Newsletter Christmas 2000


Happy New Year
March 2000 show
November 2000 show
Dates for your diary
Second poem
Lhasa Apso Breed Council
GPRA report
Amsterdam All Winners Show


When you have a quiet minute in the New Year please do not forget Membership Subscription for 2001 is now due.  Please complete and return the form together with your subscription at the end of this Newsletter.  

We look forward to seeing you all in the New Year.  

March 2000 show

Our first event of the year was our AGM and Tenth Open Show on Sunday 26th March at Stonehouse Gloucestershire.  The AGM was well attended and went well, unfortunately Lynne and Gary Horton decided to resign from the committee due to personal obligations.  We would like to thank Lynne and Gary for all their hard work and commitment whilst members of the Committee.  Lynne for being a tower of strength in the Kitchen on show days and to Gary for stepping into the breach as Acting Honorary Treasurer when Sandra Marcoveccio had to retire for health reasons.  We would like to welcome two new members to the Committee in Josie Richardson-Black and Jane Paradise.  Jane was nominated and duly elected as Honorary Treasurer. 

  The show was judged by Mrs. Hazel Gay (Hazgaye) who had drawn an entry of 92 from 76 dogs and found her BIS in Gill McNally's homebred Angadema Applause (Vaderlands Vested Interest X Kandykone Kinda Magic for Angadema).  Reserve BIS and Best Bitch was awarded to Leslie Gilfoyle and Margaret Preston's Gregval Madam Resides at Beauroi JW (Meadowvic's War Dancing Bear at Sulhasan's X Ragoosa Lady Penelope) bred by Mr and Mrs Watt.  Best Puppy in Show was awarded to Chris Lawson's homebred Rishlyn Entrapment (Ch Deelayne's Obsession for Exphials X Drivin' Miss Daisy to Rienach).  Best Veteran in Show was awarded to Madelaine Lewis's homebred Ch Deelayne Fanya (Saxonsprings Lothario X Saxonsprings Faith)

Dates for the diary


AGM and Open Show Sunday 25th March 2001

at Stonehouse Community Centre, Stonehouse, Nr Stroud, Gloucester.

  Judge Mrs Pat Noujaim

(Mimayin Tibetan Terriers)  

Nominations for Hon. Secretary and Committee and items for inclusion on the agenda to reach the Secretary in writing by 10th February, 2001  

We are also holding an Eye Testing Session at our March Open Show, details will be with the schedule.


Inter Clubs Memorial Challenge and  Gala Evening Dinner Dance

Sunday 6th May 2001 at Honiley Court Hotel, Nr Warwick (details enclosed).

Open Show Sunday 4th November 2001 at Stonehouse Community Centre, Stonehouse

Judge Mrs Jan Bromley (Jardene Lhasa Apsos)



Our second show, held on 12th November 2000, was judged by Mrs Sally Pointon (Ballito) who had drawn an entry of 93 from 82 dogs and found her BIS in Dorothy Quelch's Kutani Lionheart for Ardquin (Ch Chethang Ferdinand X Kutani Mississippi at Danton) bred and handled on this occasion by Wendy Cain.  Reserve BIS and Best Bitch was awarded to Audrey Sutherland-Bolton's Zentarr Piccadilly at Khalila (Ragoosa Simply Outragious at Zentarr X Zentarr Grace) bred by Margaret Anderson.   Best Puppy in Show was awarded to Audrey Sutherland-Bolton's homebred Khalila Hell's Angel (Ch Zentarr Michaelangelo X Ragoosa Barmy Daze at Khalila).  Best Veteran in Show was awarded to Vanessa Reece's Kandykone Konundrum (Ch & Ir Ch Deelayne Quick Dash at Kandykone X Belazieth Magic Moment at Kandykone) bred by Val Webster.


I often bred puppies, when in my youth,

They were always quite sound, in leg, limb and tooth.

I always had homes waiting, often too many,

And then I would worry - would she have any?

  The puppies all went, and were cared for and loved,

None ended in rescue, from home to home shoved.

But nowadays it's different, you cannot be sure

That the owners stand by morality or law.

  So many unwanted and ill-treated doggies,

And horses, and donkeys, and rabbits and moggies.

Why breed so many, when you don't really know,

Whether to good homes they really will go.

Puppies are lovely, whatever the breed,

But so many litters we really don't need.

I do not agree with mating each bitch

And just hoping the outcome will not have a hitch.

  I know that most breeders will want to keep one,

Because in the showring the parents had won.

But what of the other small puppies so sweet:

Will they have good homes?   Will they play? Will they eat?                                                                       Anon


I am not an active member

How did that come about?

T'was at the L.K.A

When I thought I heard a shout.


A legend in Lhasa Apso's said

“Do you think you could spare a pound?”

We desperately need some members

To get us off the ground.


“I live so far away” I said

But I will fill in a form

To make-up the requisite numbers

One Hundred? being the norm.


I am not an active member

Some entries have I sent

Don't go to any functions

But my donations you have spend!


So far away for an Open Show

It really makes me think!

I'd be an active member

If with Championships you could link.


Yes!  I am just a member

My name is on the list

But with a resignation

My contribution would be missed.

The Lhasa Apso PRA Project in the University of Cambridge

Figures Related to the Disease

By November 2000, 34 Lhasa Apsos affected with progressive retinal atrophy (PRA), and distributed in six countries has been reported to ILAC.  In addition to these, several unreported individuals are known.   

In some countries, such as Sweden, affected individuals have died, so the number of countries with living affected individuals has decreased. 

 PRA is a recessive disease.  This means that affected animals have two copies of the mutant gene, while carriers have one normal copy and a mutant one.  Each of the versions of a gene, in this case the normal and the mutant is called an allele.

 From the number of eye-tested individuals, both affected and non-affected, it is possible to estimate the frequency of the mutant allele in a population, as well as the proportion of carriers.  We know that approximately 2% of all eye-tested individuals are affected.  From this we can deduce that in the countries where PRA has been detected, 25% of the population is composed of carriers.

 Locating a Disease-Gene

When searching for a gene associated with a disease the first problem that arises is where to start looking for it; dogs may have around 40,000 genes (the precise figure being unknown), and they are distributed among 37 pairs of canine chromosomes plus two sex chromosomes (X and Y) that contain enough genetic material to span at least one meter.  In principle, the gene underlying a disease may be anywhere in that genome.  This illustrates the formidable task faced when searching for them.  However, human ingenuity has managed to devise several ways of finding those genes.  

In principle, there are three methods of finding the gene involved in PRA in Lhasa Apsos, and we have been working with the three of them:

Ÿ   the candidate-gene approach,

Ÿ   linkage analysis, and

Ÿ   linkage disequilibrium.


1.   The Candidate-Gene Approach

This involves searching for mutations in genes which can reasonably assumed to be involved in PRA.  Usually the genes that are studied are chosen because they are known to be involved in similar diseases in other species, such as Retinitis Pigmentosa in humans, or because they are known to be expressed in the retina, due to studies using model animals.

 This method has allowed dog geneticists to identify all but one of the canine genes currently known to be involved in diseases.  In our laboratory, it has enabled us to identify the two PRA genes known to date:  PDEB in the Irish Setter and PDEA in the Cardigan Welsh Corgi.

 We have performed some experiments with the candidate-gene approach during the last few months in order to find the PRA-gene in the Lhasa Apsos.  However, we have not found any abnormalities in the genes we have screened.  This approach is very inefficient, since it requires testing many genes until the mutated one is found.  The ratio of success to failure is very low.  This situation has prompted us to try other methods.

  2.            Linkage Analysis

This is a more powerful procedure.  It has been used in a very few studies since it requires a map of the canine genome, which has only been available since very recently.  The map is a set of sequences with precise locations in the genome, and each one different from all the others.  These sequences are called markers.  Markers vary between individuals, reflecting the genetic differences between them.  As the genes, each variant of a marker is called an allele.

 In linkage analysis, the pattern of inheritance of markers distributed along the genome, in known locations, is analysed in a multigenerational pedigree.  If one of these marker sequences shows a pattern of inheritance resembling the one we expect for the allele causing the disease, then we may reasonably conclude that that marker is closed to the gene involved in the disease.  The only reason (apart from chance or coincidence) why the pattern of inheritance of one such sequence may match the pattern expected for the disease allele, is because they are physically close, and thus are inherited together.

 We have done experiments using this procedure.  Results show that the method cannot be applied usefully to the Lhasa Apsos available to us.  The reasons for this are twofold.

Firstly, the affected Lhasa Apsos are not clustered together in a few families.  Instead of this, there is generally only one affected individual per family.  Affected siblings are extremely uncommon, as well as affected individuals in consecutive generations of the same family.  Given this distribution of affected animals, it is not possible to infer the inheritance of the disease allele in these families.  This means that when the patterns of inheritance of markers throughout the genome are analysed, there is no pattern to which to compare them (since it is impossible to deduct the pattern of inheritance of the disease allele). 

Secondly, even in the best families we have for study, we are missing crucial individuals who would contribute information.  In a late-onset disease, such as PRA in the Lhasa Apso, it is impossible to get grandparents, and we have also had problems tracing siblings of affected individuals.  Each missing individual in a family reduces our power to analyse it.  

3.            Linkage Disequilibrium (LD)

This is the method to which we are shifting.  It requires, as the proceeding one, a map of the canine genome. 

 We expect that alleles in the disease locus (locus is the location in the genome of a gene or any other sequence) will be distributed differently in affected and non-affected individuals:  all affected individuals will have two copies of the disease allele, and no copies of any other allele, while non-affected individuals may have different combinations of alleles for that gene, with the only restriction that they will not have two copies of the disease allele.  IN LD, therefore, we study the distribution of alleles for many markers, among affected and non-affected animals, until we find one with a distribution resembling the one described above for the disease locus.  If a marker sequence shows the distribution we expect for the disease locus, it must be because they are close to each other, and hence they are inherited together.  The only other explanation would be coincidence, but there are ways to rule this out. 

This procedure is based on the idea that the mutation that gave rise to the disease allele arose only once in the population and since then it has been transmitted to successive generations.  This means that all individuals having the mutant allele are descendants of a single ancestral individual in which the mutation took place, and they are all relatives.  When these related individuals are bred, both parents may transmit the mutant allele to their offspring which will have the disease.  Therefore, affected individuals will have two copies of the same mutant gene that originated in an ancestor common to both parents.

As mentioned, LD works by studying sequences along the entire canine genome to se if any one of them is identical in all affected individuals, as would happen with the mutant allele.  In very close relatives, a very large proportion of their genomes will be identical, since, it will have been inherited from a very close ancestor common to both of them.  For more distant relatives, the proportion of their genomes that is identical will be smaller.  The larger the number of generations that separate two relatives from a common ancestor, the smaller the proportion of their genomes that will be identical.  As generations pass, less and less of the genome will be identical for distant relatives.  Less and less of the genome will have been received from the same distant ancestor, and more and more of the genome of these distant relatives will be due to ancestors not shared by them.  This means that as generations pass, the length of the chromosome fragments that are identical for these relatives becomes smaller.  In order for alleles of a marker to show the distribution we expect for the disease allele, both, the marker and the disease locus, must reside in the chromosome fragment that is identical in all affected individuals and that has remained intact since their common ancestor.  The more distant two or more affected individuals are from their common ancestor, the smaller the chromosome fragment identical in both of them; this means that the marker and the disease locus must be very close to each other if they both are to be in that same chromosome fragment.

 We have just finished the analysis of the pattern of inbreeding in the families of affected Lhasa Apsos for which we have blood samples.  Except for one family, the parents of all affected individuals share a set of three ancestors.  This does not mean that the mutation arose in any one of them.  In fact, the presence of that single family not sharing any of these three ancestors suggests that the mutation arose in a still more distant ancestor, common to this and to the rest of the families.  If has not been possible to identify this ancient ancestor.

 A maximum of eight generations separate the affected individuals from those three common ancestors.  With this information, it is possible to estimate the average length of the chromosome fragments identical for all affected individuals.  This length may then be compared to the average spacing of the markers in the canine genome.  If this spacing is smaller than the estimated length of the chromosome fragments conserved intact since the mutation arose in the common ancestor, then there will be at least one marker within this conserved fragment.  This is crucial, since only markers located in the chromosome fragments that are identical for all affected individuals, as well as to the common ancestor, will show the same distribution pattern as the disease locus.  Our results show that average spacing between markers in the current canine genome map is approximately the same as the length of the chromosome fragments identical for all affected individuals.  This means that there may be one marker close enough to the disease locus, such that both, the marker and the disease locus, belong to a chromosome fragment that has remained intact since it was originated in the ancestor common to all parents of affected individuals 

The fact that the average length of identical chromosome fragments in all affected individuals (fragments that have remained intact despite the several generations that separate all of them from their common ancestor) is approximately the same as the average distance between markers on the current canine genome map, means that it may be possible to find a marker with the same distribution as the disease allele, although the chances are slim.  If the average spacing of the markers on the canine genome were smaller (e.g., a more dense set of markers) then the chances of finding such pattern would increase, since there would be more than one marker within the identical conserved chromosome fragment, and so more opportunities for finding the distribution pattern we are looking for.

The Plan

Given this situation, a first attempt will be made to find a marker with the same distribution pattern as the disease allele, using the set of available markers on the canine genome map. 

In parallel to this work, in the course of the following months a more dense set of markers will be developed, and then they will be used to detect that pattern.

David R Sargan, Ma PhD                                 Lecturer in Molecular Pathology

Director of Postgraduate Studies                   University of Cambridge

We are grateful to Dr Sargan for all his hard work.  The subject of DNA is not simple to grasp and I found I had to read the forEgoing a couple of times before it sank in. (Secretary)

Breed Council - PRA/DNA Appeal Fund

With your help the Breed Council has now reached it's first target of £3,000 and this has now been sent to Dr Sargan's research account at the University of Cambridge.  We have, in fact, raised a further £1,164.22 and are well on our was to our second £3,000 target.  Please keep up the good work as this sort of research does take an awful lot of funding.  Any donation should be sent Lhasa Apso Breed Council Hon Secretary/Treasurer, Mr John Quelch, “Ardquin”, The Downs, Ross-on-Wye, Herefordshire, HR9 7TJ.  Tel: 01989 562515.  Cheques should be made payable to “LABC PRA/DNA Appeal Fund”. 


Lhasa Apso Association of Wales & South West on the ‘Net'

We will shortly be having a small web site on the Internet.  We hope to put this Newsletter on it, schedules with entry forms for downloading and other useful information.  For all you avid surfers keep a look out for our site.


Showing at the 111th Amsterdam Winners Show 2000

It all started in March 2000 when I was lucky enough to get my Lhasa Apso “Buzz” (Shardlow Hakuna Matata) micro chipped at CRUFTS for free, followed by rabies vaccination by my vet. There is a possibility that Buzz might live abroad for a while at some point, and I wanted to be prepared. This done, I realised that there was an ideal opportunity to take him to the 111th Amsterdam Winners show by travelling with Johnsyl Travel. This would take all the worry of planning the trip away from me, and let's face it there was enough to do just getting the dog's papers all in order. Whilst it would have been nice to take a Briard I decided that a Lhasa was by far the easier option for a first try at showing abroad.  

Once a month had passed after the rabies vaccinations a blood sample was taken to be sent for testing and once this was back the vet could complete Buzz's PETS1 passport. I sent an Export Health Certificate application form to MAFF in readiness. As it turned out the regulations changed before we travelled and this was not necessary, but we did need a PETS5 passport in French. According to MAFF the Netherlands required a Private Vet Health Certificate so this had to be completed a few days before we travelled, but it was never inspected. I was able to visit the Koninklijke Nederlandse Kennel Club “Cynophilia” internet site ( and order a schedule ( I talked Storm Jones from Stormfield Briards into coming with me on the coach and Florence Fahey and Joe Shire from Bentarsna Lhasa Apsos were to fly from Ireland to meet us at the hotel.  

A month before our trip I used Drontal wormer and Frontline flea treatment on Buzz to make sure there were no gross adverse affects. I knew from this that he would suffer a degree of upset tummy so took some appropriate medicine with me. I also took my own Drontal and Frontline with me.



The great day had arrived to set sail. At 4.15 am on the morning of Friday 24th November Storm Jones and myself set out to meet the Johnsyl Travel coach. It was an uneventful outward trip, with Buzz being the only dog taken on the two coaches. During one of the stops I found that amongst fellow travellers on the other coach were people that I knew in Lhasas - and another Briard person, Molly, whose family had sent her on the trip as a birthday present (lucky lady). We eventually arrived at the Novotel hotel around 7pm that night and settled into our room.



Had breakfast and met Molly who came with us to the show. The walk from the hotel to the RAI where the show was held was only about as far as walking from the NEC car park into the halls. We watched the Polish Lowland Sheepdogs and Briards. The judge for Polish Lowland Sheepdogs and Briards was Hr P Sliweka from Poland.

 There were many unusual and rare breeds to be seen.


Saw quite a few familiar faces visiting from the UK and Ireland. On the way in to the show Buzz was inspected by a vet and passed to enter the show. There were benches with wonderful metal bar doors so you dog is safe. The dogs had plenty of room and even the small dogs had these pens. Our entry card was handed in at the ring table (mine was late as I did not realise it was supposed to be handed in by 10am). All dogs are graded and given a written critique, which you can collect when judging is finished for the breed. There were only 24 Lhasas entered with three males in the Open class and Buzz came third. We felt that overall the quality was mixed and quite a few of the dogs had longer muzzles than ours with head proportions of 50/50 instead of 1/3 and 2/3. The BOB under President of the Dutch Breed Club, judge Hr P Burema was a nine year old bitch from Denmark Fu-Kao Honolulu Deens.

I had to arrange with the Head Veterinarian for the flea and worming treatment to be carried out and the paperwork completed earlier than the show management normally do this but he was very helpful and was able to oblige. Otherwise we would not have complied with the treatment being carried out between 24 and 48 hours before sailing for England. Shopping followed and after the show myself, Florence Fahey, Joe Shire and Storm Jones set out for the flea market and later that evening after the obligatory visit to the Sex Museum, we were delighted to find an authentic Tibetan restaurant called the Tibetan Restaurant Lhasa, so we ate there.



The long journey home started with packing luggage onto the coach at 7.30am. En route through Holland, Belgium and France we stopped at a Chocolate Shop, a tobacco shop and a hypermarket. Everyone had enjoyed themselves. Alas, things did not go according to plan at Calais. There was Buzz waiting to be scanned and his paperwork inspected, but the French authorities were adamant that a dog could not travel on a bus - they said that buses were for people. They would not allow Buzz as a foot passenger and said that dogs were only allowed in cars. John Wright and our trusty driver were remonstrating with them as John had travelled six dogs on a coach to the Junior Handling competition earlier in the year. No budging. We missed two ferries whilst this was taking place.  The French insisted that it was an English P & O regulation. I cannot thank all the people on the coach enough for their support. There was no way they were going to leave Buzz behind and I understand that Thelma Lowe was ready to take on the French, and demonstration strategy was being organised, so we almost hit the national papers. Thankfully the French conceded, my heart stopped until Buzz scanned OK and his papers were then stamped. We all finally arrive home exhausted but exhilarated and want to do it all again (except for the Calais problems!). Buzz, bless him, was a little treasure to take. Someone commented on how good he was, and I replied that as far as he was aware he was only just down the road from home. (He has good sea legs having travelled so often to Ireland and back in September he had flown to Belfast).


Facts and Figures - Amsterdam Winner:

In 1998 there were no entries from UK, 1999 there was one entry and in 2000 there were 24.

The top entry in 200 was Golden Retrievers with 160 entered.

There were 4887 dogs entered in 2000, 2239 dogs and 2648 bitches.

3872 of these came from Holland.

BIS 2000 was a UK dog!!!!!!

 On a sad note, as I write this Ann East had been due to bring her King Charles Spaniel bitch home on the coach, having sent her out to be mated three weeks earlier. The poor bitch suffered an allergic reaction to the Frontline administered by the vet, and would not stop fitting. Ann had to leave her on a drip in the vets in Amsterdam. She was paralysed and they feared that the liver was affected. The prognosis looked very bleak. When I phoned Ann on the following Wednesday night she had just heard from Holland that the bitch had come round and had eaten a little. She had managed a couple of steps and after exhaustive tests they are hopeful that she may make a full recovery. The dedicated care she has received has been second to none and Ann has been most impressed. Thankfully the lady in Holland that the bitch had been living with for the previous three weeks is able to take her in when she can leave the vets, but few of us would be fortunate enough to have this situation if our dog was taken ill abroad. Food for thought if you intend to travel, and a warning for us all to be prepared for this eventuality. It had not previously occurred to me that my dog might be taken ill as I had been panicky enough about ensuring that his microchip and papers would be A1.