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wildairbc
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Wildair,

 

I don't know too much about CL. My understanding is that it's prevalent only in the NZ and Oz show lines -- which is not to say that other lines don't have it, but rather that is so rare that it hardly bears mentioning. I don't know of a single dog that's had it.

 

I believe that the worst health problems facing the Border collie are environmental. All but the most experienced folks seem to overfeed pups, feed them rocket fuel, and encourage lots of jumping, running, and other potentially injurious activities before the dogs' joints are fully developed.

 

When you tell someone to keep a dog lean, it's best to give them an example of what they should strive for. I took me years to learn what a Border collie should feel like; that it's important to be able to feel the ribs, spine and hip points. My first two dogs suffered because of the fact that I was so slow on the uptake.

 

Another environmental health hazard is poor training. If you don't teach a puppy limits, he's much more likely to end up under the wheels of a passing car, or buried in a neighbor's pasture because he's gotten in with their sheep one too many times.

 

In my mind, these subjects, which are so often overlooked, are at least as important as the genetic health issues that are often discussed in intricate detail with prospective puppy buyers. Probably much moreso.

 

 

 

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Bill Fosher

Surry, NH

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Guest PrairieFire

If you own Kiwi or Oz show dog lines, then CL appears to be a traceable genetic disease - the "we" you are referring to are the conformation breeders/showers that have imported those lines...

 

Perhaps the best way to eliminate CL is simply not to breed any dogs from those lines?

 

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Bill Gary

Kensmuir, Working Stockdog Center

River Falls, WI

715.426.9877

www.kensmuir.com

 

 

 

[This message has been edited by PrairieFire (edited 06-29-2002).]

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I'll second Bill's inputs.

 

CL is not a known disease amongst the working dogs in UK and US.

 

If I'm selling a pup,most handlers are quite familiar with the lines and most problems are work related,i.e.,strong eye,one sided,etc.

Majority of working dogs handlers firmly believes keeping pups extremely lean into adulthood but I cannot emphasize enough to keep pups and young dogs on a minimal feed (well balanced adult food) intake.

 

 

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Inci Willard

Clearville,PA

814-784-3414

ikw@pennswoods.net

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Guest PrairieFire

Charlie -

 

CL isn't even on the list of "genetic problems" that Dr. Denise Wall put together as a "buyer's guide" for "real" Border Collies...so you ain't dense son, you just don't hang around with enough of the "fancy"...don't y'all got no pretty dogs out there in the "land of the saints"...?

 

Actually, when I first read CL - I figured we were gonna talk about Caseous Lymphadentatis...

 

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Bill Gary

Kensmuir, Working Stockdog Center

River Falls, WI

715.426.9877

www.kensmuir.com

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Caseous lymphadenitis is also known as cheesey gland disease. It often manifests itself primarily as chronic wasting. Internal and external abcesses form on sick sheep, which often leads to the condemnation of carcasses.

 

It's apparently transmissible from sheep to goats, but not so much the other way.

 

Most of the theories about transmission of the disease involve exposure to the pus from ruptured abcesses, which is generally loaded with the bacteria. There's also some evidence that there may be some fomite transmission -- meaning that the bacteria live on equipment such as shearing gear, watering and feed troughs, barn walls, fences, etc., etc. and can be picked up by uninfected sheep that way.

 

There might even be aerosol transmission among closely housed animals.

 

Caseous is theoretically curable with long term and massive antibiotic treatments, but it's generally not practical to treat. There's a vaccine available, but once your sheep are vaccinated they will test positive for the closely-related tuberculosis bacteria.

 

It's a nasty disease, and just about impossible to rid the flock of once it gets established. It has its economic effect by limiting the useful lives of ewes, and causing them to produce weak lambs, or not enough milk to grow properly.

 

 

 

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Bill Fosher

Surry, NH

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My Cruz has CL in his ancestor's and was the reason why he was desexed and given to me, his previuos owners had no use for a desexed male dog(unfair I thought, but I have a great dog now).

Here are some facts on CL(ceroid lipofusoinosis) that I got from work.

- Rare diesease occuring in Border COllies which affect the nerve of cells of the body. Also know as Storage Diesease.

-It is an inheriated disease, not contagious.

- Identical disease also occurs in humans and is know as Batten's Disease.

-Australia's first known case was found in 1980. Since then 32 proven cases from 15 litters have been notified.

Another form of CL has been found overseas in other breeds- Salukis, English Setters, Cocker Spaniels, Dachshunds, In Devon Cattle and South Hampshire sheep and in Siamese Cats.

-Affected dogs usually display signs before the age of 21mths.

The likelihood of a Border Collie developing CL is very small whatever its ancestry and carrier dogs are not themselves affected in any way. They can be kept as non-breeding pets as they are normal healthy animals in other aspects(This is what Cruz is)

CLINICAL SIGNS AND DIAGNOSIS OF CL

animals appear normal until aged app 18mths.From the embryonic stage, there is metabolic defect which allows waste products "cl" to accumulate in the body cells.

With very little room in the brain for waste products the accumulation begins to compress and destroy healthy brain cells.

-Unreasonable apprehension of familar objects or surroundings.

- Abnormal gait- is unsteady on feet, has difficulty with jumping or climbing or placing feet.

- Lack of concentration and apparent lose of sight.

- Demented behaviour,Mania, hyperactivity and rage(aggression is usually one of the last symptons observed)

The disease progresses rapidly once the intial stages appear and distressed animals have not been kept past the age of 2 1/2 yrs.

There is no test as yet to identify dogs, which have inherited the disease or are carriers. Suspected cases can only be confirmed by post mortem examinations. No treatment.

 

Both males and females are equally susceptible.

Sire and Dam of an affected dog must be either carriers or affected.

Mating one carrier animal to a non carrier can produce carrier offspring.

 

I have a contact number for anyone interested in further info:

Dr Isabel Johnston

Small Animal Clinic

Veterniary School

Unviresity of Queensland

PH frown.gif07)33652530

 

It is very interesting reading and if anyone is interested this Dr has plenty of info on the disease.

 

Mandie

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Er Bill, katendarby was engaging in a type of humor that is rare here in New England but quite common among flatlanders: self deprecating humor.

 

Oh wait a minute! Was your reply an example of New England's own surreptitous, dark humor? Being a flatlander, if I get New England humor at all, it's usually hours later. Of course, my understanding comes with another realization: I was the butt of the joke! biggrin.gif

 

------------------

Margaret

retired terrierwoman, border collie wannabe

drumlins@adelphia.net

 

 

 

[This message has been edited by Margaret M Wheeler (edited 07-02-2002).]

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I believe that CL is a risk in ALL BCs, since they all came from the same place, after all.

There is no DNA test for CL right now, however the Australian?s are working hard on it. Hopefully within a few years there will be one. Most breeders believe this problem, CL, to be a breed problem, and not a country problem. The Australians get extra credit for noticing that there was a problem and putting so much time and energy into trying to find a test for it. But all of the known carriers in Australia can be traced back to one dog imported into Australia, R Fortunes? Scottish Victory. It is unlikely that this dog developed a problem in Australia, but more likely that he carried it from his English and Scottish lines.

There is at least one known case that was treated here in the United States from a dog of unknown pedigree, more than likely this dog didn?t not have any Australian lines in his pedigree, he was treated around 1998 or so, and he was 2 years and 7 months when he was brought in so that would make him born around 1995 or so and there were very few Australian dogs here then.

I believe also that many cases of CL go undiagnosed, since it is such a rare disease and few vets would look for it, especially if breeders don't inform them of it's presence in the breed.

Bonnie

 

------------------

What you believe has no effect on the truth.

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Guest PrairieFire

Not only "random", but fatal by two years of age...seems pretty specific...

 

And STILL doesn't answer my question that since the show lines that exhibit this traced genetic disease are well known - why not simply stop breeding these "champions of the show ring and carriers of a fatal flaw"?

 

------------------

Bill Gary

Kensmuir, Working Stockdog Center

River Falls, WI

715.426.9877

www.kensmuir.com

 

 

 

[This message has been edited by PrairieFire (edited 07-03-2002).]

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Guest C Denise Wall

First let's ground ourselves in reality. We all, dogs, humans, etc., carry a minimum of three to six harmful mutations as individuals. As a whole race or breed, there are millions of possibilities and combinations. A mutation may randomly occur in us, or it may have been passed on from one or both of our parents. From my biochemistry/molecular biology background, I can tell you that most of these genetic mutations are expressed in enzymes, the proteins that catalyze bodily functions of all types. These deleterious mutated enzymes range from partially functional to nonfunctional. Most harmful mutations are recessive and therefore the harmful effect is not expressed unless the animal has two copies of the mutated gene, one from each parent.

 

The mutation causing ceroid lipofuscinosis (CL) is thought to be in an enzyme that breaks down ceroid lipofuscin. This causes harmful accumulation of this in body cells, the brain cells being most susceptible. It's typical of one of the millions of possible mutations any of us can carry. The incidence of disease caused by any one of these millions of random mutations in a population is usually very, very low unless we are somehow joined up with another carrying the same mutation. Human medicine is filled with single case and extremely low incidence reports of illnesses causes by such random occurrences. The incidence of this type of mutation is increased by inbreeding such as that common in the conformation show dog crowd.

 

Although all breeds originate from common gene pools, inbreeding is not common in the working Border Collie community. There is functional selection for breeding prospects. There are less genetic diseases than in show breeds. We do not have the same breed as the show "Borders". The incidence of the mutated gene that causes CL may be no higher in our breed than any one of millions of other similar mutations our dogs as a breed, like us, carry. Should we worry about and develop DNA tests for them all? Where does it end? Shouldn't it be established as a significant problem in our breed first? There are no reported cases in working Border Collies. How can we consider it to be a problem when we know of no dogs who have had it? It can't be viewed as cost effective or even reasonable to say we should help develop a test and test for something just because other dogs have been shown to have it.

 

As for it being undiagnosed - possibly. However, as much as we are viewed as dumb redneck hicks, we do get upset when our dogs get sick and drop dead. Surprisingly, many people actually have them diagnosed. And once again, the working dogs and their progeny, especially frequent breeders, are out there being seen and getting discussed. It hard to keep secrets in our world.

 

Finally, there may be leakage of working bloodlines into the show crowd but I see no evidence of leakage the other direction, as in, working people using dogs from show lines as breeding stock. There doesn't seem to be anything the show "Borders" have that the working people need or want. CL seems isolated in your breed. Therefore, I, personally, don't consider CL a threat to the working Border Collie community at this time.

 

Denise

 

[This message has been edited by C Denise Wall (edited 07-03-2002).]

 

[This message has been edited by C Denise Wall (edited 07-03-2002).]

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Guest PrairieFire

"As for it being undiagnosed - possibly. However, as much as we are viewed as dumb redneck hicks, we do get upset when our dogs get sick and drop dead."

 

Yep.

 

Means I gotta go out and get 'nother $50 dawg from the ole boy down the road...and haveta take the collar offn the old dawg...and bury it in the back pasture and try ta remember a new name...

 

I thought maybe I'd jest name all mah dawgs, Shep, then I'd never haveta learn a new name...

 

Oh, and Denise, thanks for the well-written post.

 

------------------

Bill Gary

Kensmuir, Working Stockdog Center

River Falls, WI

715.426.9877

www.kensmuir.com

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>>>I believe also that many cases of CL go undiagnosed, since it is such a rare disease and few vets would look for it, especially if breeders don't inform them of it's presence in the breed. Bonnie<<<<

 

Do you "other activities" breeders actually breed your dogs at such young ages?

Those who are affected by CL seems to pass away at young ages,that tells me they take the affected genes out of the gene pool. Perhaps you should all try to wait until they reach maturity,which is between 2 1/2 to 4 years of age.

 

 

------------------

Inci Willard

Clearville,PA

814-784-3414

ikw@pennswoods.net

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Denise, thank you for such a well written reply.

 

And I am guilty. The only dog I ever had just drop dead I didn't post--figured he was 18 (years) at the time, why bother.

 

I have heard 'rumor' of 2 CL affected litters in 'US" lines. This was from an obed breeder who was quite open about it. I have been unable to get a copy of the pedigree, but understand it was from the same litter repeated w/in one year. One source claims that there were Barbie lines involved, but I have no concrete evidence so can't say. This is/was the only incident of CL in the "American" lines that I have heard of.

 

And the Aust lines have been in the US since before AKC recognition and what makes you think they do not end up in rescue?

 

Perhaps one reason the working breed has fewer of the severe problems is that the old time breeders had no reluctanct to 'culling' any inferior specimens. I cannot say the same holds true for the show breeders I know.

 

Pam

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