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IGS in Border Collies

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Recently there has been a lot of discussion among quite a few European breeders who compete on stock dog trials over there about this genetic disease and testing breeding stock for it. Does anyone know of any border collies in North America that have been diagnosed with this? I looked it up at the University of Davis site and it says that it is Beagles and Border Collies and affected dogs are unable to absorb B12. It is a recessive gene so each parent must be a carrier in order to produce affected progeny.

 

 

 

 

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We believe that this is what killed our young dog Bute several years ago. Sadly, his problem was not diagnosed (through bloodwork) until it was too late. I have been reading some information about it via FB postings and have been in touch with a couple of people who have experienced it (and been able to treat it) in multiple dogs. Those dogs were either imported or had recent imported parentage, I believe. Bute's father was an import. I don't know if it's more prevalent over there.

 

It is an awful condition, with painful ulcers, lack of good growth, inability to eat, and/or digestive problems like diarrhea.

 

His problems never spoiled Bute's delightful outlook on life but he certainly experienced pain and suffering, and we did not realize the extent of his problems, and neither did our vet. By the time we all realized how ill he was and pursued bloodwork testing that finally gave us a diagnosis, he was dying.

 

His sire was sold on, I'm sure as a stud dog, shortly after we got Bute. I hope that his breeder informed the new owner once we informed her of the source of Bute's problems. His dam had been used to produce many litters of pups, and Bute may have been from the last. I hope no other pups they produced in other breedings suffered like Bute did.

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This is why I have often brought up testing for B12 malabsorption when posts have concerned young dogs that are very picky or have frequent loose stools without an obvious reason. If my vet and I'd only known then what I know now, Bute would probably be healthy and happy and alive with proper treatment.

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I know of one working-bred (not "working lines") Border collie diagnosed with this disease. It almost died a couple of times, and the owners incurred many thousands of dollars in vet bills (which the insurance company refused to cover) in the process of diagnosing it. It's doing fine now with B12 supplementation.

 

This from the "ISDS working border collies" FB page:

 

These are some stats from a recent clinic in the UK where they did the B12/ IGS test They found....118 clear - 10 carriers and 1 affected.
That is a carrier/affected rate of 8.5% appox from this small sample.
I also tested 9 dogs and found one carrier and I know of a few others that have also found several carriers which are not included in the results above.
This is alarming news.
I would recommend to all breeders and puppy buyers to have at least one DNA tested normal parent in every litter.
I also recommend all breeders test all their dogs now.
Owners who have dogs with symptoms get their dogs tested.
It would be a good idea if all dogs were tested now so we can get a bigger picture of the carrier rate.
This test can be done at Orivet here in Australia as part of the Border Collie DNA test package (cheapest) and is also offered around the world at other labs.
This disease can lead to GI problems and also to seizures in severe cases.
Description:
Canine Imerslund-Grasbeck Syndrome, also known as cobalamin malabsorption, is a disorder which causes a dog to be unable to absorb adequate levels of Vitamin B12. Cobalamin or Vitamin B12 is normally taken in through the small intestines, but affected dogs cannot absorb the vitamin and quickly begin to show symptoms of deficiency.
Symptoms of IGS typically appear within 6-12 weeks after birth. A puppy is born with a certain amount of Vitamin B12, but after the stored vitamin is depleted, the puppy will exhibit signs of deficiency. Symptoms include anemia, lethargy, failure to thrive, and lack of appetite. While IGS cannot be cured, the disorder can be managed with regular supplementation of cobalamin.
Imerslund-Grasbeck is inherited as an autosomal recessive condition. A dog must inherit two copies of the mutated gene to have IGS, and one gene must come from each parent. Dogs that have only one copy of the mutated gene are carriers of the mutation. Since carriers do not exhibit any symptoms of the disorder, DNA testing is an important tool to ensure the optimum health of puppies.

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Thanks for sharing that, Sue. I'm often in a position where people are asking me if these issues might be a food problem, i.e. intolerance, but I haven't heard much about B12 malabsorption. I'll start suggesting testing for that. I do know someone whose BC was just diagnosed with low B12 and her vet told her it was a problem that BCs have, but he didn't elaborate or explain to her that it was a genetic problem. Fortunately, she made an appointment with a specialist.

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(Sorry for the duplication but I missed Lynn's post above)

 

Here is the quote from the FB post on the ISDS Working Border Collie page -

These are some stats from a recent clinic in the UK where they did the B12/ IGS test They found....118 clear - 10 carriers and 1 affected.

That is a carrier/affected rate of 8.5% appox from this small sample.

I also tested 9 dogs and found one carrier and I know of a few others that have also found several carriers which are not included in the results above.

This is alarming news.

I would recommend to all breeders and puppy buyers to have at least one DNA tested normal parent in every litter.

I also recommend all breeders test all their dogs now.

Owners who have dogs with symptoms get their dogs tested.

It would be a good idea if all dogs were tested now so we can get a bigger picture of the carrier rate.

This test can be done at Orivet here in Australia as part of the Border Collie DNA test package (cheapest) and is also offered around the world at other labs.

This disease can lead to GI problems and also to seizures in severe cases.

Description:

Canine Imerslund-Grasbeck Syndrome, also known as cobalamin malabsorption, is a disorder which causes a dog to be unable to absorb adequate levels of Vitamin B12. Cobalamin or Vitamin B12 is normally taken in through the small intestines, but affected dogs cannot absorb the vitamin and quickly begin to show symptoms of deficiency.

Symptoms of IGS typically appear within 6-12 weeks after birth. A puppy is born with a certain amount of Vitamin B12, but after the stored vitamin is depleted, the puppy will exhibit signs of deficiency. Symptoms include anemia, lethargy, failure to thrive, and lack of appetite. While IGS cannot be cured, the disorder can be managed with regular supplementation of cobalamin.

Imerslund-Grasbeck is inherited as an autosomal recessive condition. A dog must inherit two copies of the mutated gene to have IGS, and one gene must come from each parent. Dogs that have only one copy of the mutated gene are carriers of the mutation. Since carriers do not exhibit any symptoms of the disorder, DNA testing is an important tool to ensure the optimum health of puppies.

From my conversations via the internet with just a couple of owners of affected dogs and this information (as well as other sources), there has recently been a DNA test devised to detect this in an animal of any age. Pups seem perfectly normal at a very young age as they have been supplied with B12 from their dam. Carriers are not affected but two carriers can produce affected offspring.

 

Ulcers are a very common, painful, and horrible adjunct to this defect. This results in what we saw with Bute - being hungry, looking at his food dish, and simply not being able to bring himself to eat. Yet he would eat some very odd things - raw and cooked veggies, dead birds or mice, even mice stolen from the cat.

 

What someone understood from her experience with this is that eating can result in such pain (due to the ulcers) that some dogs can find it hard to even contemplate eating from their conventional bowls, locations, etc., even on their "good" days because of associating the pain with the normality of eating their regular food out of their dish. This could have been a reason why Bute would dive into just about any new food but lose his interest in it within just a few days.

 

Intermittent diarrhea can be an associated symptom. Since Bute also had a heavy giardia and hookworm population when I brought him home, we don't know if there was also damage to his digestive tract from his early puppyhood parasite load. His eating problems and intermittent yucky stools kicked in right after we brought him home, when he was 12 weeks of age. Up to that point, he seemed as healthy and well-grown as a pup could be.

 

Bute's ulcers caused him a great deal of pain, which we did not realize at the time. About half a year before he died, he had an episode of vomiting a large amount of blood. We took him to the e-vet who did nothing more than an exam and a couple of prescriptions, to "soothe and settle" his stomach. If I'd known then what I know now, I would have taken him to my vet and had him scoped. We would have found the ulcers that way at least, and could have treated for those.

 

In May 2009, when we'd had him three years, we noticed him being a bit sluggish when working and had some blood tests done. Those indicated that "something" was wrong (maybe a bit anemic, and odd liver and kidney values, if I remember correctly) and so we had blood drawn for more extensive testing. I went off to the Bluegrass before the results were in and that Saturday, Ed called to say that Bute was not doing well and the vet had called to say that he had "B12 malabsorption". She called late in the day and had Ed bring Bute in the next morning for a B12 injection but it was too little, too late for Bute. Sometime over late Sunday night and early Monday morning, this valiant little dog bled out and died in his sleep.

 

For the three years we had him, it was always a struggle to get enough food into him to keep him growing and he was always a skinny, scrawny little dog. Happy, active, shiny but definitely with something not right inside but neither we nor the vet could figure out what. With this defect being recognized more readily, hopefully dogs like Bute can be diagnosed and treated, and live happy, healthy lives. With a DNA test now available, this is one painful, debilitating, fatal defect that can be avoided with wise breeding choices - and something that can be treated when there is an affected pup.

 

Here is the home page for the group that is compiling a database but note that it is totally voluntary and, I believe, the PBHF is primarily based on KC dogs so you will see that most if not all are KC-registered animals but some are of ISDS breeding.

 

http://www.pbhf-dog.com/databases.html

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IGS is out there….it's not just imported dogs. However, I don't think it's terribly common….but it is often misdiagnosed and the dog dies or is euthanized….despite there being an effective and simple treatment. Easy to test for and I'll be including the test for at least one (if not both) dogs of any proposed breeding.

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No, I'm sorry, I did not mean to imply that it was something primarily in imported dogs. I'm sorry if I gave the wrong impression. The clinic (the statistics quoted) was in the UK, the database referred to was UK-located (I believe), the person raising the issue on FB was from Australia, and the person I spoke to with the most experience with this defect was talking about either imported dogs or those of fairly recent imported lines. So it is obviously present overseas as that's where the concern has recently been raised, and may be just as prevalent over here.

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I suspect that Birdie's littermate has this. She was extremely picky, apparently had some diarrhea issues. We stumbled on B vitamins because we decided to try them for their appetite stimulant properties. I don't believe her owner has had her tested, and I have no plans to breed either the dam or Birdie, but I may test the dam at some point just out of curiosity.

 

I, too, had read one of the Facebook discussions and that's what made the lightbulb go on for me regarding Birdie's sister. By the time I read about it, she was already receiving B12 injections (every three weeks I think) and was doing well, but I still don't think she's ever been formally diagnosed.

 

J.

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Does anyone know if there's any correlation between IGS, which seems from the description above to manifest in puppies, and cobalamin malabsorption that develops in adult dogs?

 

I wonder because of a couple people having this occur with adult dogs. Krisitne has mentioned it and I have a dog, though a mix, who does, as well.

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Cobalamin absorption is a complex process involving several different proteins.

 

I would imagine that IGS and the adult onset form(s) of the disease are caused by defects in different ones of these.

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I may have had a dog with it. He failed to thrive as a pup, was thin, had chronic diarrhea and low energy. He turned around with B12 injections. I placed him as a pet, so can't do the DNA test. However, a dog sired by a 3/4 brother to my dog's sire died of similar symptoms. That dog's dam was later DNA tested and found to be a carrier. That breeder suspects the dog who died had IGS.

 

I would love to see a screening done on ABCA registered dogs to estimate carrier rate in out country. That would help us know if testing of all breeding stock is worthwhile.

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UC Davis has a test for $50. You can do TNS and IGS for $70. I *think* my pup's grandfather is a carrier. I'm still waiting to hear back on confirmation for that, but I think I'm going to get him tested just to be on the safe side.

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UC Davis has a test for $50. You can do TNS and IGS for $70. I *think* my pup's grandfather is a carrier. I'm still waiting to hear back on confirmation for that, but I think I'm going to get him tested just to be on the safe side.

That sounds very reasonable. The blood work we had done was around $100 for the initial work, and somewhat more than that for the more specific testing that revealed the problem. A test like that for breeding partners could avoid any affected pups for a very moderate cost.

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My young dog has just been diagnosed homozygous for IGS which means that he is affected and that both parents must at least be carriers. I have told the breeder.

 

Like Liz P's dog he had chronic diarrhoea and has always been very thin. I wouldn't have said he lacked energy as such but his stamina wasn't great. Lack of appetite is a common symptom but that didn't apply.

 

At 12 months I changed him to a food that did improve the diarrhoea but a couple of weeks ago he was off his food, his diarrhoea returned with a vengeance and he vomited. In a very short time he deteriorated and had the staggers and head tremors. Quickly to the vets of course and in hours he had sunk so low they thought they were going to lose him but they managed to stabilise him enough for him to be referred to the Liverpool Uni Small Animal Teaching Hospital where IGS was strongly suspected and just confirmed by DNA test.

 

He perked up very quickly with a B12 injection and I now see that he really hadn't been as lively as he should have been. I thought he was just calming down a bit as he grew up.

 

I was quite relieved at the diagnosis which was preferable to the pancreatitis which my vets thought it might be.

 

The hospital vet said that they had only seen 4-5 cases and that it had only been identified in dogs in the last 2-3 years as far as she could recall, although she admitted that is could be significantly underdiagnosed generally. The test has only recently become widely available here.

 

I feel for breeders who test for everything reasonable where a test exists, only then to have their legs cut out from under them by yet another disease to test for. A friend told me a few weeks ago that she had had her dog tested for everything before thinking of using him at stud but his name doesn't appear in the list of tested dogs where I would expect to find it. I suspect that she thought she'd covered all the bases but has been caught out by this latest one. I'm sure she will test now she is aware if she wasn't before.

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Since there will always be new inherited diseases identified/recognized our best course is to breed to keep the COI (for lack of a better descriptor) as low as possible. Unrecognized inherited diseases become recognized when the incidence rate of "carriers" rises to the point that the rate of "affected" pups is high enough for us to recognize the disease as inherited.

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Excellent prognosis with B12 injections for life thanks. Inconvenient mainly. I will learn to do it myself but at present he is very wriggly and hasn't much flesh to inject into so I'll leave it to my vet for the time being,

 

I'm philosophical. There are much worse things that could be wrong with him and he's alive.

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OK. I had to do this with Tilly because of cobalamin malabsorption, though I don't think she had IGS, since it developed later in life.

 

It really wasn't a big deal giving her B-12 shots every 2 weeks. And it's inexpensive.

 

You're right. It could easily be worse.

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