The.....MBT.....TELL-AGRAM.....july/97.....Issue#2

The response to the first issue has been rewarding, surprising, encouraging & only dismaying in that many readers asked for both more content & more than quarterly issues! We’ll see what we can do. There’s certainly enough subject matter sent in and accumulated from other sources to warrant a newsletter every two months - just not enough hours in the day, days in the week, and postage monies. I was somewhat unnerved to be getting multiple calls from minibull fanciers who wanted a copy of the first issue which had only just been sent out - then a call from Wanda Moriarty to tell me she had mentioned the MBTT on the Internet. Several people thought they’d been missed - but weren’t: many more didn’t get their copy in the time they thought they should’ve, didn’t want to wait, and had their friends fax them instead. I’m gratified to see the MBTT getting the attention it deserves.

The MBTT is not a club and especially not a Bulwark Minikin home page newsletter. That Bulwark Minikin dogs feature so often is only because I have more information on them (so far) than on other dogs. As Dave Barry said to people who asked him why he talked about his dogs so much - "Well, I don’t know anything about your dogs."...Your editor is not a saint, veterinarian, or preacher - merely a breeder somewhat more outspoken than most. As such, I’m obviously going to be a target from many angles & it may well be that I’ll have to change my opinions on matters made clearer to me by higher authorities. That’s fine - that’s part of communication. It’ll be MBTT policy to publish the flak - provided the owner acknowledges it. Some comments & criticisms, of course, are not the same thing as flak - merely corrections of erroneous statements, or better explanations, or updated arguments. Let us all recognize the difference in both real life & the MBTT...

Regarding letters & other types of submissions to the MBTT - please, no ticking parcels! Seriously, if the MBTT needs to edit your offerings, it will make every effort to retain the gist, tone, length, and context of the original. I remember years ago reading a judge’s critique in which every grammatical error & spelling mistake was painstakingly reproduced and later learned that it was done on purpose to make a fool of the judge whose decisions had not been appreciated. The MBTT will correct as necessary.

Somewhere in every issue, the MBTT will publish corrections from the previous issue. I’m sure this will be one of the more popular sections. The MBTT is already planning better reproductions of your photos, and as I learn more about my disability at the keyboard & with my computer’s help, the layout should become smoother & more visually dynamic.

The MBTT will be on the Internet - if you can access it from there, please do & save us the postage.

NEWS FROM AROUND THE WORLD

AUSTRALIA/NEW ZEALAND breeders & pet owners are reeling with the impact of a fatal kidney condition affecting two major breeding lines. Polycystic kidney disease is a familially inherited defect. The disease is diagnosed with the use of ultrasound; with this disease, blood and urine testing may not pick up affected dogs early enough to keep them out of the breeding program. As with most diseases, the progress & severity of it varies with the individual animal.

Queensland & Sydney Veterinary Schools are currently doing research into this particular kidney defect. (What particularly interests me is the news from the BULLY REVIEW that test results of 30 bull terriers showed 50% affected with Polycystic kidneys "some also with heart disorders." I hope the heart defect issue won’t be neglected.)

The BULLY REVIEW suggests: A certificate system to encourage breeding from unaffected dogs; and a National Register for recording them.

Margaret Craven, the editor, says in her column: This health crisis should never have happened - it was avoidable...I plead to all other owners - start talking about the problems, work in a united way, test all breeding animals for hereditary problems (especially kidney and heart problems) but above all - remember HONESTY is the only thing that is going to save our breed.

CANADA has its first lens luxation case documented and made known to the fancy: Am.Ch. Hobbit Hills Black Magic, out of Hobbit Hill’s Ebony Ice, by Ch. Ryatti’s Yensid of Regency. Magic was certified normal at 15 months old; fully luxated in one eye and subluxated in the other eye at 4yrs/5mos. Magic’s grandsire, Ch. Hobbit Hill’s Ralph & Ready is considered a carrier with 3 PLL offspring; his sire, Ch. Darby Fair’s Firecracker, a carrier with 2 PLL offspring. There must be more cases involved, and we ask you to please submit your news so that future breedings will be made more wisely - benefiting us all, our dogs especially.

CANADA’S 2ND documented lens luxation case is that of Am.Ch.Bulwark Minikin Short Story - actually, she is only in the subluxation stage still - but we expect the inevitable. Chicklet is out of Beewau Libra at Swannymote, by Warbonnet Hypericum.

UK is involved with gene-marking and Lens Luxation research through its Animal Health Trust. Drs. Keith Barnett and Matthew Binns have offered to take on the project. Meanwhile the breed club continues eye clinics at some of its yearly shows.

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With PLL as ultimately harmful to everyone’s breeding program as are heart & kidney disease - it is, without a doubt, essential that we take steps to limit the damage present & future. This, of course, requires courage and steadfastness - traits we applaud in the terrier breed itself. It requires that we start at home with updating our test results & sharing the results nationwide. It requires full disclosure, not partial & evasive disclosure - for instance, if you say your dog tested normal, that’s great; but if you stop there and don’t mention his son, sister, uncle and you know they are not normal, that harms the breed, many breeding programs, and many individuals human & canine.

Damage control is obviously best done as prevention but we are well past that stage in this breed at this time, for which state of affairs we must all share the guilt. Who amongst us has not used a dog without asking for documented proof of his soundness? Who has not used a dog known to be a high risk? Who has not stood such a dog? Who has not asked specifically for progeny testing? Who has not used a dog with outdated test results? We have been playing the Crying Game - in which there are no winners.

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The PLL issue is primary in more ways than the obvious one. Unlike the one-time definitive BAER test for hearing, eye exams may not show up a problem right away in the very young dog. Unlike the Echo test for heart function, eye exams may not show up problems developing in the adolescent dog. Unlike the hip xray, eye exams may still be missing problems in the adult dog (2 years & up). This leaves us with PLL, kidney disease, and luxating patellas as our major breeding age problems, as all can present without notice in prime breeding years. All three of these problems are considered highly hereditary. The question of how each is inherited is, in my opinion, moot. The less we know about the mode of inheritance, the more careful & demanding we need to be regarding our breeding options. Always the very least we can do in damage control starts with the absolute ban on breeding from affected animals.

WHEN DO WE SUSPECT THAT A DISORDER IS INHERITED IN A GIVEN BREED?

WHEN THE FREQUENCY IS GREATER THAN IN OTHER BREEDS

WHEN THE FREQUENCY INCREASES IN THE BREED AS A WHOLE

WHEN THE FREQUENCY IS GREATER IN RELATED DOGS WITHIN A BREED

WHEN IT HAS A CHARACTERISTIC APPEARANCE AND LOCATION

WHEN IT HAS A CHARACTERISTIC AGE OF ONSET AND COURSE OF PROGRESSION

WHEN IT LOOKS IDENTICAL TO AN ENTITY WHICH HAS BEEN PROVEN TO BE INHERITED IN ANOTHER BREED

 

(AMERICAN COLLEGE OF VERTERINARY OPTHAMOLOGY/1996)

It would make sense for all breeders to start asking pertinent questions of each other. It would be of immeasurable help for those questioned to be forthcoming. It would be a leap of faith for me to expect both parties to contact the MBTT with results - but I’m doing

it AAAAAAA

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EEEEEE

eeeeeeee

(thump!)

THE GOOD NEWS IS THAT THE BAD NEWS IS PERMANENT.
THE BAD NEWS IS THAT THE GOOD NEWS ISN’T PERMANENT.

GOOD NEWS/BAD NEWS

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Gridiron’s expected litter from Ch. Gridiron Affairs of the Heart x Am.Cdn.Ch.Bulwark Minikin Marksman produced 4 pups: 2 male/2 female, all doing well. As per MBTT policy, both parents have normal heart status as determined by a Doppler echo exam.

Ch. Bulwark Minikin Magic Marker left the sandbox long enough to win SEVEN Group #4 (one under Jon Cole,) FOUR Group #3’s; and ONE GROUP #2 (under Betty Munden.). His co-owner Alanna Leach handles him to all his wins; she’d like to state, for the record, that at home he’s "Roo" and only Jo calls him "Markie Mark". His first litter consisted of two daughters, doing well.

The MBTT would like to thank the following people who took the time to call or write with words of encouragement, praise, thanks and/or suggestions:

Marilyn Drewes, Cathy Napoli, Patti Holt, Trudy Pizer, Dennis Harris, Regina & Terry Mays, Andrea Jackson, Victoria Corse, Peggy Morang, Elizabeth Feuz, Sue Windham, Wanda Moriarty, Barb Gradl, Janice Dolphin, Granny and many more...Special thanks, of course, to Trudy Pizer, the MBTCSC, Priscilla David & Patti Holt, for postage money for this issue - covering all of it! - and Lora Eggleston for most of the printing costs.

Am.Ch. Bulwark Minikin Small Change wants the world to know that his daughter "Lily" took not one, but two, Best in Shows/June’97. "Ferrous" is BAER and HEART normal (by Doppler echo).

Victoria Corse asked the MBTT to squelch a current misconception regarding the general inheritance of heart defects.

It is not true that unaffected parents cannot produce affected offspring. If only our life were so simplified! If it were true, then some of our currently affected minis have a defective parent we don’t know about or haven’t been told about!

PLL, on the other hand, does have a simple mode of inheritance in which a parent must be affected or a carrier. Unhappily, affected dogs may seem normal for years; and carriers in our small gene pool are readily available to match up with other carriers with disastrous results...sigh...

THE MINIATURE BULL CLUB OF SOUTHERN CALIFORNIA

IS RECRUITING MEMBERS. THIS CLUB "WHOLEHEARTEDLY" (BLESS THEIR HEARTS!) SUPPORTS THE "TELL-AGRAM". SINGLES/$15; COUPLES/$20. THE MBTCSC’S MOTTO IS: "WE PROMISE VERY LITTLE AND WE DELIVER!" HOW CAN YOU REFUSE AN OFFER LIKE THAT? JOIN THE CLUB - FIND OUR WHAT’S GOING ON AT THEIR END OF THE MAP. FOR MEMBERSHIP, WRITE:

PRISCILLA DAVID, 10937 HAVENHURST
GRANADA HILLS, CALIFORNIA, USA, 91344

AND MAYBE "BINKIE" WILL SEAL YOUR NEWSLETTER WITH A KISS!!!!!!

( or maybe Dennis will, depending on who you are and how he feels.......)

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IN MEMORIUM

Am.Ch. Hobbit Hills Black Magic, out of Hobbit Hills Ebony Ice x Am.Ch.Ryatti’s Yensid of Regency, was put to sleep June, 1997, aged 4 years/5 months. She had primary lens luxation in both eyes. For all minibulls, please, CERF yearly and breed wisely.

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QUOTES FROM THE PAST

PRESIDENT’S MESSAGE/LITTLE BULL/WINTER ‘94/5 -

"OUR SMALL GENE POOL DEMANDS COOPERATION BETWEEN BREEDERS. ANY SUCCESSES OR PROBLEMS IN BREEDING AFFECTS US ALL. IT IS TIME TO MAKE A CONCERTED EFFORT...IF WE ARE HONEST & OPEN ABOUT THESE PROBLEMS, THEY CAN BE COMBATED."

IT IS NOW 1997 - HAVE WE BEEN COOPERATING AMONGST OURSELVES? HAVE WE BEEN HONEST AND OPEN ABOUT OUR PROBLEMS?

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BULWARK MINIKIN POSTER PUPPY

"HI! MY MOM HAS LENS LUXATION - DOES YOUR'S?"
PLEASE SPEAK UP FOR THOSE WHO CAN'T

THE MBTT IS A NEWSLETTER FOR ALL MINIBULL OWNERS, BREEDERS, FANCIERS. FEEL FREE TO WRITE WITH YOUR CONCERNS, STORIES, PHOTOS, QUESTIONS, - ANY SUBJECT YOU’D LIKE OTHER OPINIONS ON. WE’RE ONLY A STAMP AWAY!!!

LENS LUXATION IS EVERYONE’S PROBLEM TODAY!

IN LENS LUXATION, THE MODE OF INHERITANCE IS
LIKELY A "SIMPLE AUTOSOMAL RECESSIVE"

HOWEVER, THIS DOESN’T MEAN SIMPLE IN TERMS OF ERADICATION, NOT BECAUSE WE CAN’T BUT BECAUSE WE WON’T - IN ENOUGH NUMBERS WORKING TOWARDS THE SAME END - APPLY OURSELVES TO THE PROBLEM.

Our breeding stock can be considered as 3 types in dealing with PLL:

the normal dog/no defect & producing none
the seemingly normal dog - the carrier/producing PLL
the affected dog/all progeny are carriers

Again, there goes "simple". For several years, there’s no way of discerning the normal (safe) dog from the yet-to-be-affected dog (unsafe).

There’s some proof that progression from a normal eye exam to full luxation takes from a year to 3 years. Should no eye exam be performed during that period, valuable information is lost & thus ultimately damages our breeding programs.

In the meantime, we could be using the most unsafe type of dog in the most prominent breeding position.

Since breeders tend to follow formula and line breedings, the chance of carrier meeting carrier is very high; factor in carrier meeting yet-to-be-affected dog, or worse, yet-to-be-affected x yet-to-be-affected and the gene for the defect becomes so firmly fixed in the genepool as to eventually infiltrate all breeding stock.

If all dogs were kept from breeding prior to their 4th year, eye exams done at that time may very well show the defect itself, or the deterioration that precedes it - in this way, the yet-to-be-affected dogs & the affected dogs could be culled at once & no offspring, automatically carriers themselves, would have been produced. This step alone could do more for the control of the problem than any other (short of finding the gene itself and being able to cull those who are carriers).

Another step in control can be made by re-testing and confirming the "safe" status of dogs older than 7 years who have had multiple litters with tested offspring 3 years & older with no signs of the defect. These dogs should, if free of other breed-related problems, be used when possible: to tested, seemingly safe, mates of 4 years & older.

A voluntary 4 year hiatus in the breeding program?! What planet does this person come from?!

Hey! Hold on there...only the youngest dogs need wait the full 4 years. The others are on their way. Their potential mates are maturing, too. There is so much to lose by being hasty, and so much to gain by proceeding with caution. Your actions would speak for themselves as never before - are you for or against breed improvements?

Every book on genetics, every breed spokesperson talking about breeding for improvement has stated, uncategorically, "Don’t breed from affected parents."

The safest breeding practices stem from and support the above advice. Here are some other steps to follow:

* if breeds have late-onset defects, don’t breed until test results prove them safe
* if the parents have multiple offspring, siblings and grandparents with known breed defects, don’t use them.
* especially don’t breed those 2 lines together
* if you choose to breed carriers, they must be worth, in other ways, the sacrifice you are making & the potential damage you will cause to your program & other programs involved with yours.
* ask questions and get results, or breed elsewhere. Don’t compromise yourself, your potential litter, or your buyers.
be brave, be honest, be open, be careful - breed improvement is in your hands.

WORDS OF WISDOM FROM MALCOLM WILLIS: PRACTICAL GENETICS FOR DOG BREEDERS/1992:

"THERE IS NO CRIME IN PRODUCING A DEFECT. CRIME, IF ANY, LIES IN WHAT YOU DO ABOUT A DEFECT. IF YOU BURY YOURS AND KEEP QUIET ABOUT IT AND I DO THE SAME WITH MINE, THEN SOONER OF LATER WE MAY USE EACH OTHER’S DOGS AND PAY THE PENALTY FOR NOT HAVING BEEN HONEST WITH ONE ANOTHER AND WITH THE BREED WE PROBABLY PROFESS TO LOVE."

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SHE STILL HAS A SWOLLEN HEAD FROM HER 1995
NATIONAL SPECIALTY BEST IN SHOW!

AM./CDN.CH.BULWARK MINIKIN MARZIPAN BISS!
Multiple Group winner!

"Marzi" is BAER normal, Eye normal at 3 years old, and heart normal (colour doppler at 2 years). Missed by Wanda, kissed by Jo. MIGHT be bred in 1998.

STILL DON’T THINK MBT PROBLEMS ARE GOING TO KNOCK AT YOUR DOOR?

WORDS OF WISDOM FROM THE INCOMPARABLE SHEL SILVERSTEIN:

THE SLITHERGADEE HAS CRAWLED OUT OF THE SEA.
HE MAY CATCH ALL THE OTHERS, BUT HE WON’T CATCH ME.
NO YOU WON’T CATCH ME, OLD SLITHERGADEE,
YOU MAY CATCH ALL THE OTHERS, BUT YOU WO---

-SHEL SILVERSTEIN

CANINE HEALTH / THE BREED CLUB / & THE FUTURE/?????

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THE FOLLOWING EXCERPTS ARE FROM AN ARTICLE BY CONNIE VANCORE, APPEARING IN THE JUNE ISSUE OF DOGS IN CANADA.

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"THE WEIMARANER CLUB OF AMERICA ESTABLISHED A HIP DYSPLASIA REGISTRY, PUBLISHING THE NAMES OF ALL OFA-CERTIFIED DOGS IN THEIR CLUB MAGAZINE. NO DOG CAN BE ADVERTISED IN THAT PUBLICATION WITHOUT OFA CLEARANCE.

THE NEWFOUNDLAND CLUB OF AMERICA HAS LONG SUPPORTED RESEARCH INTO THE CAUSES AND HEREDITY OF SUBAORTIC STENOSIS (OUR BIG HEART PROBLEM IN MINIS).

THE CAIRN CLUB OF AMERICA HAS ESTABLISHED A ‘TERRIER CONNECTION’ WHEREBY HEREDITARY PROBLEMS COMMON TO SEVERAL TERRIER BREEDS ARE SUPPORTED BY RESEARCH & INFORMATION.

HOW DOES A CLUB BEGIN TO ADDRESS HEALTH PROBLEMS IN ITS BREED? THE FIRST STEP IS USUALLY A SURVEY TO DETERMINE THE PREVALENCE OF A PROBLEM - NOT AS EASY AS IT SOUNDS BECAUSE IT REQUIRES THE MEMBERSHIP TO ADMIT THERE IS A PROBLEM AND BE WILLING TO ADDRESS IT.

THE CLUB MUST DECIDE WHICH PROBLEMS TO ADDRESS AND HOW TO DO IT.

THIS IS WHERE THE CANINE HEALTH FOUNDATION IS HELPFUL. WITH ITS ACCESS TO THE SCIENTIFIC COMMUNITY, THE FOUNDATION IS ABLE TO SOLICIT RESEARCH PROPOSALS IN AREAS OF CONCERN AND, THROUGH CONTACTS WITH MANY PARENT CLUBS, IS SOMETIMES ABLE TO PUT TOGETHER A STUDY INVOLVING SEVERAL CLUBS ADDRESSING A PARTICULAR DISEASE.

AS TESTS TO DETERMINE DISEASE TRANSMISSION BECOME AVAILABLE, THERE WILL BE NO EXCUSE TO BREED DOGS CARRYING HEREDITARY DISEASES. PARENT CLUBS ARE BEGINNING TO REALIZE THAT THEY HAVE TO DEAL WITH THESE ISSUES AND PROVIDE THE GUIDANCE AND MONEY IT WILL TAKE TO ACHIEVE THE GOAL OF PRODUCING HEALTHY DOGS."

Our parent club has over $1000 on hand and scheduled for trophies. The membership could vote to bank this money in a fund for eye & heart research. The membership is the club. Members could be acknowledged for their donations to health concerns in lieu of trinkets; it could well be your dog saved from a defective future.....

REGIONAL CLUBS - VOTE FOR THE FUTURE OF OUR BREED - NOW!

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THE HUMAN GENOME PROJECT

SOUNDS LIKE A SCIENCE FICTION TITLE, DOESN’T IT? HOWEVER, THIS IS ONGOING, WORLDWIDE RESEARCH INTO HUMAN GENETICS. IT IS A MASSIVE UNDERTAKING, DESIGNED TO IDENTIFY EVERY SINGLE GENE IN THE HUMAN GENOME, AND ANTICIPATES BEING FINISHED IN THE EARLY 21ST CENTURY (2005+?).

IT WILL IDENTIFY THE HUMAN GENE(S) INVOLVED IN ZONULE FIBRE FORMATION - THOSE SAME ZONULES RESPONSIBLE FOR PLL IN MBTS. EVEN AS I WRITE THIS, IT MAY ALREADY HAVE BEEN DONE!

SURPRISING THOUGH IT SOUNDS, THE DIFFERENCES BETWEEN HUMAN AND CANINE GENOMES ARE VERY TINY. THUS, THE INFORMATION GAINED FROM THE HUMAN GENOME PROJECT MAY DRAMATICALLY NARROW THE SEARCH FOR CANINE INFORMATION.

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GENOMES: ONE SET OF HAPLOID CHROMOSOMES AND THE PAIR OF GENES THEY CONTAIN. ALSO, HUSKIES WHO TURN RIGHT FOR NOME....

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YES, VIRGINIA, THERE IS A CANINE GENOME PROJECT, TOO! IT IS UNDERTAKING THE SAME RESEARCH FOR THE DOG WORLD. WATCH FOR MORE INFORMATION IN UPCOMING ISSUES OF THIS, AND OTHER CANINE ORIENTED MAGAZINES. THOSE WHO SURF CAN ACCESS IT ON THE INTERNET.

CAUTION! THIS ISSUE CONTAINS LANGUAGE THAT MAY BE DEEMED OFFENSIVE: THE WORD "BULWARK" APPEARS X NUMBER OF TIMES.....

THE MBTT 2ND ISSUE WILL BE A LIMITED RUN OF 125 COPIES. THOSE OF YOU WHO SURF THE NET CAN ACCESS IT FROM THERE. THIS CUTS DOWN ON POSTAGE & TIME AND ALLOWS FOR MORE CONTENT PER ISSUE.

DUE TO HEAVY SHOW SCHEDULES & SLOW MAILS, SOME PROMISED INFORMATION IS NOW SCHEDULED FOR THE NEXT ISSUE. SEE YOU THERE!

FOUND IN THE NEWS - SNACKS FOR THE PKD AFFLICTED

…FROM GRAINVIEWS/MARCH/97….A CANADIAN FARMERS NEWSPAPER…

MALCOM OGBORN, OF THE UNIVERSITY OF MANITOBA, THINKS THAT FLAX COULD BE THE KEY TO SLOWING DOWN POLYCYSTIC KIDNEY DISEASE. THIS GENETIC DISEASE, CURRENTLY THE MAJOR BULL TERRIER PROBLEM IN OZ, CAUSES CYSTS TO FORM ON THE KIDNEYS, LIMITING RENAL FUNCTION. IN HUMANS, 1 IN EVERY 400 SUFFERS FROM PKD - AND REMEMBER, HUMAN GENOMES ARE SIMILAR TO CANINE GENOMES. DAMAGED KIDNEYS PRODUCE SCAR TISSUE. FLAX SEEMS TO HAVE THE ABILITY TO REDUCE THE INFLAMMATION INVOLVED. OGBORN’S STUDY CONSISTED OF USING FLAX AS A DIETARY SUPPLEMENT IN RATS AFFLICTED WITH PKD. THE RESULTS SHOWED THEY HAD A REDUCTION IN SCARRING, AND A SLOWING OF THE DECLINE OF KIDNEY FUNCTION.

THERE’S NO REASON THIS RECIPE CAN’T BE USED FOR DOG SNACKS. DELETING THE COFFEE AND USING FRUIT JUICE INSTEAD. OR WE CAN EAT THE COOKIES OURSELVES & GIVE THE DOGS MILLED, SOAKED FLAX IN THEIR FOOD.

"NO, REALLY, THEY'RE
EASY TO BAKE -
TRY IT!"

FLAX HERMIT COOKIES/48 OF ‘EM !

ONE HALF CUP SHORTENING……….ONE HALF CUP WHITE SUGAR
ONE HALF CUB BROWN SUGAR/ONE QUARTER CUP COLD STRONG COFFEE
ONE EGG…..ONE & THREE QUARTER CUPS ALL-PURPOSE FLOUR
THREE QUARTER CUPS MILLED FLAXSEED/HALF TSP. SALT
HALF TEA-SPOON SODA…………..HALF TSP. CINNAMON
HALF TEA-SPOON NUTMEG………….ONE CUP RAISINS
ONE CUP NUTS, CHOPPED

BEAT TOGETHER SHORTENING, SUGARS, COFFEE, AND EGG. STIR IN REMAINING INGREDIENTS. MIX UNTIL COMBINED. FORM INTO ONE INCH BALLS, PLACING TWO INCHES APART ON UNGREASED COOKIE SHEET. BAKE AT 375 DEGREES/F FOR 8 TO 10 MINUTES. DONE WHEN NO INDENTATION REMAINS AFTER BEING TOUCHED. REMOVE IMMEDIATELY FROM COOKIE SHEET AND COOL.

THIS RECIPE WAS FROM: A TASTE OF FLAX COOKBOOK TWO/FLAX COUNCIL OF CANADA.

CASES OF MINIATURE BULL TERRIERS WITH PRIMARY LENS LUXATION/ FROM THE UK CONFIRMED LIST / 1992/ INCOMPLETE

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THE OFFSPRING OF THE LAST DECADE ARE NOW OF AN AGE TO BE LUXATING - WHERE ARE THEY ?

IS IT POSSIBLE THAT OUR EARLY PRESENTATIONS (2 TO 4 YEARS) OF LENS LUXATION ARE CAUSED BY PRE-EXISTING GLAUCOMA? AND THAT OUR LATE PRESENTATIONS OF LL (8 TO 11 YEARS) ARE SO LATE BECAUSE THERE IS NO GLAUCOMA? WITHOUT EQUAL ATTENTION BEING PAID TO BOTH THESE SERIOUS EYE DEFECTS, WE MAY BE MISSING KEY EVIDENCE NEEDED FOR FUTURE RESEARCH. WE ASK YOU TO ASK YOUR OPTHAMOLOGIST FOR PRESSURE TESTS (IOP’s) ALONG WITH THE ROUTINE TESTS FOR CERF.

GLAUCOMA IS AN ABNORMAL INCREASE OF PRESSURE WITHIN AN EYE. THIS PRESSURE, IF HIGH ENOUGH, CAN CAUSE DYSFUNCTION AND DESTRUCTION OF THE DELICATE NERVE CELLS OF THE RETINA AND OPTIC NERVE, RESULTING IN BLINDNESS.

INTRAOCULAR EYE PRESSURE IS MEASURED BY AN APPLANATION TONOMETER - NORMAL PRESSURE IS 15 TO 25 MM HG. AGAIN, PLEASE ASK FOR IOP MEASUREMENTS WHEN YOUR DOG GETS HIS EYES TESTED.

OVER 40 DOG BREEDS ARE PREDISPOSED TO PRIMARY GLAUCOMA - MBTs ARE NOT, SUPPOSEDLY, ONE OF THEM! LET’S COLLECT A SUFFICIENT NUMBER OF IOP MEASUREMENTS AND SEE - IN MORE WAYS THAN ONE!

THERE IS A LOT OF MISSING INFORMATION ON LENS LUXATION CASES THAT COULD BE HELPING THOSE WHO WANT TO MAKE A DIFFERENCE. BOTH MISINFORMATION AND INDIFFERENCE ARE HOLDING BACK RESEARCH. IN THE LAST DECADE BREEDINGS HAVE BEEN DONE THAT WILL CONTINUE LL IN ALMOST EVERY BLOODLINE - SO IF YOU HAVEN’T BEEN HIT YET, YOUR NUMBER’S COMING UP. THERE CAN BE NO VALID EXCUSE OR REASON TO WITH-HOLD LL NEWS FROM THE CLUB MEMBERSHIP - AND STILL PROFESS TO BREED FOR THE IMPROVEMENT & LOVE OF MBTs

AM.CH. BULWARK MINIKIN SHORT STORY WAS DIAGNOSED AS SUBLUXATING ON JUNE 27/97 AT 7 YEARS/9 MONTHS OLD. THIS WAS HER 3^RD EYE EXAM. PLEASE, GET YOUR MINIS EXAMINED YEARLY, MAKING SURE THAT YOUR EYE DOCTOR IS SPECIFICALLY LOOKING FOR SIGNS OF GLAUCOMA, LL, RETINAL & ZONULE DETERIORATION.

MEMBERS! CALL YOUR CLUB PRESIDENT AND GENETICS COMMITTEE CHAIRPERSON WITH YOUR CONCERN FOR OUR BREED’S FUTURE. THEN DO YOUR SHARE OF WHAT’S REQUIRED…..

++++++++++++++++++++++++++GLOSSARY OF TERMS+++++++++++++++++++++++++

"CLEAR" / BOTH PARENTS ARE NORMAL (NOT CARRIERS)

"CARRIER" / HAS ONE ABNORMAL GENE IN THE PAIR OF GENES ASSOCIATED WITH THE DEFECT. DOES NOT SHOW THE PHYSICAL DEFECT, BUT GIVES THE BAD GENE TO HALF (50%) OF HIS OFFSPRING.

AFFECTED / BOTH GENES ARE ABNORMAL / ALL OFFSPRING WILL BE CARRIERS

IF YOU ARE STILL CONFUSED (LIKE ME), HERE’S SOME COMBINATION EXPLANATIONS:

AFFECTED MBT X AFFECTED MBT = 100% AFFECTED LITTER. (DO NOT PASS GO)

AFFECTED MBT X CARRIER MBT = 50% AFFECTED + 50% CARRIER

CARRIER MBT X CLEAR MBT = 50% CARRIER + 50% CLEAR

AFFECTED MBT X CLEAR MBT = 100% CARRIER

CARRIER MBT X CARRIER MBT = 25% AFFECT + 50% CARRIER + 25% CLEAR

THE ABOVE TERMS APPLY TO SIMPLE AUTOSOMAL RECESSIVES ONLY.

AND NOW A POTENTIAL CURE FOR INFLAMMATORY REMARKS : EAT FLAX HERMIT COOKIES…….

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REFLECTIONS

EVEN A CURSORY LOOK AT THE PLL LIST SHOWS US THE DEVASTATING RAMIFICATIONS OF BREEDING OUR MINIATURE BTS TOO YOUNG (1 TO 4 YEARS), AND TO CARRIERS BOTH KNOWN OR YET TO BE PROVEN AS SUCH. A CLOSER LOOK SHOWS US WHERE REPEAT BREEDINGS PRODUCED REPEAT LUXATING ANIMALS. THOSE THEN ENTERED BREEDING PROGRAMS AND PRODUCED THIRD GENERATION LUXATORS BEFORE THEIR OWN DEFECTS PRESENTED. THIS ESCALATING DAMAGE CONTINUES WITH EVERY NEW GENERATION BEING BRED - FROM THE FIRST RECORDED (PLL LIST) CASE BORN IN ’71 TO OURS, IN ’97.

AN IN-DEPTH LOOK SHOWS US THAT OUR OWN FOUNDATION SIRE CAME FROM A LITTER WITH LENS LUXATING SIBLINGS - WHICH MEANS THAT HIS PARENTS WERE AT BEST CARRIERS OR AT WORST, AFFECTED - AND IF THE LATTER OUR FOUNDATION SIRE IS A CARRIER HIMSELF.

IT WOULD PROBABLY BE ONLY A SLIGHT EXAGGERATION TO SUGGEST THAT ALL PRESENT-DAY MBTS ARE CARRIERS; BUT CERTAINLY A TREMENDOUS NUMBER OF THEM MUST BE, JUDGING BY THE NUMBERS OF AFFECTED DOGS WE HEAR ABOUT.

CAN WE TELL THE CLEAR FROM THE CARRIER PRIOR TO BREEDING & THE SUBSEQUENT PASSING OF TIME? NO, NOT REALLY. THAT OLD STANDBY, TEST BREEDING, - WHERE A "CLEAR" DOG IS BRED TO AN AFFECTED DOG - REQUIRES TIME TO PROVE ITS POINT; AND IN TEST BREEDING WE ARE ALSO CONSCIOUSLY REQUIRING OUR DOGS TO SUFFER THE BURDEN OF PROOF.

THE FUTURE OF MBTS FREE OF THIS PARTICULARLY HORRID & HANDICAPPING AFFLICTION LIES IN THE HOPE OF GENE IDENTIFICATION. THIS MAY OR MAY NOT BE POSSIBLE IN OUR LIFETIME. IN GENE "TYPING" RESEARCH IDENTIFIES THE ABERRANT GENE(S) IN THE CHROMOSOMES, ONCE "MARKED" THE GENE CAN BE LOOKED FOR ON ALL DNA TESTED DOGS AND THOSE INDIVIDUAL CARRIERS REMOVED FROM THE BREEDING PROGRAM. DNA TESTING FOR "MARKED" GENES CAN BE DONE ON DOGS OF ANY AGE, AND ALSO FROM TISSUE SAMPLES, (IE:SPERM;BLOOD) PROPERLY PRESERVED FOR THE PURPOSE, OF DOGS LONG PASSED AWAY.

QUOTES FROM THE PAST

PRESIDENT’S MESSAGE/LITTLE BULL/FALL ’91

"WE HAVE BEEN SKIRTING AROUND ADDRESSING HEALTH PROBLEMS IN MINIS AND THIS MUST BE A PROJECT OF OURS…WE CERTAINLY HAVE GOOD DOGS THAT ARE PHYSICALLY AND MENTALLY SOUND…WE NEED TO BE SURE THAT THEY ARE THE ONES WE ARE BREEDING FROM…"

IT IS NOW 1997 - ANOTHER HALF DECADE AND MORE SKIRTING AROUND THE HEALTH ISSUE…HAVE WE BEEN BREEDING FROM THE RIGHT DOGS?

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The MBTCA is having an eye/heart clinic in conjunction with the Montgomery specialty. Contact Susan Hall for details: 5641 Mt. Gilead Road., Centreville, VA, 20120. It’s a step in the right direction - an eye-opener that should gladden your heart******703-631-3565*******

THANK YOU, SUSAN, FROM ALL OF US !

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PLL CASES FROM NORTH AMERICA - PLEASE SPEAK UP FOR THOSE WHO CAN’T!

HOBBIT HILLS BLACK MAGIC / RYATTIS YENSID OF REGENCY X HOBBIT HILLS EBONY ICE

BULWARK MINIKIN SHORT STORY / WARBONNET HYPERICUM X BEEWAU LIBRA AT
SWANNYMOTE

ORANJE’S MAID MARION / HOBBIT HILLS RALPH AND READY X ROVER RUN BONSAI
BUFFY

???????????????????????????????????????????????????????????????????????????????????????????????????????????
???????????????????????????????????????????????????????????????????????????????????????????????????????????

THERE ARE SO MANY MORE LL CASES IN NORTH AMERICA THAN ARE LISTED ABOVE, THAT IT IS TRULY TERRIFYING TO ENVISION ANY FUTURE FOR OUR MINIATURE BTS WITHOUT TOTAL MEMBERSHIP COMPLIANCE WITH TESTING, CULLING, AND SHARED GOALS. OUR CLUB NEEDS "LEADERS" - TO SET GOOD EXAMPLES, DISCLOSE NEEDED INFORMATION, AND IMPLEMENT PROGRESSIVE BREEDING PRACTICES. TO THAT END,

PLEASE SUPPORT THE FIRST AND ONLY ACKNOWLEDGED LL LIST IN NORTH AMERICAN: THE MBT TELL-AGRAM! THANK YOU….

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AM.CH. BULWARK MINIKIN SHORT STORY

at 8 months
already showing
the style she still
has at almost 8 yrs.

the fully mature
Specialty winning,
proven brood
bitch...

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"CHICKLET" IS BAER NORMAL, DOPPLER ECHO NORMAL, AND PATELLA NORMAL; DAM OF 8 AMERICAN CHAMPIONS; AND, SADLY, AFFLICTED WITH LENS LUXATION.

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THE MBTT WOULD LIKE TO THANK PATTI HOLT AND PAM HATHAWAY FOR SHARING THE FOLLOWING WITH US ALL:

Pam writes,

I first noticed a problem with Marion’s left eye on a Friday dog show morning. She seemed uncomfortable, and I had to clean some "matter" from it. On Saturday, it was the same. On Sunday I noticed a white circle in the eye, so on Monday I called my vet and was referred to an eye clinic. I was very upset that I couldn’t get her seen at the clinic until the Tuesday.

Thirteen months prior to all this, I had had Marion’s eyes examined and was told that she could not "CERF", and that one day she would "sublux". I was not told to bring her back for any follow-up, nor was I told how painful her condition would be when it happened. I was not told what my options would be, and how to stay on top of things and prevent the suffering she must have gone through during those four days.

Now I do know better, and she’ll have her checkups regularly.

+++++++++++++++++++++++

Ch. Oranje’s Maid Marion is six years old. Her eye exam revealed intraocular pressures of 22 and 45 (average IOPs are 15 to 25); one fully luxated lens, and one subluxated lens - for a diagnosis of Lens Luxation with Secondary Glaucoma OS, and Subluxation OD.

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If YOU LOOK HARD ENOUGH, YOU’LL FIND PROBLEMS; BUT, LOOK EVEN HARDER, AND YOU’LL FIND SOLUTIONS…

THE MBT TELL-AGRAM JULY ISSUE 1997

c/o Jo Turley, Box #4, Site #2, RR#1, Priddis, AB, Canada TOL 1WO

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