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.