role.



> Akin to the appearance of a bee with a very
> hard ("stainless steel") exoskeleton.


Don't be silly. there would still be soft bits between the armor. Don't you know anything about armor?



> Please accept that there is no such
> bee now.


I do as the idea as you have stated it is ridiculous - which is why you stated it that way.



> Please understand that the same bee would be "sting proof"
> as well as "varroa proof". Kinda like a bullet-proof deer.


If you haven't already figured it out, deer have found a way to have beer sold to ******** at a low price so as to adversely affect their aim. That is how they are becoming resistant. Problems is the ******** keep buying bud and miller and don't quite get sauced enough.

Do I think the average beekeeper is going to breed resistant bees? Nah, the gene pool to select from will need to be huge. Do I think that over time the mites will be less pathogenic and the bees less susceptible to damage by the mites? Yep, seems to the pattern in host parasite relationships. It takes a long time though and there will be losses, lots of losses. And the resistance will not be perfect.

Remember this - we are not talking about absolute resistance here, it rarely exists. We are talking about being resistant enough to get by, that is what happens. Now there is often a difference in what an animals owner will consider getting by, and what mother nature considers getting by, something some of the harder core organic minded folk have a hard time seeing - but that is another thread.

Keith

Disclaimer: I use the term mother nature as the personification of how things work in our little neck of the universe. I know it is bogus, but it saves typing a bunch more words. Take it in the spirit it is intended and try not to make too much out of it.


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## Jim Fischer (Jan 5, 2001)

Lots of nice words Keith, but they go 'round in circles.

> Remember this - we are not talking about absolute resistance here, 
> it rarely exists. We are talking about being resistant enough to get 
> by, that is what happens.

OK, 'splain it to me then... we got these varroa beasties, and they
weaken the bees, burden the bees and transmit any or all of about
18 viruses that we know of. The darned viruses can mutate faster
than you can blink an eye, and the latest example is this IAPV
virus, which clearly is a variant or descendant of Kashmir Bee Virus.

How exactly is a larger breeding pool going to help, given the limited
genetic variants for Apis mellifera that exist? Maybe try to cross-breed
with Apis ceranae? Apis dorsota?

So, the physiological attack of a varroa mite is going to be hard for
bees to resist without some sort of learned behavior thrown in, which
clearly will vary widely from hive to hive. And the viral implications,
well, they are an even tougher nut to crack.

So, we DID have a winner there.
Well done, ndvan.
I'm not sure what other questions I have not answered for you,
so please list them or point to a specific post where I can find
them.


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## TwT (Aug 5, 2004)

I thought you all were talking about bee's being able to handle mites, not viruses, I think bee's can and are evolving to handle mites ( mine have lived going on 5 years without any kind of treatments) but handling viruses is different thing, that is like human's handling mosquitoes and not malaria, two different things


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## MichaelW (Jun 1, 2005)

With a smaller breeding pool you are going to have a higher percentage crappy (non-resistant) genetics coming in from outside. With larger breeding pool, the population can handle the now lower percentage of incoming crappy genes better.

People are incredibly resistant to leaches, we simply pick them off.

Resistant bees would be bees with a "balanced host parasite relationship" such as found in Apis cerana. That balance possibly evolved over time, or varroa was just never that successful with them. Breeders are trying to get euro-bees into a balanced host parasite relationship in an incredibly rapid time frame. But take a dozen or so resistant queens and throw them to the varroa wolves among a mass of crappy bee genetics and super mites and you have what we have. 

I'm a firm believer in breeding varroa as well. Time and time again researchers have taken euro-bees from areas where there is a balanced host parasite relationship with varroa and placed them in a different location and found them to crash with varroa due to the genetic difference in varroa.


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## NeilV (Nov 18, 2006)

*Response to Jim*

Jim,

You need to look into that job opening on the Price is Right.

Unfortunately, I'm not a winner (story of my life). I was just paraphrasing what you had to say. I agree with the idea that it would be much harder to adapt to a parasite that just shows up to suck your blood. I think MBs point about external parasites not being fatal is a good one, that I had not thought of at all. I also think Keith Benson's points that there is adaptataion to external parasites are well taken.

However, my real point was that Varroa mites do not really just show up to suck blood. They live in and reproduce in the hive.

Here are the tough questions:

"The question I pose to you is much like the question about thymol that I posed to start this thread: If there is not any relevant variation in bee populations, why would varoa mites kill some hives but not others? Is there some characteristic of the hive or is it just dumb luck that some hives live?. Why do populations of untreated hives drop after being exposed to varoa and then recover?"

In other words, if, as you suggest, bees probably cannot adapt to varroa, why does is look like they do just that? See Bjorn's new "bees adapting" post, which is an offshoot of this post. Jim, how do you account for the apparent decrease in varroa in Bjorn's hives since he stopped treating?

ndvan


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## Dale Hodges (Jul 13, 2007)

SHB showed up here 8 years ago. I was getting very fustrated, the bees didn"t offer any resistance. The SHB had the run of the hive. Now I'm seeing them fighting back . The beetle isn"t gone, but the numbers are down were the bees can function. They're not doing this by thier selfs, they've got all the help I can give them. I'm hoping the mite goes the same way, I'm not niave enough to think we're going to get rid of them, just help the bees fight back. IMO the bees learned to fight the hive beetle in a remarkablebly short time. Hope for the best, prepare for the worst.


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## Kieck (Dec 2, 2005)

I think this thread is missing some significant points.

Evolution, through selective pressure, is less about the "form" of the pressure than it is about the "strength" of the pressure. The greater the pressure (in any form), the faster and more strongly selection occurs. The resulting changes are "evolution."

The selection can either be natural or artificial.

Secondly, the source of the selective pressure is important. Not the form; the source.

Let's just take a blood-sucking insect, a mosquito, on a human as an example.

The mosquito bites the human and withdraws enough blood to fill itself. Selective pressure on the human? Very, very low to none. The amount of blood withdrawn is highly unlikely to pose any threat to the human. The mosquito, and, in most cases, the allergic reaction to the mosquito bite, however, make humans desire to avoid the mosquito. So, humans have developed a defense. Slap.

Now, if our human misses a mosquito, well, no real harm done. The mosqito escapes with her life and a full meal of blood. The human survives quite nicely, and the mosquito bite confers no real loss of fitness on the human.

So, the selective pressure from the mosqito on the human is negligible, at best.

But, if that mosquito is carrying a disease -- let's just say, malaria -- the human's life is at risk because of the malaria. Loss of life, if occurring before offspring can be left, seriously reduces evolutionary fitness. So, the selective pressure is much, much higher on the human. But not from the mosquito; from the plasmodium that causes malaria. As the chances of contracting malaria increase, the selective pressure increases.

Now, a "reasoned" method of reducing the selective pressure might be to reduce the population of mosquitoes that carry malaria, or a way to reduce the incidence of mosquito bites, but selective pressures don't function that way. The selective pressure is from the plasmodium, not from the mosquito.

Same thing goes, seems to me, for Varroa on honey bees. As long as the viruses or other pathogens carried by Varroa are the source of the selective pressure on honey bees, the adaptations that will enhance the evolutionary fitness (survival) of the bees will be in response to the direct source of the selective pressure.

Same ideas apply to resistance to "soft" treatments developing among Varroa. As long as the selective pressure is low (either the mites face relatively little chance of exposure to selective pressure, or the pressure does not significantly reduce the evolutionary fitness of the mites), resistance will develop very, very slowly -- if ever. But if the selective pressure increases, the speed with which resistance (or adaptation) will develop will increase correspondingly.

Just an interesting note on mites overcoming resistance: T. L. Harvey, T. J. Martin and D. L. Seifers at Kansas State University used experimental pressure to measure the speed with which wheat curl mites (Aceria tosichilla) can overcome plant resistance to the mites. The plant resistance is frequently physical, not chemical, such as "hairy" plants preventing the mites from acquiring feeding sites. Now, these mites are not the same as Varroa, but they are both mites. The wheat curl mites were not given a chance to switch plants -- either they managed to feed on the plants presented to them, or they starved to death. The mites overcame the best forms of host plant resistance available at the time of the study in 60 days. More interestingly, 60 days represents 8 generations of wheat curl mites.


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## Robert Brenchley (Apr 23, 2000)

Human adaptation to malaria is a perfect example of the random nature of evolution. We developed a gene which confers imunity; great. Why haven't we all got the gene? Because a homozygote develops a dangerous disease; sickle-cell anaemia. In a region with significant malaria, the gene reaches a level in the population where the extra offspring born to people with a single gene (advantage) balance out the offspring not being born to people who die of sickle-cell first (disadvantage)


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## JBJ (Jan 27, 2005)

*Response to Jim's Challenge*

"Can anyone name any example of any animal developing some sort
of "natural resistance" or "ability to deal with" a parasite?" Jim Fischer

OK, Jim I will take the bait, and take it a step further, just as a heuristic conversation.

I will go out on a limb and postulate that all animals or organisms that do not go extinct due to parasitism have developed natural resistance and coping abilities to deal with parasites (& I see virus as an obligate parasite) developed through a Darwinian type of natural selection. 

Would honeybees go extinct without human intervention? I would wager they would not, but there would be a huge genetic bottleneck where the susceptible genotypes are culled by Mom Nature.

Several Varroa and virus coping mechanisms have been observed and well documented in honeybees. For example, the researcher who first documented IAPV found that in 30% of the honey bee samples the viral genome had been incorporated in the the bee genome, thus conferring disease resistance from the virus. This type of genetic phenomena combined with other genetically based traits, such as higher degrees of Varroa Sensitive Hygiene (VSH), slightly shorter larval developmental periods, propensities for high degrees of allogrooming and individual grooming will prevent the extinction of the honeybee due to Varroa and the mites they vector. It is almost impossible to talk mites with a consideration for the virus they help transmit.


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## Keith Benson (Feb 17, 2003)

Kieck said:


> The selection can either be natural or artificial.


Define artificial in this context.

Keith


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## Keith Benson (Feb 17, 2003)

JBJ said:


> Would honeybees go extinct without human intervention? I would wager they would not, but there would be a huge genetic bottleneck where the susceptible genotypes are culled by Mom Nature.


I agree with the first stament, but question the idea of a huge bottleneck, at least as I read the term huge bottle neck. To me this implies a significant bottleneck, i.e. a narrow one. I think that it would not be as bad as you think. Would there be some loss of genetic heterozygocity? Sure, but nothing akin to say, the cheetah. Why? I think the base is too wide for that and the mites don't act fast enough. Of course I am speculating, and rather wildly at that.

Keith


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## Keith Benson (Feb 17, 2003)

Michael Bush said:


> Since most external parasites usually don't kill their host, there is no reason for natural selection in this matter. Since Varroa do, there would be natural selection (assuming you aren't treating for them).


If it feeds off of you, it affects you. Something need not kill you outright to have selective pressure. Now killing you is very effective pressure, but if it does so fast enough and completely enough you will never develop resistance. Think gunshot to the head.

For a population to develop resistance (and this is always discussed in terms of populations not individuals) you have to have a parasite that is not immediately fatal, and a host population in which there is some variability in susceptibility. Then you can see some changes related to selective pressure.



> People aren't killed by leeches so why would there be any natural selection?


Who says there isn't. Just because a behavior is A) a behavior and B) has other uses doesn't mean it does not fit the definition of resistance. Pick the darn things off. Primates have been doing this for eons. Come up to the level of the monkeys and pick. All this evolution and someone needs to point out that this is what you do to be resistant to a leech?

Don't confuse the ability to kill you with the ability to exert a selective pressure One is not the other. It can be, but it is not necessarily so. All it takes is to reduce your fitness to the point where it creates a differential between your ability to propagate relative to your conspecifics. Don't make the assumption that the mechanism of resistance is not already present in some other form, recognized by humans or not. Coming up with something brand spanking new is unusual in the extreme, mother nature tends to borrow and improvise rather than engage in de novo creation. That is apparently the realm of various creator deities.

Keith


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## Keith Benson (Feb 17, 2003)

Robert Brenchley said:


> Human adaptation to malaria is a perfect example of the random nature of evolution. We developed a gene which confers imunity; great. Why haven't we all got the gene? Because a homozygote develops a dangerous disease; sickle-cell anaemia. In a region with significant malaria, the gene reaches a level in the population where the extra offspring born to people with a single gene (advantage) balance out the offspring not being born to people who die of sickle-cell first (disadvantage)


 
Well put.

Keith


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## Kieck (Dec 2, 2005)

> Define artificial in this context. -Keith Benson


I threw the "natural or artificial" comment in to point out that selection can act through either method, but the amount of pressure is the significant factor.

This context, as I read it, is that honey bees are likely/unlikely to develop "resistance" to _Varroa_. Natural selection would be simply that bees that are "resistant" to _Varroa_ have greater evolutionary fitness. "Artificial" selection could be imposed on the honey bees by beekeepers if, for instance, beekeepers deliberately destroyed/requeened/etcetera colonies that showed any evidence of _Varroa_ infestation.



> . . . you have to have a parasite that is not immediately fatal. . . . -Keith Benson


To me, that is redundant. "Fatal parasite" is an oxymoron. "Parasites," by definition, are not fatal to their hosts. Once they become fatal, they move into the realm of "parasitoids" or "predators," to my way of thinking.


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