I’ve been breeding goats for seven years now. I began with breeding five does. Over the years, I’ve expanded my herd, and last year I had twenty-one does give birth. My first year, we had nine kids, and last year there were forty kids born on the farm. It all started with my Saanen does, a Nubian cross doe and a borrowed buck. The next year I bought my own buck~Ozzy Osboer.
I kept three of Ozzy’s babies~two girls and Goliath. I even bought Goliath three little Boer girls of his own, so he’d have someone besides Mabel to breed.
I also bought Grover (You know, like Sesame) Street. He was my main breeding sire for a couple of years. He wasn’t much to look at, but his kids were beautiful, and I kept several of them.
I tend to look for patterns in my goat herd, and in the last two years I noticed a disturbing pattern. I began to lose kids. Two years ago Lily Osboer had twins, but her little buckling, Silas, died about a day after he was born. Later in the summer, just after we weaned kids, Milton and Sam died suddenly within a day of each other. It was devastating.
The next year, we had a kid born with entropion eyelids. Around weaning time, this kid also died. It reminded me of Milton and Sam, and I really began to wonder about our new buck, Jack. Until his arrival, I’d never lost a kid to these unknown circumstances, and he had sired all four of those kids.
Last summer, it became obvious we had a genetic disorder. Silas’s twin sister lost both of her twins~one at birth and one at just under three weeks. Then Helen lost her baby. My local vet agreed it sounded like I had some kind of genetic disorder going on in the herd. I sold Jack and most of his daughters…not for breeding.
I began doing research on genetic disorders. Let me tell you, there isn’t a lot of information out there on goat genetics. The horrible climax of the summer was the death of Jack’s yearling buck, Flash. I had been debating on what to do with him. I was kind of waiting to see how his kids finished before making any final decision. Yep, same sudden death with no obvious symptoms until just before death.
I made a map of the herd. Once I did this, it was very obvious where the problem started. In my color coding, yellow means they are a carrier. Red means they’re dead. I have three that are peach colored that died, but I’m not sure they were actually affected.
If you are really interested and want to see a bigger version, you can click HERE. My Saanens and Ozzy are fine. Mabel was a carrier. Grover Street was a carrier. Scarlet is a carrier. That means of all the Street girls, probably half of them are carriers, but I never lost a kid because it takes the same defective gene from both parents for a kid to be affected. I never bred Grover to Mabel or Scarlet~they were Goliath’s does. When I bought Jack, who was a carrier, I began to have kids who were affected.
I tried talking to Iowa State University vets, and they completely blew me off. The response I got was:
…talked it over with Dr. Plummer who is a small ruminant specialist here. We both agreed that the likelihood that the herd deaths are linked to genetics is pretty low. It is more likely coincidence that they come from the same buck. The reason that we say this is the following:
1. The deaths are occurring in animals of all age ranges. Most genetic abnormalities that result in death occur in very young animals.
2. The clinical signs may not be the same between animals. While you are seeing inappetance as the main clinical sign, there are many things that can cause an animal to go off feed and even to colic and have an upset stomach.
To get a better idea of what is occurring with your herd, I think it will be better for you (and your sanity since researching genetics can be hectic! J) to have Dr. Schmitz do some investigation and diagnostics with the animals that are becoming sick to find out exactly why they are becoming ill. Alternatively, we are always happy to see your animals here…
I pressed to see what other types of things they suggest I look out for since, in their expert opinion, it wouldn’t be genetics. The response:
…the first big clue that we often see is unwillingness to nurse or eat or play (in kids). They may or may not have a fever (for a goat, a temperature of up to 103 can be normal). The causes are really variable and can range from parasites to viruses to bacteria to nutritional imbalances to toxin ingestion, etc. Really, the best thing to do after you notice an animal go off feed is to take it’s rectal temperature and call your veterinarian. A simple blood test and/or fecal exam can sure help rule out (or in!) causes of inappetance and lethargy. This way you will know if it’s something to treat with antibiotics or fluids or nutritional supplements without guessing what to treat it with and hoping something works.
What they said makes sense if I hadn’t been checking for worms and hadn’t already had my vets see some of these kids and agree it was probably genetics. Obviously, they were not going to be of any help since they were acting like I’ve not been successfully raising goats for seven years. I went back to the Internet and kept researching and researching. I swear there were times I would read an article with the dictionary right beside me, or I’d Google the terms and then use the dictionary to figure out what it was talking about. It’s not fun easy reading.
Finally in November I found an article on a specific genetic defect, mucopolysaccharidosis IIID, that gave me hope. (Click HERE for article.) It is a lysosomal disorder meaning the cells don’t produce an enzyme that allows the lysosomes to break down a particular substance, in this case heparin sulfate (Source). Eventually, when the cell cannot store any more, it dies off, eventually causing the death of the animal. The symptoms sounded almost identical to what I was experiencing in my herd. Even more miraculous~there was a simple blood test for the disorder. This disease is the same as one found in humans, so goats with the disorder can be used for research on finding a cure for humans. The only catch~it is found only in Nubian and Nubian crosses. (See my article on Painted Boer Goats.) I figured it was still so perfectly describing what was happening that I had to test.
Dr. Schmitz came and drew blood from Betty Lou, whom I knew to be a carrier, and Fionn. I sent the samples in and waited. Due to my poor packaging, Fionn’s blood did not make it to the lab in Texas. Betty Lou’s arrived and was tested. A week later, I got an e-mail telling me the results were normal. I’ve never been so disappointed to have a negative test result. It meant I was back to the very beginning~nothing to go on. I assume, while not this one specific disorder, it is some sort of lysosomal disorder. Chances are, I’ll never know what it is in the herd. The only reason I care is because having that test would make it so much easier to breed the defect out of the herd.
Coming soon: The plan to get rid of this genetic defect.
Very interesting thanks for sharing
Glad you found it interesting. It makes the work and blogging worth it if I can help educate people.
you go farther than most folks would to research issues with your herd – and take effort not to pass it along.
It’s the only responsible thing I can do. I have to admit, Millie keeps me pushing to find out. 🙂
Wow…that’s a lot of research, time and heart ache for you! I’m sure it’s frustrating to have the university blow you off like that!! I hope your hard work pays off, and you can get rid of it!
It’s kind of a stab in the dark, but I’ll do my best.
Times like these can be so frustrating Teresa, especially loosing loving members of your herd and not knowing what to do next! Good luck! Hugs!
Thanks. I am trying my best to have a good plan to get rid of it.
Hi Teresa. Have you done liver copper levels on any of your dead goats? That turned out to be the underlying problem for a number of goat deaths I had a few years ago.
Donna
Copper really isn’t an issue in the area I live. There really aren’t symptoms that would indicate a copper deficiency. I have a large enough herd, any nutritional issue like copper would result in more deaths.
Oy. The Goatmother found out (after buying her) that Boo’s father carried the G6S gene – hence no babies for Boo. But that’s okay, because none of us are having any babies anyway. 🙂 I do hope you find a way around whatever your genetic problem is. Losing babies is no fun, I am quite sure – especially for someone who cares for your animals as you do.
There is a test (link at the end of the article I linked to) performed by Texas A & M that will see is she is a carrier if you did want to breed her. It is horrible to lose babies, especially when you know there is nothing that can be done. The helplessness is the worst. Do you ever breed your goats and have kids?
By the way, isn’t it awful that it is so difficult to find vets who know anything about goats?
I am actually one of the lucky ones because my vets aren’t too bad. I just struggle getting them to look past worms, but I’m working on them!
Oh, Teresa, the losses must have been completely heartbreaking. And to do all that research – that is not only time consuming, but must be so headache inducing trying to digest all the information. I wish you luck in your continued research.
That photo of Betty Lou and daughter Helen is breathtaking.
It is a lot of work, but if I can figure out how to get this out of the herd, it is well worth all the work. I love that goats spend quality family time together, even after they have grown up.
Good on you for persevering Teresa. Let’s hope there is a happy ending.
Thanks. I think I will get there eventually.
Excellent job of this! Though all so confusing.
YOU should become the premiere National Goat Vet!
Our worse death was Wee Bill who was the HUGEST kid in the herd…..displayed no problems…..ran, jumped, ate, played…never any scours. And then one day he just dropped down dead. It was so sad.
I applaude your efforts…especially in keeping us informed!
And, on a lighter note, sweet Fionn turned out to be a hottie! LOVIN’ those curls!
😉
I’ve always said those Saanen girls are determined to teach me everything a human could possibly know about goats. I just wish the lessons weren’t so hard. Fionn is a hunk for good reason~Goliath is his Grandpa and Ozzy his great-grandpa.
I’m in awe of your analyzing talents in this area. Even though the “experts” aren’t giving you any cred — I’d definitely still keep your chart. I really think you are on to something big here. Kudos, Teresa!
I’m guessing this is a fairly common defect. The research found that 25% of all Nubians are carriers of G6S, and whatever defect I have seems to be pretty common with the number of carriers I’ve ended up with in my herd. I certainly don’t have the skill necessary to figure out a test for it however.
How frustrating for you that you can’t get the vets at the University to help/listen! It seems that there is an attitude of “inferiority” towards goats in this country. We don’t even have a vet in this area that is interested in treating them. I’m curious to see what you plan will be…I learn so much from you about the goats!
I’m glad you are learning from me~hopefully it’s all good information. I am lucky that I have vets around that treat goats. I do think the attitude towards goats is changing, but it’s going to take a long time for it to make a difference. We also need to have vets actually listen to us goat owners.
Two of my first kids dies from birth defects. This is very educating, thank you for posting. I can’t wait to see what your plan is.
I’m not sure if it’s a good one or not, but I guess time will tell. Do you know what kind of defect your kids had?
They were both bucks and all I know is that their testicles never dropped and they were a lot tamer then the other bucks I had. It was really sad. They were my babies.
That is strange. I’m so sorry you lost your babies. It’s never easy to lose one, but especially so when they are your babies.
I never thought that breeding goats involves such a “science” ! They all look so good !
Those that are carriers are perfectly healthy and live a normal life. It’s only those that inherit the defect from both parents that become ill and die. Life on the farm involves science each and every day!
What an amazing amount of time and energy you’ve put into this! I can only imagine how heartbreaking and frustrating this process has been for you, but I am so happy to hear how proactive you’ve been about it all! Good luck with the rest of the process!
Thanks.
Kinda scary. Thanks for sharing. I pray this does not happen to me when I breed my girls.
The chances of something like this happening are relatively low. My goat herd is just determined that I learn everything there is to know about goats. I pass along what I learn so hopefully nobody else’s herd has to do that.
Thank you so much for your diligence on this. It is thanks to people like you and researchers that we even have large animals for disease research. My son has MPS II, which has no large animal models (only mice), so I was all ready to forward your information to researchers and families in the MPS IIID area if it had turned out to be positive. Do you know how they tested the blood? Sometimes it is difficult to find the genetic defect in MPS II at least. Thank you again.
I’m not sure how they tested the blood. I had to send it to Texas Veterinary Diagnostic Labs. It’s the only lab I’ve seen that does the test. I wish you and your son the best of luck.
UC Davis will also test using hair
I’m just reading through all the missed posts from December and this one just blew my mind. If I didn’t know who you were, I would have thought you were a researcher because of the way you are approaching this issue. It’s very interesting seeing how you are figuring all of this out on your own and without any help. I hope that the new babies this year will be better for you and that you are successful in getting rid of the genetic defect.
Hi
I bought 2 rams in Nov 2011 and put them with my ewes Dec 2012. My ewes started lambing and up to date i have 18 lambs. Of which i have 8 rams, the funny thing, it seems that all my rams are dying before 3 days of age. Of which the last one died yesterday, 2 were born today, but i am fearing for their lives. I starting looking on the internet and came across your article for genetic disorders in boer goats. That is what i have, the normal white with brown head. But you say that your genetic problem is only with nubian goats. Might it be a possibility that the boer goats can also have this disorder? Here in South Africa no one have ever heard of this problem i am experiencing now. No vets, no breeders or anyone. So i must see if i can find something. I am going to take my rams in for testing to see where this problem is coming from, but i want educate myself also, so that the vets here cant lie to me just to get me off their backs. I have had this problem, they tell you anything just so that you can stop asking questions. Even thought, they don’t even have the answer and their ego is to big to admit it. I guess, all i am asking you, is it a possibility that boer goats can also have this genetic disorder?
I am waiting for your reply.
Boer goats cannot have G6S. My goats do not have this specific disorder, but one that is very similar in its presentation. Chances are you will not be able to identify it. The best you can do is cull the buck. If you want to be even more efficient, you should cull the does that lose their kids also. It’s such a sad thing to see your babies die and feel so helpless. Vets really do try, but there isn’t a lot of research on many of the disorders goats might have. The reason I tested mine is because of the tiny bit of Nubian that was mixed in. Even though they look pure Boer, it might be possible to have a small bit of outside blood.
thanks so much for taking the time to share this. I have been reading the article. By raising awareness we can perhaps eradicate it from the goat herds.
I am trying to breed it out of mine. It’s a lot harder when there isn’t a test, but I didn’t lose a single kid from this defect last year!
I’ve been having a similar problem with my boer goats. One day they’re fine and then next they’re dead. A vet said it could be a thymine deficiency but none of the treatment worked. We lost both kids from the same doe within a few weeks of each other. They were also unusually small. Was this a problem with your goats?
I assume you’ve ruled out worms. Did you have a vet post one? Since I’ve learned more, I think it’s possible the older ones in my herd were victims to round worms, and just the newborns were the genetic defect. I have since switched bucks, and I’ve not lost a newborn since.
Consider testing for Johnnes it is a viral and causes much of what you describe…