: The Life of a Yorkshire Vet

by Norton, Julian

  Bobby was suffering from repeated bouts of non-specific illness. He would develop a high temperature, lose his appetite and become listless, but other signs were vague, and on each occasion he appeared to respond to symptomatic treatment. When I first met him he had ulcers in his mouth and was drooling. This sounds just like the disease with which I had been preoccupied for most of the previous year, but Bobby was not a calf nor a sheep so I could exclude foot-and-mouth disease – dogs were not cloven-hooved, I had learnt that ages ago. It is, though, very unusual to see mouth ulcers in a dog, especially a young pup. I arranged to admit him for an anaesthetic so that I could examine his mouth and take biopsies. The results came back quickly but the histology report from the pathologist was almost as vague as Bobby’s clinical signs. There were various diseases that could cause ulcerative stomatitis in dogs but they were rare. I took some more samples – this time blood tests – and started cautious treatment. All seemed to go well, so I was disappointed when he became ill again, a couple of weeks later. Another round of blood tests showed a high white cell count. This was an obvious sign of inflammation and probably infection. Despite a battery of x-rays and ultrasound scans, try as I might, I still couldn’t identify the cause.

  Then the story became even more mysterious. It transpired that Bobby’s brother had been treated at another veterinary practice for similar signs. He had been referred to a specialist for investigation of the mystery illness. The specialist, as it turned out, wasn’t quite so special, and had failed to get to the bottom of the illness. Bobby’s brother had deteriorated and been put to sleep.

  The next step, I decided, was to take a bone marrow sample. The bone marrow is the part of the body that makes blood cells – both the red cells that carry oxygen around the body, and the white cells that fight infection, by attacking bacteria and viruses. I was suspicious there was a problem with Bobby’s bone marrow, as he seemed prone to infections, so I needed to investigate this possibility. The samples were taken and sent off to the laboratory. The results, when they came back, appeared to be unequivocal – Bobby’s bone marrow was alive and well. It was bursting with loads of immature white blood cells, all ready to be sent out to work, to fight infection. The laboratory diagnosis was ‘immune mediated neutropaenia’. This meant Bobby’s own immune system was actually destroying its own white blood cells, once they had been sent out into the bloodstream, thereby rendering him unable to fight infection. The pathologist seemed confident in this diagnosis, but to me, it didn’t make sense. Immune mediated neutropaenia should result in persistently low levels of white cells in the circulation and should respond to treatment with steroids. Neither of these things were the case. I phoned the lab. The pathologist, who was an American lady and a world expert on bone marrow, was not in the building, but the receptionist kindly gave me her mobile telephone number, assuring me it was OK to contact her in this manner. She answered the phone straightaway and was more than happy – enthusiastic even – to talk, despite being in the middle of shopping in the supermarket. I was impressed by her commitment. She was very excited about the case because immune mediated neutropaenia was pretty rare. I told her my concerns about her diagnosis, and that I couldn’t see how it could be the case. She, on the other hand, was positive about the state of Bobby’s bone marrow – the young white cells were bursting to get into the circulation. We agreed to do a further test to see if this was an aberrant result.

  After we had done another test, a vague bell started to ring in the back of my mind, about a condition that had briefly been touched upon during our haematology lectures at vet school. I did some research, and it seemed to fit. I thought Bobby might have a very rare genetic disorder called cyclic neutropaenia. It had been documented in a small population of grey and white Border collies. It is often the case that this sort of disorder is carried by a gene linked to an unusual colour. These colours are usually recessive so problems only arise if two individuals carrying the same recessive gene produce offspring. Bobby was black and white rather than grey and white, but all the other signs matched up. The condition was characterized by cyclic variations in the white blood cells in the body, as the cells were released from the bone marrow in waves, rather than continuously. Every three weeks his bone marrow would stop releasing the bacteria-fighting cells into his blood and, in just the same way as happens in a cancer patient whose bone marrow has been zapped by chemotherapy, his blood count would fall. The result would be that his body would be overwhelmed by bacterial infection. This explained his episodic bouts of high temperature. It also explained why, once it fired up again, his bone marrow appeared to be jam-packed with baby white blood cells, waiting to be released.

  With Val’s consent, and after persuading the lab to carry out the blood tests at a very much reduced rate, we set about trying to confirm the disease, by measuring Bobby’s blood count every two or three days, and plotting the results on a graph.

  Both Val and Bobby were completely compliant in this exhaustive episode. Bobby simply stood there, or even lay, relaxed, on the floor when I approached him with yet another needle. Amazingly, his tail always wagged and he was always a happy dog, one of those dogs who seemed to wear a smile on his face. He never resented me for being the harbinger of discomfort and, like many dogs I have treated, I am sure he actually realized we were helping him. At times when he was hospitalized with another of his high temperatures, I would sit with him, stroking his head, which undoubtedly ached, but his eyes were full of appreciation. He never once refused to come to the practice and Val described how his tail would always wag and his eyes light up when she said, ‘Come on, let’s go and see Julian.’

  After a couple of months, the graphs we had made demonstrated a clear pattern. Every three weeks, Bobby’s neutrophils would plummet to dangerously low levels. Interestingly, I noticed all his other blood cells – red cells, other types of white cell and platelets – also fluctuated, although this did not seem to have the same clinical significance.

  So what now, we thought? Bobby was already a year old and had enjoyed a happy life, apart from the few days every month when he felt rubbish. He had outlived his sibling by many months, all of which had been filled with fun. He was on antibiotics and other medications to help his temperature at the times when we expected his white cells to fall, but this was only just keeping things at bay.

  I discussed Bobby with the experts, in particular Mike Herrtage at Cambridge Vet School, who was the head of the medicine department when I was a student. He is now a professor and head of the vet school. He was an amazing teacher, and all the students held him in awe. At the same time he was completely approachable, and even well into our veterinary careers he was, and still is, happy to offer advice and guidance if requested. We came up with a plan to try using the recombinant drugs used in human chemotherapy patients, to boost blood counts after toxic doses of anticancer therapy.

  I persuaded a hospital to give me some of their part-used vials of a drug used to treat human cancer patients. These opened vials would otherwise have been thrown out. With great caution, I administered these to Bobby, at the times when we predicted his white cells would be low. It worked. The next set of blood tests showed his white cells going through the roof, and we could keep him safe and healthy. Unfortunately, as predicted by Mr Herrtage, these beneficial effects were relatively short-lived and Bobby’s condition was not as controlled as we all would have liked.

  Whenever he was ill, it was me who treated him. If it was on a weekend my colleagues would phone me, and I would go in to sort out his drip and his anti-inflammatories, and rejig his antibiotic doses to make him feel most comfortable. Sometimes I called to see him at Val’s house, in the nearby town of Ripon. It was nice to see him happy in his home environment. There was a track around the garden, where the grass had been worn away by him running, endlessly, with his ball. On my first home visit, Bobby excitedly showed me his ball and his usual route around the garden.

  Sadly and inevitably, the episodes of
illness got more and more serious, and he didn’t respond as well at each occasion. We tried another novel treatment that did ameliorate the fluctuations in his cells to some extent, but during one particularly severe bout, it became evident that the decision to put him to sleep needed to be made. I phoned Val to tell her. She already knew, I think. There is always a certain point at which it is so obviously the right time to do this. It is the point when the eyes suddenly lose their sparkle, and it is always clear to any owner who really knows their dog. People often ask how they will know when it is the right time to put their beloved pet to sleep. It always sounds a bit like folklore when we say ‘you will just know’ but it’s true. When the time is right, there is no doubt.

  This was the case with Bobby that particular Monday. Putting an animal to sleep is always a horrible job for us, although we normally know that it is for the best, and we are in the privileged position of being able to prevent the drawn out and terrible suffering that often comes with terminal disease. Although we do this on a regular basis, euthanasia is never a procedure that we get used to, but we have to remain professional, and it is usually this that gets us through, and on to the next thing. However, when it happens to a patient that we have been treating intensively for a long time, when we have invested a lot of emotion, and particularly when we have become great friends, it is a wrenching process. On this occasion it was absolutely awful, and I was terribly upset.

  What I didn’t know was that Bobby had a successor, also a Border collie and also called ‘Bobby’. It turned out that it was a tradition in the family to give all their dogs the same name. Three months later I saw a Border collie called ‘Bobby’ with the same surname on my waiting room list, and my heart nearly stopped! But this was the new Bobby – the next in a long line. The small black and white and very cute Border collie was just as pleased to see me as his predecessor but, mercifully, was blessed with better health.

  There are few cases that are as emotionally charged as Bobby and, in fact, mostly our cases are happy stories, which are uplifting and pleasant to deal with. It is just as well, because we would find it very difficult to come to work each day if that wasn’t the case. It is not good to dwell on the negatives, and we are lucky that the pace of our practice is such that it is never very long before a bitch caesarean arrives and we have our hands full of squeaking newborn puppies, or a pair of kittens turn up for their vaccinations, and our faith in the vigour of life is restored.

  One of these amusing and uplifting cases involved the dog belonging to Sylvia, one of our receptionists, although I do not think Sylvia found it very funny at the time. Harvey, a robust Border terrier, had been involved in a skirmish with another dog. The offending dog had ventured into Harvey’s garden. Being the owner of a Border terrier myself, I knew this was a risky thing to do. Border terriers are very protective of their own patch. Having managed to break up the fight, Sylvia scooped up Harvey and rushed him in to be checked over for battle wounds. The biggest injury appeared to be to his pride, but he did have a number of small lacerations on his throat, which were attended to and patched up by a colleague. This was on a Thursday afternoon, and no one expected anything but a speedy return to normal. However, I saw Harvey as an emergency the very next day. The sight was extraordinary. Harvey’s entire body was inflated just like a blow-up toy. Even his head and face were distorted by the air under his skin. This gave him the appearance of wearing a ridiculous grin, because the corners of his mouth were pulled so tight.

  Unbeknown to anyone at the time, his trachea, the pipe taking air from his mouth to his lungs, had been damaged in the dogfight, and air was leaking out of it into the loose connective tissue under his skin. I took an x-ray of Harvey to check that there was no leakage of air to other places, as this could have been more serious. While he was asleep for the x-rays, I made various holes in his skin, and air came whistling out, as if he was a leaking inner tube. I also wrapped bandages around his legs, as the air was beginning to seep down there too. If it went all the way to his feet, not only would he look even more ridiculous, he wouldn’t be able to walk.

  The x-rays confirmed his upper airways were not too badly damaged. I felt confident that the leaks would soon heal over, and that there would be no serious long-term effects. Harvey certainly did not seem in any discomfort. I tried to reassure Sylvia, but she did not seem completely convinced. Her dog looked like Violet Beauregarde, the girl who was inflated in Willy Wonka’s Chocolate Factory. I jokingly suggested that she brought Harvey for his next checkup on a string, along with a bunch of balloons, rather than on a lead!

  Happily, Harvey did deflate after several days without any further treatment, but his visits during his inflated days were always hilarious, and a perfect antidote to the sad moments of our working day.

  17

  World Records and Team GB

  I have always thrived on pushing myself hard physically, whether during cross country running at school, or rowing, rock climbing and mountaineering at university, or later on my mountain bike. I throw all my energy and enthusiasm into my sports and, for better or worse, I have an overriding competitive determination. I was never content with a ‘gentle paddle’ while rowing with the college eight, or a ‘steady’ bike ride with my mates. I always have to be going hard and fast. Up until my early thirties, my greatest success had been when I was seventeen, competing for West Yorkshire, in the English Schools Cross Country Championships. I got my place in the team by a stroke of luck. I was the first reserve, and therefore I didn’t expect to get the chance to race. However, the day before the team left for Cornwall, one of the other runners twisted his ankle whilst running round the dark streets of Leeds. I got a phone call at half past nine on the Thursday evening: ‘Could you run? We leave in the morning at 5.30 a.m.’ I jumped at the chance, and had a fantastic race. I finished nowhere near the front, but just to get there was achievement enough. I trained hard in those days, as I still do, and on that trip to the English Schools, I shared a room with a guy called Mark Sesay. He was an awesome athlete – a junior international – and I quizzed him about his training regimes. As the conversation progressed, I was surprised to find that I actually did a much greater volume of training than he did!

  Competition was in my blood. My father had been a national-standard runner, had an Oxford Blue and had competed at the Bislett Games in Oslo in 1963. It was the same stadium where Steve Cram broke the world record for the mile in 1985. My maternal grandfather had been a competitive track cyclist. I was still some way behind their level of sporting success.

  But then I was reinvigorated by my change in diet. Looking back I had probably been afflicted by the insidious effects of coeliac disease for many years, which had surely restricted my athletic capabilities. I’m sure that I am not alone in this respect. I am convinced that gluten intolerance is much more common than is generally known. I feel very fortunate that my condition was identified when it was, because otherwise this chapter in both my life and in this book wouldn’t exist!

  By my mid thirties, I was finally beginning to feel as fit as I ever had. One sunny Saturday, at a wedding reception, I was chatting with a friend, Roger Brown. Anne and I had met Roger and his wife Beccy at antenatal classes, when we were expecting Jack and they were expecting their daughter Lily. Roger is very tall and quietly spoken, but has a fierce competitive streak. He rowed for GB in the Atlanta and the Barcelona Olympics, and has a Commonwealth gold medal. He has competed alongside Redgrave, Pinsent, Cracknell and the Searle brothers and his house is full of pictures of international sporting success. Roger and I were discussing the merits of the Concept 2 rowing machine, used by gym goers and Olympians alike. Roger, obviously, had his own in his garage, and after our conversation it occurred to me that maybe I should get one too. I could exercise to my heart’s content on my own rowing machine and, more importantly, I could do it while I was on call. Being on call was, and still is, the enemy of all proper training regimes. If I could row in my own garage, within s
ight and sound of my pager and mobile phone, I could do as much training as I liked. Going for a bike ride or going for a run was impossible while on duty, and since my on-call duties were every second weekend and two nights a week, it was proving hard to keep my fitness at the level I really wanted. So, soon after that wedding conversation, I acquired my first Concept 2 rowing machine, and I remain convinced that it is the best thing I have ever bought. I could train for an hour a day, even if I was on duty. Sitting for an hour on a rowing machine was the perfect antidote to a stressful day at work. The repetitive rhythm was extremely therapeutic and, as a consequence of this therapy, I became very fit and decided I would compete at the 2008 British Indoor Rowing Championships. I finished in the top ten. I was pleased with my result, but it was so very tough I felt very lucky not to have died. The race was over 2,000 metres, and it was very, very hard. I am not really big or strong enough for the explosive effort needed for sprints. Endurance has always been my forte, and I had another plan.

  I had been looking at the records for various long-distance indoor rowing challenges. I did some sums, and reckoned the British record for 100 kilometres was within my reach. The rowing had to be done in a public place, so it could be verified. The gym in Thirsk had just had a major refurbishment, so they agreed to host my attempt as part of their launch. I set about training, and with a huge degree of determination, I managed to break the record, one Saturday in the summer of 2009. It took just over seven hours, and I knocked twenty-nine minutes off the previous record. I had a collection bucket and a sign, to say what I was doing, and to try and raise some money, through my efforts, for the boys’ primary school. All the gym-goers gave me fantastic support, and quite a few people popped back several times during the day to see how I was getting on. There was some degree of incredulity at the task I had set myself. One guy commented, ‘I didn’t think things like this happened in Thirsk.’ It was true, but I didn’t see why they shouldn’t. I was just a normal guy, not an uber-athlete, and I think these things are perfectly possible with dedication, preparation and enthusiasm. I was on duty the following day, and got called to do a caesarean on a cow. I was expecting to be in all sorts of trouble with aches and pains, but found that the only part of me that was giving any discomfort was a blister on my big toe. It had been easier than I expected.