Talk to me about Mega Colon...

[Bekah-n-Tennessee]

Although my plans are to breed Silver Foxes, I picked up a trio of meat mutts this past weekend to work with and get a bit of experience under my belt before my young SFs arrive. I was paying very close attention their eating, drinking and elimination as I was concerned about the stress of transport, food change and the heat/humidity and quickly realized that my one doe had poop unlike the others. She is the youngest (10 weeks or so), was actually the first of the three to settle in nicely, ate and drank really well. The size of her fecals are two to three times the size of my buck's who is considerably larger and many are oval. On to Google I go and...

Yeah, I'm 100% certain this girl has Mega Colon Syndrome. She not only has poops that sometimes can't even fall into the tray, has an incredible appetite (although I was free feeding her regardless due to her age and assumed as a grow out, she'd eat more) but low and behold, she has the patterns that are apparently classic for those that carry these genes. Since I was so focused on the Silver Fox breed, I know pretty much nothing about color patterns and the genetics that are involved with them and I actually picked her out of the litter.

Besides a very hearty appetite for her 17% pellets, hay and a couple of small romaine leaves a day, her poops are the only sign that I can see being an issue at the moment. She's actually quite sweet, comes up to me when I approach and looks to be quite relaxed and content without signs of pain or any GI stasis.

So...what do I do now? I had hoped to breed her in the fall, that's pretty much out of the question now I'm assuming. I had planned to dispatch these three rabbits and any offspring from them produced by end of year to focus 100% on the silver foxes anyway so should I just look to replace her now and mercy dispatch? My head is telling me that's the correct answer but admit I'm holding onto a little hope I can keep with my original plans for this 'practice' trio. (The other doe is older, told proven and bred so will see if I get a litter next week.) If, on the off chance, I could still try with her knowing she's not staying in my program past this year, any recommended foods to add to assist her?


Editing to add a comparison picture between this does and my buck's poop:


Side note: These pics are from my very temporary set up on my covered patio which is cooler, shaded and has box fan off to the side. My Bass 36x30 stacking cages were ordered 2 1/2 weeks ago, my building (two 3x3 windows on the back side as well) was just delivered this week which I'm fully insulating, installing electric, a shuttered exhaust ventilation fan, linoleum flooring and am contemplating AC. I am hoping to have that all up and running within a month.

 

[Preitler]

To me, those bunny berries look rather normal, not longish, really oversized, etc. . , even small compared to what my nursing does produce. If she has a healthy appetite, I wouldn't expect something much different. That grid doesn't look that wide anyway, so I wouldn't even expect all poops to fall through.

 

[Bekah-n-Tennessee]

To me, those bunny berries look rather normal, not longish, really oversized, etc. . , even small compared to what my nursing does produce. If she has a healthy appetite, I wouldn't expect something much different. That grid doesn't look that wide anyway, so I wouldn't even expect all poops to fall through.

I should have done a comparison picture so buck's is on top, young doe on the bottom (it looks even worse to me now that I put them side by side...):

 

[tambayo]

Broken with little color is an indication for a "charlie¨, but they need both parents to be broken and both pass on the broken gene for that to be a true "charlie". So first question is : what color where the parents?
Also, it carries the high risk, but is not a 100% given. Observe and as long as she is happy to eat, move and live life i'd not do anything now.

 

[Bekah-n-Tennessee]

Broken with little color is an indication for a "charlie¨, but they need both parents to be broken and both pass on the broken gene for that to be a true "charlie". So first question is : what color where the parents?
Also, it carries the high risk, but is not a 100% given. Observe and as long as she is happy to eat, move and live life i'd not do anything now.

I know the buck was broken, I don't know about the mother.

 

[kusanar314]

Knowing the genetics but not having experience with this issue, my thought is to just grow her out, see if she starts having issues, so far she seems happy and healthy (otherwise) from what you are saying.

Now, for the genetics part... What color is your buck? If she's En/En and he's broken En/en, then every kit will have a 50/50 chance at being a charlie like mom and then have a chance of getting megacolon as well. If dad is solid, you will get 100% broken kits with no charlies.

Edited to fix my gene notation, I had broken as en and solid as En which is backwards.

 

[Alaska Satin]

Although my plans are to breed Silver Foxes, I picked up a trio of meat mutts this past weekend to work with and get a bit of experience under my belt before my young SFs arrive. I was paying very close attention their eating, drinking and elimination as I was concerned about the stress of transport, food change and the heat/humidity and quickly realized that my one doe had poop unlike the others. She is the youngest (10 weeks or so), was actually the first of the three to settle in nicely, ate and drank really well. The size of her fecals are two to three times the size of my buck's who is considerably larger and many are oval. On to Google I go and...

Yeah, I'm 100% certain this girl has Mega Colon Syndrome. She not only has poops that sometimes can't even fall into the tray, has an incredible appetite (although I was free feeding her regardless due to her age and assumed as a grow out, she'd eat more) but low and behold, she has the patterns that are apparently classic for those that carry these genes. Since I was so focused on the Silver Fox breed, I know pretty much nothing about color patterns and the genetics that are involved with them and I actually picked her out of the litter.

Besides a very hearty appetite for her 17% pellets, hay and a couple of small romaine leaves a day, her poops are the only sign that I can see being an issue at the moment. She's actually quite sweet, comes up to me when I approach and looks to be quite relaxed and content without signs of pain or any GI stasis.

So...what do I do now? I had hoped to breed her in the fall, that's pretty much out of the question now I'm assuming. I had planned to dispatch these three rabbits and any offspring from them produced by end of year to focus 100% on the silver foxes anyway so should I just look to replace her now and mercy dispatch? My head is telling me that's the correct answer but admit I'm holding onto a little hope I can keep with my original plans for this 'practice' trio. (The other doe is older, told proven and bred so will see if I get a litter next week.) If, on the off chance, I could still try with her knowing she's not staying in my program past this year, any recommended foods to add to assist her?
View attachment 41706View attachment 41704View attachment 41705View attachment 41708
Side note: These pics are from my very temporary set up on my covered patio which is cooler, shaded and has box fan off to the side. My Bass 36x30 stacking cages were ordered 2 1/2 weeks ago, my building (two 3x3 windows on the back side as well) was just delivered this week which I'm fully insulating, installing electric, a shuttered exhaust ventilation fan, linoleum flooring and am contemplating AC. I am hoping to have that all up and running within a month.

I'm so sad to read this. It always seems to be the sweetest ones, right?

I agree, those poops aren't normal, and since she's so young, she may be at the beginning stages of megacolon syndrome. Whether she's genetically a charlie or not, it's obvious she has a problem. From discussions I've had with other breeders, megacolon can kind of creep up in the rabbit's life. (That's one of the reasons we don't breed charlies; as you now know very well, it's a bummer to sell someone a bunny that ends up sick!) Several folks have told me that there is a really wide range of seriousness to the condition. They've told me that some rabbits are more or less fine till around 3 yrs old, then they will start having periods of serious problems with weight loss, hygiene and eventually GI stasis.

So, long story short, she may be a happy bunny for the rest of this year, at least. As far as breeding her once, I'd not necessarily instantly rule that out. If she was in my barn and I wanted to stick with the plan, here is the reasoning I'd use to make a choice:

- Since it seems that megacolon rabbits have problems with nutrient uptake and metabolism, that would be my first concern with breeding her. While gestation usually doesn't seem to take a tremendous amount out of does, lactation certainly can challenge them. I would monitor her weight and hygiene religiously and at the first sign of problems, scuttle breeding plans.
- I would also have to steel myself to the fact that I might have to mercy-cull her at mid-gestation or even after kindling. In theory this shouldn't be any different, but to most people (me!) it really feels different. Having said this, if I was willing to give her the chance, I'd make sure to have at least one more doe bred at the same time that would be able to take fosters.

As you've discovered, megacolon is most commonly inherited through getting a double copy of that broken gene <EnEn>, so you wouldn't have to worry much about her babies suffering from it as long as you breed her to a solid buck. Even if you do breed her to a broken buck and get more charlies, if they're terminal meat bunnies and harvested at 10-12 weeks, it most likely won't be an issue. But since there are some charlies that don't ever seem to get megacolon, there may be some modifier or gene linked to <En> that is the actual cause. So, even if you do breed her successfully, I would not keep any offspring from her as breeders, as she apparently has it, and some number of her bunnies may inherit it; whether they're actually charlies or not, there's no reason to keep it going in any gene pool.

Keeping her on a bowl instead of switching to a water bottle is a good idea since it seems to be that megacolon rabbits need more water than normal; I expect that mucous overproduction coming from an irritated gut takes the hydration out of them. Some breeders have mentioned that consistency is even more important for megacolon rabbits than usual, so don't change her diet or routine if at all possible. Avoid anything that might be an intestinal irritant (fruit or other sugary foods like carrots etc.), and it sounds like some will keep greens to a minimum. I'd be inclined to go with @tambayo's and @kusanar314's suggestions to just watch her and make decisions as you go.

If you wanted a practice run to learn about rabbit breeding, you're getting it!

 

[Bekah-n-Tennessee]

Knowing the genetics but not having experience with this issue, my thought is to just grow her out, see if she starts having issues, so far she seems happy and healthy (otherwise) from what you are saying.

Now, for the genetics part... What color is your buck? If she's en/en and he's broken En/en, then every kit will have a 50/50 chance at being a charlie like mom and then have a chance of getting megacolon as well. If dad is solid, you will get 100% broken kits with no charlies.

This is my buck, was told he had some Rex in him but I really don't know. Apologies for the fuzzy picture, I haven't wanted to disturb them during this first week taking them out...

 

[kusanar314]

This is my buck, was told he had some Rex in him but I really don't know. Apologies for the fuzzy picture, I haven't wanted to disturb them during this first week taking them out...View attachment 41716

Ok, so, he's broken, which means that the kits will be 50/50 broken (like dad) and charlie (like mom) and as discussed in this thread, the gene or gene modifier that causes megacolon is linked to the En gene (I had it wrong earlier, En is broken and en is solid, I'm going to go edit for clarity) so 50% of her kits will have a chance to express megacolon and all of them will likely carry the modifier.

 

[Bekah-n-Tennessee]

I'm so sad to read this. It always seems to be the sweetest ones, right?

I agree, those poops aren't normal, and since she's so young, she may be at the beginning stages of megacolon syndrome. Whether she's genetically a charlie or not, it's obvious she has a problem. From discussions I've had with other breeders, megacolon can kind of creep up in the rabbit's life. (That's one of the reasons we don't breed charlies; as you now know very well, it's a bummer to sell someone a bunny that ends up sick!) Several folks have told me that there is a really wide range of seriousness to the condition. They've told me that some rabbits are more or less fine till around 3 yrs old, then they will start having periods of serious problems with weight loss, hygiene and eventually GI stasis.

So, long story short, she may be a happy bunny for the rest of this year, at least. As far as breeding her once, I'd not necessarily instantly rule that out. If she was in my barn and I wanted to stick with the plan, here is the reasoning I'd use to make a choice:

- Since it seems that megacolon rabbits have problems with nutrient uptake and metabolism, that would be my first concern with breeding her. While gestation usually doesn't seem to take a tremendous amount out of does, lactation certainly can challenge them. I would monitor her weight and hygiene religiously and at the first sign of problems, scuttle breeding plans.
- I would also have to steel myself to the fact that I might have to mercy-cull her at mid-gestation or even after kindling. In theory this shouldn't be any different, but to most people (me!) it really feels different. Having said this, if I was willing to give her the chance, I'd make sure to have at least one more doe bred at the same time that would be able to take fosters.

As you've discovered, megacolon is most commonly inherited through getting a double copy of that broken gene <EnEn>, so you wouldn't have to worry much about her babies suffering from it as long as you breed her to a solid buck. Even if you do breed her to a broken buck and get more charlies, if they're terminal meat bunnies and harvested at 10-12 weeks, it most likely won't be an issue. But since there are some charlies that don't ever seem to get megacolon, there may be some modifier or gene linked to <En> that is the actual cause. So, even if you do breed her successfully, I would not keep any offspring from her as breeders, as she apparently has it, and as her bunnies may inherit whether they're actually charlies r not, there's no reason to keep it going in any gene pool.

Keeping her on a bowl instead of switching to a water bottle is a good idea since it seems to be that megacolon rabbits need more water than normal; I expect that mucous overproduction coming from an irritated gut takes the hydration out of them. Some breeders have mentioned that consistency is even more important for megacolon rabbits than usual, so don't change her diet or routine if at all possible. Avoid anything that might be an intestinal irritant (fruit or other sugary foods like carrots etc.), and it sounds like some will keep greens to a minimum. I'd be inclined to go with @tambayo's and @kusanar314's suggestions to just watch her and make decisions as you go.

If you wanted a practice run to learn about rabbit breeding, you're getting it!

I really appreciate the time you took to break it down for me, incredibly valuable information and I absolutely concur with you on needing to steel myself on a possible mercy-cull mid gestation should we get that far. I know it would hit me harder.

With everything I have read and following other people's experiences, I will definitely be breeding two does at the same time come fall and thereafter. And yes, any offspring that may come, will be heading to freezer camp.

In the meantime, I'll continue to watch her like a hawk, make sure she is getting plenty of good, all she can eat, quality pellets. I'll start weighing her as well to better monitor her weight and make sure she is clean.

And good Lord yes..."they" always say be careful what you ask for and I asked for experience! And I guess I'll name her Charlie...poor thing.

 

[Bekah-n-Tennessee]

Ok, so, he's broken, which means that the kits will be 50/50 broken (like dad) and charlie (like mom) and as discussed in this thread, the gene or gene modifier that causes megacolon is linked to the En gene (I had it wrong earlier, En is broken and en is solid, I'm going to go edit for clarity) so 50% of her kits will have a chance to express megacolon and all of them will likely carry the modifier.

Good to know what I'm looking at, thank you for helping me understand. (And now I have another reason for sticking with the solid silver foxes...)

 

[Alaska Satin]

Good to know what I'm looking at, thank you for helping me understand. (And now I have another reason for sticking with the solid silver foxes...)

Breeding brokens isn't any trickier than breeding solids, now that you know about charlies. You just breed brokens to solids and there shouldn't be any problem related to the broken gene. You'll always get a combination of both patterns that way. And I've found that there is a large subset of people who really like broken colored rabbits, if you're thinking you might sell some bunnies in the future.

All of Charlie's bunnies would get at least one copy of the broken allele <En>, but it's not necessarily the case that all of her bunnies will inherit the tendency toward megacolon. If it is a modifier linked to the <En> allele (as far as I know, nobody has shown that conclusively, but it makes sense given observations over time), that does not mean it's automatically inherited along with the allele; linkage-based inheritance is commonly under 100%. However, you can predict that some of them will carry it, and it won't necessarily be the charlies or even just brokens - solids can carry and pass on modifiers too (though she won't produce any solids).

Some people actually like to keep a healthy charlie around as a breeder since that way they can get 100% broken colored litters. And there are some breeds that are charlies by design: Blanc de Hotot and Dwarf Hotot. Interestingly, a good friend who has been breeding Dwarf Hotots for about four years now has never had a case of megacolon, which I interpret as more evidence that the tendency to develop megacolon isn't 100% linked to a homozygous <En> gene.

Here are some charts that might be helpful in predicting what you're dealing with in breeding broken-colored bunnies.

 

[Bekah-n-Tennessee]

Breeding brokens isn't any trickier than breeding solids, now that you know about charlies. You just breed brokens to solids and there shouldn't be any problem related to the broken gene. You'll always get a combination of both patterns that way. And I've found that there is a large subset of people who really like broken colored rabbits, if you're thinking you might sell some bunnies in the future.

All of Charlie's bunnies would get at least one copy of the broken allele <En>, but it's not necessarily the case that all of her bunnies will inherit the tendency toward megacolon. If it is a modifier linked to the <En> allele (as far as I know, nobody has shown that conclusively, but it makes sense given observations over time), that does not mean it's automatically inherited along with the allele; linkage-based inheritance is commonly under 100%. However, you can predict that some of them will carry it, and it won't necessarily be the charlies or even just brokens - solids can carry and pass on modifiers too (though she won't produce any solids).

Some people actually like to keep a healthy charlie around as a breeder since that way they can get 100% broken colored litters. And there are some breeds that are charlies by design: Blanc de Hotot and Dwarf Hotot. Interestingly, a good friend who has been breeding Dwarf Hotots for about four years now has never had a case of megacolon, which I interpret as more evidence that the tendency to develop megacolon isn't 100% linked to a homozygous <En> gene.

Here are some charts that might be helpful in predicting what you're dealing with in breeding broken-colored bunnies.

View attachment 41729

All really incredibly interesting (you should know I've printed all of the info in this thread)! I really enjoy learning about the genetics and it's probably a good thing I'm not independently wealthy as I'd have multiple barns dedicated to different breeds and mixes...this is truly addictive.

 

[MsTemeraire]

Ok, so, he's broken, which means that the kits will be 50/50 broken (like dad) and charlie (like mom) and as discussed in this thread, the gene or gene modifier that causes megacolon is linked to the En gene (I had it wrong earlier, En is broken and en is solid, I'm going to go edit for clarity) so 50% of her kits will have a chance to express megacolon and all of them will likely carry the modifier.

I'm not sure it is a separate gene, more like the mechanics involved when a rabbit inherits two EN genes. Certain parts of the anatomy require the presence of pigment cells - melanocytes - to develop normally. A classic example of this is deafness in white cats - the inner ear hasn't received the melanocytes during embryonic development needed for hearing. It's a similar thing for Charlies, they have very little colour and therefore no melanocytes migrate to the intestines from the neural crest to enable the nerve cells there to develop, so they don't have normal peristalsis.

 

[MsTemeraire]

Here's something I found a while ago and bookmarked - it's a whole page with links to Megacolon in rabbits, case studies, research papers etc. Very useful if you're looking for more information.

Megacolon - The curse of the 33 spots

 

[Bekah-n-Tennessee]

Here's something I found a while ago and bookmarked - it's a whole page with links to Megacolon in rabbits, case studies, research papers etc. Very useful if you're looking for more information.

Megacolon - The curse of the 33 spots

Thank you so much for this, I'll definitely be combing through it.

 

[kusanar314]

I'm not sure it is a separate gene, more like the mechanics involved when a rabbit inherits two EN genes. Certain parts of the anatomy require the presence of pigment cells - melanocytes - to develop normally. A classic example of this is deafness in white cats - the inner ear hasn't received the melanocytes during embryonic development needed for hearing. It's a similar thing for Charlies, they have very little colour and therefore no melanocytes migrate to the intestines from the neural crest to enable the nerve cells there to develop, so they don't have normal peristalsis.

Is there no megacolon in solid rabbits? I honestly don't know.

I was assuming it's a modifier that tends to hitch a ride on the En gene but can be bred out by breeding exclusively charlies and culling anything and any lines that have the issues. Then you get perfectly healthy charlies eventually like with the Hotots

 

[MsTemeraire]

Is there no megacolon in solid rabbits? I honestly don't know.

I was assuming it's a modifier that tends to hitch a ride on the En gene but can be bred out by breeding exclusively charlies and culling anything and any lines that have the issues. Then you get perfectly healthy charlies eventually like with the Hotots

It is directly associated with the lack of melanocytes in the gut. It can also be late onset, so unless you kept all offspring for 3+ years you may not know if it has been bred out. Selecting for pattern along the spine would potentially help, as this is where the neural crest is located, from which the melanocytes migrate. It's the lack of pigment cells in that area which causes the megacolon.

It can be found occasionally in other rabbits but Charlies have a predisposition to it due to that lack of pigment.

Hotots are not Charlies. They also have the Dutch gene. Rabbits with white bodies that do not have megacolon would have a spotting pattern that allows the melanocytes to migrate normally, but then not produce pigment. The EN gene prevents them from migrating at all, hence the gut issues.

 

[Scooter1A]

I really appreciate the time you took to break it down for me, incredibly valuable information and I absolutely concur with you on needing to steel myself on a possible mercy-cull mid gestation should we get that far. I know it would hit me harder.

With everything I have read and following other people's experiences, I will definitely be breeding two does at the same time come fall and thereafter. And yes, any offspring that may come, will be heading to freezer camp.

In the meantime, I'll continue to watch her like a hawk, make sure she is getting plenty of good, all she can eat, quality pellets. I'll start weighing her as well to better monitor her weight and make sure she is clean.

And good Lord yes..."they" always say be careful what you ask for and I asked for experience! And I guess I'll name her Charlie...poor thing.

I think you will be fine. Good idea breeding both does at same time once they are of age. If you have room for all those babies for 10 weeks before processing. That's alot of babies coming your way ha. Anything you have questions about can be answered on this forum. These are very cool people. Have fun, happy summer!

 

[Alaska Satin]

It is directly associated with the lack of melanocytes in the gut. It can also be late onset, so unless you kept all offspring for 3+ years you may not know if it has been bred out. Selecting for pattern along the spine would potentially help, as this is where the neural crest is located, from which the melanocytes migrate. It's the lack of pigment cells in that area which causes the megacolon.

It can be found occasionally in other rabbits but Charlies have a predisposition to it due to that lack of pigment.

Hotots are not Charlies. They also have the Dutch gene. Rabbits with white bodies that do not have megacolon would have a spotting pattern that allows the melanocytes to migrate normally, but then not produce pigment. The EN gene prevents them from migrating at all, hence the gut issues.

That's really interesting about the spine marking possibly minimizing the problem - it would make sense. Although with the broken gene being the one blocking the coloration you'd normally get posterior to the saddle, and that blocking precluding any spine marking, I'm still not sure that explains why at least some lines of hotots don't develop megacolon.

As far as I can tell, some/many hotots are in fact charlies. Yes, they have the dutch gene as well, but observing the litters of my friend's Dwarf Hotots when crossed with solid Polish (for type), we've seen that every litter is entirely broken/dutch marked; she never gets solids. She always breeds correctly-marked animals in her line - the Polish crosses were someone else - and you would expect to get charlies if you were breeding correctly-marked hotots together, even if the stock were originally <Enen>. What I find so interesting is that she does not have problems with megacolon in her rabbits. She's been raising them for 5+ years now, and it's a pretty small community up here, so she has access to information about many/most animals she sells, and has never had any reports of issues.

On the other hand, a friend who raised Blanc de Hotots did have problems. In fact she was so frustrated by the constant GI issues and reproduction problems - which certainly looked like incipient megacolon, although I never got a chance to examine them internally - that she quit raising them.

The take-home we've settled on in discussions here (meaning locally, not on this forum), is that the modifiers that determine where the markings end up - regarding both broken and dutch effects - may be the drivers that determine the propensity for megacolon. The Dwarf Hotot breeder I know apparently got the "right" set of modifiers!

Here's an article with a lot more information about dwarf hotot genetics by a Dwarf Hotot breeder that I found really helpful:
https://www.adhrc.com/Forms/Color Genetics of the Dwarf Hotot.pdf

Is there no megacolon in solid rabbits? I honestly don't know.

I was assuming it's a modifier that tends to hitch a ride on the En gene but can be bred out by breeding exclusively charlies and culling anything and any lines that have the issues. Then you get perfectly healthy charlies eventually like with the Hotots

There can be several different causes of megacolon, including injury and disease, so it does occur occasionally in solid-colored rabbits. It's the congenital condition that seems to be mostly associated with charlies.

Yeah, breeding out the associated modifiers does seem to be what's happened in my friend's Dwarf Hotots. Although it's not as simple as weeding out many other characteristics, because as @MsTemeraire points out, megacolon can sometimes lurk asymptomatic for years.