The Bearded Collie Club of Canada
Home The BCCC About Beardies History Events Education Contact Us
BCCC Member Login     
Judges' Education Program
Caring for Your Beardie
• Autoimmune Disease
• Vaccination
• Vaccination Protocol Revised
• Feng Shiu for Beardies
• Pre-Breeding Testing
• Diagnosis
• When the Dog Bites...
• The Eyes Have It
• Stem Cell Therapy


by Linda Aronson DVM

In a perfect world a vet or even an owner could look at an animal and come up with an accurate diagnosis of whatever is troubling him – maybe there would be one of those magical instruments that Dr McCoy pointed at his patients in Star Trek that gave him an instant diagnosis – even if the problem was new to then medical science. In the real world many diseases present alike and yet their medical management may be impaired if the wrong label is put on the underlying disease. We often hear, "If only he could talk and tell me what’s bothering him, I could help him." Even if he could it’s doubtful our diagnostic ability would be significantly increased. Most human doctors have this benefit, and yet, as often as not are groping in the dark along with their veterinary counterparts. Referred pain makes even saying where it hurts a questionable exercise.

These thoughts have come home to me rather a lot of late. Those who know me may have been bored this past year with the saga of my daughter, Sarah’s, lame horse. OK, so Caliban isn’t a Beardie, although the girls like to ride on his back, but his case illustrates many of the points I wish to make. Having started the last season’s show circuit in style, the best dressage score in the show, a clear jumping round and offers from the dressage judge and several others to buy him, we looked like having another good year. Then one day Sarah said he didn’t feel right, the same the next day, and the next day he looked like a non-believer trying to cross the molten coals on tender feet. Everything seemed to hurt. Cal being the biggest wimp about needles makes everyone wish to be as conservative as possible about spending my money in finding the cause of his problem. There is no heat in his feet, no pulses, no sensitivity to hoof testers etc. Well, there are people who don’t believe Lyme Disease exists in horses, but if you do he sure looked like a good candidate. We’d also been pulling dog and deer ticks off his anatomy in decent numbers. So we drew blood and did Western Blot and ELISA tests for Lyme. They came back borderline and equivocal, but it seemed a good place to start, so we treated him for over three months with doxycycline for Lyme. Sarah rode him lightly during that time, and while his improvement wasn’t dramatic and wasn’t even smoothly progressive at the end of that time he was serviceably sound again and he started back into work. He did quite well for several weeks, and resumed jumping. Then he was lame again. During the treatment for Lyme the lameness seemed to settle in the front legs, sometimes shifting from one to the other. We saw his toes point in on whichever leg was most painful; sometimes it was both. Now he was consistently lame in his left fore. A vet friend and I put our heads together, did flexion tests and decided (nothing seemed to particularly help or increase the lameness) he probably had torn a suspensory ligament in the back of the leg. OK so normally we’d have used local anesthesia to progressively numb the leg from the hoof on up until we knew where he was lame, we figured we might block one joint and then it’d be open season, so we thought the treatment for suspensory ligament injuries won’t hurt him – 4 weeks to 4 months rest. We did let him go out and be a horse in the pasture during his approximately 6 week lay up. He appeared sound throughout the period, and came back seemingly raring to go. A few weeks later he was well enough, we thought, to participate in a clinic. The instructor was not a good choice. She thought she knew everything and wouldn’t listen to Sarah when she explained how she warmed Cal up to spare his leg. Result a horse that could barely hobble for the next three weeks with someone on his back or not. Time to get serious, we loaded him on the trailer and went to a new diagnostic centre in Acton Massachusetts. Here we examined his whole body with digital infrared thermal imaging (DITI). Popular in Europe this technique is just reaching the US. It will be as applicable in dogs, I believe, as in horses. DITI enables you to scan the whole body and see relative areas of heat – which appear redder - and cold – which appears bluer. The whole horse can be imaged in about 15 minutes. The most notable things about Cal’s DITI was that he had intense heat in his right neck, lesser heat on the left, centred in the region of his 6th cervical vertebra. His front feet looked hot, I thought the left more than the right, but when Mary Kahan, the vet operating the equipment, reviewed the images later she felt this was less significant. His legs above the hooves though were deep blue and therefore stone cold. We continued with our exam. Cal was feeling brave, and so was Mary, so we blocked his foot, and most of his lameness disappeared. We X-rayed his foot. There were profound changes in a little bone at the back of his foot called the navicular sesamoid bone. Navicular disease is a popular diagnosis for lameness in the horse, and one would have said Cal’s changes were classic, except that nothing that looked like navicular disease showed on his DITI. Also other bones in his foot and lower leg seemed to be losing density. We ultra sounded his legs and his suspensory ligaments looked fine – normal wear and tear only. Finally we drew blood for further Lyme tests. Mary pointed out that Cornell, despite the fact that at least 50% of vets don’t believe horses get Lyme disease, use three times the dose of doxycycline to treat the disease that we had used on Cal (results of these tests are still pending.) So what did we conclude? Since she first saw Cal, Mary has suspected he has Wobbler’s syndrome, a narrowing of the spinal column so that there is pressure on the nerves. In Cal this expressed itself as appearing to lose conscious awareness of where his feet were, or even it seemed sometimes that he had feet at all. Most of the time he was fine. The heat in his neck seems to confirm this suspicion. The alternative explanation is that he was abused or injured his neck at some time. We believe that the narrowing of the space is also affecting the conduction of the sympathetic nervous branch of the autonomic nervous system to Cal’s front legs, especially the left one. The autonomic nervous system controls functions in our bodies we don’t have under conscious control - in this case, the flow of blood to the fore legs. Diminution of the blood flow has resulted in loss of bone mass and secondary navicular disease. We were able to show that when we exercised Cal in hand the blood flow to his leg increased. Instead of rest, exercise would help him get better. Of course exercise is only part of his treatment, he is also fitted with special shoes to relieve the pressure on the navicular bone, magnetic boots while he’s inside to increase the flow of blood to the feet, and a non-steroidal anti-inflammatory drug, which not only provides pain relief but also increases blood flow. If he agrees to co-operate he’ll also be acupunctured. This diagnosis is an uncommon one to be sure, but it does underlie the importance of finding out what is causing a problem rather than treating it empirically. OK so I always want to know the outcome of cases. So far, 8 days after the testing, Sarah is riding Cal again. He’s not completely sound, but he is enjoying himself, and we hope he will be restored eventually at least to where he was before this very bad year. I also don’t discount that all this really started out with Lyme disease, and the reduced work load then made the Wobbler’s more apparent. In veterinary school we are always told to look for one disease or problem to cover all the signs rather than multiple laundry lists of causes. Another point to be made is that last spring Cal’s signs were definitely very different than they are this winter. Often owners ask why their vet missed a diagnosis. One very good reason is because the animal they saw then isn’t the animal I am seeing now. Another, when it comes to my behaviour patients, is because I have taken the time to get extra training in my little niche of veterinary medicine, and by seeing things more often I may be more likely to pick something up than the general practitioner who gets a very different case load. In Cal’s case, Mary and her husband Joe have only had the DITI a month, and to diagnose Cal previously it would have cost at least 10 times the cost of a DITI to get a soft tissue and bone scan, not to mention filling the horse with radioactive chemicals. Veterinary medicine is advancing by leaps and bounds, where the use of CAT scans and MRIs in animals was most unusual as little as 5 years ago, now it is becoming far more common. Maybe we aren’t too far from Dr. McCoy’s little hand held diagnostic tool.

Diagnosis can also be a problem with canine Lyme disease, and for Beardies it may be especially problematical. Recently the veterinary literature has contained a number of reports of mistaking Lyme disease for systemic lupus erythematosus (SLE) and other autoimmune diseases and vice versa. Diagnosis of SLE in Beardies seems to have increased dramatically in recent years. SLE has been described as the great imitator, but the same name could also be given to Lyme and other tick borne diseases. SLE is an autoimmune disease in which antibody-antigen complexes circulate in the blood and become lodged in various tissues of the body; these can include the kidneys - where they lodge in the glomeruli where the process of waste filtration begins; the joints - leading to signs of polyarthritis; the skin, subcutaneous fat and mucous membranes - where they can cause ulcerative lesions (these will be felt as nodules under the skin when the complexes invade subcutaneous fat – a condition called panniculitis); or the brain - where abnormal behaviour or neurological signs may result. A diagnosis of SLE relies upon two major signs plus a positive titer on the antinuclear antibody (ANA) blood test. While many consider the ANA test specific for SLE it can also be positive with a number of infectious, inflammatory and neoplastic diseases as well as a less common type of pemphigus (P. erythematosus). Clearly too, the major signs associated with SLE are not unique, glomerulonephritis can occur also in various infectious diseases such as hepatitis, endocarditis, brucellosis, heartworm, rickettsial diseases like ehrlichiosis or Rocky Mountain Spotted Fever, Lyme disease, pyometra, leishmaniasis, trypanosomiasis, chronic bacterial infections and septicemia; inflammatory diseases such as pancreatitis, polyarthritis and prostatitis; endocrine diseases like diabetes mellitus or Cushing’s disease or long term administration of corticosteroids; as well as neoplastic, familial, and idiopathic (unknown cause) cases. Joint pain can be seen in many or single joints and be indistinguishable from osteoarthritis. Certainly rickettsial diseases like ehrlichiosis and Rocky Mountain Spotted Fever as well as Lyme disease are associated with similarly painful joints. Dermatological conditions are not always identifiable by cause, even with skin biopsy. Usually SLE is left after everything else has been ruled out. Panniculitis can be caused by a great many things, including trauma – including injection sites; bacterial or fungal infection; degeneration; pancreatitis or pancreatic carcinoma as well as SLE. If a needle aspirate contains primarily lymphoplasma-histiocytic inflammatory cells it is suggestive of SLE, but positive ANA and direct immunofluorescence tests would be needed to confirm diagnosis. Brain lupus occurs in about 40% of human patients. To date, I believe, the only case of canine brain lupus reported in veterinary literature is my report on the case of my Beardie, Tell. If a dog has SLE, treatment must be directed towards suppressing the immune system and initial therapy at least usually includes high doses of corticosteroids, like prednisone or dexamethasone.

Cases of SLE can be further complicated because they are frequently accompanied by other autoimmune diseases, like autoimmune thyroiditis or immune mediated thrombocytopenia (ITP) and occasionally immune mediated hemolytic anemia (IMHA – also known as autoimmune hemolytic anemia AIHA). Thrombocytopenia is a condition in which the number of platelets circulating in the bloodstream has been reduced. Platelets are those little anuclear cells in the blood that stick together to plug up tears in blood vessel walls. While we are not aware of this, our internal blood vessels are constantly springing small leaks, which the platelets block off before we lose much blood. In ITP antibodies are formed against the antigens on the platelets so that they are prematurely removed from circulation, thereby reducing their numbers. The designation ITP is also used to denote idiopathic thrombocytopenia, which means a reduction in platelet numbers (thrombocytopenia) of unknown cause. While that cause may be autoimmune it is not always the case. Thrombocytopenia can have many causes, and it is frequently seen in cases of Lyme disease as well as other tick borne diseases such as the rickettsial diseases ehrlichiosis and Rocky Mountain Spotted Fever.

Are we beginning to see a pattern here? A recent case report in a veterinary journal told about a dog that had fallen down stairs. This dog was found to have joint pain, a fever and was lethargic. The dog had evidence of an infectious disease, and a moderate/high titer for Lyme disease. He was negative for Ehrlichia canis and Rocky Mountain Spotted Fever. The dog also had thrombocytopenia and a positive ANA. Two positive signs for SLE with associated ITP, if he had also had glomerulonephritis would the reporting vet have assumed that to be the correct diagnosis? As it was he ran further tests for other members of the Ehrlichia family. The dog was negative for E. risticii and E. platys but had a very high titer for E. equi. A bone marrow biopsy showed secondary damage. E. equi is transmitted by deer ticks, as is Lyme disease, E. canis by dog ticks. E. equi is often transmitted with Lyme disease yet is rarely tested for routinely. I have heard of many dogs, including Beardies, diagnosed with Lyme disease that are also said to have ITP, although as in this case the thrombocytopenia is likely to be secondary to the Lyme disease. The reporting vet felt the Lyme disease was less important in this dog than the ehrlichia. The excessive damage to the marrow suggested a severe chronic form of the disease. The dog in the case report, survived, but it took a very long time for the organism to clear his body, and treatment was maintained for far long than most vets treat either Lyme disease or Ehrlichia. If he had only had E. equi, and had shown signs of kidney disease it is highly likely that this diagnosis would have been missed. Perhaps a diagnosis of SLE and ITP would have been made, even with the Lyme disease a seriously considered rule out. Without antibiotic treatment the true cause of his problems, which were considered minor throughout treatment, would have been missed until he developed the ocular lesions, seizures and coma seen as this disease progresses.

Getting an accurate diagnosis is rather like sleuthing out a criminal case. Dead ends and red herrings abound. Often negative findings are as significant as positive ones. Money is clearly a factor. While most people’s immediate reaction is to "make him better no matter what it costs," the cost can mount up alarmingly quickly. Quality of life must also be considered along side life itself. Sometimes time is against those trying to diagnose the problem. Disease progresses too rapidly for a cure – in the next column I’ll look at two of the most common causes of dog poisoning, and we will see that unfortunately by the time owners realize their dog has a problem, it may be too late to save him. Other factors can enter into the picture. Sadly, in my field of behaviour, tincture of time is often needed while the dog’s behaviour is modified. Even where drugs are appropriate they may take several weeks to reach therapeutic levels. If the problem is an aggressive dog the owners may not be able to grant the dog the time to find the right diagnosis. Other problems can be almost as destructive and frustrating while a diagnosis is reached, and therapy instituted. I think most vets enjoy the challenge of an unusual or complex diagnosis; sadly we don’t always like the outcome.

Good health to you and your Beardies.

Copyright © 2000 [ Linda Aronson DVM].
All rights reserved 


© Bearded Collie Club of Canada 1997 - 2010
All rights reserved

Last revised: November 11, 2010