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G6S

7833 Views 38 Replies 12 Participants Last post by  Aja-Sammati
Can someone explain this disease completely to me please.
I have never heard of this in the goats that I have in my pedigrees, yet I purchased an outside doe from a semen collector in my area and then sold a buck to someone in Oregon and bam! that buck is a carrier.
The sire is not a carrier, the dam died last year. Her daughter passed this spring from kidding complications. The only other offspring out of her is fat and healthly and has never had any kids with any complications. He has sired over 90 kids so far, most over a year old now.
Please explain this disease to me.
Jennifer
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Read the article and then would love to start a discussion on it. Vicki
OK G6S discussion then.


I was very disturbed to see this happen to a goat that came from me.
Dam was
Diva-Cam's Menagerie DY Diva N1180278
Sire was
Pete-All 4 Winds ET Mountain Elk N1335365

I have had roughly 40 kids from Pete that are in my herd and other peoples or butcher bucks. I have never lost one of his kids from a discription of G6S. We have 4 milking daughters here that are 2 and 3 yrs old and 7 doelings that we are keeping this year.
ALL of these does are fat healthy and beautiful to behold. We also retained a buck this year.

Diva on the other hand,
We purchased her from a close girlfriend that needed milk and when she had purchased her from Mr Faircloth earlier that summer, she had raised a buckling and he thought that she would milk for this woman. She dried off from the move and so the woman sold her to me, I was glad to have her BoK lineage in the herd to cross with another buck that I had. After getting her here, I called Cam and talked with he and his wife about her. She had never had a doeling for them and they still have her full sister, so they sold her. She had raised a couple of meat kids for them but most of her kids that had nursed ended up with a COCCI load and they lost them.......
Now that I know more about G6S that last statement rings a bell to me. What do you think?
I have called the Faircloths twice now and have not been able to reach them. I know that they are busy with collections this time of year, they have Mega Bucks semen works. I will still try to get ahold of them and maybe be able to talk to them over the weekend about this.


The buck that we sold to Oregon for breeding was just an excellent specimen.
He really did things for her herd and had been shown and also retained his first leg.
What bothers me is that this woman was so quick to destroy this buck when she loved him so much.
She has also destroyed most of the kids without testing. She did test her favorites and retained 1 or 2, but only to put them down after kidding she says.

Can anyone else shed some light on this attitude for me.
Jennifer
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She had raised a couple of meat kids for them but most of her kids that had nursed ended up with a COCCI load and they lost them.......
Now that I know more about G6S that last statement rings a bell to me. What do you think?
What is this supposed to mean? What does cocci have to do with G6S?

I am missing something here.... Have the two animals Diva and Pete been tested as a carrier or positive for G6S?
Nobody can even understand let alone explain how one person runs their farm over another....it's her farm. We all have to make decisions about our own management, and then purchase from those who have similar management or philosphies about genetic disease and communicable disease.

I will be only using G6S negative bucks, and eventually want to test all my does, I do know Babbett is a carrier, and I know how she has it, mostly because I don't think anyone owns as much of the bloodline as I do and via testing of sisters out of the line, it is her dam line.

Tim she means that the unthrifty appearance and failure to thrive that G6S kids have is usually blamed on poor kid rearing or cocci/worms or all of the above.

None of us keep all the kids we have born, none of us can even keep track off 1/2 of the kids born out of our bucks, so to say that all his kids are fine isn't true. Further yearlings can still be carriers, or they can be positive, they don't have to die young, they can be bred and kid. So it is not self limiting in every situation. Vicki
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Any buck that I purchase or any buck that I keep as a replacement sire will be tested for G6S. Testing the whole herd right now is cost prohibitive. $30 a pop plus shipping and Vet bill is a whopping amount when you multiply it times every animal in the herd.

From Jennifer's post, I am assuming Pete turned up a carrier and was destroyed. A carrier buck is still healthy and can produce healthy offspring but he must be used on non-carrier does.

However, if this was the case that Pete was a carrier and this lady decided to "put him down", it was her way of managing the disease in her herd. I wouldn't do this with a buck who has thrown excellent kids, but I would have to test every doe he was bred to and then at least every buck kid I kept or sold from him. There is 50-50 chance of his offspring being a carrier.

Cam may be like a lot of breeders, they haven't seen the disease because they passed it off as an unthrifty fluke, or stunted from parasites or something. He probably can't give you any answers because he hasn't recognized the symptoms.

If you know Diva is the carrier in the pedigree then you can just still only guess that those cocci kids might have been G6S kids instead. How could you know unless the kids were tested as affected? It is really just a guess... Again I can almost guarentee that the breeder of Diva don't know her G6S status because if he did, he would be selective as to who he bred her to.
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What Tim said is what I was talking about concerning the cocci look of Diva's kids the kidding that we got her.
Pete is MY buck, he is G6S neg.
Diva is undetermined, but it had to be her as Pete is neg.

BUT, it says in the research posting that it would be possible to use a good buck still, just be cautious on whom is he is bred to.

SO, is this the facts.....
If you breed a carrier to a normal, part of the kids will be carriers?
Carrier to carrier would beget affected?

If only the affected goats are a health risk and not the carriers and the carriers never will, then why is this such a big deal?
Just test you goats once in their life and breed accordingly.
If they are carriers, then they are, breed to normals.

CAE, TB and Bruc are tests that we have do every year, at least G6S is a once in a lifetime test. It is actually less expensive that any of the above per goat.

Another thing that we can discuss is does anyone know of carrier bucks that there is only semen available from or such so that we can breed informadly with all of this OLD semen in the tanks?
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There is a list of carrier bucks and does on Nubian Talk. It's a list that needs to be on the INBA website, hmm Tim and Sara :)

Since you can test semen, you can always sacrifice a straw for the testing.

Testing your carrier does kids is going to be expensive, especially since they have to be done before shipping at 3 weeks. And why I would rather have a carrier female only having 1 to 4 kids, rather than carrier males who have many many more kids per year. I know for myself since I will have to test Babs kids anyway, I won't keep any carrier doelings out of her and won't sell any carrier bucklings. And even with her disclosed on my website, I still have two deposit's one for a non carrier doeling and one for a non carrier buckling, and they are paying for the tests if they come up negative. Positive I will pay for the test and the kid will then not be for sale. It's just how I am going to do it. Vicki
You could breed a carrier to a carrier and never have an affected or carrier kid- the odds are against it, but it is possible ;) Odds are that 1 in 4 will be normal, 1 in 4 affected, and 2 in 4 carriers.

And I think lots of Nubian breeders know there are Nubian lines that are carriers, that are supposedly untested that no one talks about... If you are really worried about it, only buy from people who test and declare, and declare what you know on your own animals. I think many people might test and not declare...and it is very fair to test for someone that requests it if they are willing to pay for it, but that is a personal opinion :D

I have a yearling that is smaller than my 7 month old kids- she has lots of issues that point to being G6S affected, but she can't be- her sire is tested normal- but even the appraiser thought she looked like an affected kid, though he had never seen one...

Michelle
have a yearling that is smaller than my 7 month old kids- she has lots of issues that point to being G6S affected, but she can't be- her sire is tested normal- but even the appraiser thought she looked like an affected kid, though he had never seen one...
I think my curiosity would get the best of me and I would HAVE to know what her G6S status is...
Michelle- I'm confused- you said

I have a yearling that is smaller than my 7 month old kids- she has lots of issues that point to being G6S affected, but she can't be- her sire is tested normal- but even the appraiser thought she looked like an affected kid, though he had never seen one...
But if only her sire is tested, how can you be sure she's negative?
Read the original paper on this. Both would have to be carriers to have an affected offspring. The only thing this doe could be is a carrier with a negative sire, which is supposed to be unsymptomatic. Vicki
I have read it, and I do understand the method of inheritance.

Inheritance is not the only way to get metabolic disorders. Nonsense mutations occur all the time, and it is possible to have a first generation mutation for a known disorder where both parents are negative, or one is positive but the gene contributed by the normal parent is the one where the mutation occurred.

So unless youve actually tested the animal, although its unlikely to have a first gen mutation, it is possible. Its actually quite common in the human form of the disease, which has been studied a bit longer than the recently identified caprine form.

Another potential, if tested and the kid came up with two positive genes, is that the first test on the buck was a false negative. I'd consider that possibility far more likely. Thats actually one of the things I was wondering about when I asked the question.

The more esoteric thought is that this a genetic disorder that is known to produce a constellation of disease expression in humans- in other words, the exact same genetic sequence may produce barely noticable symptoms in one individual and severe disease in another. Since the reserach on the caprine form is really in its infancy, it would be very interesting if you identified an individual that appeared symtomatic with only one abnormal gene.

It might be an expression of another genetic fault in that individual, or a hint that disease expression in a heterotypic individual may be dependant on enviormental infuence. Or a dozen other subtleties. But the researchers might just find it worth looking at, if all other cause for the symptoms are ruled out.
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Laura I am soo glad I found you...but girl you have to speak in English!!! :) Vicki
Sorry to bump this so late :blush I don't get on here very often...playing catch-up.

I should also have mentioned that the doeling I mentioned was a 7-10 day preemie that we suspect has congenital issues- most likely the cause of her size issues. I'd rather spend the money to have her dam tested, lol, as the doeling will never be bred, but yes we are curious...

If you are testing for a specific gene marker, than how could you come up with a false negative?
I don't think you can come up with a false negative. Barring someone in the lab just not reading it right or reporting it wrong....so I guess it could happen. It is not a disease it is a genetic defect. Our foundation doe is a carrier. I cannot bear to get rid of her, I also cannot afford to test all of her kids. I did test her georgeous daughter and she was not a carrier. Her full brother was fine for the first couple of months and then became very unthrifty and ended up dieing at the home that her was sold to. So it is a bit hard to say the reason he died because he was not under my own management. This was way back in the beginning of our goat adventure. So I have been in the process of culling all carriers. I did breed our foundation doe to our normal buck. I figure that if she had any kids that I absolutely love, I will test them. Otherwise they get sold as pet quality and unregistered. I was told that the lines that have this most prevently are also some of the old lines that are known for their heavy milking ability, probably due to the heavy line breeding. (not saying that linebreeding caused it) Carriers do tend to be on the small side. If your status is unknown and you have a doe that is small for what is considered the norm she is most likely a carrier. I would like to say that everyone should test and cull the carriers but it is so very expensive and I myself have that favorite doe that I cannot bear to part with. It's a dilemma. Shannon
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I also don't think, barring lab error that there will be false negatives. You can see Babbette on my website, she is a carrier and there isn't anything small about that doe. Vicki
This is all very interesting. Could you tell me at approxmately(sp) what age you would decide that maybe your does has this defect. I have two nubian doelings at ages 81/2 months. At the first of September one weighed 45 lbs and the other weighed 50 lbs.Have not grown much since then. They are very small but show no signs of illness. Very healthy. I know most people breed at this age but I have decided to wait until next year to see if they will grow anymore.
Part of size is definitely breeding & management, too. Are they from smaller parents? Have they been raised on cocci and parasite prevention? Some goats are just slower growing- I have some, too.
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