More French Great Danes

Source 

Source

Source 

Please. Someone tell them to stop.

See also The Demise of the Great Dane

Pug Tea Party

Just in from the Royal Veterinary College...

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A Pug Tea Party With Difference. 

Saturday, 5 September 2015 from 09:00 to 16:30. 

An opportunity for your Pug (or Pug cross) to have a free eye exam with a Specialist Ophthalmologist at the Royal Veterinary College, as part of our research project into pigmentary keratitis. By taking part, you will be contributing to the future health and wellbeing of this charming breed. There will be a chance for you to socialise with other Pugs and Pug owners, over Tea Party refreshments, in addition to a presentation about Pigmentary Keratitis in Pugs, given by one of the Ophthalmology Team. There are limited places available so please book one ticket per pug if you would like to attend.  https://www.eventbrite.co.uk/e/a-pug-tea-party-tickets-1826…

FAQs

What is Pigmentary Keratitis?

Pigmentary keratitis describes a condition in which the front of the eye becomes gradually obscured by a dark pigment, often causing visual impairment or blindness. Pugs appear to be predisposed to pigmentary keratitis and the prevalence seems to be high. Currently, it is unclear what causes pigmentary keratitis, but it is thought that several factors are involved. We hope to shed more light on the condition as part of this research project

Who is supporting this project?

We are very fortunate to have received a grant from the Kennel Club Charitable Trust, without whose support we could not be carrying out this important work. The West Peninne Pug Dog Club, the Wales & West of England Pug Dog Club, the Pug Dog Club and the Pug Dog Welfare & Rescue Association have all kindly welcomed us to a number of their events, where we have set up an Examination Tent for show attendees.

What does the examination involve?

Your pet’s examination will be carried out by a specialist veterinary ophthalmologist. The examination is similar to a routine eye examination for dogs and should last approximately 10 minutes. 

We would also like to take a DNA sample from your Pug, in the form of a cheek swab. A soft brush is rubbed along the inside of the cheek for approximately 45 seconds. This procedure is well tolerated and will be carried out by a qualified veterinary surgeon.

Are there ID requirements or an age limit to enter the event?

There is no minimum or maximum age for Pugs that you would like to enrol in the project. We would appreciate a copy of your Pug's Kennel Club registration for the DNA part of the study, but this is not mandatory and we welcome non-registered Pugs to this event. Your Pug does NOT need to be microchipped to attend. 

May I bring more than one pug?

Yes please! Just remember to book one ticket per pug. 

The event will take place at The Royal Veterinary College, Hawkshead Lane, North Mymms
AL9 7TA, Hatfield

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A request to the RVC.. Could the next one be for Boston Terriers please? Better title... ;-)

Fix the Face!

Especially for Australian vets... a workshop in November 2015 in New South Wales (download pdf here) to help you earn more money from your clients who have been stupid enough to have bought a Bulldog or other brachy breed in need of surgery (i.e. loads of 'em).

Here's the schedule:

Cost? $2400 Australian Dollars. But don't worry.

Big business Bulldogs. The pups sell for between £1000 - £2500, sometimes more. They are terrifyingly expensive to insure because they are at such a high risk of health problems. Vets make a small fortune out of them - and as we can see, those who teach vets do all right, too.

It helps promote a conspiracy of silence.

Stuck in the middle of it all, meanwhile, is the poor lumbering, gasping, short-lived dog.

Here's one that was made earlier - currently being used by the Kennel Club to - ta-daaa - promote responsible breeding.

Check it out on Facebook here.

Busted Bostons

Click to enlarge

Have a really good look at these two dogs as it's revealing for a host of reasons.

The UK dog on the left won Best of Breed at Crufts this year. The US dog on the right won Best of Breed at Westminster 2014. So same breeds, almost the same time.. and same breed standard!

As you can see, they are enormously different once you get past the similar markings.

Now it's by no means always true that the US show-dogs are always worse than the UK show-dogs - and not all Bostons in the US look like the dog on the right. But, boy, the Westminster winner is just awful.

First look at the heads.

Leaving aside that the US dogs' ears have been cropped (why would you do that in a breed with naturally erect ears?), the US dog has a shorter muzzle and a rounder, more domed head with a shorter back-skull - all features that predispose to syringomyelia (which sadly is increasingly documented in this breed). Note too the rounder, more prominent eye; another potential health issue.

Then see the difference in how the necks flow from the head - and how much thicker the US dog's neck is, too?

Would you expect this man to snore at night? You betcha. And in a soon-to-be-published paper from the Royal Veterinary College, we will see that thick necks (whether from obesity or selective breeding) are a predisposing factor to breathing problems in brachycephalic dogs like the Boston.

Now to the feature that I expect first grabbed people's attention - the terrible "posty" rear end on the American dog.

I am at a loss as to how anyone could think that's a good idea. We know that straight back legs in dogs can cause cruciate ligament injuries and, ta-da... what's the most common orthopaedic problem in Bostons according to the Boston Terrier Club of America? Luxating patellas.. which lead to cruciate tears (see here).

That shorter back is a worry too as it is linked to hemivertebrae (a painful, sometimes paralysing spinal problem caused by misshapen vertebrae). And, guess what? Hemivertebrae is a common problem in Bostons.

The 2014 Westminster winner is not a one-off... Here's the 2015 Westminster BOB, showing a better length of body, but still a very short muzzle, prominent round eye and those bizarre back legs.

Of course, when you point out the obvious link between particular physical features and disease in breeds, you are met with a wall of denial from breeders - and videos which are supposed to prove that the whole breed is entirely healthy. Or if they're not, they've been bred by those awful backyard breeders. In fact, those awful back-yard bred dogs are usually way more moderate, especially when it comes to the length of their muzzles.

Here is how today's show Boston compares to a champion Boston from 1933 and a modern show x pet Boston.

Click to enlarge

Bostons are also a mess on the inside - the KC's 2004 health survey found that a whopping 92 per cent of them had been delivered by C-section.

But here, to cheer you up is a great video showing just how athletic Bostons can be.

Now Rosie here does have raspy breathing, but there wouldn't be much to complain about if all Bostons were like this. 

And how great would it be to see a balloon keepy-uppy competition for Bostons at Crufts and Westminster?

 
Source: High flying Boston Terrier plays 'keepy-up' with balloon by RoseandBruiser on Rumble

Gordon Setters: ouch!

A whopping nine per cent of Gordon Setters in Norway suffer from an immune condition which causes all their claws to fall out.

Wow!

And guess what?

The same bunch of genes that researchers found are linked to this condition - called  symmetrical onychomadesis - may help protect Gordons from another immune-mediated condition:  hypothryoidism (which commonly causes hair loss as well as lethargy, weight gain, muscle loss, sluggishness and a slow heart rate).

The new findings from researchers in Norway (read the open-access paper here) present breeders with a dilemma. Do you select against one condition at the risk of heightening the risk of another?

Well let's have a look:

Symmetrical onychomadesis (also called Symmetrical Lupoid Onychodsdrophy or SLO) varies in severity, but the lesions can be very painful, treatment is often not successful and some dogs have to be euthanised. English Setters, Whippets and Bearded Collies suffer from it too.

Hypothyroidism, meanwhile, is treatable (if tricky and expensive to keep on top of) and is found in Gordons at a lower prevalence than the claw-loss (2.9% compared to 8.9%).

So... select against the claw-loss!

Well no. The authors stress that a lot more research is needed before breeders could start using the new info in a way that could help improve the health of their dogs. In other words...

But actually...

Immune-mediated disease (heck almost all disease) in dogs is on the rise because of the way we breed them: closed gene pools, overuse of popular sires, over-emphasis on looks to the detriment of health (as much as the loonies would prefer to deflect the blame on to vaccines, dog food and vets conspiring with big-pharma).

This new Norwegian paper looked at a specific part of the dog genome called DLA (dog leukocyte antigen).  DLA codes for the immune system and it is made up of different haplotypes (bunches of genes).

The number and distribution of haplotypes is considered to be an indication of overall genetic diversity in a breed.

Broadly speaking, the more haplotypes, the better. Your immune system needs a diverse armoury with which to fight disease/foreign invaders.

And, generally, the more inbred the dog is,  the fewer the haplotypes.

The Norwegian researchers found 10 different haplotypes in Gordons and seven in English Setters in the dogs they studied - not the worst compared to other dog breeds, but low. A high incidence of immune-mediated disease is found in other breeds with a low number of DLA haplotypes, such as the Bearded Collie, Standard Poodle and Nova Scotia Duck Tolling Retriever.

Seriously, the answer is not that difficult. And there is no need for paralysis while we wait for the researchers to come up with the definitive answer. Because there is already one out there.

We need to increase diversity in these breeds. And where it isn't possible to do it within the breed by going out to different lines, then it's time to outcross... to dilute the poisoned rivers that are today's closed gene pools.

Because, frankly, I'm sick to death of paper after paper finding yet another breed-related disease at the kind of rate seen for symmetrical onychomadesis in the Gordon Setter.

Read it again.

Almost one in  10 Gordon Setters in Norway suffer from a hideous condition that makes their claws fall out. 

Want to have a guess at how it feels to walk with that?

Which dog is most inbred?

Reckon you know your stuff when it comes to co-efficients of inbreeding (COI)? Have a go - or a guess... is it X, Y or Z?

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The answer is here... And if you got it wrong - or even if you got it right and are keen to learn more... there's a fantastic current offer from the Institute of Canine Biology.. a free online course - COI Bootcamp - for breeders.

Help make epilepsy history in Golden Retrievers

This extremely distressing footage is of a working Golden Retriever called Buddy having seizures. Buddy lives in Germany but unfortunately epilepsy is widespread in Goldies and it is thought to be inherited.

Buddy's owner Regina Enzinger has made the footage public to help raise awareness and funds for research led by Professor Dr Tosso Leeb at the University in collaboration with canine epilepsy guru Prof Dr Hannes Lohi at the University of Helsinki.

Their aim is to isolate the gene or genes and develop a new DNA test for Goldies.

More about the project and how to donate here.

Purina feels the heat

Nicked from Purina's Facebook page this morning...Other than making me itch in a grammarly kind of way, I thought it could be improved.

Goodbye Zak - "He was my world"

Zak last week - the morning of the day he was PTS

I was really sad to hear of the death of Zak the Boxer who featured in the first Pedigree Dogs Exposed.

The footage in the film of Zak's epilepsy (he suffered from cluster seizures) caused controversy.  First, it was extremely distressing; second some thought it inappropriate for a film crew to have been present (in fact we weren't there; we had given a camera to Joan and her partner Fred to film it themselves.)

There were accusations too that Zak wasn't show-bred so shouldn't have been in the film as PDE focused mainly on the damage done by KC breeding of show-dogs. Others maintained that although Boxers can and do suffer from epilepsy, there are certainly other breeds that are worse-affected (as indeed, we did state in the film).

Poor Joan got a lot of flak after the film but she always stuck to her guns that it was important for people to see what it was like for owners to deal with epilepsy - which in some breeds is frighteningly common due to inbreeding and a breeder-culture of brushing it under the carpet.

It has been a terrible, terrible last 12 months for Joan. Last September, she lost her long-term partner Fred. Joan nursed him at home and he died surrounded by their three Boxers.

Fred with Boxers Zak, George and Tasha

Then, just 16 days after Fred died, Joan lost her younger Boxer, Tasha, aged 7 to a brain tumour.

Tasha (left) with Zak

Now Joan has lost her beloved Zak and is left with just Georgie, her white, deaf rescue Boxer.

"Zak was my world," says Joan simply.

Joan did a truly amazing job of caring for Zak given how severe his epilepsy was - something her vets have applauded her for,  too.

Joan was also very brave to let us use the footage of Zak in PDE. 

She has my admiration and heartfelt thanks. 

Zak in his younger years 

Zak with Fred in Pedigree Dogs Exposed

Walk like an Egyptian... GSD

Spotted on Facebook... posted by Egyptian Amr Ismat on his Facebook page.

Ever so proud of his new imports, he is - unaware that he got fleeced. But of course the real tragedy are these two dogs with broken backs and collapsed rear ends. They look so traumatised, too.

In fact, I think these dogs might be Chinese-bred as they breed GSDs like this there - and Mr Ismat also has pictures of grossly overdone Tibetan Mastiffs on his page.

Breeding dogs like this is animal abuse - as bad as beating a dog with a stick.

Impossible to watch and not weep.

New hope for Shar-Pei... coming soon

There is news today about a long-awaited DNA test for Shar-Pei that could revolutionise the health of the breed - as long as breeders are willing to accept less-wrinkled dogs.

Shar-Pei expert Dr Linda Tintle confirms on her Facebook page that a new test has been validated  - but warns breeders and puppy-buyers that, for the sake of the health of their dogs, they may have to learn to love the breed without the over-abundant wrinkles that are a hallmark of the breed in the West (but not a feature of the original Chinese dog).

Four years ago, Dr Tintle was part of an international team of researchers led by Mia Olssen in Sweden. The team reported some key findings - and has been working on a DNA test ever since.

• the Western "meathmouth" Shar-pei has a different version of  the hyaluron-coding gene HAS2 to its less-wrinkly original cousin (also known as the "traditional" or "bonemouth" Shar-pei) 

• the "meatmouth"mutation - when numerous copies of it are present - is linked to health issues. Geneticists call this a 'copy-number variant/variation'' or CNV. (In humans, CNVs are often associated with disease and the same phenomenon is thought to be linked to an elevated risk for cancer.)

• Although not perfectly correlated, the more wrinkled a dog is, the more likely it is to have more copies of the mutation (which figures... more copies of a gene that codes for hyaluron production is likely to result in over-production of hyaluron. It is excess hyaluron that is linked to many Shar-pei health problems.)

•  The "traditional" Shar-pei, meanwhile, has a different version of the gene and appears to be much less susceptible to the classic Shar-Pei health issues.

(You can read the 2011 paper here.)


In the West, the breed is based on a tiny number of dogs exported from China in the 1970s. Their wrinkly puppy faces were an instant hit and they were bred (and inbred) profligately to meet the demand. The more wrinkles the better... which led to the selection and breeding of ever-more wrinkled dogs - to the extent that in some parts of the world today you can find poor creatures like this (this dog is in Uzbekistan).

You are much less likely to find such extremes being produced by breeders in the US/UK - but, nevertheless, you still see some very padded dogs in the show-ring and many Shar-pei puppies have to have their eyes 'tacked' to prevent their rolled-in eyelashes ulcerating their eyes.  No doubt too that there are many breeders (not all pile-em-high pet breeders) still selling these dogs by the wrinkle. Some adult dogs' eyes are so obliterated by rolls of flesh that facelifts have to be done to save their sight.

Even when they are not as horribly-wrinkled as the Uzbekistan dog above, the modern Shar-pei's health problems are rife.  Excess hyaluron builds up in the dog's body prompting an inflammatory response that manifests itself in a number of clinical signs, ranging from unpleasant to life-threatening.

• Familial Shar-pei Fever - sudden agonising fevers during which the dogs can barely move
• Amyloidosis - leading to kidney/liver failure
• Arthritis - immune mediated
• Recurrent otitis - ear infections (not helped by the selection in the breed for tiny ears/ear canals which hinder air-flow)
• Hereditary Cutaneous Hyaluronosis - or mucinosis as it is sometimes called.

Yes, it's that disgusting...

The above conditions are now lumped under the umbrella of SPAID (Shar-Pei Auto Inflammatory Disease) - with a number of other symptoms also thought to be linked, including Inflammatory Bowel Disease (IBD), allergic dermatitis, streptococcal toxic shock syndrome/necrotising fascitis (yep, that flesh-eating bug), lymphedema and Swollen Hock Syndrome.

My view has always been that the Western Shar-pei is such a genetic/medical basket case that it is unethical to breed it.   But the new DNA test should be a help, just as long as breeders are willing to use it and just as long as it does finally make it to market.

The test will reveal not just that a Shar-Pei carries the meatmouth mutation but, critically, how many copies of the mutation it has, allowing breeders to choose to breed from those with fewer copies. (Again, the lower the number of repeats, the less likely the dog is to suffer from hyaluronosis. As these are also likely to be less phenothypically extreme dogs, it should over time lead to more moderate dogs).

Well there's the hope, anyway. And the DNA test is taking an age. The reason for the hold-up is unknown, but likely due to scientific and commercial manoeuvrings . It is hopefully not due to a challenge published in Animal Genetics last year by a team in Hanover which asserted that the 2011 findings were flawed.

Certainly, there has been a very robust response from Linda Tintle's team (reproduced in full below for those interested*). Given the stature of the scientists involved in the original study (they include canine genetics royalty Kerstin Lindblad-Toh), I know who my money is on.

I am also encouraged that there is more interest in the  traditional dog, which common-sense tells you is sounder than the overdone Western version.  There are now some trad dogs in the UK - and below is the stunning Maxim, owned by Kikka Posti in Finland.  Maxim has been a great ambassador for the traditionl dog, particularly on social media.

Compare Maxim to this year's Cruft's winner - and, in particular, check out the dog below's hock area. There is a bagginess there likely due to excess hyaluron and it isn't something that - in my opinion - judges should be rewarding. (Or those posty back legs which predispose the breed to cruciate ligament tears - although it should be said that they are often a feature of the trad dog, too.)

Kennel Clubs could play their part here, too, with a class for the traditional Shar-Pei in which longer legs, less padding and only slight wrinkling won't get the dog thrown out of the ring for not being a real Shar-Pei.

(And yes, sadly that's happened...)

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Linda Tintle

Our collaborative veterinary and genetics team has been working tirelessly for almost ten years to dissect the genetics of what was known as Shar-Pei fever, but is now recognized as Shar-Pei Autoinflammatory Disease (SPAID). This key driver of our work has been to understand the mechanics of this disease, from genetics through to clinical presentation, with the ultimate goal of developing a reliable test with which to help the community. Together with Shar-Pei owners, we have collected samples from more than 500 individuals and with this level of personal and professional involvement, we take our reporting responsibility seriously. 

We feel in light of the recent publications that we need to clarify what we have learned about this disorder and how our scientific findings differ from that reported by others. 

In 2011 we published a paper where we described the correlation between a breed-specific genetic variant (a copy number variant) in Shar-Pei and the higher activity of one of the genes encoding hyaluronan (HAS2). The same genetic variant was also correlated to a higher risk for an individual to suffer from periodic fever (reference 1). Taken together with other studies (reference 2-4), this copy number variant also appears to underlie the folded and thickened skin of Shar-Pei, which we know is a result of increased deposition of hyaluronan in the skin. 

We followed this in 2013 with a breakthrough paper for this disease (reference 5). After the meticulous examination of veterinary medical records from 255 Shar-Pei, we realized that fever was only one of the clinical signs of inflammatory disease seen within this breed. We coined the term Shar-Pei Autoinflammatory Disease (SPAID), to cover a spectrum of inflammatory signs including fever, arthritis, ear and skin inflammation and amyloidosis. Our research showed that SPAID is one genetic locus, meaning that one region of the genome is correlated to all these clinical signs. 

We welcome the evaluation of our work by others, as reproducibility is key to scientific validation. However in order to “refute” our research, as was claimed by Metzger & Distl (2014), the same methodology in terms of techniques and disease classification must be employed. In this case, that simply was not done. Let us take you through our most important point of contention, the classification of healthy and sick Shar-Pei. 

As we illustrated above, we have invested a great deal of time and effort in order to strictly classify healthy and sick individuals prior to the commencement of genetic studies. This process involves the combination of interviews with owners and veterinarians, plus the study of each dog´s medical records. This is extremely important, as in complex diseases such as SPAID, an individual can be a carrier of the genetic risk factor without being ill. For this reason, we excluded all “healthy” dogs with sick relatives. We also excluded “healthy” individuals with vague or more mild signs of inflammation, such as a reluctance to move for one or two days as this observation can be easy to miss or interpret as something else, while it is in fact disease symptoms. On top of this, we required “healthy” individuals to be five years of age or older. This was to avoid the misclassification of dogs that had a later onset of fever events as “healthy”. 

These are just three examples of our very careful approach to ensuring healthy and sick dogs were properly characterized before studying what differentiated them on a genetic level and is in clear contrast to Metzger & Distl who state only “47% of the analyzed Shar-Pei dogs were older than 3 years at the time of investigation". It is likely that “silent carriers” or dogs with a later disease onset were classified as healthy in their investigation and this could be a possible explanation as to why they failed to see a correlation between disease and genetic variant. 

Our research has shown that we are not dealing with a single clinical symptom, but rather the syndrome of SPAID. This means that the genetic test we developed needs to be evaluated for understanding not only Familial Shar-Pei Fever, but rather a raft of inflammatory conditions. We are finalizing our results using a new technology that offers greater precision in measuring the copy number variants in each individual. This technique has greatly increased our understanding of how variants are passed down from parent to offspring over generations of breeding. 

With help from engaged and generous dog owners world-wide, we have been able to replicate our results in more than 200 Shar-Pei dogs and are confident that our results hold and will be useful for the breed’s health. 

Jennifer Meadows, Ph.D.
Dept. Medical Biochemistry & Microbiology (IMBIM)
Uppsala University, Uppsala, Sweden

Kerstin Lindblad-Toh, Ph.D.
Professor in Comparative Genomics, Uppsala University, Sweden
Co-director of Science for Life Laboratory, Uppsala, Sweden
Scientific Director of Vertebrate Genome Biology, Broad Institute, USA.

Mia Olsson, Ph.D.
Faculty of medicine, Department of Pediatrics
University of British Columbia, Vancouver, Canada

Linda J.M. Tintle, D.V.M.
Wurtsboro Veterinary Clinic, P.C.
Wurtsboro, New York, USA

Åke Hedhammar, D.V.M., M.Sc., Ph.D., Dipl. Internal Medicine-Companion Animals
Senior Professor, Department of Clinical Sciences
Swedish University of Agricultural Sciences
Uppsala, Sweden

References:
1. Novel unstable duplication upstream of HAS2 predisposes to a breed-defining skin phenotype and a periodic fever syndrome in Chinese Shar-Pei dogs. Olsson M, Meadows JRS, Truve K, et al. PLOS Genetics 7: e1001332, 2011.
2. Cutaneous mucinosis in shar-pei dogs is due to hyaluronic acid deposition and is associated with high levels of hyaluronic acid in serum. Zanna G, Fondevila D, Bardagí M, et al. Vet Dermatol 19; 5, 314–318, 2008.
3. Hereditary cutaneous mucinosis in shar pei dogs is associated with increased hyaluronan synthase-2 mRNA transcription by cultured dermal fibroblasts. Zanna G, Docampo MJ, Fondevila D, et al. Vet Dermatol 20(5-6):377-82, 2009.
4. Increased HAS2-driven hyaluronic acid synthesis in shar-pei dogs with hereditary cutaneous hyaluronosis (mucinosis). Docampo MJ, Zanna G, Fondevila D, et al. Vet Dermatol 22; 535-545, 2011.
5. Thorough investigation of a canine autoinflammatory disease (AID) confirms one main risk locus and suggests a modifier locus for amyloidosis. Olsson M, Tintle L, Kierczak M, et al. PLOS ONE 8:e75242, 2013.