The Independent Voice of the Afghan Hound Breed
43rd Year Of Publication

"The Deadly Blues"
by Gary Sinck
Our Afghans Aug 2005
As presented at the 6th World Congress, South Africa

What is it about genetics that makes people shudder, claiming not to understand it? It is not hard. Like most things people do not accept or claim not to understand. It is mostly a case of their refusing to do it. Like me being a computer minimal. A computer is a machine. Ergo, it is out to do me in, sane kindness, with a vengeance and probably messy electrical burns, shriveled fingernails and frizzled hair. So far my computer hasn't bitten me, shocked me (although some of the emails have been surprising), or done any bodily harm at all. Mentally it's way ahead. Especially when I hit the wrong button and can't figure out how to correct my error. Then AOL comes along and boots me off line for some reason. I pay the bill too! I can empathize but it doesn't mean I have to like it.

As people in a society chuck full of other people, we recognize dominance. Regardless, given two people 9a small chuck full society) one of them will be dominant over the other person to some degree. Than, given a group with many people in it, like your kennel club, you can recognize who is dominant, who takes over when the dominant person is absent etc. Right down the line, there will be someone new to take over, thus becoming the dominant individual

That is the basis of genetics. One gene is dominant over the rest of the genes (people) in the society (locus). It is an interactive society in which a person at another site may or can influence what happens at the location where you are. As in, "Oh yes! I want to take off my clothes and dance naked at this beach party." Then the thought "Mom will kill me," occurs and you can't do it. Genes work the same way. A gene at a totally different site can influence the expression (deeds, interesting or not) of a basic gene in another location. The topic of this presentation is just such a case.

In Afghans, black is dominant over read and black and tan. At another locus, there is a dilution factor turning black into blue. However, this is not a real color change. It is an optical illusion. The blue dilution factor restricts the airspace inside the hair follicles. The black pigment, melanin, clumps rather than being evenly spread out along the hair follicle. This clump9ng is seen as blue (gray) rather than black due to the way the light is absorbed into the hair.

Visually, it is hard to tell gray from blue. The resulting color is the same. In Afghan Hounds, a gray gene is present in at least two alleles, different modes of expression or color. The mutation with the gray gene appears to be dominant, causing the black pigment tot turn gray. A report in AARP magazine mentioned what happens with graying hair. Medical doctors Emi Nishimura and David E. Fisher (AARP, Dec 23, 2004) from Harvard Medical institutions, found stem cells generating melanocytes (the pigment producing cells) die off with aging or function improperly. The melanocytes are sent to the wrong site in the hair follicle and no pigment is produced. I think this type of activity or lack of proper malenocyte function, results in the black dog that turns (gray) as he ages.

This event also appears in the black-masked reds and creams. The black muzzle color becomes gray at an earlier age and suddenly your three-year-old animal now has a gray muzzle and appears to be a hundred and six!

Blues were rare for many years. When I started in Afghans in 1964, the first and only blue Afghan I saw was Ch Balkwod Colonel Mosbey. The Akaba era was beginning, and Top Brass had taken his first BIS in 1962. Lois Boardman produced blues right and left. People discovered or learned how to breed for the blue color at this time

First you need a black dog. If the black color isn't present, there are going to be no blues. The next step is adding the blue dilution factor into the mix. This is a recessive factor so an animal needs to receive the gene from each parent. An example from my own breeding applies her. Ch Dureighs Golden Harvest was blue factored although he was not black or blue himself. The blue factor passed through two generations from Golden Harvest, ending up in a third generation dog. He was a black masked cream of my own breeding which produced blues. It was a great surprise when there were two blue pups in his first litter, although we knew the dam was a blue factored black.

The origin of the blue factor in our pedigrees, those from Great Britain and the United Sates, comes from two sources. The first, an original import into England, Khan Of Ghazni, carried the blue dilution factor. Through him, via Turkuman lines, it passed into the Grandeur breedings.

The second source of the color comes from Saki of Paghman and Tazi of Beg Tute. Saki, a blue bitch and Tazi, a self-masked cream dog, were imported directly from Afghanistan to Pork Blakely, Washington U.S.A by Lawrence Peters and his wife in 1934. Peters was a foreign news correspondent. The couple became enamored of the Afghan Hound while in Afghanistan.

After much searching and frustration, they were able to procure these two animals; Saki and Tazi are the source of the defects under discussion here.

As far as I know, the blue syndrome was strictly an American problem. With the exporting of AKC Afghans around the world, starting in the 70's and picking up steam since then, I am sure the genes causing the problematic defects are being disseminated around the world. As in my examples of Golden Harvest, he received the blue gene from Turkuman (Khan of Ghazni) ancestors. He is an example of how the gene can pass through several generations before meeting up in the correct mix to express itself. The same unknown transmission of the "bad" blue factors can also occur, passing through several generations before the right combination of genes are matched.

The spread of descendants of Saki and Tazi is surely carrying the hidden defects in their germ plasm. Not every descendent carries the defects. Unfortunately for the breeders who own those that do carry the defects, there are some gruesome surprises awaiting them.

Just so you don't feel Afghans are especially cursed with these problems, the defects are not restricted to Afghan Hounds alone. The defects are actually linked to the color "blue". Do not panic, if you have blue or gray animals. Most are fine and wonderfully healthy. This information is only about the bad effects, if they occur. When they do, one has to accept the fact and decide on your course of action. As breeders, this is very important. With the ones maintaining the breed and passing along new generations to the fancy.

This quote from a Chinese Crested publication (Fernandez and Rhae p 168) demonstrates the problem exists in other breeds. "Over the years, researchers have identified several types of inherited hairlessness in dogs, including color mutant alopecia hair loss linked to the gene for blue coat in many breeds such as Doberman and Chihuahua.." The following breeds also exhibit color mutant alopecia, called Blue Dog Disease - fawn Irish Setters, some red and fawn Dobermans (besides blues). Blue dogs in these breeds also have problems; Dachshunds, Chow Chows, Standard Poodles, Great Danes, Italian Greyhounds, and Whippet." "Observation has shown the color mutation to be heritable and the skin defects to be associated with the coat color" (Muller, Kirk and Scott 1989)

Any mammalian species with the blue gene present appears to be affected. Certain breeds of cats, including blue point Siamese, have problems. The issue is not whether the problems exist, but trying to get information from the breeders.

I read an article (Goodwin 1972) about the variety of effects between mammalian species and would like to share the review of my summary notes. First, the effects vary greatly from one mammalian species to the next. The author's discussion did not contain any mention of gross anatomical defects. However, he did make the statement, dogs, with no specific breeds mentioned, were high on the problem list. He stated that the most work was done with guinea pigs, rats, and mice. These animals are widely used in lab situations because maintenance is easy and generational times short, and that came as no surprise.

Here's what he has to say about effects in human beings. "A number of pathological conditions have been discovered in which there is a genetically determined metabolic block.. of an amino acid.." This causes breakdown products to collect in body tissues. In humans, phenylketoruria is the resulting disease. The liver isn't able to create the proper enzymes to complete the metabolic process. High levels of incompletely used proteins collect in the body, causing several mental retardation (Goodwin 1972).

There are two things to note about the human disease. First, for my purposes here, the infants or children with this condition have a gray streak in their hair. Second, a good thing, if detected early enough, retardation is preventable with correct medication. The "black diaper" test is used to determine if this malfunction is present. A urine soaked diaper is placed in a chemical solution. If the defective metabolic process is active, the diaper turns black. Placed on corrective medication, retardation is prevented. After a certain age, the child is no longer threatened and medication can be stopped.

Although the metabolic breakdown in humans can be corrected, however, in our dogs, it cannot be corrected as far as I know. Once the defects begin to activate, there is no cure or magic fix. You can treat only the symptoms; there is no permanent cure. The animal will die regardless of how hard you try to avoid the outcome or the amount of money is spent on medical bills.

These are the defects that I've been able to gain knowledge about from owners, breeders and personal observation. It is very hard to find people with affected dogs who are willing to discuss the problems. Many don't realize it is an inherited problem, associated with only the color blue. They react like it's an insult to their reputation, breeding stock, or their plans.

Dealing with defects is difficult. The defects are not consistent, even within the same litter. There are multiple factors, affecting the severity and the number of defects occurring within a litter. Because it's a multiple factor inheritance, the problem could come from many places (loci or gene locations). One has to deal with the defects actually occurring,. One thing that makes a study difficult is that I do not call it "lethal" for nothing. There is probably no way to discover the number of conceived puppies vs. puppies actually delivered. I think in severe cases, many fertilized eggs die and are re-absorbed. This makes for a reduced number of puppy births. Reduced litter size is something not recognized when it happens. A litter of three of four is not uncommon where the average number of pups is around six or seven. It's a case of what one doesn't see, doesn't hurt one

1. Defect number one can be listed as in utero death. At birth, worse case scenario, are gross physical defects. Some pups are born with their abdomen open, intestines hanging out. A condition close to Spina Bifida is common. The entire central nervous system may be exposed. The nerve tissue was never encased in bone for some reason. The degrees of exposure vary greatly. It may include the brain and spinal cord in totality or smaller portions. Seeing these physical manifestations is extremely upsetting to owners or breeders. The good thing is these pups are stillborn or die at birth, unable to survive once the umbilical cord is severed. As a result, mortality rates are high at birth.

2 The next high mortality peak comes at about three days. At this time, the inborn food supply is used up. This results from an inability to adjust to independent life. Many pups expire, whether it is caused by a lack of digestive processes to breakdown milk, absorption, or other internal physical problems.

3. The next age at which pups experience increased mortality is at weaning. Again, I think it is an inability to adjust to a diet of solid food. This is not to discount other metabolic problems being activated with increased maturity. If the pups were autopsied or necropsied, an expensive procedure most people wont pay for, we would know a lot more about the actual cause of death. Now the pups are weaned and on their own.

4 The next really dangerous period seems to arrive by four months, often sooner. The most common symptoms are a combination of anemia and chronic gastric enteritis, neither responds to medical treatment or dietary changes. The combination is deadly. In many cases, this will be the first sign the blue syndrome is present and active. If you have a blue puppy and it develops this combination, you might as well bite the bullet. Your pup is going to die. There is no successful record of treatment saving an affected pup that I am aware of.

At these ages, these life-threatening events most often develop. These are also the most common problems and have occurred in all the litters I am aware of exhibiting the syndrome. I am sure there are other diseases or symptoms of which I am unaware. Again, these are the common problems.

Now, to consider the viable blue pups. These are the survivors. These are the Afghans who will carry on the bloodlines if bred. Not all animals will pass on the bad stuff but some will.

However, there are specific problems with adult blues. Often they have temperament problems. They are shy, exhibiting many behaviors associated with it. Uncontrollable fight or flight reactions are common behaviors. An Afghan bouncing like a yoyo on the end of a lead is not a good thing. Blues are often untrustworthy, fear biters at least and others just vicious.

Blues are often reluctant breeders, especially noticeable in males. They just don't appear to be interested in sex. This behavior is not limited to blue males from defective lines. Of course, not all blue males act this way, but lack of interest or sexual drive is not uncommon

Bitches are not exempt. I can attest from personal experience regarding my one and only blue, a bitch. Her dam did come from a "hot" line, but her father's side was a clean one. She got to travel to the East Coast on several occasions to be bred. She went many times, the freight people got to know her. When the owners of the stud dog came to pick her up, they were met with "Oh she's right over here. No asking who or what they were coming to freight terminal to remove. She never conceived. My vet said she was cystic, which means she didn't ovulate. This was prior to the days of the hormone treatments that are now available. Therefore, (probably fortunately) she never produced.

Reluctant breeding behaviors, sterility, lowered conception and reduced fecundity rates are common. If you're into blues and breeding them, you have to deal with these issues, None of them are insurmountable, just problematic. The good news is there are plenty of perfectly normal blues indistinguishable in temperament and behavior from any other Afghan.

Often another commonality found, in affected but viable blues is a slower growth rte and smaller size. Even Saki Of Paghman was recognized as a small bitch. These dogs aren't midgets or too small to be shown. They are however on the small end of the standard. Unless they have an extra edge such as good or flashy movement (not quite the same thing), or are truly Maltese blue, I think judges would tend to penalize them for being smallish.

The blues I'm concentrating upon are not the majority of blues, which are normal in every way. Don't take this presentation as a denouncement of all blues. I am not here to badmouth any blues, just to shed some light upon a problem with a few specific dogs.

Personally, most of the defective blues and their parents I've known have been most desirable animals. I can be green-eyed with envy on the best of days. Just look at the pictures of the descendents of Saki and Tazi. The Felt's dogs still make my teeth fall out when I see pictures of them. Elegant, typey, that piercing gaze, truly haughty expression, a look to covet. They remind of a cobra, poised and ready to strike, a truly spine shivering experience.

Here's some information from Afghan history that Conni Miller share with me many years ago. Readers who have studied the breed, know Kay Finch's first Afghan was Felt's Thief of Bagdad, a direct descendent of Saki and Tazi. With his get and grandchildren, Kay started two generations of out crosses with Ch Taejon Of Crown Crest, taking his daughters to Ch Ophaal Of Crown Crest, an import from the Holland kennels of Eta Pauptit. This was done to get away from the problems Kay was having with the blue syndrome. By breeding two generations of outcrosses away from the Felt's stock, she eliminated the problems in her kennels. However, the descendants from these crosses still carried the defects forward in specific cases. Generations later, the problem resurfaced here and there. They are most certainly still being passed long. Hidden they may be, the problems are still there.

Gary Sinck

Fernandez A and Rhae K (June 1999) Hairless dogs - the naked truth (from Chinese crested xoloitzcuintl and peruvianj inca orchid (p 168) Privately Published

Goodwin B.C.(1972) Tyrosine Catabolism, the biological phsysiological and clinical significance of Hydroxphenylpyruvate oxidase. Oxford Clarendon Press

Miller C and Gilbert Jr E M (1972) The Complete Afghan Hound (2nd edition). New York, Howell Book House (p 72)

Muller G H D.V.M. Kirk R W D.V.M and Scott D W D.V.M (1989) Small animal dermatology (4th edition) Philadelphia; W B Saunders Company. Harcourt Brace Jovanovich. Inc (p 677)

Nishimura E M.D. and Fisher D E M.D. (2004, Dec 23) Science on line, AARP, Washington DC. AARP Publications.

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