One of my Afghans is particularly “reactive”.  As a show dog, he was very sensitive to specific stimuli, but I took that as part of being an Afghan, part of being from a dam who was a bit on the nervous side (and really, I do still think of it that way).  He’s still sensitive, but experience and training has helped a great deal, though he still is fearful in unusual circumstances (like when a man entered the house carrying a king-sized mattress on his shoulder).  He’s the smartest dog I’ve been around, with the exception of one Border Collie I shall never forget.  He’s sweet, gets along with all dogs, and is a superior companion.  We’re impressed with his temperament.  I trust his assessment of humans implicitly—if he doesn’t like someone, there’s something wrong with that person.

His breeder was forthright about the existence of hypothyroidism in his pedigree, and having another Afghan, from unknown background, at home with hypothyroidism, with no other real health problems than hip dysplasia, I thought that was acceptable, for I didn’t plan on using this dog for breeding (though I thought the breeder might). 

So, when his health screenings showed Autoimmune Thyroiditis, I was not surprised nor alarmed.  I thought it meant the same thing as “hypothyroid”.  I ignored the “autoimmune” portion for a number of years.  Readings told me that it was thought to be an autosomal recessive.  Of course I told the breeder so she would know, and a littermate owner, so she would know since she was breeding that littermate.

I was trying to collect this dog for the breeder, and had been unsuccessful.  A reproductive vet advised putting him on thyroxine, explaining that the thyroid gland would be destroyed and he would become sterile.  A doctor who has never met a dog he could not collect was unable to collect him.  I tried various environments, including home.  I became proficient.  As far as we could tell, he was sterile.  In the end, I gave the dog a vasectomy to ensure no accidental breedings, should we be mistaken (he was no longer being shown).

Radiographic screening showed nice, tight hips (PennHip). He was 28 months old. It also showed some arthritis in both hocks, which explained why he would start coursing, but basically stop after pushing off hard. He loved the baggies, so it had been confusing.  It had been hard to get him to push forward in a stack (and I regret not seeing that he was in pain, but he is very stoic).  I don’t know why there is arthritis in both hocks.  It explains the strange movement I was seeing in the ring.  I will note that his angulation in the rear is excessive, and he is not a square dog, being several inches taller than long.  But, that could be totally unrelated.  I’ve raised other Afghans who have not developed arthritis in the hocks (or anywhere else, knock on wood).  He’s almost 7 years old at present.  His new veterinarian noted right away that he didn’t seem comfortable, and that his hocks have limited flexion.

My reactive dog develops hyperplasia.  During his vasectomy, the veterinarian removed much excess tissue from his gums.  Recently, what appeared to be a mass at the base of a canine, turned out to be hyperplasia.  The tooth had to be removed as well, unfortunately.  A pocket of pus was in the mass, though he’d been on oral antibiotics. 

He’s had cysts removed from all four feet (they were painful, and there were many), and the report noted the intense inflammation. 

He’s had an abscessed anal sac.  A spot on his tail develops an acne-like condition, and has to be expressed regularly or it will abscess (it has in the past). 

His ears develop dark, waxy gunk, deep, which I clean.  I had assumed this would get better after supplementation of thyroxine, but it continues to be a problem, though less severe than prior to beginning supplementation. 

Though our yard was surrounded by a brick wall, if the neighbor sprayed weed killer, he would have a seizure.  Of course, we didn’t use pesticides or weed killers ourselves.

The first rabies vaccination was met with vomiting.  The second vaccination was met with a seizure.

At 18 months or so, he developed hygromas on both elbows.  In general, minor trauma to his body is met with a large, inflammatory reaction. (I’m not saying that dogs with hygromas have autoimmune disease!) 

I’ve learned to expect a pronounced, reaction from this dog to normal, run of the mill things.  We continue to monitor his thyroxine supplementation, feed a raw diet, give rabies vaccine as required by law (with pretreatment) and try to stay on top of whatever his body decides to react aggresively to. 

I do give ivermectin, according to his weight, monthly for heartworming, and use panacur (fenbendazole) for regularly scheduled dewormings (northern hookworms are a problem here, as are whipworms).  Other chemical dewormers are done as needed based on fecals.  I don’t want to add up the amount we have spent on veterinary care to take care of his body’s overreaction. 

I have come across material that states that cases of autoimmune thyroiditis have been linked to exposure to toxins and other insults.  And I’ve read that it’s simply genetic.  It’s my guess that once there, it can be passed on.  Surely it makes sense to test for it (early, when the dog still has auto-antibodies) and try to breed away from it.  I don’t understand what relationship, if any, autoimmune thyroiditis might have to any other autoimmune diseases.  I think all breeders should test for this, because knowledge is power. 

COPYRIGHT (C)2005-SHOW DOG DESIGNS