Description: This is a problem that I really don't hear much about outside my own herd and the herd that some of my foundation animals came from. Please contact me if you think you have seen it in your herd! It's called hydrocephalus, which just means "water on the brain" or that something is abnormal about their brain.
It is present at birth. The kids almost act blind, not following the herd or staying with their dam. But they do react to light and motion, so they are not actually blind. They go to a corner and push when they are hungry and they often push so hard that they take an abnormally hyper-extended posture (shown below.) Each affected kid shows different degrees of these behaviors. Some are very slow to learn things and appear "dumb."
We have tried to raise them by bottle-feeding (few would ever learn to nurse their dam), but they never learn to eat hay, so we have had to put them down. We had the Utah Veterinary Diagnostic Lab necropsy the bodies after death and they found an obvious part of their brain that was abnormal or missing/filled with fluid. They also seem prone to pneumonia but that could be because of abnormal feeding practices because they won't take a bottle nipple on their own. You have to open their mouth, push the nipple in, and support their stretched out body until they start sucking and relax.
(Video available.)
It is present at birth. The kids almost act blind, not following the herd or staying with their dam. But they do react to light and motion, so they are not actually blind. They go to a corner and push when they are hungry and they often push so hard that they take an abnormally hyper-extended posture (shown below.) Each affected kid shows different degrees of these behaviors. Some are very slow to learn things and appear "dumb."
We have tried to raise them by bottle-feeding (few would ever learn to nurse their dam), but they never learn to eat hay, so we have had to put them down. We had the Utah Veterinary Diagnostic Lab necropsy the bodies after death and they found an obvious part of their brain that was abnormal or missing/filled with fluid. They also seem prone to pneumonia but that could be because of abnormal feeding practices because they won't take a bottle nipple on their own. You have to open their mouth, push the nipple in, and support their stretched out body until they start sucking and relax.
(Video available.)
Inheritance: We stumbled upon this when doing some line-breeding in the first couple years of owning goats. Two of our foundation animals, who were related, produced affected kids in two successive litters. It appears to be genetic and follow simple recessive rules descending from certain relatives. But we see it so rarely, even when doing a lot of very close breedings, that we are not sure exactly how it works.
It should be interesting to note that most carriers we have seen trace back to Dawnland Tabby's Halifax, grandson of Goodwood Tom Thumb and Goodwood Water Lily. However, those are foundation animals found at the back of many pedigrees.
There is no genetic test. It would require DNA sequencing on multiple affected kids, carriers, and relatives until you can hopefully find the defective/mutated allele.
In order to get affected kids, both parents have to be carriers. And even then, you are looking at about a 1 in 4 of offspring being affected. So, looking at the Punnett square below, both parents are normal but carry the same recessive gene.
It should be interesting to note that most carriers we have seen trace back to Dawnland Tabby's Halifax, grandson of Goodwood Tom Thumb and Goodwood Water Lily. However, those are foundation animals found at the back of many pedigrees.
There is no genetic test. It would require DNA sequencing on multiple affected kids, carriers, and relatives until you can hopefully find the defective/mutated allele.
In order to get affected kids, both parents have to be carriers. And even then, you are looking at about a 1 in 4 of offspring being affected. So, looking at the Punnett square below, both parents are normal but carry the same recessive gene.
The 4 squares show possible offspring:
1. Non-carrier (DD-25%): Light blue is a normal kid who could never carry or pass on the recessive problem, even though they are directly descended from 2 carriers. And even when bred back to a known carrier, kids from this goat will always be normal. We feel like we have seen this from Barbeillon and Niolo, who were both bred to known carriers but had 4 normal offspring in each litter. But that's not really enough offspring or dice to "know" they aren't carriers. Of course the only way to be 100% certain that they are not carriers would be to develop a genetic test. Niolo has 2 parents and a full brother who are all carriers, but it appears he is not a carrier. Unrelated goats from other herds may also be "non-carriers." We don't know how often hydrocephalus occurs in the general Nigerian Dwarf population, but we don't hear about it much. For example, Giulianni, Mimolette, Jude, etc are from unrelated herds and are not carriers, but do have those same ancestors.
2. Carrier (Dd-50%): Orange shows kids who appear normal and healthy but when bred to each other or other carriers will have some affected kids. We had one doeling (D'Affinois) who was slow to learn how to take a bottle from the bottle rack and was just a little slow to learn things. But she did learn to eat hay and is living a normal goat life. We suspected she might be a carrier and bred her back to her grandfather (D'Ambert) who is a known carrier. That breeding resulted in one normal kid and one hydrocephalus or affected kid. However, we have not felt like other carriers (D'Ambert, Tumacacori, or Cantal) showed signs of being abnormal as a kid. Once a goat has an affected kid, they are easily identified as a "known carrier" from that point on. Many of the goats in our herd are "unknowns" and have never been bred to a known carrier, but once they have affected offspring, they are then carriers.
3. Affected (dd-25%): Pale yellow shows the percentage of kids who are born affected from two carrier parents. These are the abnormal kids who have to be put down. We don't see very many of them. See chart above.
1. Non-carrier (DD-25%): Light blue is a normal kid who could never carry or pass on the recessive problem, even though they are directly descended from 2 carriers. And even when bred back to a known carrier, kids from this goat will always be normal. We feel like we have seen this from Barbeillon and Niolo, who were both bred to known carriers but had 4 normal offspring in each litter. But that's not really enough offspring or dice to "know" they aren't carriers. Of course the only way to be 100% certain that they are not carriers would be to develop a genetic test. Niolo has 2 parents and a full brother who are all carriers, but it appears he is not a carrier. Unrelated goats from other herds may also be "non-carriers." We don't know how often hydrocephalus occurs in the general Nigerian Dwarf population, but we don't hear about it much. For example, Giulianni, Mimolette, Jude, etc are from unrelated herds and are not carriers, but do have those same ancestors.
2. Carrier (Dd-50%): Orange shows kids who appear normal and healthy but when bred to each other or other carriers will have some affected kids. We had one doeling (D'Affinois) who was slow to learn how to take a bottle from the bottle rack and was just a little slow to learn things. But she did learn to eat hay and is living a normal goat life. We suspected she might be a carrier and bred her back to her grandfather (D'Ambert) who is a known carrier. That breeding resulted in one normal kid and one hydrocephalus or affected kid. However, we have not felt like other carriers (D'Ambert, Tumacacori, or Cantal) showed signs of being abnormal as a kid. Once a goat has an affected kid, they are easily identified as a "known carrier" from that point on. Many of the goats in our herd are "unknowns" and have never been bred to a known carrier, but once they have affected offspring, they are then carriers.
3. Affected (dd-25%): Pale yellow shows the percentage of kids who are born affected from two carrier parents. These are the abnormal kids who have to be put down. We don't see very many of them. See chart above.
* of course when you breed a carrier to a noncarrier, you would have all normal kids, but roughly 50% would carriers and 50% would be noncarriers.
So it really depends on your breeding goals. If you outcross a lot, then you may never see it. If you breed an "unknown, possible carrier" to any relative or progeny, no matter how many generations away, you may get an affected kid.
So it really depends on your breeding goals. If you outcross a lot, then you may never see it. If you breed an "unknown, possible carrier" to any relative or progeny, no matter how many generations away, you may get an affected kid.
Parents involved:
Known Carriers: Tumacacori, ES D'Ambert, J Cantal, GL D'Affinois, Eagle Scout, ES Cendre
Suspected Non-carriers: (bred to known carriers and all kids were normal)
Mimolette, Raclette, Zoella, ES Niolo, D'A Barbeillon, Jude, Giulianni, Zufi, Zola, Zimbro, Gorgonzola, Brie, Daisy, ES Faisselle?
Suspected Non-carriers: (bred to known carriers and all kids were normal)
Mimolette, Raclette, Zoella, ES Niolo, D'A Barbeillon, Jude, Giulianni, Zufi, Zola, Zimbro, Gorgonzola, Brie, Daisy, ES Faisselle?
* because D'Affinois is a carrier, her dam Cantal is also most likely a carrier. I assume there are several other carriers in our herd, but there's no way to know who it is without breeding them to known carriers and getting affected kids.
Probability of unknown goats in my herd to be carriers: (as each generation gets further away from known carriers, then it's less likely the goat is a carrier, but it can change anytime they are bred to a known carrier. For example, D'Affinois had a 25% chance, being 2 generations away from a known carrier, until she was bred to D'Ambert and had an affected kid.)