Mac’s AIHA Journal

This is a long story but after hearing that there are quite a lot of auto immune system diseases popping up in the UK right now, I choose to share a journal detailing Mac’s AIHA journey so far, hoping it could help another pet owner to save their beloved fur babies. Indeed, Irish Setters (with 9 other breeds) are genetically predisposed to primary AIHA (primary in this case means no known cause). Unfortunately, AIHA as well as all other types of auto immune diseases take time to be identified, and in case of anaemia, time we do not have.

Back to the 1 of May, my birthday boy was celebrating his 4th birthday, and his best present of course was to go out with his dad for a 2 to 3 hours run on the beach and dunes. Mac is a boy with incredible stamina, full of energy, happiness and fun. For Mac, life is just wonderful, always in good health and does not know the face of his vet as he never had anything wrong in 4 years. As one of the consultant vets told me later on; Mac is a very strong boy.



Then suddenly Mac stopped eating. The first day I just acknowledged it, although he was not eating his meal he never said no to a treat. However, when the fast was continuing the next day, I started to be concerned and was closely watching my dog. Beside not eating, he was still the same bouncing around boy, but when day 3 of fasting started, as expected his energy started to decline. I got into worry mode and decided to go to the vet first thing on that morning of the 3rd fasting day.


Tuesday 5 of May. Strangely enough, that very morning, I was with my telephone in hand and ready to dial the vet number when my phone rang. It was Dorothy Park. Never ever Dorothy phoned me on the morning, but she wanted to involve us in a Setters rescue fundraising car boot sale and was running short of time in her call’s list. I informed her I was on the point to phone the vet about Mac, and explained all the symptoms. The symptoms were mainly a lack of appetite, starting his 3rd days without eating and being a bit lethargic, which is never to be seen with Mac. “Right” Dorothy said, let me phone to make the appointment – Dorothy is well known and the vet knows that it is not a panicking pet owner phoning but someone with over 35 years of experience in breeding setters. Hardly 5 minutes later, she told me the time of the appointment and that she will meet me there. After examination, the vet thought that Mac’s belly was a bit sensitive and that he was probably having crystals in the bladder, so urine sample was sent to the lab. Most dogs refuse to eat when they are in pain, injections of antibiotics and anti-inflammatory, then back home. But that day Mac was getting more and more lethargic, I could see the difference almost by hours.

Wednesday 6 of May.

That morning Mac didn’t want to get out of bed (my bed) to do his business. I gently lead him out, and luckily he peed against a white wall and just beside me …. I could see that the urine was colour of the rust, reddish brown and very dark. I look at his eyes and the white part was yellow and so was his gum. I was convinced my boy was suffering from poisoning (ticks, lepto, etc.) When I took him back home, the poor mite was standing in the middle of the lane, not moving, not responding to me, I had to lead him inside. I rushed to the phone, took an emergency vet appointment and phoned Dorothy who said she will meet me there again. Mac was lowering his head very low and hardly had the energy to jump in and out of the car. A different vet was working that day and she took a blood sample, sent it to London, informing us that we will have the results first thing next morning, but this time she kept Mac at the clinic to monitor the evolution and put him on the drip as he was seriously dehydrated.

Thursday 7 of May.

The results of the blood analysis were arriving one by one and by lunch time that day, the vet phoned me to say that they need to do a blood transfusion straight away as the lab results are showing that Mac was very anaemic. However, his liver and kidneys were perfect. Things were getting seriously wrong, from having crystals in his bladder to being anaemic in one day, this was a bit hard to understand. That evening, the vet told me that she is still investigating what could be the cause and sending more blood to London to confirm her diagnosis. More results expected on the morning of the next day.

Friday 8 of May.

That morning when I phoned, again a different vet was working that day and to resume our conversation, she said that Mac was so very critically ill, that I should come to discuss with her the way to say goodbye and nicely let him go!!!!
I froze and couldn’t trust my ears, so I said: are you telling me that my boy is dying? She confirmed I understood properly, adding that the blood’s results are showing an auto immune system disease and he was far too anaemic to survive. How come a bouncing boy could die from anaemia within 3 days???

Nothing was making sense, David was away for a week, I desperately needed someone to tell me that I did not hear properly. I phoned Dorothy Park and let the message on her answering machine – Mac is dying!
Five minutes later Dorothy phoned me back to know more, I was so devastated that I am still not sure what I told her, so she phoned the vet and 10mn later Dorothy phoned me back saying – right Chantal, get ready, I am coming to pick you up and we are taking Mac to Earlswood Veterinary Referrals Hospital in Belfast, I am taking my young boy Charlie to give Mac more blood.

Today I can definitely say that this very decision of Dorothy Park and her active participation have saved the life of my boy!!!! If it wasn’t for Dorothy Park, my boy would have crossed the bridge by now. She knew where to go and what to do in an emergency crisis. That day, I realise how very important it is to have the support of a breeder. Breeders – good ones of course, have seen and dealt so many times with so many problems, they know their breed and are the most precious ally a pet owner could have. Do not worry if your breeder lives far away from you, Mac’s breeders are based in England but Mac lives with us in Northern Ireland, so not really possible to help me physically. Any good breeders will always help you, so I would strongly advice all pet owners to contact their closest breeder and start a good relationship with them. Luckily for us Dorothy Park is a local breeder, she knows very well the breed and the line, and very important, she lives only 15 mn away from us.

Belfast Hospital

Mac arrived at the hospital around lunch time Friday 8 of May (day 3), extremely anaemic, put straight away in the intensive care section and declared by the Belfast consultant Ian Millar as very critically ill, but by this time the type of auto immune system disease was finally fully identified …. AIHA – Auto Immune Haemolytic Anaemia , one of the most critical auto immune system disease, and for Mac it was paired with a serious jaundice.
“AIHA is a disease in which an animal’s immune system destroys its own red blood cells. Antibodies produced by the immune system to fight pathogens instead target the body’s red blood cells and destroy them. Red blood cells are necessary to carry oxygen to the tissues of the body, and animals cannot survive without adequate oxygenation of all of the body’s tissues.”
End of quote
The adequate oxygenation is measured with a test called PCV. The PCV or “Packed Cell Volume” is calculated in % and ranges from 45 to 55% in large dogs like Irish Setters. It takes a full year for a puppy to build its immune system to that level.
For a young Irish setter male, 50% is a good average. Mac was so anaemic his PCV (red blood cells count) was 7%. To give you an idea, at 6% for a large dog like the IS, the lack of oxygen which is carried to all the organs by red cells, make the blood thick and clots are forming everywhere and consequently the animal die very quickly. To avoid the risk of clots, Mac was given aspirin and the first week his stomach had a very hard time, no food and plenty of medications ….
Mac’s case was so critical, he couldn’t have survived the day without another blood transfusion.

Thanks to brave young Charlie (Redclyst Jean Valjean Lestannons) from Dorothy Park, turning into a dog blood donor, it gave Mac one more day of life, a bit more time allowing the strong auto immune suppressor medication to start its work and preventing the red cells to be destroyed systematically. After the blood transfusion, that evening, Mac’s PCV (Packed Cell Volume) went up from 7 to 10%. The consultant wasn’t happy with this result, so a medicine specialist consultant was called and they change Mac’s medication. Mac was then on a massive dose of corticosteroids to suppress the immune system faster, hoping that his immune system would stop soon killing its own red cells.

That Friday afternoon, when we left Mac at the hospital, we drove home with a rather sleepy Charlie boy – blood dog donors are lightly sedated to keep them quiet during the process. But as soon as she was home, busy bee Dorothy Park was contacting local Setters owners to find more blood to buy more time for Mac. Fortunately Mac was rhesus positive and could take any blood. The response was amazing; everyone was ready to drive even up to 2 hours one way just to give blood to Mac. I never realised I was surrounded by such a wonderful Setters community. I am extremely humble and grateful for all the support and help Mac received.



Saturday 9 May

The medication was not yet working and Mac’s PCV dropped down to 8% during the night. Early morning the hospital phoned directly to the owner of one of Mac’s blood donors. This time it was Liz Boal (Mac’s groomer and handler) who has one girl – Madison (Sabrejil She Who Dares), the same age as Mac. It is important that the dog donor is young and not on any medication. Madison is so much like Mac, as bouncy and full of energy as normal Mac. When Liz and I arrived at the hospital, my boy was lying flat on his side, eyes open but not moving, not responding to his name, nor to my touch, totally lifeless. An horrible and nightmarish image which, I am afraid, will stick in my mind for ever.

We left super energetic Madison with the staff and went for a coffee. We were called back 20mn after instead of 2 hours like for Charlie. I froze again, something is wrong, Liz was ready to drive back home and take another of her girls. We went directly to Madison and Mac and to my total amazement, this “She Who Dares” girl was done in no time and came out of the vet room bouncing and jumping. I needed to see that as a good omen, that Madison must have given some of her punch and dynamism to Mac. The taking of the blood from Madison lasted less than 20 minutes, and the transfusion to Mac was done in 3 hours. Mac’s PCV went up to 14% that evening.

Although Dorothy Park found plenty of dog blood donors, the vet informed me that he wants to stop giving Mac more transfusion. Mac had 3 transfusions already, surely it gave Mac new good red cells to carry oxygen everywhere on his body but at the same time it was also stimulating his white cells to kill more red cells …. The transfusions were given to Mac to buy time until the medication kicked in, but not as a solution and for the vets it is a very delicate balance to manage.

To make things more difficult, Mac was far too weak to drink or eat, so, on drips and fed by tube directly in his stomach. In addition to the weakness, unfortunately nothing could stimulate his appetite.

Sunday 10 May

Mac’s PCV dropped down from 14 to 12, then 10 and stabilised at 8%. At that point, the only hope was that the medication started to do its job. I beg the vet to give him a fourth blood transfusion, although he was very reluctant knowing that it wasn’t a solution, he agreed to do it as the last resort if it came to it. For the time being, Mac was in the intensive care room supervised 24 hours a day by specialised nurses and the medicine has to start working.
Sunday evening, suddenly there were little signs that the medication started to work!!!!! The signs were so subtle that it took 2 days and many tests to be absolutely sure. Mac’s PCV was still very low, oscillating between 12 and 8%, but at least not going lower. New worry though, the ultrasound were showing that his kidneys were enlarged but this was explained from the harsh medication and returned to the normal size before he was given the permission to leave the hospital.

From that day on, I was hanging after all minute signs, like drinking again, his first piece of chicken fed by hand after being fed with a tube for days, lying down with his head on his front paws instead of only lying flat on his side, lifting his head, being able to stand up (shakily) for 1 or 2mn, walking 3 meters out of his crate, his first mini meal by himself, getting out to do his business, getting out at least 5mn to take the fresh air as the nurse said, etc. every little signs was raising my hope but the boy was still on the intensive care room and classified as very critically ill. Then the miracle happened, suddenly Mac’s PCV went to 15, then 18 and one day to even 22%. Nevertheless, we spend 14 very long days anxiously waiting the glorious moment when the vet told us – Mac is out of the critically ill zone!!!!!! Meaning SAVED.

14 long days and 14 long nights since the local vet called me to say goodbye to my boy and the consultant team of Belfast hospital declared Mac out of the critically ill zone ….. It seemed like centuries! David and I were smiling to everything; the clouds, walls, etc. and of course so many tears of joy running along our faces!!! We knew that even though, anything could happen, Mac having no immune system working to protect himself – we also knew what will happen soon …… the boy will come back home!!!!

Saturday 23rd of May

Mac was transferred from the Intensive care unit to a new room with a much bigger crate. At that point they have reduced the frequency of the PCV, his blood cells count was done only once a day.

Tuesday 26 of May



Mac had a battery of tests and everything came back even better than expected. His PCV was at 35%, liver and kidneys ok, he had lost some weight of course, now at 28kg, but has gained a monstrous appetite and thirst now, due to the steroids. He needs to go out every 2 hours, days and nights, as well as being fed every 4 hours, etc. The good news is that they had already reduced twice his corticosteroids, so the boy was ready to go back home, and home he went on the afternoon of Wednesday the 27 of May!!!. He was away from the 6th, 2 days in Coleraine clinic and 20 days in Belfast hospital!!! We were informed that the next 6 months/1 year will be quite intensive in care, Mac cells count will still be done once a week, that he will have once a month a big check up at the hospital, but the boy is alive and with us, so life is wonderful again. The local vet team call him Mister Miracle.


As said, Mac has AIHA (Auto Immune Haemolytic Anaemia). The anaemia makes it the worse of all the auto immune system disorders. This disorder can be classified as primary or secondary. Primary means no known cause, or idiopathic (that is with no known trigger/cause). Secondary means there is an underlying cause.
There is NO CURE, it is a life time condition and both, primary and secondary form can and most probably would come back again.

Quoting here:
AIHA – Auto immune haemolytic anaemia can be either a primary or secondary disease. If it’s a primary disease or idiopathic, there is no underlying cause that can be identified. In secondary AIHA, the immune system produces red blood cell antibodies in response to an underlying condition such as cancer, chronic inflammatory disease, a drug reaction, or exposure to an infectious agent. Newborns can acquire this disease from their mother’s first milk, which is colostrum, although this is pretty rare.
The surface of the red blood cells becomes altered by an underlying disease process or a toxin. These alterations catch the attention of the immune system, which sees them as foreign invaders or pathogens. The immune system targets the altered red blood cells and destroys them through a process known as haemolysis, either within the red blood cell vessels or as they circulate through the spleen or liver.
Some of the known underlying triggers for secondary autoimmune haemolytic anaemia are infectious agents like leptospirosis, babesia, ehrlichia, and the feline leukemia virus. Also heartworm disease, IBD, certain drugs like the sulfa drugs, heparin, and quinidine, hypersensitivity reactions (for example, to bee stings), and vaccines can all over-stimulate the immune system and cause AIHA.
End of the quote

In the case of Mac, we simply don’t know what has triggered the disease, which is seriously annoying as the probability for AIHA to come back is very high.


We have two IS, Mac and Darwin who is 10.5 years old and has a very fragile liver. So I asked no less than 4 vets and consultants if I should have a full blood test done for Darwin before Mac is coming back home. The answer was very clear – NO – the AIHA is an individual internal disease, like thyroid or heart problems, it cannot be passed to other dogs or humans. It is a genetic condition. However, the dog affected should avoid contact with other dogs at the beginning since part of the initial treatment is the suppression of its own immune system. The AIHA dog should be protected from anything carried from humans and dogs.


As usual, one cannot avoid thinking, could it be hereditary. However, all the consultants and vets I have asked were very strong at disregarding this option. It is not hereditary but purely genetic and individual. For AIHA, unfortunately Irish Setters and some other breeds mentioned below are simply genetically predisposed. Breeds predisposed to primary immunodeficiency disorders include basset hounds, Cardigan Welsh corgis, Jack Russell terriers, Beagles, German shepherds, Chinese shar-pei, Doberman pinschers, dwarfed Weimaraners, gray collies, and Irish setters.

However, there is an increase of evidence linking vaccines to AIHA which I could accept, but it was absolutely not the case for Mac as he had no booster since 3 years.  

I will end this post by thanking so very much Dorothy Park and her Charlie boy, Liz Boal and hyper Madison She who Dares, and of course all the wonderful super vets and their team from Earlswood in Belfast, without whom Mac would have not been here today. During this period, I was like a zombie and couldn’t speak to anyone. My mind was in complete denial and I wanted everyone to think of Mac only as the bouncy happy boy he always was. I couldn’t utter any words such as sick, very ill, and even less “dying” although it was part of the reality. I wanted to think of Mac only alive and happily bouncing around as I am a believer in positivism and that our thoughts create our reality. Well I am nuts anyway, but new quantum physics studies support this idea, although I haven’t a clue about Quantum physics, this is the domain of David.

However, behind the scenes, without me knowing it really, there were a net of wonderful friends, informed by Dorothy & Liz, and today I would like to thank them so very much for all the support, willingness to give your dogs’ blood, sending prayers and positive thoughts, crossing all your fingers, etc. A special thank you to Mary and her prayers to St Francis of Assisi, and to Brian who had a good word with St-Anthony and consequently knew the very first day that my boy would be alright.

I send you all the energy of my love and my deepest gratitude.

The aim is to inform as many blessed IS owners, and raise the awareness of these immune system diseases currently popping up in the UK and help you to protect your fur babies.

Chantal Mcilveen-Wright

Bloat & Gastric Torsion

Bank Holiday Monday 28th May 2007 will stay etched sharply in my mind for the rest of my life. My Irish Setter, Geordie, who was just five years old, otherwise known as ‘Cymbeline Fallon By Hooley’ (sire: Twoacres Fergus, dam: Timadon Miss Irresistable) had Gastric Torsion and Bloat. His mother had Bloat when she was 7 weeks in whelp and tragically was later found dead in the whelping box, when the pups were just 14 days old. So I took Geordie, always knowing that because of this, I could never use him at stud and have turned down several offers of stud work for him, being totally honest about my reasons for doing so, as it has always been my policy to be open and honest about any health problems concerning my dogs.

I have always believed that Bloat & Gastric Torsion happens very quickly and is a dire emergency, but this was not my experience. I watch my dogs like a hawk, so am always immediately aware if they are not well, even if it isn’t obvious what the problem is.

Geordie was not himself for 48 hours prior to this happening. If I let him out, he wanted to come striaght back in, but once inside, he just wanted to go back out again. He just couldn’t settle, clinging to me like limpet, feeling very sorry for himself and generally not knowing where to put himself, or what to do. His appetite during this time remained normal……nothing distracts him when there is food around, eating is his favourite activity: unusual for an Irish Setter.

One of the reasons that it wasn’t immediately obvious that Geordie was bloating, was because he has another health problem and his behaviour could have signaled the onset of that quite easily. Geordie started fitting when he was 18 months old, eventually being diagnosed with Idiopathic Epilepsy after an MRI scan of his brain and a spinal tap, at the Animal Health Trust in Newmarket. This ruled out the possibility of the fits being caused by anything other than Epilepsy, such as a brain injury, a virus, a brain disease, or another diseased organ. This is not a particularly pleasant procedure for the dog to experience and is not the first diagnostic test the vets opt for to diagnose this disease, but I felt that it was imperative as, not only hadhis father been used at stud and his mother whelped another litter, but Epilepsy is not the only reason for fitting. As you can imagine, I was absolutely devastated by the diagnosis.

Geordie’s Epilepsy progressively became worse, until he began to have cluster fits, severely enough to need hospitalizing in order to stop him fitting. On Bank Holiday Monday 28th May, Geordie hadn’t fitted for eight months and as any change in his behaviour pattern could indicate that he was going to begin another bout of cluster fits, his behaviour that weekend did not immediately scream Bloat at me.

Geordie did not swell up suddenly, but very gradually, over the course of 48 hours, until by the Monday morning, the day he bloated, I noticed that he seemed fatter than normal and made a mental note to tkae him to the vets after the holiday for a check up. His twice daily medication regime of Epiphen and Potassium Bromide for the Epilepsy, has caused him to steadily gain weight, so he is on a restricted diet and never has titbits, so there was no apparent reason why he should have been getting fatter,

As the morning wore on, he just wouldn’t leave me alone, to the point of becoming a nuisance, though it was obvious that he was desperately trying to tell me something. At this point, he wasn’t huge, just slightly fatter than normal, he was salivating a lot, but the Epilepsy medication often caused him to salivate heavily, so alarm bells didn’t ring. He didn’t seem to be unwell: he just wasn’t his usual bouncy, happy self. It is worth noting that he was not at this time, exhibiting any of the other signs of abdominal discomfort usually associated with Bloat & Gastric Torsion.



Then a couple of hours later, I noticed that he was trying to be sick without success, though he only did this once and he was uncomfortable when he walked, moving very stiffly on his back legs. It was so similar to watching someone trying to move whilst suffering a severe bout of colic, that this was when my instinct kicked in, BLOAT shouted at me and I called the emergency vet. However, it also occurred to me that he might have an abdominal obstruction, though to my knowledge he hadn’t had anything which could have caused this.

Never before have I been so relieved to discover that my own vet was the duty vet that weekend. Although Geordie’s abdomen, by this time, was enlarged and tight like a drum, his back end being wider than his front end, when viewed from the head down to the tail, the other symptoms of phase two, were not present.



At weekends and Bank Holidays, the local surgery, which is literally 5 minutes down the road, is closed, we always have to travel to the main surgery, a nine mile drive away. It was a nightmare journey with every red light being against us. Geordie is normally so good in the back of the car, even on his own, just laying down and keeping still, he is so quiet that several times, I have thought that I must have left him behind, as it hasn’t been obvious that he is in the back. This journey was not like that, he spent the entire journey moving around and throwing himself all over the place. The further we traveled, the more acutely aware I became, that he could very well be bloating and having gastric torsion in the back of the car and there was nothing I could do about it. I felt totally helpless and useless, but tried to stay calm for Geordie’s benefit.

My vet arrived at the surgery at the same time as me and as he lives further away than I do, he must have driven like the proverbial clappers, for which I will be eternally grateful. When he examined Geordie, he said he didn’t think he was in dire straights yet and he didn’t think his stomach had started to twist, but there was a possibility that he could actually have torsion later, if he sent him home, so he would have to x-ray him and release the gas anyway, as he was full of it and blown up like a drum. He did note that Geordie had a shaky stance whilst being examined. He is not normally anxious when at the vets. This shakiness was probably due to shock.

My vet wasn’t able to release much of the gas by tubing him, so had to perform abdominal surgery to get rid of the gas. He explained that quite often Bloat creates lots of frothy foam, which blocks the exit from the stomach, making it impossible for the gas to escape. When he opened him up he was astounded to find that the stomach had already started to twist, because Geordie had not presented as if he was in this stage of Torsion.

He stressed that if I hadn’t phoned when I did, then the organs inside would have been damaged by the blood supply being cut off as the stomach twisted. This is what causes the damage and is why some dogs do not recover. I’ve never had a dog with Bloat before, or seen one with it, but knowing my dogs as I do, I instinctively knew that he wasn’t right. I was surprised to hear from my vet that Bloat and Gastric Torsion can also be caused by a blockage, or a tumour, as I didn’t know this could happen.

Geordie’s liver was very swollen, so some was sent away for analysis, but found to be normal. He had a much bigger operation than normal, as his stomach had to be cut open to remove the contents, because my vet couldn’t get them out any other way and his stomach needed to be completely empty to stop him bloating again after surgery, so Geordie was stitched all the way down his abdomen. Whilst Geordie’s stomach has now been stitched down in an effort to reduce the chance of him having Gastric Torsion again, (an operation called a Gastroplexy) my vet was at pains to point out that he could probably bloat again and that if this happened, then it would be a battle between the gas and the internal stitches. Unless the internal stitches break down, he will hopefully not experience Gastric Torsion again, though of course there are no guarantees.

No one knows the definitive reasons, or cause of this dreadful disease, but there are several well known risk factors. In the thirty years that I have owned Irish Setters, I have always been scrupulous about following a strict management code, doing everything that we are supposed to, in order to limit the possibility of this happening, but yet disaster still struck.

As a matter of course I have always:

  • Fed my dogs twice daily, staying with them after they have eaten
  • Used a head-height stand for both water and food dishes
  • Limited the amount of water available immediately after eating
  • Avoided rigorous exercise, stress and excitement for 1 hour before and 2 hours after eating, even making them go to bed if necessary
  • Any diet changes have always been made gradually over a period of 7 days.

After 7 days in intensive care, Geordie was allowed home. So far so good, he is managing to eat without further problems, but now, much to his delight, he is eating four small meals a day, the biscuit being soaked to avoid it swelling and fermenting in his stomach. The vet is very pleased with his progress. He says this is helped by the fact that I got him there so quickly, right at the start of it, so there was no damage to the internal organs. Geordie was lucky that his Bloat and Gastric Torsion was a ‘slow burn’ and not the rip roaring type that we all think of when we hear those dreaded words. Because of his other health problem, it would have been so easy to miss this, or not recognize it for what it was. If I had not followed my instinct and had thought that I would see how he was in the morning, he would have been dead. I am so very grateful for the skills of my vet and the support I received from my friends. Knowing they were all there for me helped tremendously.

© 2007 Michelle Webster

Canine Herpesvirus

A Canine Herpesvirus (CHV) infection can prove devastating to entire litters of newborn pups. Thankfully however the disease does not strike too frequently. Despite the similar name, CHV has not been shown to be related to the human herpes simplex virus. The virus appears to infect only domestic and wild dogs.

Despite the fact that a CHV infection means almost certain death for a dog less than 1 week of age, the viral particles are sensitive to most cleaning agents and survive for only a short time outside the dog. Thus, disinfection of kennels or homes is possible and the disease does not claim an exorbitant number of victims.


Transmission of CHV occurs only via direct contact with bodily fluids or secretions. Adult dogs, and even those puppies more than 2 or 3 weeks old, may contract and carry the virus without suffering from any adverse symptoms. Though they lack symptoms these infected animals will retain and periodically shed viral particles for some time. It is when a pregnant female becomes infected that the disease is truly dangerous.

Infected females may occasionally transmit the virus to her puppies in utero, leading to spontaneous abortion, or stillborn litter. More commonly however an infected mother will pass the virus to her offspring via mucoid secretions during, or after birth.

Upon infection, CHV particles first attack the nasal passages, pharynx, and tonsils of young pups. During the 6 to 10 day incubation period the virus replicates and then spreads via the bloodstream to the liver, kidneys, lymphatic tissues, lungs, and central nervous system. Once in these organs the virus proves deadly in nearly 100 percent of cases in pups less than 2 weeks of age.


Clinical signs of CHV infection in young puppies include loss of appetite or disinterest in nursing, shortage of breath (dyspnea), tender abdomen, inco-ordination, soft yellow-green faeces, and possibly a bloody nasal discharge.

Death occurs rapidly after onset of symptoms and many owners do not notice anything is amiss until they find a dead puppy. Diagnosis is thus often post-mortem and involves autopsy findings. If however symptoms are caught early, a veterinarian may reach a diagnosis based almost solely upon observable symptoms and exposure risk. Blood tests may occasionally reveal the presence of antibodies in the bloodstream, but such procedures are somewhat unreliable and not always feasible.


As previously mentioned, many owners do not realize that their puppies are ill until it is too late. For cases detected early enough however, treatment is mainly supportive and almost always futile. Keeping the puppy warm by using lamps or heat pads is the major goal of treatment, as one reason young pups are so susceptible is that their body temperature tends to be too low to kill the virus.

Beyond this, treatments are at this point, experimental and controversial. Further information should be obtained directly from your veterinarian.


A new vaccine is available in the UK by Merial Animal Health Ltd, best known as the makers of Frontline®. The vaccine, Eurican® Herpes 205, cannot prevent infection but if given during pregnancy it has been shown to significantly improve fertility rates and reduce early puppy death. Even bitches that already have the virus can be vaccinated.


Puppies that survive a CHV infection may excrete the virus for several weeks after recovery. Isolation of sick dogs and a rigorous disinfection routine are imperative to protect other young dogs. Since the viral particles are easily killed my most household cleaning agents, disinfection is relatively uncomplicated.

It is important to note that if a female has given birth to one infected litter, she will develop immunity and all future litters should be safe from infection.


Untreated Canine Herpesvirus can infect:

  • Liver
  • Kidneys
  • Lungs
  • Central Nervous System

Canine Herpesvirus (CHV) is specific to domesticated wild dogs.  As with other herpesviruses, CHV becomes latent and is carried by the affected individual for life, though they may not show any clinical signs.  The infection may flare up and become a clinical problem during periods of stress or immunosuppression.


Dogs are infected in one of the following ways:


  • In foetuses, across the dam’s placenta
  • In new born pups through contact with the birth canal
  • During mating
  • Via the respiratory route

A dog’s normal core temperature is 38.3 – 38.7C CHV is a virus that grows best at a temperature slightly below the normal core temperature of a dog, meaning that it is usually restricted to the nasal passages, where the temperature is lower.  If a puppy is chilled, or has few maternal antibodies, it is more susceptible to widespread infection.

A puppy may acquire protective antibodies against CHV from the mother across the placenta, as well as in the colostrum.  The bitch will only have antibodies to pass on if she has either been exposed to the virus, or if she has been vaccinated recently against it.  Vaccination has not been shown to give lasting immunity; live vaccines might be more effective, but could result in a lifelong carrier status.

If a foetus is exposed while in utero, the effects will depend upon the stage of pregnancy – those infected earlier are unlikely to survive to term, though pups infected later, may also be aborted, mummified, stillborn, premature, or born weak.  Some pups may be born apparently normal, but succumb within nine days of birth.

If a newborn pup is exposed to CHV, the virus first reproduces in the nose and the tonsils; then it travels through the blood and spreads to the other organs.  The virus can affect blood clotting, causing bleeding problems within the organs.

These pups infected after birth, may become acutely affected with a fatal illness between the age of one and three weeks.  Affected puppies often fail to suckle and may cry persistently.  Some may have a nasal discharge and some develop pinpoint bleeding on their gums.

Puppies that have antibodies from the dam are not fully protected, but are less likely to develop a severe infection.  A bitch may give birth to a severely affected litter and then, because she develops antibodies against CHV, may have normal litters subsequently.

Puppies infected after the age of three weeks, are less likely to have a severe infection, but instead show milder signs of upper respiratory tract infection and sometimes genital lesions.

Infected dams seldom show any signs of a problem unless they lose a litter.

Prevention is currently largely based around management, such as keeping puppies warm to reduce the likelihood of systemic infection.  Routine testing is not carried out, even when puppies are lost, so there is no concrete data on how many puppies are lost to CHV every year.

Currently the main tests available for CHV are:

  • Blood tests for antibodies (serology)
  • Viral isolation

Serology simply proves exposure to the virus, but not whether it is a clinical problem.  Viral isolation requires live virus to grow in cell culture.

PCR  (Polymerase Chain Reaction)

Is a technique that can be used to detect CHV DNA.  This has been done on tissue samples, but in theory, could be applied to nasal swabs from live dogs.


Canine Herpesvirus (CHV-1) is a virus that has been largely ignored for many years. However, it is becoming increasingly clear that the virus causes many more problems than was first thought. Like all herpes viruses, CHV is highly infectious, and a recent study showed that more than 80% of dogs in England have been exposed to the virus at some time in their lives.


For most dogs CHV is not thought to cause any significant problem, so for a long time is has largely been ignored by both breeders and vets. However, it is now clear that CHV can be a significant cause of death in young puppies, and also smaller litter size and weight.


CHV attacks the placenta of the mother, starving the foetus of nutrients. This can lead to abortion, stillbirth or re-absorption of the foetus (seen by the breeder as infertility).


If the puppy is infected before birth and survives, it may be underweight at birth and have a weakened immune system, making it vulnerable to early puppyhood infections. If the puppy is infected soon after birth, CHV is known to be one of the factors in “fading puppy syndrome”, in which the pup fails to suckle, loses weight and fades away despite intensive care.


In the dog, CHV can cause painful lesions on the genitals. In the bitch, there may not be any external signs, but the bitch seems infertile, or gives birth to undersize and weak litters. In both males and females, CHV is also known to be a cause of kennel cough.


There is no cure for an animal that has CHV – infection is probably life long and can flare up repeatedly during periods of stress. Antiviral drugs do not appear to be effective and are very expensive.


A new vaccine is available in the UK by Merial Animal Health Ltd, best known as the makers of Frontline®. The vaccine, Eurican® Herpes 205, cannot prevent infection but if given during pregnancy it has been shown to significantly improve fertility rates and reduce early puppy death. Even bitches that already have the virus can be vaccinated.

Canine Herpesvirus (CHV), also known as “fading puppy syndrome,” is a viral infection that affects the reproductive organs of adult dogs. While adult dogs infected with CHV usually do not show any symptoms, the infection is the leading cause of death in newborn puppies. One puppy in a litter may be affected and death may occur abruptly, with little or no warning, or an entire litter may perish within a 24-hour period. If the disease is contracted when the puppies are older than three weeks, it is often less severe. Older puppies have a much better chance of survival, but may have long-term effects of a persistent CHV infection.


Canine Herpesvirus lives in the reproductive and respiratory tracts of male and female dogs. In adults, the disease is transmitted via aerosol and direct contact, including sneezing, coughing, nosing, sniffing, licking and sexual activities between an infected and an uninfected dog. Puppies usually contract the disease in the birth canal or from nasal and oral secretions of the mother shortly after birth. Puppies can also spread the virus to one another. Just because one puppy in a litter is infected with CHV does not mean they all are.


  • Often there aren’t any symptoms
  • Occasionally raised genital sores may be seen
  • Abortion
  • Stillbirth
  • Kennel cough


  • Sudden death of newborn puppy
  • Weakness, lethargy, crying
  • Lack of suckle reflex/appetite
  • Painful abdomen, bruising of the abdomen
  • Soft, yellow/green faeces
  • Respiratory difficulty, nasal discharge
  • Haemorrhages, such as nose bleeds and small bruises
  • Older puppies may develop nervous system abnormalities, including blindness and seizures


No. Humans are not at risk of catching Canine Herpesvirus.

Coefficient of Inbreeding

In their quest to produce happy, healthy puppies, many breeders run genetic reports, or pedigree analysis on a potential breeding, looking for both pitfalls and strengths.  These reports give us a lot of data- but what exactly are these numbers, what information do they give us, and how should they be used?

The pedigree database on the site, shows the COI, or Coefficient Of Inbreeding, for each dog when you bring up a pedigree.  This is also sometimes referred to as IC, Inbreeding Coefficient.  It does this automatically and is not something that I have set it to do.  The database uses Wright’s Inbreeding Coefficient Program to calculate the COI for each dog, being set at default to calculate this over 10 generations.  It can calculate the COI for each dog using anything up to 60 generations.   The Inbreeding Coefficient is expressed as a percentage.  The more common ancestors there are in a pedigree and the closer they are in terms of generations to their descendant, then the higher the Inbreeding Coefficient of that descendant will be.

The KC’s recently launched Breed Mate Select web site does the same thing and uses the same program, but does not state how many generations are used to calculate the COI.  There are several different programs available for calculating the Coefficient Of Inbreeding, but the Wright’s program is widely considered to be the most accurate.

Whilst most breeders recognize that a mating between half siblings, or cousins, represents inbreeding, not everyone understands which one is the closest relationship.  The standard definition of ‘Inbreeding’ is that it is any scheme which results in the sire and the dam having common ancestors.  The parameter used to express this common heritage, is called the INBREEDING COEFFICIENT and was first proposed by Sewell Wright in 1922.  Designated ‘F’ by Wright, but more commonly known as ‘IC’, or ‘COI’ by breeders.  It can theoretically range from 0 to 100% but as a general rule, the lower the number, the less inbreeding there is.

When looking at the same dog’s COI on different web sites, there can often be differences in the results.  This is due to missing ancestors in the pedigree.  However many generations are used to calculate the COI of a dog, each of the generations in the pedigree, needs to be 100%.  If the ancestors are not 100% present for each generation, then this will ultimately affect the end result.  Put simply, to calculate the COI and receive an accurate result, there should not be any missing ancestors in the pedigree.  Once the missing ancestors are added, the result will go up or down accordingly.

When using a pedigree database, the COI% for that dog can often be seen, but this is only part of a Pedigree Analysis.  When breeders ask for a Pedigree Analysis, or Genetic Report for a particular dog, or planned litter, they are given other information as well.

PEDIGREE ANALYSIS DECIPHERED by Tina Porter, explains the information contained in such a report.

The following table is a sample pedigree report for the hypothetical mating between:

Lakeways Its Yours Truly Sierra (Tru) & Lakeways Take A Chance On Me (Joss)

The top line: TEST:: Tru/Joss:: 091707 is the data for the hypothetical puppy

NameCOICORCountMin GenMax Gen% of BloodCov AX
#TEST :: Tru/Joss :: 0917079.70%100%1000%109.70%
Lakeways Its Yours Truly Sierra0.03%57.01%11150%59.72%
Lakeway’s Take a Chance on Me13.61%59.57%11150%66.50%
Lakeways It’s Simply Simon-Zion14.97%42.08%12225%47.26%
Lakeway’s Bailey Lady of Zion16.69%38.59%12225%43.67%
Twincedars Desparado – OTX0%23.92%12225%25.05%
Indy Woods of Sierra11.51%42.73%12225%47.25%
Shiloh’s Wolfin Sasquach3.77%34.05%84724.22%36.33%
Crane’s Our-Tribute-To Contessa11.23%32.31%23418.75%35.69%
Jnk Smoke’N Black Bear Of Zion10.83%33.18%23418.75%36.58%
Shiloh’s Easy Rider3.91%21.80%125815.63%23.27%
Morris Good Morning Mona0%24.48%95813.67%25.64%
Snow’s A Tribute To Pax-Zion7.90%28.33%13312.50%30.82%
Sierra’s Close Encounter16.25%28.08%13312.50%31.72%
Twin Cedar’s Northern Dancer0%12.02%13312.50%12.59%
Twincedars Adorable Adelaide0%11.95%13312.50%12.51%
Zion’s Winnie-The-Pooh6.99%30.80%13312.50%33.37%
Shenandoah’s The Phantom V Zion14.97%37.13%13312.50%41.70%
Super Sweet Sabrina Selah26.34%13.21%125912.30%15.55%
Shiloh’s Kara Lobo Of Emmview2.15%15.69%1861110.94%16.60%
Shiloh-GuardianStill Smokin’21.44%21.94%146910.55%25.33%
Campaigner’s Gunsmoke3.13%16.76%6071410.55%17.83%

The following explains the content of such a report.


  • A number created by calculating how many times (and in what generation) shared ancestors appear in a pedigree of a specific dog.
  • The higher the number, the more ancestors a pup’s Sire and Dam have in common.  COI’s are 0% for dogs with no common ancestors.
  • The number also tells you the probability that both alleles for any given gene come from the same ancestor.  (This is called having a homozygous genotype.)
  • The higher the number, the greater the chance of locking in a trait – either good or bad.
  • The higher the number, the more you risk the effects of inbreeding.
  • Any trait your dog is homozygous for, it will pass that allele on to its pups.


  • This number doesn’t tell you which ancestor is contributing the alleles that are being doubled on.  Is it the one on the dam’s side that produced the problem, or the fabulous great-great- grandsire who lived to be 16?
  • COI doesn’t tell you which particular alleles you might be doubling up on.  Is it a “good” allele for a trait, which you want the dog to have?  Or is it a “bad” allele that causes disease and structural faults?
  • Due to events during sperm and egg cells production, the COI is only a “guesstimate”. (A guide).  The reality is, it could be higher or lower than this number, depending upon which specific alleles are inherited by each dog in the pedigree from the common ancestor.


  • An approximate percent of the genes passed down from a specific ancestor to the dog whose pedigree you are studying.
  • The higher the COR value, the more genes the ancestor and hypothetical pup will have in common, and the greater the chance they will share a trait.
  • COR values are influenced by the dog’s COI number, presence of other relatives in the pedigree, and pedigree position.


  • Again, this is only an approximate percentage of the genes.  When the dam “passes” her genes to the puppy the COR expects that 50% are coming from her dam and 50% from her sire.  But this may not be the case.  Of the genes the dam passes to the pup, anywhere between 0 and 100% of them may come from her dam, not just 50%.  This is why siblings don’t all look alike (and are genetically different) – they are getting different combinations of genes from their parents.


  • The number of times this individual shows in the pedigree.   Higher the count, the higher the possibility of locking in traits from this ancestor.


  • While this number can be quite large and the ancestor’s genes are found in the dogs we are breeding, it is more important to look at his COR and Cov AX numbers to determine his true genetic influence. If for instance, this dog first appears in the 8th generation, and his genes have been filtered through his offspring to our current breeding pair, it is the genes being held by the dogs in the first 4 generations and their immediate relatives that are more likely to be of worry.


  • The first generation where the dog appears in the pedigree.  The lower the generation number, the more recent the dog.  The 1st generation are the parents, 2nd generation are the grandparents etc.


  • The last generation where the dog appears in the pedigree.


  • Another method of showing the possible genetic contribution of each ancestor.
  • Based on the calculation that each dog passes 50% of its genes on to the next generation.  So for the planned puppy – the parents each contribute 50%, the grandparents contribute 25%, the great grandparents contribute 12.5% and the great-great grandparents contribute 6.25%, etc.
  • Dogs that appear more than once in the pedigree will have % of Blood number that doesn’t follow this pattern.  Their contribution from each appearance in the pedigree is combined into one number.


  • This is different from RC (Relationship Coefficient) in that the calculation for RC uses the IC (Inbreeding Coefficient) for the dogs.  % of Blood is based only on the dog’s position in the pedigree.
  • Problems with this data are the same as the ones for RC (Relationship Coefficient).


  • It determines the extent to which the planned puppies will resemble that specific ancestor.
  • COR, (Relationship Coefficient) COI (Coefficient of Inbreeding) and % of Blood are used to calculate genetic covariance.  The more homozygous the dogs genes (COI), the more of that dogs genes get passed on to its offspring (COR), and the closer that dog appears in the pedigree (Min Gen), the more of its genes the puppies will carry (% of Blood), therefore, it is more likely its offspring are going to look like that dog.


It is only as accurate as the numbers used to create it – so the “Keep in minds” are also true for this one.  If the stud looks like his great grandpa on the sire’s side, that great-grandpa may be a greater influence than the numbers suggest.

Each of these numbers can give useful information when planning a litter.  While it would be nice to think that there could be a magical formula, or combination of COI, COR & CovAX numbers that would create the perfect litter of puppies, it simply is not true.  An IC (Inbreeding Coefficient) of less than 10% will not guarantee you a healthy litter, just like an IC of over 30% does not mean all the puppies will be sickly.  Instead, these numbers are best used to help us to identify important individuals (those who will make a large genetic contribution to our puppies).  Then it is up to the breeders to research those individuals, find the plusses and minuses associated with them, and then make the best decision possible.


The most useful COI number is the one for the planned puppy.  Having a low COI lessens the risk of doubling on a nasty hidden recessive allele, suffering from inbreeding depression; helping to keep the gene pool healthy.  The COI’s for the rest of the dogs in the pedigree are interesting, but only useful in that they are used to calculate COR and CovAX.


Are all are excellent for pointing out dogs in the pedigree that we should know more about.  The higher these numbers are, the more genes they will give to the puppies, the more they will determine what your puppies will look like, therefore the more important they are to investigate.  This is why it’s important to also look at the ancestors (and their littermates), especially the 2nd and 3rd generation, so you can see some of the traits they have and get an idea of some of the genes they carry.


What are some of the health issues associated with:

  • This dog?
  • This dog’s siblings?
  • This dog’s offspring?
  • This dog’s ancestors?

Pedigree report numbers do not tell you what they look like, what they act like, or how healthy they were.


Pedigree Analysis Reports are valuable tools that can help give us a sense of which dogs in the pedigree will be the largest genetic contributors to a litter.  Once those individuals are identified, they can be researched further to get a sense of which genes they do carry.  However, it is not the only tool a breeder should rely upon.  These numbers alone do not give enough information about the dogs to be the sole basis for planning a litter.  Breeders must always take into account the actual dogs that are being considered for breeding.  In addition to their individual health, temperament and structure, breeders must also attempt to learn as much information as possible about their siblings and parents.

Coefficient of Inbreeding, or COI, as it is more commonly known, is just a way of determining the level of inbreeding for the chosen dog.  Whilst it seems to be the latest buzz word on the Internet, amongst those interested in dog breeding, it should be remembered that it is only one of many useful tools to help the breeder produce a healthy litter, in the same way that Hip Scores and DNA test results are useful.  Obviously when breeding a litter, or planning a litter, all other aspects should be taken into consideration.  The COI should be seen in context with everything else and not used as the only deciding factor.  Bear in mind that it is perfectly possible for a dog with a high COI to not have, or to not produce health problems and equally it is perfectly possible for a dog with a low COI to have, or to produce health problems.  It is after all just another useful tool for the breeder.


I don’t intend to be flippant, but having an Epileptic dog often feels rather like needing to attend confessional therapy, like alcoholics, or gamblers anonymous, such is the stigma surrounding this condition. Generally, people won’t talk about it, doing their utmost to keep it under wraps. It’s almost as if they are ashamed of owning an Epileptic dog. Of course, in reality, this is utter rubbish. Epilepsy is an illness, just like any other, it just happens to affect the brain. If the dog had any manner of other illnesses, owners and breeders would not be affected by the well known ‘Ostrich Syndrome’, in other words, they wouldn’t stick their heads in the sand……….they would talk about it. Of course there are those who could not be open and honest about problems with their dogs, even if their life depended on it, but I would hope that they are in the minority. Breeding an Epileptic can happen to anyone and is no ones fault, unless they have knowingly bred from affected lines, it’s how they then deal with it that matters. To knowingly breed from affected dogs and their siblings, is in my opinion, unforgivable. Adopting such a cavalier attitude, displays a total disregard for dogs and owners and shows a complete lack of concern for the future health of the breed.

Geordie, otherwise known as Cymbeline Fallon By Hooley, had his first fit, or seizure, when he was 18 months and two days old. This was the first time I had seen a dog having a seizure and it was extremely distressing. Although I had experience of children with this condition from my teaching days, I didn’t immediately recognize that this was happening. It was vastly different, not least because it was happening to MY beloved dog and there were no warning signs. One minute he was his normal self and the next, he was being sick, bringing back the wild mushrooms he had eaten in the garden a couple of hours earlier. Then he collapsed on the floor and was desperately clawing at his throat as if he was choking. It was only when he went rigid, then started to paddle his limbs and involuntarily urinated, that I realized he was having a seizure. The howling screams that accompanied this behaviour were chilling, cutting through me like a knife. I felt completely and utterly helpless, knowing there was nothing I could do to help him, I just had to wait for the seizure to end. Instinctively, I got on the floor with him, stroking him and talking to him all the time to reassure him, being careful to keep my face away from his, as some dogs can become aggressive during and after fits, though Geordie never has.

My knowledge of this condition was extremely limited, but I knew that when in the throes of a fit, although he could not see me, he could hear me. I also knew that it was important that I note everything I could about the fit and also how long it lasted. The entire episode didn’t last very long and as soon as he was back to normal, I contacted my vet, so that she could note it on his record. If there are several dogs in the household you need to be aware that the others could possibly attack the Epileptic dog whilst it is fitting, as they often feel threatened by this strange behaviour. It is testament to the good temperament of my boys that I never experienced this. Whenever Geordie had a seizure and the other boys were there, they would just take themselves to the opposite side of the room and watch him, all the while looking very concerned. Once he came round and seemed normal, they would check him over and show their delight that he was behaving normally once more.

The classic time to develop Idiopathic Epilepsy is between 18 months and 7 years of age. So at this stage it seemed as if this could be the reason for Geordie’s siezure. However, my vet was adamant that dogs are usually sick after they have fitted and not before, as Geordie had been and because he had eaten the mushrooms, she was of the opinion that the seizure had probably been caused by toxic poisoning. I fervently hoped that she was right. As the days went by, I searched my memory for anything that I might have missed, that would have warned me of Geordie’s impending seizure. No matter how hard I wracked my brains, I didn’t remember him behaving any differently to normal. I did, however, remember that six weeks previously he had run full pelt into the conservatory door from the bottom of the garden 100 feet away. At the time, the bang on impact with the glass door was deafening and Geordie appeared to be concussed, but as a normal x-ray wouldn’t reveal anything, it was pointless asking the vet to give him one. The next day he seemed his usual self and until he had the seizure, I forgot about the incident. Like my vet’s theory about the seizure being caused by toxic poisoning, I hoped that the bang on the head was the reason for this dreadful state of affairs. In fact, to be totally honest, I hoped that there was a reason for this development, the last thing I wanted to hear was that Geordie was an Epileptic.

In the light of the fact that I have already said that Geordie had fitted, this might seem rather odd, but there are many different reasons why dogs have seizures. Just because a dog has a fit, or seizure, this does not mean that it has Epilepsy. There are a variety of problems which can cause fits, such as brain injury, a virus, a brain disease, a tumour, diseased organs, or several degenerative diseases. Unless the dog is fitting on a regular basis, at least once every four weeks, vets are reluctant to medicate, as the medication can have severe side effects and can cause liver damage. Consequently, it was a case of waiting to see what happened next. Whilst the scientist in me could see the sense of this, as a dog owner, I found it extremely frustrating and worrying. I had no idea if and when this would happen again, or indeed, why it had happened at all. Waiting to see if Geordie had another fit, was rather like having the sword of Damocles hanging over my head.

The first lesson I learnt, was that with this condition, there is no easy, quick route to diagnosis, it can take a long time to get the answers you’re looking for and Geordie seemed determined not to follow any set pattern, following the usual rules was just not in his remit. He continued to have seizures at irregular intervals; every fit was different to the one before and there never seemed to be any signs beforehand that would indicate that he might be going to fit. In retrospect, I was always able to see, that in fact, his behaviour for a few days beforehand each time had been different, though this didn’t help very much, as again, each time he behaved differently. He could be very tired, quieter than normal, extremely hyper, very naughty, or could be extremely unco-ordinated and clumsy. Eventually, I realised that any departure from his normal behaviour could be an indication that he was going to fit and I gradually learnt to recognize the signs, so was prepared for the inevitable. I kept very detailed notes each time Geordie had a seizure. Not only did I need to be able to give a detailed account of what had happened to my vet, but it also helped me to see at a glance, how regular, or irregular, they were and if there were any patterns emerging.

The only way to determine the definitive cause of Epilepsy, is with an MRI scan of the brain, a spinal tap and full urine analysis, as it is able to rule out the possibility of fits being caused by anything other than Epilepsy. This is not a particularly pleasant procedure for the dog to experience and is not the first diagnostic test the vets opt for in order to diagnose this condition. It is not usually suggested unless the dog is on medication and has been fitting regularly for more than a year and then probably only because there is a suspicion that there are other factors at play. However, I felt that it was imperative that Geordie have these tests as soon as possible. Not only had his father been used at stud and his mother whelped another litter, but Epilepsy, as previously stated, is not the only reason for fitting.

So eleven months after his first seizure, at my request, my vet arranged for Geordie to visit the Animal Health Trust in Newmarket. The consultants at the AHT were wonderful, putting both of us at ease and explaining everything in easily understandable terms. They also gave me a detailed account of the worst and best scenarios, for which I was extremely grateful, I wanted to be prepared and not have any nasty surprises. It soon became clear why the AHT is regarded as a Centre Of Excellence for Epilepsy and Neurological problems. All the procedures are carried out under general anaesthetic and a large area of hair is shaved from the dog’s head and neck to facilitate the spinal tap. The dog is able to go home at the end of the day, but can often be quite unwell for up to two weeks afterwards, as sometimes it can cause them to be rather unco-ordinated and wobbly. The cost was prohibitive, so I was relieved that Geordie was covered by his Pet Insurance, but so anxious was I to discover the cause of this, that I would have gone ahead, even if he had not been insured.

After what seemed like an endless day, I was given the news that Geordie had Idiopathic Epilepsy. In other words, his seizures were not being caused by brain disease, a brain injury, a tumour, a virus, diseased organs, or a degenerative disease. The consultant told me that she believed that the condition was inherited and could be passed on. She stressed that under no circumstances should Geordie or any of his siblings ever be used for breeding. As you can imagine, I was absolutely devastated by the diagnosis. At the same time, the diagnosis made a lot of sense. As a puppy he had been extremely hyper and was a lways very different to any other Irish Setter I’d had. He was very clumsy and unco-ordinated, often walking straight through, or over something, rather than going round it. Although it was obvious that he was highly intelligent, he didn’t approach problems, or learning in the same way as the others, often giving the impression of being slow, though he got there in the end. We often used to joke that he was wired differently to the others; how near to the truth we were! At the time, I put the difference down to his coming from different lines to my other boys, thinking that he was just developing in a different way and that it was because I had no experience of the lines he came from. Being given the diagnosis was like someone turning on a light switch……everything suddenly became crystal clear and I could understand why he had behaved in the way he had. Talking to others with Epileptic dogs, it soon became apparent that this sort of behaviour is fairly common amongst Epileptics.

One of the difficulties with this condition is that although you may learn to recognize the warning signs and know when the dog is in the Aura stage, before they actually begin to fit, you have no way of knowing exactly when they will fit. But when they do begin to fit, everything has to go on hold while you deal with it and the ensuing after effects, which can sometimes last for several weeks. Epilepsy is regarded as a CONDITION, rather than a DISEASE. The difference is that a DISEASE has a known cause; a CONDITION can have many different causes and therefore can be much more difficult to diagnose and treat. Many think that if Epilepsy is a CONDITION then it isn’t as bad and can be dismissed, they are also under the miss-apprehension that it is not hereditary. They are wrong on all counts. If anything, a CONDITION is often worse, as by definition it has many different causes.

Having Epilepsy is hard for the dog and the owner. Life as you knew it no longer exists, your life changes forever. When the dog is initially started on medication, they can seem to be much worse, as the drugs can have severe side effects. They are often extremely tired, only waking up in time for their next dose of medication, before falling asleep again and they are often so unco-ordinated that they are very wobbly and constantly fall over; they can also be very shaky and it can be like watching someone with severe MS, or Parkinson’s Disease. These side effects do eventually disappear, if you are prepared to persevere. The medication makes them permanently ravenous, so weight gain could be a problem, if you were not made aware of this. The first three months are dreadful, whilst the body adjusts to the effects of the medication and of course, during this period, the dog will continue to have seizures, so it is not an easy time for dog or owner. It can take up to two weeks for the medication to take effect. The vet will then take blood tests to determine whether the levels of medication in the blood stream are correct. Once you receive the results, the medication will then be altered accordingly and the whole procedure starts again, continuing until the correct levels are indicated by the tests and an improvement in the dog can be seen. There is no cure for Epilepsy, the best we can hope for at present, is that we can control it with medication, by reducing the severity and frequency of the seizures. Achieving this can be a very long, slow process.

Sadly, many people feel that they can’t cope, they just cannot see the light at the end of the tunnel and so decide to have the dog put to sleep. For me this was never an option. unless my dog had no quality of life and there was nothing further that could be done for him, then I would do whatever it takes to help him in any way that I could. He didn’t ask to come to me, I chose him and I feel that as a responsible owner, it is my duty to afford him the very best care for his entire life, I would never dream of giving up on him because I found it difficult in any way, I feel that he deserves better. Any dog that comes to me, stays, no matter what, they are never re-homed and they are certainly not put to sleep unless there is nothing further that can be done for them, or they no longer have quality of life. I would never chose this as an easy option, or because it made life easier for me.

Towards the end of 2007, two years after Geordie was prescribed medication for his Epilepsy, I began to notice that he was having tremors, was once again quite unco-ordinated and was sleeping deeply for long periods, as he had done when he first started taking the medication. My vet assured me that it was caused by the side effects of the medication and that there was nothing that could be done about it. Then I noticed that his skin had several areas that were covered in spots and his hair was not only thinning, but was actually falling out. We tried every possible remedy, but to no avail and my vet tested him for everything she could think of that might be causing it, but again, it was to no avail. By Christmas he resembled a very bad RSPCA case. His skin was covered in itchy spots, there literally wasn’t an inch of him that didn’t have a spot on it and in addition, he had numerous bald patches and he no longer had any undercoat. The tremors had become much worse, so that once again, it was like watching someone with severe MS and he couldn’t move without falling over.

I was convinced that this was it, he no longer had any quality of life and I decided reluctantly that I would have to bow to the inevitable. However, my vet contacted the consultant at the AHT, who suggested that it could be due to the medication and of so, it could possibly be altered. She advised me to stop his Potassium Bromide completely for five days. I knew that doing so would mean that he ran the risk of having another seizure, but I felt that I had only one other alternative and I didn’t want to go there! So with my heart in my mouth I followed the consultant’s advice and was astounded to discover that five days later, he was co-ordinated and no longer had any tremors. The improvement was so dramatic, that when she then advised me to re-introduce the Potassium Bromide, but halve the dose, I was worried about doing so. Once he began taking the Potassium Bromide again at half dose, he began to have tremors, but only mildly and very infrequently. Eventually, as his system became used to the medication again, the effects lessened, until he only had the occasional tremor. However, the skin problem, loss of coat and tiredness continued, so my vet carried out more tests for the suspected cause. Her feeling was that he had a thyroid problem, but the tests came back as clear. At this point she drew a blank, so contacted the consultant at the AHT once more for advice. She is an extremely experienced vet, but admitted that she was surprised to learn that Epilepsy and Epilepsy medication can actually mask other problems and cause false test results. The AHT consultant explained how to perform the same tests differently for an Epileptic. All the tests were repeated and Geordie was diagnosed with an Under Active Thyroid Gland. Apparently, the two problems often go hand in hand, it is very common for Epileptics to have an under active thyroid, caused by the condition and the medication; likewise, apparently it is very common for a dog with thyroid problems to go on to develop Epilepsy. Once the thyroid medication levels were established for Geordie, he became a different dog within weeks and three months later , he was once more dripping in shiny coat and looking the picture of health.

As I have already said, the best you can hope for with an Epileptic dog, is that with medication, you can control the condition. I was delighted that we seemed to have achieved this with Geordie, as at the beginning of 2008, he hadn’t had a seizure for more than 18 months. I have discovered that in his case, there can be many different trigger factors that will cause him to fit, or to lower his fitting threshold. If something lowers the fitting threshold, this means that it increases the dog’s chances of having a seizure. A change of routine, excitement, stress, flashing lights, loud noise, fireworks, thunder storms, because of the change in atmospheric pressure, a change in hormone levels, anaesthesia, some medications and food, can all be trigger factors for Epileptic dogs. In Geordie’s case, there is no one factor that will cause him to fit, any of the above factors could result in him having a seizure within a few days of the event.

I was thrilled that we had been able to stabilize Geordie’s Epilepsy and that he had been well for so long, but it didn’t last, as it never does. I didn’t know at this point, that for an Epileptic dog to be free of seizures for the length of time he had, was extremely unusual. Apparently, the longest period that an Epileptic dog will go without having a seizure, is normally no longer than 12 months. In February 2008, our area was rocked by quite a large earthquake, the noise was deafening and the walls of the house literally shook. At the time, Geordie appeared to be unaffected, but exactly seven days after the event, he had a seizure. Things settled back down again, until two months later, one evening, we had a power cut that lasted for several hours. We had used torches and lit candles, but each time a candle was lit, you could actually see his eyes ‘sparking’, though I didn’t make any connection with this and his Epilepsy, as Geordie has always been extremely light orientated, almost to the point of obsession with torches, even opening the cupboard door to get at the torch! I learnt to my cost that this was indeed a trigger factor for Geordie, as he had a seizure the following morning.

Three weeks later, Fergus, his father, died suddenly. He was always very close to him and had never known life without at least one other dog, so the stress of losing Fergus and finding himself without his beloved canine companion was a very stressful situation for him. He had previously fitted a few days after my other dog, Flynn, had died suddenly in 2006, so I expected that he would probably do so again after losing Fergus, but nothing prepared me for what actually occurred.

Exactly one week after Fergus died, I was woken up very early by the sound of Geordie having a very bad seizure. Once he was over the fit, he slept soundly for the rest of the day and appeared normal the next morning. He seemed to be following the same pattern of behaviour as he had done after Flynn died, so I was relieved that he had gotten the seizure ‘out of the way’. Apart from the fact that he was more clingy than usual and was determined not to let me out of his site, he was his normal self and I put his behaviour down to losing Fergus. I thought the worst was over, when in fact, it was still to come. Like a bolt out of the blue, a month later, he had another seizure, only this time he didn’t have a single fit, he had a cluster fit. This is when they have more than one fit, often having several within hours and sometimes can go straight from one fit into another, so there is no chance to fully recover before the next seizure begins. Every seizure causes damage to the brain, so the more they have, the worse it is and the longer it takes them to recover properly. They can be rather strange after these episodes for up to three weeks and often have to re-learn basic behaviour. It is as if they forget their manners. Soemtimes it can even affect their movement and it can be like watching someone, who having recovered from a stroke, is left with a slight limp.

After the third seizure in 24 hours, Geordie was admitted and put on a drip in order to stop the fits. The drip enables the Epilepsy medication to get into the system much more quickly and the vet is able to administer stronger medication. There is always the risk that the vet will not be able to stop the fitting, but I felt that we had to try. If he ever reached this stage, then it would be time to let him go. Whilst there, the vet re-checked his phenobarbitone levels in his blood to make sure that his medication dose was correct and she also tested his liver functions to make sure that the medication hadn’t damaged his liver.

I was horrified that this experience was not a one off, as Geordie continued to have cluster fits every two weeks until the beginning of November, having to be admitted each time. After a few weeks of this, I decided that enough was enough and asked if he could be referred to the AHT for another MRI Brain Scan and Spinal Tap in case there was another cause for Geordie’s sudden decline. I had begun to think that I was going to have to let him go, but wanted to exhaust every possibility before hand and I also wanted to be certain that I was doing the right thing.

It was with a very heavy heart that I took him back to the AHT, for I was convinced that I would hear the worst. The consultant was amazed at the detailed notes I handed her and also that I had thought to take a complete list of his foods and medication, in case there was anything that we hadn’t realized may be making matters worse. I was equally amazed when she told me that Geordie was by no means a hopeless case and that there was far more they could do for him before we had to give up. I learnt so much that day and to my astonishment, when my vet received the report from the AHT, so did she. She was honest enough to admit that despite going on the latest course about this condition only two weeks earlier, she did not know about some of the information in the report. That is actually quite worrying, considering that our vet is the one who we rely on at such times. Geordie’s scan and spinal tap results were clear; they showed no change in the brain activity since his previous visit and no evidence of the seizures being caused by anything else.

The consultant at the AHT told me that generally when Epileptic dogs become worse, vets automatically increase the medication. Her response to Geordie’s problem was to halve his Phenobarbitone and add in two more drugs, both for humans and neither had been used by my vet before. She stressed that if this regime didn’t work effectively, then there were other combinations and other drugs that could be added to the equation and stressed that we were a very long way from giving up. In fact she told me that roughly around 90% of Epileptics respond to treatment. Apparently, if a dog has a cluster fit and for whatever reason it is not treated, or medicated correctly, it will cause a domino effect and cause yet more cluster fits. She was convinced that this is what had happened to Geordie, with the initial recent fit being caused by the stress of losing Fergus. I also learnt that salt intake is important, as Epileptics are not able to deal with it as effectively as non Epileptics. Not realising that I live at the seaside, she informed me that Epileptics who swim in the sea, or visit the seaside, can fit due to the excess intake of salt in the air!! I also discovered that Epileptics cannot have Oil Of Evening Primrose, as it lowers their fitting threshold, making it more likely that they will have a seizure. This is something that most of us give on a daily basis to our dogs to enhance their coats, without even realising that it could have disastrous consequeneces. In short, I realized that with an Epileptic dog, every aspect of their life had to be given very careful consideration.

I had begun my visit to the AHT in the depths of despair, thinking that really I was probably clutching at straws, but at the end of the day, I left in a more positive frame of mind, I knew that there was hope and I had begun to see the light at the end of the tunnel. It took a further two months of administering the new medication and testing to see if the dosage was correct, during which time Geordie continued to have cluster fits every two weeks. Suddenly everything came together and he stopped fitting. Slowly, his body recovered and his old character and personality returned. The new medication regime is slightly more difficult to administer. It is imperative that Epileptics are given their medication every 12 hours on the dot, rather than twice a day. it has to be precise, so that the phenobarbitone levels in the blood stream do not fall, as that would cause them to fit. The new medication has to be given every 8 hours on the dot, so now my life revolves around the clock, as he has to have Epilepsy medication five times a day. Whatever I am doing, Geordie has to have his medication on time. He can never now be left alone, he has to be with someone at all times, to ensure that he has his medication on time and also in case he has a seizure. This has of course altered my life, it is no longer possible to be spontaneous and I no longer make plans in case I have to alter them at the last minute. I actually don’t mind being grounded in this way, it’s all part of caring for a dog that I adore and I’m not selfish enough to ignore his needs in preference for my own.

Three months after his visit to the AHT, Geordie had returned to normal. As I write this, he has not had a seizure for more than seven months, he is stable once more. Many friends, even those with Epileptic dogs, have been amazed at Geordie’s recovery and have admitted that they would have given up. I am so pleased that I chose not to do so and that I persevered. Geordie has a good quality of life, you would never know to see him that he has been so ill, he looks the picture of health and it is sheer delight to see his zest for life once more. There are now several other dogs in the practice who are also on the same medication regime, so he has helped others as well.

Those who think that Idiopathic Epilepsy is not a problem within the breed would be wrong. My vet informs me that it is in fact, very common in Irish Setters and this is borne out by my own experience of talking to others within the breed who have Epileptics. I am pleased to say that attitudes are beginning to change, but far too slowly, at least people are now talking to others who have had the same experience, which didn’t happen even only a few years ago. History has proven that when faced with a major health issue, the breed has the ability to work together to solve it, as they did with PRA rcd1 and CLAD, so in theory, the same could be done for Epilepsy, or any other major health problem. It is rather more complicated to develop a DNA test when faced with something like Epilepsy, as it is multi factorial and there are several genes involved, but that doesn’t mean it can’t be done. Now that attitudes are beginning to change, we have taken one small step towards solving this problem. Having now had the experience of living with an Epileptic dog, I wouldn’t wish it on anyone and certainly do not wish to repeat it. I think it is by far the worst and the most distressing health problem that I have experienced, for there is no hope of a cure, we can only hope to keep it under control and we never know when the next fit will occur. If I, as an experienced dog owner, find Epilepsy so distressing, imagine how a first time pet owner would feel and bear in mind that the majority of puppies are sold to pet homes.

I belong to a Setter discussion forum and was recently asked by a Dutch member who owns an Epileptic dog, why it was that all the English members would only communicate with her about this problem, using the private messaging service, rather than the usual ‘comment’ option which is open for all to see. Her question, whilst innocently asked, spoke volumes about our attitudes in the UK to Epilepsy and other major health problems faced by our breed. As I understand it, attitudes in Holland are very different; problems are discussed openly, the main Breed Club has a health database which is available for members to view, so that they can obtain as much information as possible before breeding litters. Therefore, armed with the information, they can make informed decisions about their breeding. However, before this is possible in the UK, we have to be ready to admit and accept that Epilepsy does exist within the breed and then we have to talk openly about it. We have taken the first small step towards this; how long will it be before we are ready to take the next step and how many more Irish Setters will have to suffer unnecessarily with this distressing condition before we do? As owners and breeders, we are the guardians of this beautiful, exuberant breed. Quite frankly, I feel that they deserve better.

© 2009 Michelle Webster

Tuesday 21st February 2012 began just like any other day, there was no indication of what was to come.  As usual I got up just before 7 am and gave Geordie his first lot of Epilepsy medication.  There was nothing different or unusual about him, or his behaviour, so I had no reason to think that things would alter as dramatically as they did.

Just before 8 am Geordie began to fit without any warning.  He had begun having fits, caused by Idiopathic Epilepsy when he was 18 months old, so I was well tuned to the warning signs and usually knew that a fit was imminent.  This time however, I was completely taken unawares.  By 8.15 am Geordie had had another fit, two in total, but neither were bad fits nor lasted very long and he seemed to recover very quickly.  Normally when he had a cluster fit like this and it was obvious that he would continue fitting, he would have to be admitted to the vets to stop it.  There is only so much medication that I as an owner am allowed to give him and when this doesn’t work then the next option is to admit him and have stronger drugs administered via a drip.

The two fits left him very tired, but he didn’t seem as if he would have any more, so I let him sleep.  When he woke up he seemed normal, bright and alert so I breathed a sigh of relief, fed him and let him down the garden.  When he came in he lay down at my Mother’s feet and suddenly, again without warning and almost four hours after his last fit, he had another one.  Again it wasn’t bad and but lasted longer.  I could tell from looking at him that there would be more to come, so I phoned the vet to say we were on our way.  As I pulled into the car park Geordie was in the throws of another fit in the back of the car. As soon as we were able to move him, he was taken in and admitted.

The signs were good as he didn’t fit again for more than 24 hours and then it was so quick the vet wasn’t concerned.  Whenever this happens my vet keeps him in until he has been fit free for at least 24 hours and to make sure that he is well enough to come home.  He seemed to be making progress that day, but was very tired after the fits.  This wasn’t unusual so no one was worried, the cluster hadn’t given Geordie any side effects such as loss of movement, or hyper activity, he was just very tired.

When I phoned the next morning, I was concerned to be told that he’d had two small fits in the night and didn’t want to eat.  One thing that Geordie never did was to refuse his food, so the fact that he wasn’t eating worried me.  A few hours later at lunch time, he seemed to be making progress, albeit very slight and he had eaten a small amount of food. I was less worried, thinking that although he was making slow progress, it was stillprogress, so he was going in the right direction and I knew from experience that recovery from some cluster fits could take longer than others.

A few hours later at 9 pm on 23rd February, my life changed in an instant.  The phone rang and as soon as I heard my vet’s voice I knew instinctively that the news would be dire.  He wouldn’t have phoned me otherwise.  The half hour drive to the surgery seemed to take forever and was the worst journey I’ve ever had to make, especially knowing what I was facing when I got there.  Geordie was comatose, but obviously in distress.  His breathing was very rapid and it was heartbreaking to see him like that.  Having been told only a few hours earlier that Geordie was recovering and making progress, it was a tremendous shock to see him so ill and hear my vet say that he had suddenly deteriorated just before he phoned me.  He explained that he had tried everything at their disposal to help him, but nothing had worked and he felt that it was time to let Geordie go.  Having come back from the brink so many times, there was a part of me that thought he could do so again.  I hoped so much that my vet was wrong, but in my heart I knew this couldn’t be and very reluctantly made the only decision I could, the worst decision for me, but the best decision for Geordie.

Geordie didn’t die because of his Epilepsy, but because of an indirect result of it.  His body had literally had enough and he had developed Disseminated Intravascular Coagulation (DIC).  This is when the blood spontaneously begins to clot in the veins, causing them to block and effectively stopping the oxygen getting through to the major organs, which then begin to fail.  If left long enough, the clotting stops and the veins haemorrhage all over the body, causing a truly horrendous death.  I didn’t want Geordie to suffer a second longer than he had to and so, although distraught to have to let him go, I was grateful that my vet had acted swiftly and minimised his suffering.

Many who know his story may think that as an Epileptic, Geordie was fitting frequently, this was not the case.  During the last twelve months of his life, Geordie only had three cluster fits.  I always said that he had to have a quality of life.  I didn’t want him drugged so much that he spent his days in a zombie like state just to stabilize the fits.  With the help of my vet and the wonderful consultants in the Neurology department at the AHT we managed to achieve a drug regime for him that stabilized the fits, making them less frequent, whilst still enabling him to have a quality of life, living it to the full.  When he died he was just 17 days short of his tenth birthday and the youngest Irish Setter I have ever lost.  But as an Epileptic, he did incredibly well to live as long as he did and to have the quality of life that he did.  I know that I did the very best that I could for him, but I also know that because I was always open about the problems he had and shared his story, there are now other Epileptic Irish Setters who, having adopted the same drug regime as Geordie, are now still alive and leading quality lives.  They were on the verge of being put to sleep because their condition was so bad and they were not responding to the drugs they were given.  I am proud to think that by being so open, Geordie has helped to improve the lives of others, this is his legacy.

When Geordie came into my life, he was a very lively, promising puppy.  Like the others at Hooley, he quickly qualified for Crufts, winning BOB’s & RBOB’s during his short show career.  I stopped showing to care for him and make sure that he had a good quality of life, devoting myself to his every need for the next eight years.  He repaid me tenfold.  He had a wonderful temperament, loved everyone and everything, never had a bad bone in his body and loved life with a passion as only an Irish Setter can.

Geordie was the only Irish Setter that I had.  This is the first time for 32 years that I have been without an Irish, so the house is dreadfully quiet and empty.  Everyone who met him fell in love with him, not only was he stunning to look at, he was also a gentleman and such a character.  As I held Geordie in my arms for the last time, stroked him gently and spoke softly to him to say my goodbyes, he calmed immediately, opened his eyes and looked straight into mine.  Farewell my darling.

Michelle Webster

Reading Michelle Webster’s article in the winter 2012 ISBC Newsletter moved me to write about my own  experience of living with an epileptic dog. Whilst mine is not an Irish Setter the condition is the same in all animals, humans included.

I’ve been involved with dogs since 1975 but until my Welsh Springer Spaniel became a fitter when he was 3 years old I’d never seen a dog fit before. It was a hot summer’s day and he was stressed and panting heavily; symptoms I now know are archetypal of fitting. Strangely enough I was very calm about it and got the others out of the way until he came round. He went through the paddling stage and then he lay still, breathing deeply until he eventually tried to stand; and then the pacing started. He walked round and round and round unable to see clearly and stumbling into things. This I find the most distressing feature of fitting.

Naturally we went to see the vet and it was decided to start him on a course of Epiphen.  The fits were sort of under control, becoming milder and shorter in duration and recovery time was much quicker but nevertheless they were still occurring. I felt so very sorry for him although his day to day life was no different from what it had always been.  His fits always happened when he was coming round from sleep; another classic trait.

So, it was decided to put him on Libromide as well. Because of the nature of Epiphen it has to be given every 12 hours and so our lives became ruled by 8 o’clock, morning and evening. The side effects of the medication make him thirsty and hungry although he is never drowsy or slow.

And so our lives continued; revolving around 8 o’clock with constant soul searching for an answer or cure.

And now for the reason why I am sharing this with you; I believe in fate and after a visit to Crufts my catalogue fell open at an advert for The Canine Epilepsy Support Group.  I gave them a call and spoke to Secretary Anne Morley. Here was someone who knew exactly what we were going through and offered all the help and support that we needed. Ann is a diviner and asked me to send her a list of everything that we fed him on. She came back to me shortly afterwards with the instructions that he was to be given no dairy, no rice and no poultry but surprisingly he was not wheat intolerant. He was to be taken off complete food and fed on Laughing Dog Terrier meal with either Butchers Tripe, Chappie or only certain kinds of Winalot.

She sent me recipes for making biscuits for him and we were to be sure to give him no additives whatsoever. Slowly things started to improve and we settled into a pattern of having one slight fit every month.

I rang Anne to give her an update of his progress and mentioned this to her. She asked if these fits were at the time of the full moon and to my astonishment they were! ‘OK’ she said ‘Now we have an answer and this is what you do’.

I was instructed to buy a homeopathic remedy Cocculus Indica 30C and to give him one tablet morning and evening 3 days before the full moon, on the day of the full moon and for 3 days after.

Of course he was still taking his regular medication and we approached the next full moon with trepidation. Nothing; nor for the next; nor for the one after that. And so it has continued with only one slight blip. He had 2 fits in January 2012 with only the second one being on the full moon. The soul searching began once more and I realised that it must be down to the branded oil high in Omega 6 oil that I had given him to improve his coat. I stopped it immediately and he has not fitted since.

I must add at this point that his coat was already in gleaming condition and he was a picture of health. The medication has not affected his appearance in the slightest and since he started fitting he has won C.C.s and Best in Show. It just seemed like a good idea at the time.

Whilst there may well be a pre-disposition to epilepsy I am firmly convinced that the occurrence of fitting can also be linked to diet. When the Summer Newsletter came from the CESG there was a warning that Omega 6 oil is highly dangerous for epi-pets and should never be given. Before he became a fitter he had been fed for 18 months on a complete food based on salmon and potato and therefore high in Omega 6. Coincidence? I believe not particularly as I have helped people with dogs of other breeds by referring them to the CESG and their dogs have been managed by diet alone.

If by writing this article I can help anyone at all, even by you passing it on to someone else, then it has all been worthwhile.

So, if you or anyone you know, has a fitting dog please, please tell them to contact:

The Canine Epilepsy Support Group on 01903- 784263 or

Those who run this group fall just short of being saints as far as I am concerned.

I repeat that I firmly believe that food additives play a major role in the cause of fitting and I am obsessed with what he is given to eat; that along with the 8 o’clocks, oh, and of course the full moon.

Christine Morgan

The Story Of ” Kenmilfore Red Pepper ” 

DOB 7th May 2004

In October 2003 my grandson died at 8 months, this left a very large hole in my world. I had been considering getting an Irish setter for some time and in July 2004 I got Abbie to help fill that gap, (maybe not the right reason to get a puppy).

I saw a litter advertised in June and arranged to go and see them. I arrived at a lovely country house with a large garden and there were seven beautiful 5 week old puppies and mum, some in the garden, some in the kitchen, one laying across the doorstep; this was Abbie. I was not hurried and the breeder was so helpful as she knew that I had not had a setter before. I left a deposit and she asked me to visit if I wanted to before I collected her, and if I took an old jumper or towel she would put it with the litter so that I could take the smell of the litter home with Abbie.

Three weeks later I went to collect my darling Abbie, the breeder had all the paperwork in place, gave me a diet sheet, worming history and other information on Irish setters. This is what I would now expect from a good breeder. Over the next 2 ½ years I communicated regularly with the breeder, exchanging pictures, letters, Christmas cards etc. Abbie was a normal naughty puppy .

In August 2006 Abbie had her first fit, I didn’t know what to do, I rang my vet and she was very helpful explained what it was and said she would come out if I wanted but there was little point as there was nothing she could do at that time, adding that if she had another one then call her straight away and to visit the surgery the next day. When I took her they decided it would be best not to put her on medication straight away as she may only have one fit and also this would help them with the dosage. I phoned the breeder to let her know what had happened as she had kept one of the litter to breed from, I spoke to her daughter as the breeder was not in and asked that the breeder rang me back. I never got a call back and rang her on several occasions but she was never available, and that was the end of my relationship with Abbie`s breeder.

At this point I would like to describe her fits, as fits vary in intensity:

When Abbie fits she will shake and claw for about 1-2 minutes, emptying her bladder and expressing her anal glands while foaming heavily from her mouth. She then lays motionless for another 3-6 minutes. When she comes round she visits every room in the house, then outside and walks around the perimeter of the garden before coming back in to drink about 1 ½ litres of water, after an hours sleep she returns to her normal self. Should her fit last longer than 3 minutes I have to quickly administer Diazepam into her back passage to help bring her out of it, and lessen the possibility of brain damage.

Over the next six weeks Abbie had a further 5 fits; it was then that the vet put her on Epiphen.

I kept a diary for Abbie for 3 years listing each time she had a fit including; possible link to her seasons/ time of day/ what she ate that day/ where she had exercised/ how long for/ length of fit/ recovery time etc…. hoping to find a common factor, but with no success.

In November that year she had a major stroke, could not walk, lost all her memory, didn’t know who she was, what biscuits were or where she lived, when we got to the vets she thought Abbie was blind because she was so vacant. I really didn’t think we were going to take Abbie home again, but the vet said we must give her a chance. It took a month for her to get over this, not being able to walk for a week and when she did I took her for very short walks and she was everywhere didn’t know what to do at the road, or know people who she had known for a long while. In the house she would walk around trying to get out as if she shouldn’t be here (we worked it out later she thought she lived in the car, as this was her first memory after the stroke).

We were lucky in that she had no more fits in this month, but a week after her recovery they started again. The fits came every week or two in clusters of up to 7 in 2 days. The vet altered her medication when she had a longer period between her fits, the medication would drop if only by ½ tablet and the fits would come again.

She has blood tests every 4 months to monitor her liver function and toxin levels. At this time she was put on a low fat / low protein diet and 240mg. Epiphen + 1950mg Potassium bromide per day, as well as the Diazepam when required (she is still on this dose).

This went on until June 2009 when she had a single stem tumour removed from the base of her neck, she built up fluid and had another operation and a drain fitted. September that year Abbie had another stroke, this time it was minor and she recovered from this very quickly, only a week. In November that year at a routine check-up the vet was unhappy with her eyes; after examinations he told me she was losing her sight.

August 2010 when I took her for her boosters, and my concerns that her fur was getting very thin the vet said she has probably got Cushings Disease, he was only 90% sure and would need to run tests and scans to confirm this. (I refused these tests as it meant two days of blood tests, sedation, scans, feeding her and more blood tests). He was not going to give her the booster, he said “It is as good as it gets, if you get to Christmas make the most of it.” That day I went home and decided that if she had so little time left that I would let her have what she wanted, I took her off the vets diet and as she loves fish, put her on 80% fish diet. Within two weeks of her new diet she was much better, even wanting to go for short walks which she had not done for so long. Her fits have been few and far between since then. We have ups and downs, sometimes I get concerned for her but most of the time now she greets me when I come home.

Having a dog with Epilepsy is not easy, social life is out the window but we still have holidays in English cottages as I can’t leave her in kennels. I would have liked her to have a litter but that really doesn’t matter either. I now have another two Irish setters aged nearly six and nearly seven months. We don’t have expensive carpets or furniture, we have towels around the house so if she has a fit we put one between her rear legs.

It is now January 2013 and we still have Abbie, she may be slow but she still has “QUALITY OF LIFE”

Thank you for listening.

Giving a Rescue Remedy Sundae can be helpful following a seizure. The Rescue Remedy Sundae is made by putting a little Recue Remedy (available from Boots) on a small amount of vanilla ice cream as soon as the dog is safely able to eat following a seizure. If your dog does not respond to Rescue Remedy, you can use plain ice cream.

You should use a good all natural, preservative free ice cream, such as Hãagen Dazs. Only use Vanilla ice cream. You only need a small amount – too much can do more harm than good. For dogs under 50 lbs, a teaspoon or two is plenty, 50 – 100 lbs can handle about 1 or 2 tablespoons and dogs over 100 lbs can have ¼ of a cup.

The reason behind this is that blood sugar levels often drop drastically before or during seizures and the ice cream will bring the blood sugar level back to normal. The way it works is the sugar in the ice cream will bring the blood sugar level back to normal while the butter or fat holds the sugar in suspension, so that it doesn’t cause a sugar rush, which plain sugar, or honey, or molasses would. Bringing the blood sugar level up too quickly is not good, which is why ice cream is recommended. Also, bringing the blood sugar level up to normal can help to prevent additional seizures. Low blood sugar itself can cause seizures. If your dog has very obvious pre-seizure behaviour and you give a little ice cream before a seizure happens, this can sometimes stop the seizure altogether.

Please be sure to thaw the ice cream a bit by letting it sit out on the kitchen counter, or ‘zapping’ it in the microwave briefly – you don’t want to chill your dog too much, or have him gulp down frozen ice cream.

Recently in a prestigious Veterinary Journal, an article appeared that described using an ice pack to stop seizures, or avoid them altogether. The idea of using ice to stop, or avoid a seizure makes a lot of sense. Most dogs get so hot during a seizure that putting an ice pack on the small of the back (NOT the neck) could stop, or slow down a seizure.

We all know that helpless feeling when our dog goes into a seizure. Besides protecting our dog from harm during the seizure and getting post-seizure medications ready, there seems little else we can do except wait for the seizure to end.

The article on using an ice pack to stop seizures is about an exciting new technique that may be able to help you shorten or even stop your dog’s seizure before it begins and may even help reduce the mount of post-ictal (after seizure) recovery time, thus returning your dog to full function more quickly.

The technique was tested, both in an ER and a regular veterinary hospital, as well as by people in their own homes on 51 epileptic dogs. In all 51 cases, the technique either stopped the seizure, or shortened the usual duration of the seizure and in many cases; the post-ictal recovery time was also shortened. These results were published in an article by H. C. Gurney DVM and Janice Gurney B.S. M.A. The article is entitled, “A Simple, Effective Technique For Arresting Canine Epileptic Seizures”. It appeared in The Journal of the American Holistic Veterinary medical Association, in the January-March 2004 issue, pages 17-18.

Probably the most exciting part of this discovery is that the technique is not in any way harmful to your dog and it does not involve giving extra medications. It is as simple as applying a bag of ice to the lower mid-section of your dog’s back (the small of the back) and holding the bag firmly in position until the seizure ends. It is advisable to first wrap the bag of ice in a tea towel or something similar. The exact area on the back is between the 10th Thoracic (chest) and the 4th Lumbar (lower back) vertebrae (bones in the spine). What this means is that the top of the ice bag should rest just above the middle of your dog’s back, following along the spine and drape down to the lower-midsection of the back. The ice bag should rest between the middle of the Thoracic Vertebrae and the middle of the Lumbar Vertebrae. See Diagram below.

  • Thoracic vertebrae: the bones forming the dorsal part of the thoracic cage.
  • Lumbar vertebrae: the bones of the lumbar region of the back.

With a properly sized ice bag, you should not have to worry about being too exact: aim for the middle of the back and the correct area will be covered. Application of ice to other areas of the body (head, neck, legs and other areas of the spine) was NOT found to be effective. Ice bags placed on the middle of the back was the only area found to work.

The article reports that the sooner the ice is applied, the better the results. So you should have an ice pack ready and prepared. If you have a small dog, fill a small sized (quart) ziplock freezer bag with cubed or crushed ice and keep it in a particular spot in your freezer. When you see or hear a seizure begin, run for the ice or, if you live with another person, have one person run for the ice while the other runs to help the dog. Place the ice bag in the lower mid-section of your dog’s back and hold it there firmly until the seizure stops. If this technique works as reported, you should not have to wait as long as your dog’s usual seizure and you may also see an improvement in the post-ictal period’s duration.

The article reports that people who tried using a bag of frozen vegetables instead of ice had less success than those who used ice, so keep a bag of ice ready, or a commercial ice pack used to keep soft drinks cold in a cooler. The article also indicated that dogs with cluster seizures are a special case and may need their usual medications after a seizure, so if your dog has clusters, follow your vet’s instruction for using oral valium or rectal diazepam.

We are very excited about this discovery and would be so pleased if it turns out to be as effective as reported. If you decide to use this technique on your dog, please let us know how it turned out; was it successful or not, by E-mailing: We would like to be able to add more testimonials from those who have used it and whether or not they found it effective. If it is effective, it will be a godsend to many of us who now feel we can do nothing for our dogs but comfort them until a seizure ends.

If your dog has seizures, you may want to try Taurine, an amino acid. As with any supplement you consider trying for your dog, please do not do so without first discussing it with your vet. You may want to print this and give it to your vet with a note that you would like to discuss this supplement for your dog on your next visit.

Taurine is considered very safe for use in dogs. It is not effective for reducing seizures in all dogs, but it is safe. In the USA Taurine is routinely given to Epileptic dogs, but in the UK it has only been used for cats who lack this amino acid. However, that is now beginning to change as more vets are suggesting the use of Taurine for Epileptic dogs.

Taurine is one of the most abundant amino acids in the mammalian brain, which Epileptics do not produce in sufficient quantities. Several studies exist that document the positive affects and the anti-convulsive activity of Taurine. One study documents that epileptics have shown significantly lower levels of Taurine in their blood platelets than non epileptics.Clinically, Taurine has been used with varying degrees of success in the treatment of epilepsy and other seizure disorders. Caroline Levin’s Canine Epilepsy: An Owner’s Guide To Living With and Without Seizures (2002) has a very short statement:“Taurine is considered to be a long-lasting anticonvulsant, which is excreted through the urine in times of stress. It acts by stabilizing the nerve cell membranes.”Dr. Roger Kendall (in Complimentary and Alternative Veterinary Medicine) recommends dosing dogs with 200 to 1000 mg per day. “Magnesium Taurinate supplies both Taurine and Magnesium and plays a large role in raising the seizure threshold.”Many owners of Epileptic dogs are convinced that Taurine has contributed to their dog’s long seizure free period. The length of seizure free periods vary, ranging from around 11 months to just over 6 years! Many have reported that once their dog was on Taurine, they seemed much less susceptible to the stress of sudden noises. Some have reported that their dogs used to jerk violently, rather like a one second seizure, sometimes at random, sometimes when sleeping and anytime there was an unexpected noise. Whilst taking Taurine the jerking decreased. If the Taurine was stopped, the jerking increased and once the Taurine was started again, the jerking decreased accordingly.Giving your dog Taurine is not meant to replace any of their Epilepsy medication, instead, it is an addition to this and should be given three times daily at regular intervals. Your dog may have to take Taurine for a few weeks before you notice an improvement. Just because Taurine works for many Epileptics, doesn’t mean that it will work for your dog, but it is certainly worth trying and it is safe.
Things to look for when shopping for Taurine are:
  • It is a capsule NOT a tablet. Tablets have binders that capsules don’t
  • It does not contain any preservatives
  • It does not contains any other supplement except Taurine.

If your dog is having seizures between 11 pm and 6 am then you might like to consider trying MELATONIN. It has been known to virtually stop the “after bedtime, early a.m.” seizures in some dogs. It is important that you discuss this with your vet first to make sure that taking melatonin will not cause any adverse reactions with any other drugs your dog may be taking.

Many Epileptics who experience seizures during these hours are also often restless sleepers, often getting up several times during the night to pace. Ask to go out, sniff around and want to come back in. Given Melatonin at bedtime, it works to create a normal sleep pattern, ensuring the dog sleeps through the night, with the added bonus of a decrease of night time seizures.

Many owners of Epileptic dogs have had amazing results with Melatonin in helping them sleep at night, reducing restlessness and reducing seizures that happen between bedtime and a.m. Melatonin works in about 90% of dogs. If your dog is having seizures after bedtime, it would be useful to try Melatonin. If there is no change after a couple of weeks then discontinue, but it is worth trying to combat seizures after bedtime.

You can purchase Melatonin anywhere vitamins and supplements are sold. Natrol is the vegetarian brand of Melatonin and comes in 1 mg & 3 mg tablets. Generally, a dose of 3 mg is appropriate for a 35 – 100 lb dog. Smaller dogs get 1.5 mg and larger dogs may get 6 mg.

Melatonin is produced in the body by the pineal gland in the brain. Tryptophan, an amino acid found in food, is taken in by the body and made into serotonin, a neurotransmitter (conductor of nerve signals). The pineal gland takes the serotonin and makes it into melatonin, but only during the night. The enzymes in the brain which change serotonin into melatonin are inactivated by light. Norepinephrine is another neurotransmitter which assists in melatonin production. It acts as a catalyst to melatonin production by stimulating cells in the pineal gland to begin making melatonin in the absence of light. Sometimes, for one reason or another, the body does not produce adequate amounts of melatonin for its needs. This can result in insomnia and depression, among other symptoms. The body’s ability to synthesize melatonin may decrease with age.


By Phyllis Croft


  • Epilepsy is a condition, not a disease.
  • This means that the dog has an underlying problem that is causing the fits. A simple analogy would be to compare fits to a headache. You get a headache for various reasons – stress, fever, brain tumour, etc. and the same idea should be applied to fits, or seizures.
  • To understand why a dog is having fits, he needs to be given a thorough veterinary examination. This will look at the whole patient. Diagnosis is by elimination of possible causes by considering history, symptoms and the results of blood tests.
  • Euthanasia should be a last resort. There are only three reasons why an Epileptic dog is put to sleep: ignorance, the owner cannot cope, or because the most severe fitting cannot be controlled.


  • To be diagnosed with Epilepsy, the dog must have suffered a SERIES of seizures, or fits.
  • Epilepsy can occur in any breed.
  • Epilepsy is twice as common in dogs as in humans. An estimated 1% of dogs suffer from it, with incidences as high as 5-6% in some breeds.
  • Dogs can start fitting at any age.
  • The onset of hereditary (also known as Primary, or Idiopathic) Epilepsy is given in books as between the ages of 1 and 5 years. This is not a very meaningful concept, as it has been discovered that dogs can suffer late onset Primary Epilepsy and puppies have been diagnosed with primary Epilepsy.


  • A recessive gene, or genes, is thought to be responsible for gentic Epilepsy. The pattern of inheritance appears to vary between breeds.
  • Please DON’T breed from dogs that have suffered any form of seizures. You will be condemning an unsuspecting owner to devastating stress and worry at some time in the future. They may not be able to cope.
  • Dogs with Epilepsy will pass on the tendency to fit to future generations . Even dogs with Secondary Epilepsy; i.e. where an underlying cause is found for the fits, have the potential to pass on a low fit threshold.
  • Epilepsy may only be discovered once dogs are well into their breeding lives – and it can happen to anyone.


  • Diagnosis of the cause of fits is often difficult and usually made by eliminating possible causes. Resources are limited, but include blood testing, an MRI scan which is expensive, a spinal tap, or examination by a Neurologist.
  • Treatment with drugs is only necessary if the dog is fitting frequently.
  • Drugs most commonly used are phenobarbitone and potassium bromide, but alternative therapies can help reduce the frequency, or severity of fits in some dogs.
  • Epilepsy can be successfully treated in many cases – if the owner is willing and if he/she has the support of their Veterinary Surgeon.


During a typical fit, an animal will lie on its side and perform rigid, jerking and paddling movements. There may be partial, or complete loss of consciousness, as well as a loss of control of motions and urine. Some dogs may vomit, or salivate during a fit.

In addition to the fit itself, a dog may appear restless, or behave oddly before the fit and may be sleepy, or restless afterwards. Some dogs become very affectionate, while others seem abnormally hungry or thirsty. Each dog will have its own individual signs.

Intervals between fits will vary greatly between dogs, from one fit every few months, to several fits in one day. Sometimes a pattern will emerge.


  • Fits usually only last a few minutes and for 99.9% of the tiime, most affected dogs can lead a perfectly normal life. Fits vary in severity and a Grand Mal in a small dog, will be easier to manage than one in a Great Dane.
  • A dog will not need medication if fits are mild, or infrequent. In those dogs that need drugs, fits may be completely controlled, or their severity alleviated and frequency decreased.
  • Based on human experience, the dog does not know what is happening to him and provided he cannot injure himself (e. g. fall down stairs), is not suffering, or in pain during a fit. Most dogs with fits will die in old age of something else – if they are allowed to.


There are two types of Epilepsy:

  • PRIMARY, or IDIOPATHIC, or GENETIC EPILEPSY – is a defect in the dog’s genetic makeup. This is the term that is used when a Veterinary Surgeon cannot find an obvious cause for the seizures.
  • SECONDARY EPILEPSY – is triggered by something else that is going on in the dog’s body. This could be the result of a neurological accident, e. g. trauma due to a head injury, or birth incident, or the result of infection, inflammation, tumour, poisoning, liver, or kidney disease etc.




  • Primary Epilepsy (also known as Idiopathic or Genetic)
  • Secondary Epilepsy caused by: Progressive Brain Disease, such as Brain Tumour
  • Static Brain Disease, such as Scarring after Head Trauma


  • Toxins – Outside the body – Poisons & Inside the body – Liver/Kidneys
  • Excess/Deficit – Glucose , Electrolytes

Translated from a paper written by Veterinary Surgeon Ph. Bogaerts

Many dogs may develop convulsions at any time during their lives, irrespective of their age, or their breed. However, it is important to be able to distinguish the cause and the type of these convulsions.

The term EPILEPSY refers to a convulsive state with the repeated appearance of fits, resulting from an Intercranial condition, where symptoms do not follow a regular pattern. This unorthodox definition means that we cannot solely apply the term to convulsions due to IDIOPATHIC EPILEPSY(hereditary, primary or secondary), as we often tend to do. In fact, some convulsions can be the result of a viral ENCEPHALITIS, or intoxication, even though their development or their frequency could indicate IDIOPATHIC EPILEPSY. Convulsions can, therefore, be caused by Intracranial, or Extracranial conditions. We have various ways of diagnosing and examining these changes, as well as, of treating them. Conversely, when these convulsions cannot be explained by any specific cause, we describe these fits as being IDIOPATHIC EPILEPSY, or simply, Epilepsy. The precise mechanism which triggers a fit, is not yet fully understood. The nervous system functions as a result of the production and propagation of electrical charges.

This electric activity is controlled by chemical substances called neurotransmitters. These neurotransmitters circulate from one end of the nerve to the other and in this way, they transmit nerve impulses along the entire length of the nerves. Some neurotransmitters have a stimulating action, whilst others have an inhibitive one: in other words, some of these chemical substances transmit the message carried by the nerve impulse, whilst others block it. Normal muscular activity is continuously modulated by the interaction of these opposing effects. It is in this way an individual is able to control the contraction of his/her muscles. It is, thus, easy to see that any abnormality in the release, or the action of these neurotransmitters has an effect on the normal functioning of the muscles. Convulsions can, therefore, develop when the stimulation of certain nerves is increased following a rise in the quantity of stimulating neurotransmitters, or a decrease in the number of inhibitive ones, or even following the attack on the metabolism of certain cells.

Often we can associate the onset of the convulsions with a specific occurrence, such as a sudden noise ( a storm, an explosion, television etc.), or certain visual stimulations (a flash etc.), however, we do not yet know how these act on the brain and how they manage to disrupt the control mechanisms.

The convulsions that we see in the dog can be divided into two categories: (A) Localised, (B) Generalised. It is essential to distinguish between these two types because their origins, clinical signs and prognosis are different. We must also not overlook the important differences in these two types of Epilepsy when it comes to the possibility of using the affected animals as breeding stock.

Localised convulsions, which only involve a single or limited group of muscles, are due to an acquired cerebral condition, whether it be traumas at the time of birth, NEONATAL HYPOXIA, Postnatal Trauma, ENCEPHALITIS, or a Trauma etc. This group includes psychomotor convulsions as well as JACKSONIAN EPILEPSY. We will not go any deeper into this type of Epilepsy because, fortunately, these conditions are only encountered rarely in the dog.

The two types of Generalised convulsions are:


PETIT MAL – is not found frequently in the canine species. It invloves a temporary ‘loss of conscience’ of very short duration (30 – 60 seconds) and very often there are no visible symptoms.

GRAND MAL – is the most usual type of convulsion. This fit, or ictus, is a paroxysmic malfunctioning of the central nervous system, which develops suddenly, is totally abnormal and which disappears just as quickly. There are always four typical phases:


During this phase, which can last several hours, or even several days before the appearance of a convulsion. Slight changes in the animal’s behaviour may be noticed.


This phase is usually very short (several seconds) and is very quickly followed by the convulsion. During this stage behavioural changes are more noticeable – the animal becomes more rigid.


This phase usually lasts from 30 seconds to 2 minutes. The animal lies on it’s side, struggles, defecates and urinates. It is unconscious.


This phase, which of course follows convulsion, is a period of recuperation. The animal appears to be to be disorientated, ravenous, or thirsty and very nervous. There may even be temporary blindness.

This type of convulsion can be due to many different factors, ranging from hypoglycaemia and lead poisoning, to ENCEPHALITIS and of courseIDIOPATHIC EPILEPSY. As I have already mentioned, we can only make a diagnosis of IDIOPATHIC EPILEPSY, after we have excluded every other cause open to investigation.

IDIOPATHIC EPILEPSY appears, generally, between 1 – 3 years of age, though exceptions are possible. In humans the incidence of IDIOPATHIC EPILEPSY is approximately 0.5% – that is 5 cases in a 1,000. In the canine species this incidence is believed to be higher – about 1%. As indicated by the term IDIOPATHIC, we do not know the cause, or causes of this type of convulsion. it would appear, however, that there is an important genetic influence.

Even though Epilepsy has been recognised as a disease for a long time, the first genetic studies were only carried out in 1964, on the Keeshund. Afterwards it was shown that this condition was also to be found in other breeds, such as the German Shepherd, the Poodle, the Cocker Spaniel, Retrievers, the Tervueren, the Irish Setter, the Beagle, the Collie and the Boxer.

Eventually, Epilepsy was found to be present to a greater or lesser degree in all breeds of dogs, including mongrels and cross breeds. Wherever one looks one can find it. The incidence of this disease within the various breeds, varies greatly and the statistics that have been published are somewhat questionable, since the genetic study of Epilepsy is very difficult to carry out. In fact, when he is not having a seizure, an Epileptic animal seems completely healthy and sometimes, in the case of Epileptic dogs that are kennelled, their owners never actually witness the dogs having a fit and therefore, these dogs are not included in the statistics. This means that, in all good faith, they could be used in breeding stock and as a result, transmit the genes responsible for Epilepsy. Even the electro-encephalogram cannot be considered as a reliable test because some Epileptic individuals will effectively show an abnormal graph, whilst others will have a perfectly normal result. Nevertheless, as a result of several studies, it seems that the condition is to be found slightly more frequently in the male than in the female. Depending on the breed, this difference could mean that from 3 to 5 times more males are affected than females.

Finally, the most plausible cause of the condition, would appear to be the genetic one, even though up till now the genetic link has not been identified – in other words, the gene, or genes responsible. At the present time the following theory seems to be the most probable: Several genes appear to be responsible for Epilepsy, either in the form of major genes, or in the form of modifying factors. In addition, there may be the influence of a limiting factor linked to the sex of the animal.

What this means, in fact, is that there would seem to be an ‘Epileptogene’ potential, (a predisposition, or nor, to develop Epilepsy), inherited by the animal and which would appear under certain conditions.

As is the case in all inherited conditions, it is obvious that when breeding, we must strive to avoid the genes responsible. Strict progeny testing would, of course, be expensive and slow because the condition appears on average at the age of two years.

Without knowing precisely the genetic mechanism and it’s mode of transmission, it would, perhaps, be a little premature to undertake a real programme of eradication. However, to avoid, or at least reduce the risks, it would be wise to identify and isolate the individuals affected and, at any rate, avoid using them in breeding programmes which include a high degree of in-breeding, or line breeding.


IDIOPATHIC – Any disease of unknown origin

ENCEPHALITIS – Inflammation of the brain

NEONATAL HYPOXIA – Deficiency of oxygen at birth

JACKSONIAN EPILEPSY – Symptomatic Epilepsy produced by injury to the brain (as by trauma or toxic agents) and manifesting symptoms that vary according to the part of the brain injured.

GRAND MAL – A form of Epilepsy characterised by a loss of consciosness for up to five minutes and violent convulsions.

PETIT MAL – A mild form of Epilepsy characterised by periods of impairment or loss of consciosness for up to 60 seconds.

Taken from an article written by

Dr. de Launta DVM, PhD.

Epilepsy is no longer the scientific mystery it has been for centuries, yet even today, owners of dogs subject to convulsions and seizures are frightened and alarmed by what the animal experiences.

Such natural questions as the following occur spontaneously:

  • Is the dog in pain during seizure?
  • Will it suffer permanent brain damage?
  • Is there any cure?

To answer these and other frequent inquiries about the cause and treatment of seizures and Epilepsy, Alexander de launta, DVM, PhD, of Cornell’s Department of Clinical Sciences, has brought together all the most recent information on the subject. Dr de Launta has written extensively on the neurological system and its disorders and is the author of the widely used textbook, ‘Veterinary Neuroanatomy and Clinical Neurology’.


The pet owner may find the use of terms confusing at times, but usually has no difficulty recognizing when a dog is subject to an attack, be it termed a convulsion, a fit, a seizure, or what is to many lay persons, the most ominous sounding Epileptic episode. All those words, however, apply to the same event: a sudden, transitory disturbance of brain function that is usually short and from which the dog recovers spontaneously, although the disturbance usually has a tendency to recur. The term Epilepsy, is most often used to designate recurrent seizures that are Idiopathic – without a recognised structural, or metabolic brain disease as the cause.


The brief disturbance of brain function, can be manifested in different ways, although all the signs involve abnormal function of the cerebral hemispheres. Usually, there is a generalized disturbance that includes loss of consciousness, a stiffening of the limbs and trunk, falling over and violent thrashing of the limbs, accompanied by chewing and salivation. Occasionally, the animal will defecate, or urinate during the episode. Most seizures last less than a minute and complete recovery occurs in the following few minutes, or after a period of drowsiness, abnormal behaviour such as circling, or pacing, or inability to recognise the owner and often a period of blindness. This period usually lasts from a few minutes to an hour, but in some cases, may be considerably longer before complete recovery is observed. The stages of a seizure can be divided into three relatively distinct events. In the PRESEIZURE, or AURA stage, the animal may exhibit restlessness, pacing, seeking attention from the owner, or more obvious abnormal behaviour, such as uncontrolled hysterical running, or barking, or growling at no visible object. The seizure itself, is termed the ICTUS(Latin for stroke, or attack). Whereas loss of consciousness and muscle spasm are common manifestations of this stage, the dog may also display excitement, violent movement, vomitingg, etc. The period after the seizure itself, is called the POSTICTAL or recovery stage. Some animals may continue to display signs of inco-ordination and disorientation for many hours: others, however, appear to recover quickly.

It should be obvious that there is no ‘Typical’ kind of attack, nor an altogether typical response from the dog. Some dogs may exhibit abnormal limb stiffness, inco-ordination and falling for prolonged periods, yet never lose consciousness. More rarely, the seizure is limited to the episodes of abnormal behaviour, during which the animal may run in circles, or act as if it intended to bite itself.

All these manifestations reflect the abnormal, uncontrolled neuronal discharge in various parts of the cerebral hemispheres – in effect, an inappropriate burst of electrical activity that momentarily disrupts the extraordinarily effective control that the central nervous system usually exercises over every organ of the body.


There is extensive research under way to understand the basis for seizures at a biochemical and molecular level. Fundamental to all seizures is a sudden, abnormal, spontaneous depolarization of a group of neurons – the cells of the nervous system located in the brain. Each neuron receives a large number of terminations of other neurons. These terminations are called synapses. Each synapses acts by means of a chemical neuro-transmitter substance; some of these inhibit the synapse’s function while others stimulate activity. The sum of this activity determines the ultimate activity of the neuron.

The environment of the neuron itself, is extremely complex, being affected by the movement of such ions as sodium and potassium across the cell membrane and also by the energy level generated within its core. Almost any alteration in this environment can result in a spontaneous discharge that becomes the basis for the clinical signs of a seizure. Some discharges are too limited and minor to be observed, although they may be apparent on an electroencephalogram.


The environmental alterations to the neuron may be structural, biochemical, or of unknown (Idiopathic) origin. There are, therefore, three possible ’causes’ of seizure. Structural alteration includes that associated with with inflammatory diseases of the nervous system. An example of this would be the Encephalitis that occurs from an infection with the canine Distemper virus. Other structural alterations that can result in seizures, are Cancer of the nervous system, ( more common in older dogs) disturbance of the nerve tissue, associated with poisoning, (for example; from lead, organophosphates, ethylene, glycol, chlorinaated hydrocarbons and compounds used in paints, antifreeze, rodent poisons, insecticides, etc.), injuries to the nervous system from automobile, or other accidents, malformations of the brain, such as Hydrocephalus, a condition in which there are excessive fluids in the brain and may cause separation of the cranial bones. In more rare instances, inherited deficiency of specific enzymes causes a disturbance of neuron function that is referred to as Storage Disease.

Biochemical disturbances of brain function and seizures, can be the result of diseasesthat effect other organs of the dogs body. The most common of these is Hypoglycemia, the disturbance of carbohydrate metabolism that results in decreased levels of blood sugar. This decrease may result from excessive insulin production when the pancreas, which produces insulin, is affected by a tumour. because neurons need a steady source of blood sugar to function normally, Hypoglycemia results in dysfunction, which commonly mainfests itself in a seizure. Severe Liver Diseases, sometimes, but rarely, leads to a build-up of metabolites in the blood that are toxic to the neurons. Finally, heart disease may produce a severe decrease in the oxygen content of the blood (Hypoxia), which in turn can cause disturbed neuron metabolism and seizures.

When the seizure cannot be associated with any structural, or biochemical disease, it is termed Idiopathic Epilepsy. The uncontrolled discharge of neurons that cause the observable Epileptic episode, appears to be related to what is called the ‘seizure threshold’. In technical terms, the seizure threshold can be defined as the sum of events that affect neuronal excitability. These events include the cell membrane of the neuron, the number and kind of synapses on the neuron and the environment of the other cellular elements (neuroglia). This threshold varies among individual animals and is apparently exceptionally loww in animals that suffer from Idiopathic Epilepsy. Generic factors are believed to determine the threshold levels, because it is obvious that some animals have lower thresholds than others.


The concerned owner is perhaps reluctant to accept the first step in aid of a dog having a seizure – that is, leave the animal alone. Trying to hold the dog will certainly have no effect on the attack itself and it is more likely to result in unintentional injury to the owner. The dog will usually not injure itself, except for biting its lip, or tongue. The notion that it can ‘swallow it’s tongue’, is false. Most seizures stop in less than a minute. When it is over, the dog should be taken to the vet for an examination. If the seizure does not stop within a few minutes, the dog should be wrapped in a blanket, (again to protect the owner, as well as the pet) and transported to the vet.

The most common cause of seizures is Idiopathic Epilepsy – which is a diagnosis of exclusion — exclusion of all other known causes of seizures. There is no test that will confirm the diagnosis of Idiopathic Epilepsy. The vet does have routine instruments and blood tests that will help diagnose various structural and metablic causes of brain disturbances. These should be done after the first seizure. Examination of the cerebrospinal fluid, which requires general anaesthesia, should be done if clinical signs warrant it, or if more than one seizure has occurred.


Treatment is obviously directed at whatever specific cause of the seizure has been diagnosed. For example, surgical removal of a tumour of the pancreas will correct hypoglycemia and the seizures resulting from that condition. There is, however, no ‘cure’ for Idiopathic Epilepsy. Treatment in such instances is aimed at attempting to control the seizures with anti-convulsant drugs. The owner should understand that it is unusual for these drugs to stop the seizures altogether. The goal of therapy is rather to decrease the incidence and severit to one that both the dog and the owner can tolerate. The most critical part of the therapy is the co-operation of the owner in maintaining a consistent routine of drug administration. If the owner is not willing to assume the responsibility of giving the medication on a regimen that is always daily and even two to three times a day, therapy should not be started. Haphazard administration of these drugs is worse than no therapy at all.

Whether to begin therapy at all, is often a difficult question to answer. Perhaps the following will prove helpful for the pet owner in deciding:

  • If the dog has had only one seizure and no specific structural, or biochemical cause is diagnosed, anti-convulsant drug therapy should NOT be started.
  • If the dog has a brief seizure every four to six months, the dog should NOT be treated.
  • If the seizures are severe, prolonged and very frequent, the dog SHOULD be treated.

The vet will have to rely on the owner for accurate details on the frequency and severity of the episodes.


A wide variety of drugs are available for the control of Idiopathic Epilepsy, but no single drug, or dosage will be effective at all times and for each individual dog. The most reliable anti-convulsant for most dogs, however, is phenobarbital. Another commonly used barbiturate, is Primidone. When control cannot be achieved with these, the vet can use phenytoin, valporic acid, paramethadione and diazepam. The owner should be aware of potential side effects, including increased thirst, urination, or appetite,, drowsiness & hyper-excitability. These effects can be temporary, or longer lasting, but in most cases will not be serious. nevertheless, a dog on anti-convulsant drugs will require periodic physical examinations and some laboratory tests.


Idiopathic Epilepsy can occur in any breed and also in mongrels. It has been defined as an inherited disorder in only a few breed lines, including lines in German Shepherds, Belgian Tervurens, Keeshonds, Beagles and Dachsunds. The disease is reported to be common among Miniature Toy Poodles, St Bernards, Cocker Spaniels, Irish Setters, Alaskan Huskies, Siberian Huskies, Wire-haired Fox Terriers, Labradors & Golden Retrievers.


Seizures and Epilepsy are a common problem in the dog. it has been established that 60 to 70% of these dogs can be controlled to some extent with anti-convulsant drugs (the percentage may be much lower in certain breeds). Control, however, may require experimenting with different drugs and different dosages — and it always requires strong commitment on the part of the owner, to follow the regimen of daily drug therapy. The owner must also realise that some seizures can be life threatening, particularly if the dog goes into the type of continuous seizure referred to as STATUS EPILEPTICUS. This is often difficult to stop and the physical exhaustion and metabolic consequences may result in death, or severe damage to the dog.

A realistic attitude towards the disease, also recognizes that a seizure does not mean that the dog has a devastating and terminal brain disorder. Many dogs live a normal, full lifetime on anti-convulsant treatment. The seizures themselves are, as far as can be determined, not painful to the dog. The screams given out in some attacks appear to be involuntary and not caused by pain. The dog does, of course, frequently exhibit anxiety and discomfort in the aura, or pre-effect stage and is often disorientated after the episode…..but these responses are transient and without permanent effect on the dog’s well being. In dealing with seizures, as in so many other aspects of pet ownership, it is the degree of involvement on the part of the owner, that determines the outcome of the condition.


Seizures are one of the most frequently seen neurological problems in dogs. A seizure is also known as a convulsion or fit. It may have all, or any combination of the following:

  • Loss or derangement of consciousness
  • Contractions of all the muscles in the body
  • Changes in mental awareness from non-responsiveness, to hallucinations
  • Involuntary urination, defecation, or salivation
  • Behavioural changes, including non-recognition of owner, viciousness, pacing and running in circles


Seizures consist of three componants:

  1. THE PRE – ICTAL PHASE, or AURA, is a period of altered behaviour, in which the dog may hide, appear nervous, or seek out the owner. it may be restless, nervous, whining, shaking, or salivating. This may last a few seconds to a few hours.
  2. THE ICTAL PHASE is the fit, or seizure itself and lasts from a few seconds to about 5 minuted. During this period, all of the muscles of the body contract strongly. The dog usually falls on its side and seems paralysed while shaking. The head may be drawn backward. Urination, defecation and salivation often occur. If it is not over within 5 minuted, the dog may be in status epilepticus, or going from one seizure into another without respite.
  3. THE POST – ICTAL PHASE. During this phase there is confusion, disorientation, salivation, pacing, restlessness and or temporary blindness. There is no direct correlation between the severity of the seizure and the duration of the post-ictal phase.


Despite the dramatic signs of a seizure, the dog feels no pain, only bewilderment. Dogs do NOT swallow their tongues. If you put your fingers into it’s mouth, it will not benefit your dog and you will run a high risk of being bitten very badly. The important thing is to keep the dog from falling and hurting itself. As long as it is on the floor, or on the ground, there is little chance of harm occurring. If seizures continue for longer than a few minutes, the body temperature begins to rise. If hyperthermia develops secondary to a seizure, another set of problems may have to be addressed.


There are many types of seizures. Epilepsy is the most common and of least consequence to the dog. The other extreme includes severe diseases such as Brain Tumours. Fortunately, most seizures are due to Epilepsy.


When a seizure occurs, the Vet begins by taking a thorough history concentrating on possible exposure to poisonous or hallucinogenic substances, or history of head trauma. The vet will also carry out a full physical examination, including blood tests and an electrocardiogram (ECG). These tests rule out disorders of the liver, kidneys, heart, electrolytes and blood sugar level.

If these tests are normal and there is no exposure to poison, or recent trauma, then the Vet may refer you to a Veterinary Neurologist for further tests and examinations, which could, conceivably, involve more sophisticated tests, including MRI, CAT scans and an Electroencephelogram. Fortunately, these additional tests are usually not needed.


Vets generally prescribe 1-2 weeks of anticonvulsant therapy. If there are no more seizures during that time, the anticonvulsants are then gradually discontinued. The next treatment is determined by how long it takes for another seizure to occur. That may be days, months, or years. At some point, many dogs have seizures frequently enough to justify continuous anticonvulsant therapy. Since that means that medication must be given every 12 to 24 hours for the rest of the dog’s life, your Vet will not recommend medicating until the seizures occur about every 30 days, or unless the fits last for more than 5 minutes.

It is important to avoid sudden discontinuation of any anticonvulsant medication. Even normal dogs may be induced to seizure if placed on anticonvulsant medication and then abruptly withdrawn from it. Your Vet would fully discuss with you, any withdrawal of medication before beginning withdrawal.


Status Epilepticus bears special note. it is characterised by a seizure that lasts more than 5 minutes. When it occurs, the dog’s life is endangered. Unless intravenous medication is given promptly, the patient may die. If you think your dog is in Status Epilepticus, you should seek urgent veterinary treatment immediately.

The Animal Health Trust in Newmarket, Suffolk, have a DNA Archive for Epilepsy and also other health problems.

If you or anyone you know, has an Epileptic dog, or a dog with any other health problem, then please click on the link below to find out how to obtain your kit to produce a DNA swab.


These are different kits to those provided for LOPRA rcd4 DNA swabs


Announcing the official launch of the Canine Epilepsy Network web site!

This devastating problem can affect any breed. It is our hope that this site can provide information for those who have an epileptic dog, or have produced this problem and the research will help concerned breeders, to eliminate this
problem from their breed, while keeping all the good traits breeders strive for. This site, sponsored by the niversity of Missouri College of  eterinary Medicine, provides a resource for breeders, owners, veterinarians and researchers concerned with canine pilepsy.

The site includes:

Basic epilepsy information

An invitation to participate in Canine Health Foundation funded research into the genetics of inherited epilepsy

Updates on the research

A discussion panel

And links to additional information

We invite you to visit the site at:

We would welcome your comments.

If you need additional information not provided in this site, or have any questions, please contact me. Thank you in advance for sharing this
information with others in your breed! 

Liz Hansen
Co-ordinator of Veterinary Information
Dr. Gary Johnson’s Lab-Dept. of Vet. Path.
209A Connaway Hall
College of Veterinary Medicine
University of Missouri
Columbia, MO 65211
573-884-3712 (office)
573-884-5414 (department fax)



  1. Doug Gage says:

    Thank you for this site. My Iris, Chloe had two fits yesterday. It was the most gut and heart-wrenching thing to witness. After losing my last Irish 2 years ago to gastric torsion, I thought for sure I was going to lose Chloe as well.

    When my vet checked her out immediately after she ‘came to’ ( I live 5 minutes from his office ) he noted that her gums were dark. Has this ever been reported as an indicator of an impending seizure, or is it possibly and after-effect ?

    She is currently on Zonisamide (cant remember how much right now).. have studies proved this to be effective ? I read that it is somewhat controversial and that it is not generally used as the ‘go to’ medication, rather it is used if a dog is not tolerant to other treatments ?

    I am hopeful she won’t have another fit for a long time. The information you have provided is very assuring and helpful, and I am grateful to you for it. Both of us are.

    Doug Gage
    Shortsville, NY

Five Star Care for Canines

Claire Keeton reported in the Sunday Times of 15.11.2015 that:

‘It’s not a dog’s life, no ma’am, definitely not for pets who live in the suburbs.

Owners are spending more time and money on them than ever before and services for animals are booming.  This breed of owner will pay for surgery and Reiki healing, plan holidays and play dates for pets and even swop cars for them.

“Fur kids are the new kids and their owners will do almost anything for them” said Julia Davies, a Johannesburg animal behaviourist with four rescue border collies.  Their food bill comes to more than that of Julia and her husband. “I know people who employ full-time staff for their dogs.  They look at their animals as emotionally intelligent beings.” she said.

But pets eating habits may not reflect this intelligence and vet’s bills can run into tens of thousands of Rands.  A Labrador in Cape Town has had three operations after twice eating baby dummies and finally a baby’s bottle top.  His owner, Lauren Tuohy said “He cost us about R20,000 for those ops and so we nicknamed him ‘Mauritius’.  He was the cost of a holiday.”

These days, vets can perform virtually any surgery done for humans, imaging (such as MRI and CT scans) has improved and treatments such as chemotherapy are available.

Owners are prepared to pay specialist fees and are increasingly taking out pet insurance.  Johannesburg veterinary surgeon Dr. Bruce Irvine-Smith opened a practice with his brother 45 years ago, now they have 10 vets in a hospital in Bryanston with three theatres, an ICU, a lab, sophisticated machines and many wards.  “When I bought the first ECG machine I wondered if we would use it enough.  It has paid for itself 100 times over,” he said. “We have done open-heart surgery here.”

Dr. Michael Gray works at the Panorama Veterinary Clinic and Specialist Centre in Cape Town and is impressed at the resilience of pets.  “I am still amazed that the wheel of a 4×4 can ride right over a maltese and it often survives, with fractures,” he said.  “Cats that fall from flats mostly survive with relatively minor injuries.  The higher they fall from often the less the injury.”

The rehabilitation of pets is becoming more common.  Therapist Natercia Camara of Doggy Paddle, which offers treatments such as hydrotherapy says some pet owners take their pets for a session every week.

Johannesburg career woman Michelle Caldeira moved houses to accommodate her two Cavalier King Charles Spaniels. “When getting upstairs was tricky for their hips, I found a ground-floor house with a beautiful garden.  What makes them happy, makes me happy too,” she said.

To make sure his two Rottweilers got exercise, Johannesburg chef Richard Loubser bought them a treadmill.  “I walk them every day, but when I’m away, no-one else can.  They are friendly, but strong.  It took treats and a lead to get them on the treadmill, but now my female will walk on her own.”

An underwater treadmill is one of the tools used by vet Tanya Grantham, who specialises in rehabilitation and pain control.  “I’ve even had a Persian cat on the underwater treadmill,” she said.

Another therapy which gives relief for chronic pain is gold beads inserted into acupressure points.

Look Into My Eyes - The Oxytocin Rush

The Washington Post’s Rachel Feltman reported from New York USA that you and your favourite dog may be locked in an oxytocin feedback loop – a chemical boost for the both of you that leaves both parties better at bonding and reading social cues – every time you lock eyes.

And it’s no mistake Scientists think this is one of the evolutionary turns that took modern, domesticated dogs away from their wild wolf ancestors.  Their findings were reported in a study published in Science.

Oxytocin isn’t the “moral molecule” that some have sold it as, but this hormone is important. Researchers are pretty sure that it has something to do with pair bonding, particularly between mothers and infants.

A recent published study found that oxytocin causes virgin female mice to respond to the cries of unrelated young the way a mother would, suggesting that it might make us recognise stimuli that might otherwise be ignored.

“Rather than virtue incarnate, oxytocin is more of an all-purpose social molecule,” Ed Yong wrote in his blog at National Geographic.  “It probably acts as a spotlight that draws our attention to social cues.  We then react differently depending on our temperament or whether those social cues are positive or threatening.”

Now it seems that dogs and humans may benefit from the chemical in a similar way.  In the new study, researchers found that dog owners and their dogs had higher levels of oxytocin in their urine after sustaining eye contact with each other.  Wolves that were raised as pets didn’t show the same boost when interacting with their owners.  The study also found that exposure to oxytocin spray before interactions with humans led to more eye contact from dogs (and higher oxytocin levels in the humans gazing back at them), but this only held true for female dogs.

In the same way that dogs are known to respond to pointing in ways that wolves do not, it could be that they’ve developed the ability to gain meaning from eye contact.  For humans, making eye contact is a valuable social tool and one that promotes bonding between parent and child.

“The origin of the function of oxytocin is breast feeding and nurturing” study author Takefund Kikusul of Azabu University (Japan) said. “ However, in our study we demonstrated that a non-reproductive relationship – a human and dog – show the same positive loop.”

Kikusui and his colleagues believe that this feedback loop explains the warm feeling humans have towards their dogs, and the animals’ ability to relieve stress.

 They suspect that some dog ancestors were able to interact with humans by way of eye gaze – something not many cross-species pairs can manage – and that over time we selected for ones that were able to bond with us this way.

“There’s a possibility that dogs unknowingly utilise a natural system meant for bonding a parent with his or her child,” Kikusui said. “On the other hand, humans are also unique in using eye gaze with other species, namely dogs which suggests that both humans and dogs co-evolved during this process.

(This article was also published in The Cape Argus 25.04.2015)

Megeosophagus (M.O.)



Harvey is an Irish Setter who has M.O. or Megeosophagus. His owner, Sarah recently came across a collar which helps dogs with this dreadful condition.





In Sarah’s words, this is how it works.

Having M.O. Harvey would constantly regurgitate whenever he lay down, and consequently he had 4 serious bouts of aspiration pneumonia which all involved a few days stay at the vets, on lots of medications, and on each occasion it was touch and go whether he would survive. These pneumonia bouts would come on so, so quickly. He would literally go from being fine, to being on deaths door, within one hour! I quickly learned the warning signs and could literally tell just from a ‘look’ in his eyes, and I’d race him straight to the vets. They’ve said he wouldn’t be here today if we hadn’t acted so fast. I joined an MO Facebook group and a lot of people in the States swore by a Neck Hug, which was a big, soft, stuffed collar. It holds the head up and lessens the regurgitating. The only place these can be bought though is from a website in America and they were about £50-£60 plus shipping. Purely by chance I saw these inflatable collars in our local pet shop, and in our vets practice, as a comfier alternative to the medical cones that dogs wear after operations, and I figured they would do the same job, and they’re priced at £12 – big difference! So I bought one from the vets, blew it up, popped it on him, and he’s never regurgitated once since!!! He’s been wearing it since November 2014, and we haven’t had a single MO issue since (July 2015). He wears it more or less 24/7. We only take it off him when he’s out on walks, or if we’re taking a photo of him, or we give him the odd half hour break from it to have a good scratch, otherwise he wears it all the time. We have to top it up with air once every week or two (and recently had to use a puncture repair kit on it after he popped it!) but it’s given him much more freedom to just be a dog. We always used to have to keep him standing upright after meals, or prop his head up with pillows etc…but this does that job, so he does what he pleases. Occasionally in the night we hear him wretch, and when we turn the light on we discover it’s because his inflatable collar has come off. So we pop it back on, and immediately he’s fine. It’s an absolute god-send. It’s like he doesn’t even have MO anymore, it’s brilliant and it doesn’t restrict him in any way, he adapted to wearing it no problem. I’ve seen some people on the MO support group use babies blow-up swimming rings as a quick alternative while they wash and dry their expensive ‘neck hugs’. Just Google Comfy Collar on the UK sites, and you’ll find them, all the vets are now starting to stock them as an alternative to the plastic cones. 



South African Irish Setter Health Review 2015

 Specialist Veterinary Opthalmology

Sava Clinical Eye Examination

Despite their being DNA tests which genetically identify Progressive Retinal Atrophy rcd 1 (early onset blindness) and LOPRA rcd 4 (late onset blindness) there are NO other genetic tests available for eye disease in Irish Setters yet The Kennel Club Centre of Animal Health Trust in Newmarket, UK has reported that a third form of PRA  exists in Irish Setters which is yet to be identified.

This is known due to an initial ten dog’s DNA samples sent for analysis which revealed 7 were affected by LOPRA rcd4 while 3 DID NOT carry either the Progressive Retinal Atrophy rcd1 or rcd4 mutation, meaning their PRA must be due to another mutation.  There is evidence that this third form has an earlier age of onset than LOPRA rcd4, but more blind dogs needed to be analysed to identify the mutation.  Currently the only way of diagnosis is by clinical examination of affected blind Irish Setters that have been genetically DNA tested and cleared of PRA rcd1 and LOPRA rcd4.

Breeders and owners can also only rely on clinical eye examinations of their Setters for the diagnosis or clearance of such conditions as Entropion which manifests as the edge of one (usually the bottom) eyelid turning inwards to the eyeball which causes damage to the cornea, Posterior Polar Cataracts (particularly in Irish Red & White Setters) and a wide range of other mild defects which may or may not be inherited such as persistent pupilliary membrane.

Clinical examination with South African Veterinarian Association Certification is undertaken by Drs. Goodhead, Venter and Lo-An Odayar who commute between their Fourways, Johannesburg Animal Hospital (011-4651237) and Cape Animal Eye Hospital , Panorama (021-9036632). Clinics in the major cities of Durban and Port Elizabeth are also held periodically throughout the year.

SAVA Examination certificates can be submitted to KUSA for capture on their data base with the request for an updated KUSA Health Screening Certificate which is an annexure to the dog’s KUSA registration Certificate.

Further information can be obtained from KUSA website under Health Schemes and website

DNA Testing for Adverse Inherited Conditions


Progressive Retinal Atrophy rcd1 is an early onset blinding condition.  As a result of genetic research, The Kennel Club Centre of the Animal Health Trust (UK) developed the first canine DNA test for Irish Setter PRA rcd 1 in the mid 1990’s. With the mating of tested CLEAR parentage it could be guaranteed their progeny would not develop nor carry the condition.

Initial research by Upsala University, Sweden led to the development of a DNA test for Canine Leucocyte Adhesion Deficiency (CLAD) a lethal auto-immune condition which gave pups in a litter little chance of survival as they were prone to any opportunistic infection.  Like PRA rcd1 the condition is also the result of a defective simple recessive mutant gene.  In 1999 a more robust test was developed by the Animal Health Trust.

Testing Laboratories for both PRA rcd 1 and CLAD are available worldwide and in South Africa are currently undertaken by Inqaba Testing Laboratory.   Such results are recognized by The Kennel Union of Southern Africa and the UK governing body of dogdom, The Kennel Club.  The local SA testing facility uses Whatman Cards which only require a few drops of blood collected from the ear of the dog by the breeder or Veterinarian for testing.

A properly structured scheme was instituted by a Group of Irish Setter Breeders in South Africa in 2006 and proved highly successful, thus in the nine years of operation we can report:

326 (three hundred and twenty-six) Irish Setters currently appear on the PRA rcd1 and CLAD National Registers as either DNA Tested Clear or Inherited Clear by virtue of tested ancestry.  In 2010 Irish Setters were the first breed to be issued with The Kennel Union of Southern Africa Health Screening Certificates which is an annexure to the KUSA Registration Certificate and currently reflect the status of the parentage and the pup together with all other health screening results.

NO cases of PRA rcd1 or CLAD have been reported and NO Carriers or Affected Irish Setters are currently recorded on KUSA Irish Setter Breed Registers or the group’s National Registers. Irish Setters imported into SA from anywhere in the world MUST be proven CLEAR of PRA rcd1 and CLAD before Breed Registration will be effected by the Kennel Union of Southern Africa.



In the latter half of 2011 Animal Health Trust  announced that a new form of Progressive Retinal Atrophy had been identified, initially in Gordon Setters and later in Irish Setters, which affected dogs showing rod cone degeneration (initially night blindness) beyond mid-life and blindness in later life. To distinguish this from any other form of PRA it is termed Late Onset Progressive Retinal Atrophy rcd4 (LOPRA rcd4).

Initially it was estimated that between 30 to 40% of Irish Setters were involved as Carriers in UK alone and this sent shock waves around the world as some very prominent sires were implicated. 

From August 1st 2011 The AHT offered a DNA test to Irish Setter breeders and owners which examined the DNA of each dog being tested for the presence or absence of this precise mutation.

Previously the only means of diagnosis was Clinical Eye Examination by a Specialist Veterinary Ophthalmologist of affected dogs which displayed symptoms of blindness in later life (carrying two copies of the defective gene)  Carriers (one copy of the defective gene) show no symptoms and would thus be considered clear on clinical examination. It is reasonable to assume that the mutation silently developed over a period of at least ten and probably nearer twenty years, before affected dogs were identified by Clinical Eye Examination in any numbers.

By DNA testing prior to mating any Irish Setters together the breeder acquires the knowledge to avoid breeding any pups that are LOPRA rcd 4 affected and reduce the number of Carriers, who will remain normally sighted. Those breeding clear tested mates together can guarantee Clear progeny.

CLEAR – These dogs have two normal copies of DNA.  Clear dogs will not develop LOPRA rcd 4 nor pass defective genes to progeny

CARRIER – These dogs have one copy of the simple recessive mutation gene and one normal copy, they WILL NOT DEVELOP LOPRA rcd4 but will pass one mutated gene to approximately half their progeny

AFFECTED – These dogs have two copies of the LOPRA rcd 4 gene (one inherited from each parent) and WILL GO BLIND in later life.

Immediate steps were taken at the beginning of 2012 to institute a Scheme for South African breeders and owners.  As is the case with CLAD and PRA rcd1 proposals were made to the Kennel Union of Southern Africa to prohibit the Breed Registration of any imported Irish or Gordon Setter from being placed on the respective breed register unless DNA tested Clear or proven Inherited Clear (by virtue of being the progeny of tested clear parentage) of  LOPRA rcd4.  At that time the LOPRA rcd4 status of local Setters was unknown, but it was necessary to protect SA’s limited gene pool from being further compromised. The proposals were approved by Provincial Councils and Federal Council and appear under KUSA Sch. 2 Appendix E.

Protocols and Procedures to be followed by owners/breeders participating in the Scheme were also compiled, distributed and are subscribed to on a voluntary basis. These, importantly, indicate that:

Ideally, only DNA tested CLEAR or INHERITED CLEAR parentage should be mated together to produce 100% INHERITED CLEAR PROGENY.


If a CARRIER is used for breeding purposes the following is mandatory:

ONLY CLEAR DOGS TO BE MATED TO CARRIER DOGS producing a litter which would average 50% LOPRA rcd 4 CARRIERS and 50% CLEAR progeny.

If such a mating is undertaken by a breeder it is obligatory to DNA test the ENTIRE LITTER after micro-chipping at SIX WEEKS of age.  KUSA to be requested not to Breed Register such a litter until this process is complete.

All pups to be sold with Breeders Restrictions and it should be emphasized that LOPRA rcd4 CARRIER pups from such a mating WILL NOT go blind.

LOPRA rcd4 CLEAR Setter pups from such a mating can enter the breeding gene pool with impunity and should only be mated to clear dogs within the breed.

This pattern of CLEAR to CARRIER dogs must only be undertaken in exceptional circumstances and for a limited period NOT EXCEEDING TEN YEARS FROM DATE OF COMMENCEMENT OF THE SCHEME (2013)

Irish Setters DNA tested as AFFECTED should NOT BE BRED UNDER ANY CIRCUMSTANCES neither to CLEAR and definitely NOT TO CARRIER dogs. They unfortunately will go blind and encourage the spread of the LOPRA rcd 4.

Those Setters DNA tested as CARRIERS should NOT UNDER ANY CIRCUMSTANCES be bred together (i.e.Carrier sire to Carrier dam) approximately a quarter of the litter will be AFFECTED.

To date the local Inqaba Genetic Testing Laboratory have been unable to offer a DNA test for LOPRA rcd 4 so initial testing was undertaken by the University of Missouri, America from DNA samples collected from Irish Setter owners and breeders prior to the end of 2012. Subsequently the testing laboratory was switched to Animal Heath Trust UK due to the tardiness of the University of Missouri in effecting the testing and providing proof of results.

The first batch of 27 (twenty-seven) results were received in 2013 from Missouri University and were of great concern as it was revealed that the South African gene pool had been compromised and Carriers were identified albeit that there was only one dog affected – an import from UK which had not been used at stud.  The balance tested Clear of LOPRA rcd4.

The co-ordinators of the Scheme, Mark & Bridget Simpson, advised all those who had participated of the results and, in so far as could be ascertained the direction from which they inherited the mutant LOPRA rcd4 gene.

All reports and results were subsequently forwarded to the Kennel Union of South Africa for capture on their data base and updated Health Screening Certificates were issued reflecting the status of each dog with regard to LOPRA rcd4.

With great fortitude breeders accepted the results and have juggled their breeding plans to make the best possible use of LOPRA rcd4 Clear Irish Setters to add to the pool of Inherited Clear pups. Thus we conclude 2015 with National Registers reflecting:

  •             15% Irish Setters DNA tested Clear of LOPRA rcd4
  •             66% Irish Setters Inherited Clear
  •             17% Irish Setters DNA tested Carriers
  •               2% Irish Setters DNA tested Affected

A total of 108 Irish Setter KUSA Health Screening Certificates indicating the above LOPRA rcd4 status of each dog have been issued by The Kennel Union of Southern Africa.

Progress has undoubtedly been made since the commencement of the LOPRA scheme and most breeders have elected to breed only DNA tested CLEAR or INHERITED CLEAR partners to produce Inherited CLEAR progeny. DNA LOPRA testing has been thwarted this year by the South African Postal Strikes as Animal Health Trust mail the saliva testing kits to participants.  Given SA’s “Snail Mail” when the Post Office is running normally it is advisable to courier the dog’s saliva swabs to AHT for testing albeit that this adds to the costs.

Breeders have been even harder hit by the unfavorable foreign exchange rate of Rand with the most recent hikes catapulting the Rand to Pound Sterling exchange rate to R22.50 to one Pound Sterling.  Thus the AHT £40.00 cost of the LOPRA rcd4 test per dog amounts to R900.00.  To this must be added courier fees to ensure safe arrival of samples for analysis at AHT. While expensive for South Africans, owners and breeders one hopes that all remain committed to rid the breed of LOPRA rcd4 during 2016.  It would be tragic to lose ground now when our goal is within our reach.

For further information and details of how to procure the LOPRA test kits, etc., contact Mark or Bridget Simpson

Note The full Irish Setter National Registers of DNA Testing are available and will be e-mailed on request. These indicate the PRA rcd1 – CLAD –  LOPRA rcd4 status of dogs and their progeny under the headings CLEAR – CARRIER – AFFECTED (Tested dogs) and INHERITED CLEAR dogs and progeny..



No DNA test is available to determine the degree, if any, of Hip and Elbow Dysplasia in parentage prior to breeding thus no guarantee can be given by any breeder, in any breed, that progeny will be Hip and Elbow Dysplasia free. The best any breeder can do is join the KUSA/SAVA Control Scheme for diagnosis of Dysplasia whereby parentage of progeny are hip and elbow X-rayed and clinically scored by a panel of expert Veterinary Radiologists.

The commitment by the majority of Irish Setter breeders to enter the KUSA/SAVA Scheme has paid dividends. The overall mean average of Irish Setters Hip X-rayed and scored since the mid 1990’s when the scheme was opened to all breeds gives a mean average of B2:C1/C1:B2 but on review of the results in the last five years the average score has improved to B1:B2/B2:B1 interpreted under the FCI criteria as ‘near normal hip joints’ with almost half the number scoring A1’s or A2’s for each hip ‘No signs of hip dysplasia’.

KUSA Table illustrating interpretation between the “Old” South African HD Scoring System and the “New” SA internationally accepted FCI Scoring System  


Hip Score Comparisons

Over the years Countries and Continents developed various methods and symbols to indicate scoring results which need to be interpreted when imported dogs are being used for breeding or form part of a South African dog’s pedigree ancestry        and although comparisons cannot be completely accurate the following table of the American Orthopedic Foundation of Animals ( to which has been added the “old” KUSA scoring system for Hip Dysplasia is a useful aid:

OFA                            FCI                       KUSA                 BVA                    SV

America                  European &           Old System        UK/Australia       Germany                             

                            Current KUSA 

Excellent                     A-1                        0                     0-4 (no0 > 3/hip)     Normal

Good                           A-2                        0                     5-10 (no > 6/hip)     Normal

Fair                              B-1                        0                    11-18                        Normal

Borderline                   B-2                    0 or 1                 19-25                     Fast Normal

Mild                            C                           1                     26-35                Noch  Zugelassen

Moderate                    D                           2                     36-50                        Mittlere

Severe                         E                        3 or 4                 51-106                      Schwere

The addition of Elbow X-raying for dysplasia and scoring is a relatively new practice and is undertaken at the same time as X-ray of the hips while the dog is under anesthetic.  In total twenty-two Irish Setters have been X-rayed, nineteen in

the last five years  three had 0:1/1:0 scores which indicate ‘Minimal bone change along anoconeal process of ulna – less than 2mm while the balance achieved 0:0 scores ‘no signs of elbow dysplasia’.

Thus the breed is in good shape regarding Hip and Elbow Dysplasia, but only continued vigilance and commitment to X-ray and join the KUSA/SAVA Scheme will maintain this position.

On entering this Scheme there is agreement by owners that the results of scoring will be  notified, by Onderstepoort’s Prof Kirberger, who heads the panel of scrutineers, to the Kennel Union of Southern Africa for capture on their data base and subsequent update of KUSA Health Screening Certificates which are conveyed to the owner.

Further information concerning the scheme can be obtained from one’s home Veterinarian, the KUSA website under Health Schemes or ourselves at for recommendations of Veterinary Radiologists in your area.


At the commencement of 2014 a new dimension to the breeding of healthy Irish Setters in South Africa was introduced thanks to the generosity of Miss Michelle Webster and her Hooley Pedigree data base at to which she has added over 1,000 KUSA registered South African Irish Setter pedigrees. As a result, in addition to other relevant information, each dog’s Coefficient of Inbreeding is expressed as a percentage by the Wright’s Coefficient Programme which is the same system used by the Kennel Club (London) for their Breed Mate Selection site.

This is particularly helpful to SA breeders which, of necessity, work with a relatively small genetic pool compared to those in UK and Europe.  While most breeders understand that a mating between half siblings, or cousins represents inbreeding many do not understand which is the closest relationship.

Simply described “inbreeding” is that which results in progeny where the sire and the dam have common ancestry.  The parameter used to express this common heritage, is called the INBREEDING COEFFICIENT and was first used by Sewell Wright in 1922.   Designated ‘F’ by Wright, but more commonly known as COI by breeders, it ranges from 0 to 100%, the lower the percentage the less inbreeding.  Obviously the greater number of common ancestors in the pedigrees of the parentage the higher the percentage of inbreeding.

To be as accurate as possible in calculating the COI of progeny currently bred the maximum number of ancestral generation are captured and to this end the earliest SA pedigree submitted for inclusion on Hooley’s data base dates back to an exported UK dog born in 1932 and imported into SA.  Many more SA Irish Setter pedigrees of dogs imported or bred in the post world war II period have followed, up to and including those bred and KUSA registered in the course of this year. As a result breeders are now able to gain insight into the degree of inbreeding of prospective parentage by typing the name of a South African dog into Hooley Pedigree search engine.  As SA Irish Setters also have strong links to UK bred dogs it is also possible to access their ancestry and that of many other Setters around the world.

The Kennel Union of Southern Africa have been approached to include the Coefficient of Inbreeding of SA Irish Setters on their data base and on the breed’s Health Screening Certificates, but as usual the wheels of KUSA turn slowly and we await the application of this information on these certificates.

Any owner/breeder can submit Irish Setter Pedigrees of KUSA registered dogs deceased or living with any other relevant information i.e. siblings names, progeny, etc. for inclusion on Michelle’s Hooley’s data base by e-mailing a scanned copy of the KUSA certificate of Registration to  No fee is applicable for this service.




From the above it can be seen, that while South Africans face enormous challenges to effect health screening tests for their dogs, the majority remain committed to ensuring the future wellbeing and protection of the breed in South Africa.

Motivated by this quest a referendum was held during 2013 amongst all Irish Setter KUSA breeders and stud dog owners who were KUSA members to amend and update the existing version of the KUSA Advanced Registration Certificate for Irish Setters.  At the KUSA Federal Council Meeting In December 2013 the New Advanced Registration was approved and became applicable at the beginning of 2014.

This indicates the following:

  • 1. Positively identified by tattoo, microchip or DNA;
  • 2.Over twenty four (24) month of age;
  • 3.A Kennel Union Breed Champion;
  • 4.The registered name of the dog contains an affix (Kennel Name);
  • 5.Hip X-rayed and scored under KUSA/SAVA scheme at or after 12 months of age for dysplasia and scored no worse than C2:C2
  • 6.Elbows X-rayed and scored under KUSA/SAVA scheme for dysplasia at or after 12 months of age and scored no worse than 0:1/1:0;
  • 7.Genetically clear (normal) of Canine Leucocyte Adhesion Deficiency (CLAD) either by DNA testing or by virtue of being the progeny of DNA tested parentage (inherited clear);
  • 8.Genetically clear (normal) of Progressive Retinal Atrophy rcd1 (early onset PRA rcd1) and Late Onset Progressive Atrophy rcd4 (LOPRA rcd4) either by DNA testing or by virtue of being the progeny of DNA tested parentage (inherited clear);
  • 9.The holder of a valid SAVA Clinical Eye Examination Certificate (issued in the year of application for an ARC) stating ‘unaffected’ by any obvious eye disease or other disorder


In closing we wish to thank all owners and breeders for their co-operation during 2015  and the staff of KUSA, particularly Pascale Midgley (General Manager) and Cynthia Ross, who ensure the recording of data on KUSA systems and the issue of Health Screening Certificates so that all Irish Setter Health Screening Schemes run smoothly.

This Report is compiled and written by Mark & Bridget Simpson Irish Setter Health Screening Co-ordinators South Africa.                    

The First Six Months of Puppyhood

Pastel of Irish Red & White, English, Irish and Gordon Setter Puppies

This simple article was written by Neil Campbell and sponsored by West’s Dog Biscuits. It was first published in Women’s Value issue of August 1992 but the basic timeline it gives to prospective new owners regarding normal puppy development is just as valid today.

‘The first six months of a puppy’s life fall into four distinctive phases, starting with total dependence on the mother and progressing to his own useful measure of independence.

After an average gestation period of 63 days, the pups are born with undeveloped eyes and ears, no teeth protruding and limbs unable to support the body.  Growth follows rapidly, however, with the puppies doubling their birth weight in seven day.  A puppy weighing 360g at birth will in a medium to large breed tally some 4.5kg by eight weeks.

One to four weeks:  The eyes start to open when the puppy is 10-14days old, and the ears have developed and hearing is present by about 21-25 days, when the pups may bark for the first time but after a few days in the litter, this may cease and some do not bark until almost into adulthood. Weaning occurs from two-and-a-half weeks old, when baby teeth are through and can cope with solids.  Most puppies walk by three-and-a-half weeks.

Four to eight weeks:  Most puppies should be running by five weeks.  In medium to large breeds, eight-week-old puppies are ready to go to new homes  Within seven days of changing ownership the puppy should be responding to its name and should know where its bed is and retire their voluntarily when tired.

At eight weeks the healthy puppy should be able to eat from a dish, walk and run, balance on its hind quarters to defecate and be playful and willing to respond to gentle and friendly overtures from people.  It will also require lots of sleep, having periods of furious activity for up to an hour-and-a-half, followed by several hours sleep.  Do not rouse the puppy, for sleep builds steady nerves and a good temperament.  At this stage the pup should be on four or five small meals a day.  The pet’s training and education should begin now, so time should be set aside for this.

Four months:  By this age, certain skills such as running, jumping, scenting, digging and carrying should be fairly well developed.  However, teething problems begin as baby teeth are shed and the adult set of 42 teeth break through the gums.  This causes the puppy variable pain which maybe expressed by compulsive chewing.

Six months: By this age the normal puppy should be completely house-trained and eating two to three meals per day.  It should also be capable of walking on a lead and staying alone for short periods during the day. Large breeds will not be fully grown until two years or even more.

In adolescence, large breed males may challenge their owner’s dominance.  Be alert to this challenge and handle it quickly and firmly by making the dog strongly aware of its place in the family pecking order.