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In Loving Memory

My Kerry Named Britni

August, 1989 -  April, 1997

Morwins Britni Genevieve (AKA Britni) died after
seven years young,  as a result of a genetic defect
that is called factor XI deficiency.
This is her tragic story.

For more information on Kerry Blue Terriers in general,
please visit the Official Kerry Blue Terrier Home Page.


Morwins Britni Genevieve (A.K.C. No. RB327692), AKA "Britni", was whelped on August 13, 1989.  The sire was CH. Ruan's True Grit (A.K.C. No. RA555346) and the dam was CH. Kerrytrayl Star of Hope (A.K.C. No.RB054461). The breeders were William J. Morris (Morwin's Kennel) of St. Cloud, MN and Mrs. Robert W. Powell of IA.

August 1989 to April 1997


I have owned two Kerry Blue Terriers prior to Britni. The first was Candy.; I grew up with her as a child and well into my teenage years. I have fond memories of her antics and loyalty (She was put to sleep after 15 years young, due to Kidney failure, but what a wonderful companion!).

After that experience, I insisted that if we (my wife and I at this time) owned another dog, it would be a Kerry Blue Terrier. During our early years we were living in southern California and for several years we watched the Classified ADs for Kerry Blue Terriers, after deciding that we wanted our children to grow up with a Kerry Blue – a warm, loving, protective breed.

Finally, an AD appeared. Well, one sight and the deal was done, despite the fact that we were told that she was not "show quality" due to her small size (at the time the minimum size was 17–inches). We dubbed her Kassie. She was very protective, as some Kerry Blues are, and she was very aggressive. Anyone knocking or ringing the door bell would be greeted with a hearty barking. She even took on any dog in the neighborhood that looked like a threat, even a local Great Dane.

Eventually we moved back to our native land in Minnesota, where Kassie loved the outdoors, and the freedom that L.A. did not provide. We had to put her to sleep, however, after 17–years due to arthritis. It got to the point where she required a shot of cortisone every day in order to move. It was a very sad day.

Soon after, my wife, Mary, started looking in the Classified newspaper section for another Kerry Blue Terrier. Every time she would find an AD for a Kerry Blue, I'd hem and haw, but the ADs were far and few in between. Years pass.

Our 21st wedding anniversary was fast approaching in the year of 1989. And for the last several years, Mary kept asking me for a fur, after all, all of her sister's–in–law had one. Wouldn't you know it! She found an Ad in the Classifieds for a Kerry Blue Terrier about the same time. So on November 9th, Mary finally had her fur.

Britni was a sassy pup when I first saw her at 3 months old. The breeder indicated that she was the dominate female in the litter, although he felt that she was going to be a tad small to be "show quality".  It didn't matter. Sold! The breeder also indicated that she liked to chase squirrels. Boy was he proven right. Britni would sit and bark and chase the squirrels until we disciplined her (which was quite often). But it was the chipmunks that really galled her. They would sit right in front of the basement sliding glass door, sometimes only 2–feet away, eating bird seed that fell from the overhead bird feeder.
It was amazing, but from day one, I can't recall ever potty training her. It seemed like she trained herself.

Within a year her coat turned a beautiful silver – A great show quality coat! But, the breeder was right. She only measured 16–1/2 inches. One–half inch away from the standard (although I've heard that it has changed these days). So thoughts of breeding her and showing her slowly disappeared. Unlike Kassie, Britni was far more even tempered. She had an amusing way of greeting people with her "wo, wo, wo" kind–of–bark. It made most newcomers laugh. She always wanted her way and it took quite a while for her to figure out that I was the "leader of the pack", although she would continually test me to see how far she could get. For the most part, she would just ignore Mary, sensing subordination to the "leader of the pack".


After work and supper, I would normally settle on the couch and either watch TV or I would finish work that was left over from the day. Britni had a habit of sitting right next to me and snuggle as close as possible, waiting for me to pet her. She liked me to rub behind her ears and throat. This routine happened practically every night after work. Then one evening while rubbing her throat I noticed a lump. Since we had already had decided to have her spayed, we made arrangements with a local veterinarian to take care of both. She was three years old.

My wife brought her to the vet early in the morning. Late that afternoon I get a phone call from the veterinarian. They informed us that they could not stop Britni from bleeding and since they do not have a 24–hour staff, we would have to pick her up and take her to a 24–hour emergency hospital. What was about to unfold was the nightmares, of nightmares.

We picked her up at the veterinarian and brought her to the emergency hospital. On the way there, she was vomiting blood (I can not, to this day, understand why she had blood in her stomach. Where did the blood come from! Did the surgical knife slip? What happened?).

The veterinarian on duty kept track of her vitals every hour, until morning.

She survived the night.

The tentative diagnosis was hemostasis.

The emergency veterinarian on duty recommended that we take Britni to the intensive care hospital – Metropolitan Veterinary Referral Services (MVRS). We picked her up that morning and brought her to the intensive care hospital. She was clinging to life. The vet immediately checked her vitals, did a blood workups (Her platelet count had dropped to 20,000. Normal is 200,000), and administered a plasma transfusion. We were in constant contact with the veterinarian, calling every several hours. By that evening she had stabilized.

Both Mary and I were beside ourselves. How could this happen? What had gone wrong with the seemingly standard and routine operations? My suspicions were growing.

The next day, Dr. Goullaud of MVRS, suggested that we do extensive testing of her blood to try to determine the cause of her bleeding. We consented. But as it turned out, the testing was not as extensive as we were led to believe – we did, however, eliminate "von Willebrand's" factor as a cause, which is somewhat common in Kerry Blue Terriers and has a similar effect. After three days we took her home – relieved – but still wondering what had really happened and if or when it will happen again.

Still wondering and suspicious, the next three years were happy years for Britni.  The squirrels and chipmunks kept Britni busy. She loved fish though – while fishing, when I would catch a perch, I'd throw it at her and she would paw at it a few times, bite it once or twice and then drop and roll until the fish smell covered her coat. The next step was obvious.  A swim in the lake. She also had a fascination with candy. Didn't matter what kind – any kind. She would pick it up, taste it, drop it to the floor and do the drop and roll routine until we stopped her. It was sometimes hilarious, her antics.

Then in September of 1996, we noticed blood in her urine (we changed veterinary services, still suspicious). This was not good! Dr. Skinner of Prairie Village Pet Hospital informed us that the probable cause was stones in her bladder that must be removed. We related our last experience to him. This time there would more precaution. The first step was to increase her platelet count by giving her prednisolone, which helps to inhibit her immune system from attacking her platelets. Over the next two months her platelet count increased from 15,000 to well over 100,000 and the blood in her urine stopped. We also had a complete blood analysis done by Cornell University and finally learned the cause – factor XI deficiency!

It was December and it was time to remove the stones. Before the operation she was given one bag of plasma and during the operation, another. The operation went smoothly and we brought Britni home the next day.

Everything seemed to be going well for Britni, but by the middle of February we started noticing that Britni was lethargic most of the time. We took her back to the vet and analyzed her blood. Her platelet count was dropping despite the drug prednisolone. Towards the end of March there was a definite change. Her stools were black, indicating internal bleeding. Despite a mega dose of prednisolone and three plasma transfusions, she was not getting better. She was bleeding from her eyes, mouth, toenails, urine, just about everywhere. The end was near (tears). We told our three sons to go and say goodbye (tears).; We put her to sleep (tears).


Comparative Hematology Section
Diagnostic Laboratory
Cornell University
Ithica, New York
(case number: 7708-96)

The following is an excerpt of the report.
( smaller pink text indicates comments for clarity)

"Deficiency of factor XI, a member of the contact group of coagulation factors, is expected to cause prolongation of all intrinsic systems tests (APTT, PT, TCT [all clotting time factors are extended]). Inherited factor XI deficiency is an autosomal trait" (a chromosome other than a sex chromosome), "therefore" (both) "males and females are at risk for expressing a clinical bleeding disorder. The inheritance pattern (in humans beings) is thought to be incompletely recessive" (i.e. it does not always require both parents to have the recessive gene. Upon occasion, a single parent may pass on the factor XI deficiency). " There is variable severity of bleeding associated with factor XI deficiency. Most reports describe infrequent spontaneous bleeding, but severe bleeding after surgery or trauma. In affected individuals, the level of factor XI fluctuates, and severity of observed bleeding does not always correlate with measured factor XI activity or antigen (this is what happened to Britni). Factor XI deficiency has been reported in this breed.  It would be ideal to screen for factor XI deficiency in relatives, in order to try and reduce prevalence of the defect."

"Management to limit hemorrhagic episodes should include avoidance of invasive procedures and drugs known to affect hemostasis (aspirin, sulfas etc.). Transfusion with fresh whole blood, fresh plasma and fresh frozen plasma, will supply active factor XI." (Our veterinarian, Dr. Skinner, also put Britni on the drug, Prednisolone, which suppresses the body's immune system from attacking blood platelets [normal factor XI inhibits the immune system form attacking blood platelets]). "Multiple plasma transfusions are often needed to control a hemorrhagic crisis." (in our case, three transfusions were not enough and we exhausted the local supply of plasma).



A.K.C. No. RA555346
CH. Ruan's Dark Victory CH. Ruan's Blue Victory CH. Ruan's Irish Emblem
CH. Ruan's Miss Rapsody
CH. Wedgewood's Spoonful O'Sugar CH. Kerryglen's Quinn O'grady
CH. Downtheak Cob Keepsake
Blusand's Lil Bit O'Heaven CH. Kerrymear's Cleasai CH. Kerryglen's Quinn O'grady
CH. Kerrymear's Abhagail
CH. Ruan's Naughty Marietta CH. Ruan's Blue Victory
CH. Wedgewood's Spoonful O'Sugar

A.K.C. RB054461
CH. Kerrytrayl Supreme Hope CH. Kerrytrayl Major Event CH. Kerrytrayl Patrick O'Grady
CH. Kerrytrayl Special Event
CH. Kerrytrayl Luin's Supreme CH. Kerrytrayl Patrick O'Grady
CH. Elbrley's Rio Grande Zepher
CH. Pendregon Draioct Siofra CH. Kerrytrayl Major Event CH. Kerrytrayl Patrick O'Grady
CH.  Kerrytrayl Special Event
CH. Kiskevin Lady Guinevere CH. Kearnach Kayne of Kiskevin
CH. Kearnach Kenda of Kiskevin


After several weeks I decided to inform the AKC, as well as, Mr. Morris of Morwin's Kennel, of Britni's plight. Mr. Morris, the breeder, only offered his condolences, expressed sympathy, but no explanation why he offered for sale a dog with a genetic defect.

The AKC, however, wrote a rather long explanation. I quote the following from the letter:

"There is a widely held belief that "AKC' or "AKC papers" and quality
are one and the same. This is not the case. The AKC is a registry body."

Jeffrey S. Dorl, Correspondence Department, May 13, 1997

While informing me that the AKC is only a "registry body", they sent me a pamphlet that expounded upon the AKC Mission Statement as follows:

  • Maintain a registry for purebred dogs and preserve its integrity
  • Sanction dog events that promote interest in, and sustain the process, breeding for type and function of purebred dogs.
  • Take whatever action necessary to protect and assure the continuation of the s port of purebred dogs.

Based on this "Mission Statement" I challenge the AKC to answer the following questions based upon the following assumption.

Any dog, of any breed, can not be considered a purebred if it has a genetic defect. There is one thing, about the "state-of-health" (as you pointed out in your letter)  due to disease of an animal and quite another about the issue of a genetically altered animal, being classified as a "purebred".

1.  It is known that the Kerry Blue Terrier Breed is plagued by two known
     genetic defects:

  • factor XI deficiency, and

  • von Willibrands disease

2.  Why doesn't the AKC require a known genetically defective breed, to require
     a report from a reputable laboratory indicating the absence of genetic
     defects, in order to register the dog as "purebred". This is folly!!!!!!!!!! Based
     upon the mission statement of the AKC

3.  As far as I'm concerned any animal that has a genetic defect, is not a
     purebred and should not be registered and sold as such!

I feel very sorry for other owners who have purchased a genetically altered
Kerry Blue Terrier from Morwin's Kennel.  The pain and suffering to all parties (especially the Kerry) is enormous and at times overwhelming, especially when the problem can be prevented.  I think that Cornell University said it best:

"It would be ideal to screen for factor XI deficiency in relatives,
in order to try and reduce prevalence of the defect."

I Challenge the AKC
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Date Created: February 18, 1998
Last Modified: April 5, 2004
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