4/28/08
From Magda Omansky, Dignpop Norwich
I have two comments about the relationship between early whelp and the breathing problems later in life. First, it is really important to understand the definition of an early whelp. It is a scientifically proven fact, not an opinion, that the due date has nothing to do with a breeding date. The due date is strictly related to ovulation. Only when the exact ovulation time has been pinpointed (progesterone tests are the most reliable method) the precise whelping date can be established, which is 9 weeks from ovulation date (63 days from ovulation, not mating). Sperm not manipulated by freezing or chilling lives on an average 7 days, and the eggs need to mature for 2 days after ovulation, so mating time gives an error factor of many days. Scientists have been able to film canine sperm "parking" itself on uterine walls waiting for mature eggs for a week or even longer. To add to that factor, most bitches start flagging and accepting male at the time of luteinizing hormone surge, which occurs about 4 days prior to eggs being fully mature. Some bitches do it even earlier. LH surge is followed about 2 days later by ovulation but the eggs do not mature for another 2 days and they live about 48 hours after that. I know for a fact that one of my bitches had LH surge 3 days prior to ovulation, so the 2 days time-frame of ovulation following LH surge is just an estimate, otherwise all theriogenology specialists will be advocating LH surge prediction. Instead, they ask us to pinpoint ovulation date. I have a litter right now bred 4 days post ovulation (due to all kinds of mishaps). If I calculated the due date from the mating the pups would have appeared to be 4 days early. They
were not! They were born precisely 63 days post ovulation but 59 days post- mating. This is my long answer to say that the relationship between breathing problems and early whelp can be investigated only with proper
definition of what is an early whelp. That is the first problem I see with jumping on the band wagon of linking respiratory problems with early whelp. It cannot be based on anecdotal and often incorrect reports.

My second thought is to make a distinction between UAS (a cluster of interrelated physical abnormalities of the UPPER airways) and under-developed lungs in early-whelp (true early whelp) that matured with
hypoplastic bronchioles and alveolar sacks. The respiratory problems stemming from being born too early are related to LOWER airways, not the UPPER airways in all medical literature. Being born too early has nothing
to do with elongated soft palate, or everted laryngeal saccules, or stenotic posterior nares, or enlarged tonsils- all the things we see in UAS. Please, please learn to understand UAS. It has nothing to do with lung function. I
know, we all would love to find one reason and call it a day. But everything we know about UAS shows a complicated set of anatomic abnormalities, most likely a very broad set of genes, possibly with some
environmental triggers but I very much doubt that early whelp, even accurately calculated, is one of them. There is no scientific basis for thinking that.

4/17/08
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.

3/26/08
It isn't always easy to get accurate information about dogs for pedigree evaluation. Unfortunately, not all breeders are forthright with genetic information for fear that admitting a carrier or affected dog may blacklist one's bloodline or kennel. However, reporting this information to open health registry databases is a viable way these genetic problems can be reduced or eliminated.

3/14/08
From Magda Omansky
Dignpop Norwich Terriers
CLEFT PALLETES 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.

3/1/08
Continuing Dr. Bell's Relative Risk Analysis theory, statistically. The offspring of an affected dog has a 100 percent chance of being a carrier.

2/22/08
Continuing Dr. Bell's Relative Risk Analysis theory, statistically • The clinically normal full sibling of an affected dog has a 67 percent chance of being a carrier.

2/12/08
Jerold S. Bell, D.V.M., clinical assistant professor of genetics at Tufts University School of Veterinary Medicine, Bell says • The parent of an affected dog has a 100 percent chance of being a carrier.

2/2/08
Jerold S. Bell, D.V.M., clinical assistant professor of genetics at Tufts University School of Veterinary Medicine, Bell says: If a breeding female has X amount of risk of being a carrier, breeding it to a low-risk mate can cut the carrier risk up to 1/2 X in the offspring, he says. However, if you breed three offspring, then you have added three times 1/2 X into the population. With relative-risk assessment, you have to combine the analysis with replacing the higher-risk parent and limiting the number of reproducing offspring

1/26/08
For a defective recessive gene to be passed on, there must be a carrier parent in each generation. However, unless the ancestral carriers have produced affected offspring or were the offspring of affected dogs, they cannot be identified. If four generations separate the carrier sire and an obligate carrier ancestor, then it is possible the shared ancestors between them could be carriers.

1/23/08
More factors for a Relative Risk Analysis Pedigree to be effective include:
There must be an established open health registry database, such as the American Kennel Club Canine Health Foundation�s Canine Health Information Center (CHIC), that records the confirmed affected and carrier status of dogs.

1/9/08
Important factors for a Relative Risk Analysis Pedigree to be effective include:
* The mode of inheritance must be proven to be recessive
* The pedigree information must be accurate and verifiable

12/29/07
Jerold S. Bell, D.V.M., clinical assistant professor of genetics at Tufts University School of Veterinary Medicine, says that when there is no genetic test for carriers of an undesired genetic trait, the most objective tool for selection against recessive disorders is a relative-risk pedigree analysis

12/1907
It is more difficult to predict affected and carrier dogs for some genetic disorders than others. Polygenic traits, meaning two or more pairs of genes involved in heritability, can be extremely challenging for scientists to develop a genetic test. Hip Dysplasia is an example of a polygenic disease for which no genetic test has been developed. It is easier to predict affected and carrier dogs for disorders having an autosomal recessive mode of inheritance. In these cases, both parents of an affected dog are carriers, even though they may appear normal. As the number of carriers increase, so will affected dogs. Fortunately, it is possible to evaluate pedigrees for recessive trait risk and use this information to make informed breeding decisions.

11/21/07
Relative-risk analysis does not identify carriers, just risk. Through pedigree analysis, you can lower your chance of producing carriers with each generation, but you must limit the number of breedable offspring, so as to not increase the carrier risk of the population.

11/13/17
From www.PurinaProClub.com: Using Relative-Risk Pedigree Analysis in Breeding
Responsible breeders are selective about choosing the best dogs to breed. Beyond considering physical characteristics, temperament and colors, breeders try to avoid passing on genetic disorders. Unfortunately, breeders don’t always have the tools and information necessary to make educated decisions.

It is more difficult to predict affected and carrier dogs for some genetic disorders than others. Polygenic traits, meaning two or more pairs of genes involved in heritability, can be extremely challenging for scientists to develop a genetic test. Hip Dysplasia is an example of a polygenic disease for which no genetic test has been developed. It is easier to predict affected and carrier dogs for disorders having an autosomal recessive mode of inheritance. In these cases, both parents of an affected dog are carriers, even though they may appear normal. As the number of carriers increase, so will affected dogs. Fortunately, it is possible to evaluate pedigrees for recessive trait risk and use this information to make informed breeding decisions.

(11/7/07)
POLYGENIC 
These traits are more complex than the typical dominant or recessive genetic trait. The additive interaction of the genes can cause variable results and the gene can be easily passed on to other generations without being identified. 
Canine hip dysplasia and elbow dysplasia are believed to be polygenic defects. 
1. As with the recessive trait, both the sire and the dam must contribute one or more of the genes that cause the abnormal phenotype in the offspring. 
2. Unlike recessive traits, the contribution from the sire and dam need not to be equal. 
3. Since we do not know the number or the specific effect of the genes involved in polygenic traits in dogs, no predictable Mendelian ratios are associated with these traits. 
4. Both sexes are affected with polygenic traits (excluding sex-limited traits), but not necessarily in equal numbers. 
5. The trait may skip generations and may appear to be erratic in occurrence.  

Especially when it comes to polygenic defects it is hard to tell which one of the parents is mainly responsible for the defect in part of the offspring. It is throughout possible that the bitch and the sire are equally responsible, but it could be that the bitch’s part is 99,5% and the sire’s part is 0,5%, or the other way around. A breeder might exclude both animals from the breeding stock, but this could mean that he would exclude a valuable animal that would produce normal puppies if mated to another partner.  

(10/17/07)
SEX-LINKED RECESSIVE 
(Hemophilia A, for instance, is a sex-linked recessive defect.) 
1. On the average half the male offspring of a carrier dam are affected. 
2. On the average half the female offspring of a carrier dam are carriers. 
3. The trait may skip generations. 
4. The pattern of transmission is often called oblique, because the gene goes from phenotypically normal dams, to affected sons, and then to phenotypically normal carrier daughters. 
5. Affected males transmit the gene to all of their daughters and to none of their sons, because the sons receive the Y- and not the X-chromosome. 
6. If both parents are affected with the trait, all offspring are affected. 
7. For an affected female offspring to emerge, the dam must be at least a carrier, and the sire must be affected with the trait. 
8. Most affected offspring in a typical pedigree are male. 
9. There may be related affected males on the maternal side of the pedigree, but only rarely (if ever) on the paternal side. 
10. All male offspring of an affected female are affected with the trait when the sire is normal, and all daughters are phenotypically normal carriers. 

(9/26/07)
AUTOSOMAL DOMINANT 
Some forms of epilepsy and deafness are autosomal dominant. 
1. At least one parent of an affected offspring must show the trait. 
2. The trait occurs in successive generations (no skipping). 
3. Males and females are affected equally. 
4. About 50% of the offspring of an affected parent will be affected. 

(6/3/07)
Autosomal Recessive
PRA and brindle, for instance, are autosomal recessive traits.
1. Both parents are proven carriers, but generally show no phenotypic manifestation of the trait.
2. The trait tends to occur in one generation and then skips one or two generations until carrier descendants are again mated, allowing the genes to be expressed.
3. Males and females are affected equally.
4. Matings between carriers (heterozygotes) on the average produce 25% affected (homozygous recessive), 50% carriers (heterozygous) and 25% that do not have the mutant gene (homozygous dominant).

(7/7/06)
Inbreeding: Inbreeding is defined as the mating of animals "more closely related to one another than the average relationship within the breed." Inbred pairings would include brother/sister (the closest form), father/daughter, mother/son and half-brother/half-sister.

(6/21/06)
Linebreeding and Inbreeding involve the mating of animals within the same family. Breeding relatives is used to cement traits, the goal being to make the offspring homozygous (pure) for desirable characteristics. Homozygous dogs tend to be prepotent and produce offspring that look like themselves (Walkowica & Wilcox 1994)

(5/31/06)
Linebreeding is frequently misunderstood and miscommunicated; in fact, it is not altogether uncommon for an outcrossed pedigree to be mistakenly viewed as linebreeding by the novice. We can more clearly define linebreeding and how we can more accurately describe our linebred litters.

(4/15/06)
The effects of linebreeding: Good shoulder and stifle angulation and good temperament are considered Recissive traits by most authorities. She temperaments and poor angulation are theoretically considered dominant traits. Breeders need to understand Dominant and Recessive genes in order to promote the positive traits and decrease the negative traits in our breeds.

(4/12/06)
Recessive Traits
HEAD: Pronounced parietal crest and occiput, Large skull size, Short ears, Fine skull, Light eye, Bulging eye, Overshot/Undershot Bite
BODY: Good shoulder, Angulation, Good stifle angulation, Long, reaching gait, Low tail set, No feathering on tail, Kinked tail, Long coat, Longer, straight leg (correlates with light bone)
MENTAL: Mild, non-aggressive temperament, Lack of intelligence

(3/29/06)
Dominant Traits
HEAD: Low set ears, long ears, long head, wide ear leather, dewlap, dark eye, correct bite, black nose, short face.
BODY: Sternum, deep chest, straight top line, straight tail, high tail set, good spring of rib, heavy bone, Achondroplastic short leg with crook (correlates with big bone), compact foot, short coat, weight, body height, poor shoulder angulation, poor stifle angulation, short, choppy gait.
MENTAL: Intelligence, shy and/or vicious temperament

(3/8/06)
Dominant and Recessive Traits
Dog breeders should understand two concepts: (1) aside from coat length and color, the trits of interest to us are for the most part polygenetic (controlled by many gene pairs), and (2) polygenetic traits are generally composed of a mixed bag of dominant and recessive genes. Although research in canine genetics lags behind that of other species, and some authorities disagree on whether certain traits are indeed dominant or recessive, there are dominant and recessive traits agreed upon by a majority of geneticists and breeders (Willis, 1989, Seranne, 1980). Most of these traits are controlled by numerous gene pairs (polygenetic) and factors such as incomplete dominance and penetrance. For our purpose, the most important task is to familiarize yourself with the list in general and make note of traits you wish to improve in your breeding program. We will publish the list with the next update.

(2/12/06)
Puppies and Peas. Our job as breeders would be greatly simplified if traits like good shoulder layback, temperament and reaching gait were controlled by single pairs of genes, such as those in Mendel's plants. Unfortunately, this is not the case. Outside of straight-forward traits like coat color and length, which are determined for the most part by single gene paris, most of the intricicate traits we desire in our dogs are controlled by complexes of genes which are called polygenes. Polygenes usually combine mixed patterns of dominant and recessive genes. Although we do not know how many thousands of genes are involved in polygenetic traits such as skeletal structure and gait, geneticists feel that such traits follow a bell-shaped curve, with most animals falling in the middle (Willis, 1989) Based upon this theory, two excellent individuals will usually produce slightly less outstanding offspring and vice-vversa Regarding size within a breed, most animals will be average sized, with excessively large or small animals being less common.

(2/10/06)
Breeding would be simpler if genes consistently played by the rules. Genes, however, are not always predictable. Several phenomena that can affect the action of genes include:
Incomplete Dominance, where a gene does not totally mask a recessive version (usually relates to temperament, intelligence, body height and length of leg).
Incomplete Penetrance, generally occurring in a heterozygous gene pair such as Aa, where the dominant gene A does not always show itself in a dog's outward appearance.
Modifying Genes which combine with other genes, accentuating the effect of a trait or changing it altogether (control polygenetic traits such as sholders, stifles and sternum).
Lethal Genes, which rsult in death of the embryo when they are passed on by both parents
Mutations, which are destroyed at birth but those such as the short legs of the Basset Hound and Dachshund were viewed as favorable and deliberately selected for.

(1/17/06)
Phenotype & Genotype. How a dog looks on the ouside does not always predict what genes he is carrying and what he will produce.
Example: A dog inheriting the gene pair Tt from his parents will have ticking, but because he "carries" the gene t for non-ticking, he is capable of producing dogs with non-ticking when bred to a bitch carrying the Tt or tt gene pair. The non-ticking would occur in any puppy that by chance happens to inherit his sire's t gene and a t gene from the dam.

(1/16/06)
Homozygous & Heterozygous Genes.
Heterozygous gene pair example: Tt (members are dissimilar)
Homozygous gene pair examples: TT and tt (members are alike)
Breeders goal: To "arrange" good genes in homozygous pairs to ensure that no matter which member of a gene pair a parent happens to pass on to a puppy, it will be a "desirable" gene.

(1/8/06)
Dominant & Recessive Genes. There are two gypes of genes whose interaction help determine which trait will be passed on to a new-born puppy:
Cominant genes "win out" over recessive genes
Use capital letters for dominant genes (ex T for ticking)
Use lower case letters for recessive genes (ex t for non-ticking)
Example, a dog inheriting T from the sire and t from the dam will have the gene par Tt and will have ticking.

(12/30/05)
Chromosomes & Genes are hereditary components in every cell that determine how a dog will look and act.
Chromosomes are made up of genes, which carry hereditary information. Chromosomes and genes are inherited by a puppy in related pairs, one member of each pair coming from the sire, the other from the dam. Each parent passes on a random, chance assortment of chromosomes and genes inherited from his or her ancestors.