the bluebonnet norfolk terrier club
Breeders Corner
 DataDawg 2015
Kafka said, "All knowledge, the totality of all questions and answers, is contained in the dog."
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Inheritance & Genetics
The Bluebonnet Norfolk Terrier Club does not recommend, guarantee, endorse, nor rate these recommendations or contributors, their kennel or their stock. The purpose of this section is to share the knowledge and experience of breeders who have vast experience in whelping and raising puppies. The tips and tricks below are intended to augment qualified veterinarian care, not as a substitute for qualified veterinarian care of the dam and puppies.
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Contributed from Dr. Andrew Kramer: Basically, if you're a Fluffy then you are homozygous for the long-haired gene and testing is irrelevant. This leaves those dogs who are phenotypically short-haired. The proportion of short-haired dogs that carry the long-hair gene (i.e. heterozygotes) is a function of the frequency of the long-hair allele in the breed and the level of inbreeding. If the frequency of the long-hair allele is small and/or inbreeding is high, then the vast majority of short-hair dogs will not carry the gene for long-hair. Since inbreeding is high in our breeds and fluffies are rare, the chance of a short-hair carrying the long-hair gene is very small. IMHO I would only test if I had a fluffy in the litter, and wanted to know if the other pups were carriers.
Jerold S. Bell, D.V.M., clinical assistant professor of genetics at Tufts University School of Veterinary Medicine, Bell says • The clinically normal full sibling of a carrier has a 50 percent chance of being a carrier.
From Magda Omansky  Dignpop Norwich Terriers CLEFT PALATE Good news is that bitches who were bred again after giving birth to pups with cleft palates did not have any other puppies with the problem when they were supplemented with Folic Acid. I spoke about the problem extensively with Dr. Padgett's team at Michigan State( the most definite authority on the subject) who believe it's an autosomal recessive traits with modifiers. Dr. Padgett's theory is that an environmental trigger must be present but it's an inheritable trait. Once a bitch, or a stud produced a pup with the problem, the future breedings should take it into consideration and ideally not double up on known carriers. Having said that, it's possible to have even multiple repeat breedings without a problem if the environment is highly controlled (eg. low dose of Vit A in food, high doses of Folic Acid, absence of pesticides in dog's environment etc.). Since the defect needs an environmental trigger you can avoid it, but you must be aware that in pairing dogs who produced cleft palates we're passing this to all offspring and they become carriers. If we breed a dog that produced it to the dog that never did, while supplementing with Folic Acid, we have a 50-50 chance of getting clear progeny and carriers, and no affected dogs. Probable high numbers of affected dogs being born recently has mostly to do with higher percentages of environmental triggers: lawn pesticides, dog food full of allergens, not enough Folic Acid in the diet etc. The genes have been there for a long time, but now we "activate" them with our more polluted environment and less natural food.
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