SYSTEMIC DISEASE AND LOSS OF PERFORMANCE IN THE RACEHORSE ...

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  • 1. Systemic Disease and Loss of Performance in the Racehorse SYSTEMIC DISEASE AND LOSS OF PERFORMANCE IN THE RACEHORSE - and its potentially devastating effects on trainers! The symptoms and descriptions attributed to “Lyme Disease” below may well be associated with various different systemic diseases, any one of which can adversely affect the racehorse and contribute to serious loss of performance. Lyme has been chosen as the label of choice because, once the veterinary profession did eventually accept that there might be something wrong with our horses, a high percentage of them registered off- the-scale positives for that particular infection. Unfortunately once what was then supposed to be the definitive treatment failed to deliver any great improvement, there was a tendency to adopt the view that false positives were well documented and that “they” had been right all along - the problem had been born of my overactive imagination. The appended statistics [p. 25] presumably demonstrate that, particularly by 1990, I had sufficient appreciation of what racehorses should and should not do that my suspicions should have been taken more seriously. Information, case histories and other notes have been added piecemeal over an extended period, so this discussion needs to be better organised into a proper format in order to be of value as the basis for scientific investigation, however there is a lot of information here for anyone who is interested in knotty problems and who really understands training racehorses. That is a very, very small target group. Bill O’Gorman Page 1/26
  • 2. The three stud farms and the training stable involved in this "study" consistently produced horses demonstrating various abnormal behavioural and lameness patterns. Eventually tests on many of these horses returned high positives for Lyme Disease, therefore it seemed reasonable to investigate to what degree this particular infection might account for their symptoms. I have added various notes and updates as and when things which appear to me to be relevant have come to my attention – including, lately, the stud names now that Cedar Tree and Woodditton have both closed down and Deerfield, having bred a Derby winner, will not feel the discrimination so badly! All three stud farms consistently produced very disappointing horses, which displayed similar and often bizarre characteristics, over some considerable time. There have been a few very good ones – which, Superlative being a case in point, might have been really good had they been normal. The fact that this is a relatively obscure syndrome in horses does mean that animals from many other studs and stables might be similarly infected, without the infection being recognised simply because the effects are so varied. However it does seem likely that these particular studs, and possibly many others in similar circumstances, have achieving their true potential until more research is done and some positive action is taken. Systemic disease provides a more logical explanation for the irreversible decline which some very good trainers have suffered in recent years than does the commonly quoted catch-all excuse of being stricken by “the virus”. 2005 update. Motivator - very good, but very lightly raced and, apparently, delicate to train – to be fair he was by Montjeu which in itself might present some problems. High Accolade obviously very useful on his day but had very much two ways of going. Both came from Deerfield Farm. Of the Cedar Tree horses, In Excess was a very good horse but a bundle of nerves. Provideo was an extremely awkward horse to deal with, but was actually a very tough racehorse. Konbola was not quite as good as In Excess, but was even more delicate. Raami was both high class and an easy horse to train, but he was the exception. Several siblings proved very disappointing, often after showing a lot of early promise. It has been demonstrated that Borrelia Burdgorferi infection is spread through the urine splashing of both cattle and infected rodents [1]. Burdgorferi has been isolated in newborn and aborted calves [2], and in the brain of a three day old foal [3]. If similarly compromised horses appear
  • 3. Systemic Disease and Loss of Performance in the Racehorse regularly from one source then it is reasonable to suppose that those premises may be an ongoing reservoir of infection. Moving stable has often failed to revive the fortunes of trainers, which could indicate that any infection in the transplanted horses soon colonises the new address. Because biting flies and mosquitos have also been identified as vectors, [4] there is probably no absolute requirement for tick bites in order to spread Lyme disease, as is often reported. *2004 update to above [5] The Center for Equine Health, U.Ca. Davis, released updates on studies which “Determined that adult insects, which are ingested by horses orally as they graze pastures, can transmit Potomac Fever....the caddisflies used in the experiment contained flukes that were infected with Ehrlicca risticii” Obviously, the worst possible scenario is where the traffic between the suspect studs and a training yard is constantly completing a circle. If any horses purchased at auction [which may, or may not, come from a clean source] also spend time in the suspect environment before entering training then the chances of escaping a devastating whirlpool effect are poor. The training intake is likely to have its chance of being compromised increased to virtual certainty. If the stud is retaining fillies as broodmares whose own racing careers showed every sign of infection the overall prognosis will be grim indeed. The cycle needs to be broken both by culling obviously undesirable broodmare prospects and by aggressive antibiotic therapy. The possibility of human infection should also be considered, particularly in the present climate of workplace safety. Dairy farmers have been demonstrated to be at increased risk of infection [6]. Farmers as a whole commit suicide far more often than the national average! Many American yearling purchases, which had not visited W., C.T., or D.F. studs also seemed badly affected there would appear to be some question as to [a] whether the disease is very common also in America, [b] whether it is easily spread even in a training stable where there is little direct physical contact, or [c] whether there may be little practical difference between this infection and others, probably including E.P.M. The fact that the American breds tended to show symptoms a little later in the season than did the locals might tend to support [b]. With hindsight Tom's Verdict [USA]* [* indicates an individual in training before we were able, in 1995, to put the label of Lyme infection to the problems which had plagued us for some years.] behaved like a typical Bill O’Gorman Page 3/26
  • 4. Lyme infectee, however this horse was actually destroyed in 1991 as an E.P.M. wobbler. Later Society Times[USA] tested negative for Lyme, although he showed definitive symptoms both temperament wise and in loss of ability. It seems that testing for Lyme notoriously produces false results, and unfortunately he was never tested for E.P.M. The comforting belief that the horse is the end host in these infections may be preventing studs from taking it seriously. This is probably not the case. Research indicates that herdmates are at risk from direct contact with infected cattle, however evidence of infected siblings might just as easily indicate the infection having crossed the placenta or indirect infection by a vector which had itself been contaminated directly or indirectly by previous stock. Roc de Feu and Arctic Zipper[USA] showed a high Lyme positive which dropped to a negative following treatment, however they continued to display symptoms of erratic behaviour; both these horses had brothers which followed closely in their footsteps as far as behaviour was concerned. Treatment did not seem to guarantee a reformed attitude and changes to the nervous system might not reverse even if the infection is destroyed. [2004 n.b. This was treatment as per the conventional wisdom at the time - 10 days oxytetracycline. Very long term broad spectrum treatment has seemed much more effective in later instances- and less risky. Arctic Zipper should have been pretty good based on his early works]. Possibly those animals which did show dramatic behavioural improvement following short term treatment were actually misbehaving due to feeling unwell in a lesser manifestation of the disease, as opposed to displaying irrational tendencies due to their central nervous system having been compromised. Apparently in some cases of plant poisoning, such as “loco weed”, horses may make a reasonably complete recovery but may continue to display erratic behaviour, particularly demonstrating “spooky” tendencies. M.E. in humans can often be traced back to a viral or bacterial infection, and it appears that the immune system remains stuck in a state of red alert because the genes which were switched on in the immune system in order to fight the original infection are not switched off. [38] [2003 update to above [7] Dr. Linda Mansfield, head of Emerging Parasitic Diseases Lab. at Michigan State U. reported on a 4 month old cross bred colt which was euthanized due to severe neurological problems from E.P.M. Mansfield found mature parasites in the brain and spinal cord and mature sarocysts [ contained in muscle cysts] in the tongue. Mansfield said that this finding is "suggestive that horses have the potential to act as intermediate hosts". This might lead to a re-evaluation of the comforting position of the
  • 5. Systemic Disease and Loss of Performance in the Racehorse horse being a "dead end" and might lead to revue of E.P.M. being perceived to be a purely American problem. Previous to my seeing this article Dick O'Gorman had already said that he had seen in his 2003 sales inspections several horses from one particular stud over here which he suspected of E.P.M. type lack of co-ordination and a racetrack vet at Santa Anita had suspected E.P.M. in Needwood Blade which had only been there a matter of weeks and was fine on arrival - however the vet. did not appear to have registered that he was making history by diagnosing it in an English animal, so unless he thought that E.P.M.can become a problem within weeks of first exposure, it may well have been flannel! - further update Needwood Blade ran well in his first U.S. start about 5 weeks later, later won Grade Three and now back here as a sire] [2004 Update [8] Julia H. Wilson et al. at U. Minnesota found that 40% of their subjects were still experiencing gait and behavioural abnormalities 6 months after being diagnosed with West NIle Virus - previous work done in Florida had suggested that only 15% of WNV survivors did not completely regain neurologic soundness.] [2004 update [9] Dr. Kevin Keegan, U. Missouri-Columbia Coll. Vet Med. Reported that a handful of diseases cause spinal ataxia, which is very difficult to diagnose in it's early stages, although their computer system helps. Systemic infections may now be enjoying a resurgence in more virulent variants following several decades in which they, like Tuberculosis and Malaria for example, had been largely defused by the general use of antibiotics. The timescale on which the widespread acceptance of “The Virus”, subsequently amended to “a virus”, was adopted as a cover-all explanation for loss of performance in racehorses, perhaps because various syndromes were no longer readily recognised - especially those not widely described in medical and veterinary text books - would probably support this hypothesis. Those credited with the recent discovery of Lyme Disease may well have attained their recognition under fortunate circumstances; the syndrome might equally have been identified as being similar to the already, but not recently, well-documented Relapsing Fever. This is in no way intended to be a technical study, and is merely an attempt to make some sense of a set of circumstances which had a devastating effect on a previously very successful "hands on" training establishment. It became increasingly obvious from 1985 that something was seriously wrong in the stable, although as mentioned elsewhere, there had always been an Bill O’Gorman Page 5/26
  • 6. awareness of the odd horse which demonstrated these characteristics. Some types of infection may have always been fairly common and under normal circumstances might come and go in a stable - as long as the annual intake had no more than a random chance of being carriers. Even though we still enjoyed periods of considerable success, it was obvious that more and more of it's horses tended not to thrive under a fairly rigorous training regime. The stuation became increasingly serious as the graduates and boarders of the three stud farms began to dominate the annual intake. The fact that those fillies which failed the racecourse test, whether through being compromised by disease or simply through lack of ability, were readily accepted into the broodmare band predictably compounded the disaster! Lyme disease was not diagnosed in the stable until 1995, despite very detailed discription of the various symptoms mentioned here, and despite the fact that the severe onset of the problem clearly appeared to date from the time when graduates of Woodditton and Cedar Tree [at that stage, Deerfield came later ] stud farms became the bulk of the intake. That these catchment areas might be a factor was dismissed as paranoia on my part. These two farms regularly exchanged stock, although they may both have had a problem individually. Both farms made considerable use of grazing by sheep. When subsequently a third farm was added, although built from new, it boarded it's stock on the other two farms whilst it was being completed. WD. And DF. also carry a significant wild deer population. The whole area surrounding Newmarket is also heavily stocked with pheasants, which have been implicated in studies of Lyme disease in humans [10]. Any yearlings bought at auction by the owners of the farms tended to spend several weeks at one or other premises before coming in to be broken. In such circumstances it seems likely that the rodent, and probably both bird and insect populations, of the training stable will become infected and efforts should be made to eliminate danger from these scources as far as possible. The possibility of saliva containing the infectious agent is probably serious and may present another easy method of transfer throughout the whole of the training stable once there is a steady supply of infected horses. This is necessarily a rather subjective examination of the problem based as it is on the horses in only this one training yard, however it does include a considerable number of horses and in many cases their offspring and even the next generation of followers. Other trainers have not, by and large, shown much understanding of, or indeed interest in, the matter. This may be due to several reasons; from simple lack of observation, through
  • 7. Systemic Disease and Loss of Performance in the Racehorse unwillingness to admit to an illness in their team, to an easy acceptance of the premise that most horses are simply not talented, but as they all generate the same training fees, there is no need to look a gift horse in the mouth. The fact that British racing presently caters so well for appallingly low-grade performers does little to encourage trainers to maximise the potential of their charges, and during the lengthy process of "establishing a handicap mark " it is easy to gradually abandon any expectation of meaningful ability. The early disappearance of many high-class runners to stud is no longer considered to be detrimental to their subsequent career and this again leads to an easy acceptance of shortened and/or erratic racing careers. A survey undertaken by the A.H.T. and Liverpool University [1995] , to some degree at our instigation after Neil Steven’s original diagnosis of Tame Deer, reported seropositive animals in 50 of 54 yards surveyed. They noted that the trainers seemed unaware of a problem, and based on that fact one can appreciate a certain lack of urgency in taking a difficult investigation further! Under normal circumstances consistency and progressive form was extremely high amongst this string as a whole. Increasingly however a pattern emerged of horses, good, bad and indifferent, which were quite unable to stand the rigorous training essential to maintaining such results. The horses from the studs involved would appear to be generally disappointing and very uneven in their performance wherever they are trained. Although the problem was not confined to graduates of those farms, as they came to represent a greater proportion of the team, so the stable as a whole became increasingly compromised as far as developing serious runners was concerned. In themselves many of what it would now appear be regarded as indications of these illnesses are relatively minor, however the fact is that cumulatively they are likely to be associated with marked loss of performance. Any stable suffering persistent niggling problems should certainly give some thought to the possibility of some systemic disease. Update 2003 Henry Cecil's fortunes have declined dramatically in recent seasons. It is unlikely that he has forgotten how to train horses, and, given that the usual ["viral"] avenues of explanation for the horrendous falling off in the stable's results will have been explored, it is far from impossible that some similar systemic infection has invaded Warren Place and that the hoped for resurgence will not take place unless it is dealt with. Henry himself merely says that he doesn’t get good horses nowadays. The main manifestations from which we suffered are listed below. Bill O’Gorman Page 7/26
  • 8. Temperament. Infected horses tend to be at best uncooperative. They often seem unable to follow a normal learning curve. "The New Care and Training of the Trotter and Pacer" [11], an excellent book, and far in advance of any similar work on thoroughbreds, suggests on p. 149 that "slow learners" be got rid of, being at best unlikely to attain a respectable standard as racehorses . At worst these animals tend to be erratic and stupidly "ignorant" - some of them are unpredictable to the extent of being unsafe to work with. This state of affairs may however not be recognised by handlers, due to there own lack of awareness of normal parameters of equine responses - see ref. to lads and trainers elsewhere. On the other hand lads may be suspected of causing behavioural problems through mis-handling their charges without this necessarily being the case. In the case of Cedar Tree’s yearlings, their bad manners was originally attributed to rough treatment on the stud, however in hindsight it is likely that there will have been some degree of “ chicken and egg” as to whether they were wild because they were roughly handled or roughly handled because they were wild. Neurological manifestations in Lyme infected humans may apparently be subtle, and may present as mild encephalitis with mood changes, difficulty with memory and concentration [12]. B.B. has been isolated in the brain tissue of a horse with signs of neurological disorder [13]. Presumably such symptoms would tend to become more compromising in proportion to the stresses imposed upon the victims by their circumstances, so the complete change in lifestyle combined with a severe athletic training regime which a racehorse experiences would prove to be very challenging. An apparent inability to cope normally with starting stalls seems common in infected horses. This may typically involve the horse lying on the side of the stall and dwelling when the gate opens. Unfortunately attempts to remedy this with stalls-practice have usually proved to make things worse. This pattern has several times been accompanied by reluctance to go in and out of stable door , which was not apparently attributable to any previous slip or collision. Ben K. Green refers to horses which have apparently recovered from loco weed poisoning but which will always be reluctant to step over, for example, a rope on the ground. Some of these animals give the impression that they are abnormally conscious of small spaces and they seem very apt to crowd against the wall of the stable in an attempt to avoid going through the door. Possibly there might be some eyesight involvement,
  • 9. Systemic Disease and Loss of Performance in the Racehorse such as light-sensitivity, in this problem. “Head pressing” is well documented as evidence of neurological disorder in cattle. The stable has never had a horse which required a "Stalls Certificate" in thirty years, and it might be reasonably supposed that there is some understanding of what constitutes normal behaviour in this area . Infected horses sometimes show periodic examples of extremely headstrong behaviour, often with potentially disastrous results. Sometimes these occur out of the blue with animals which have never shown similar tendencies! The Equine Vet. Journal [14] reports an instance where the subject “suddenly became extremely excited and was subjected to euthanasia by shooting after crashing through a stable door”. Some of these horses, even some not normally considered to be hard to hold [Sayyaf*, Saseedo[USA]*, Top Fella[USA], In Character, Dance Focus, etc.], have run away with their riders and have seemed prepared to keep going until they were ready to drop. The only safe thing to do seemed to be to get them round in a circle straight away before they ran into something . This happened on several occasions with good riders - in fact usually with good riders [conceivably because the passenger type of rider is unwittingly doing the right thing in these circumstances]. A century ago "Blind Staggers" , which appears to have involved a similar sudden loss of composure [although more likely to result in a fit than in a runaway ], was well documented in horses. It is not difficult to imagine some of the animals described in this study going berserk and then lying exhausted and apparently senseless until the harness was cut off! Animals which had suffered an attack of staggers were regarded as likely to re-offend and were disposed of quickly by those lucky enough to be able to do so. The prognosis for a permanent return to normal behaviour is often questionable even after prolonged treatment, although in some cases there is no sign of a repeat performance [15]. Good results have recently [1998] been achieved with erratic horses which we kept on antibiotics full time, however these particular horses may not have already suffered severe neurological damage. In such cases it might be worth reviewing the situation periodically, say after three months, in order to determine whether or not the problem has been resolved The Rules of Racing only allowed horses to run on anti-biotic treatment fairly recently, or many more experiments could have been done. Some horses [Moonstrike[USA]*, Roc De Fer, Echo] ran a temperature of up to 105, and got "stacked up" legs when placed on antibiotics, even though Bill O’Gorman Page 9/26
  • 10. they had previously registered normal or very slightly raised readings for Lyme. This is presumably the Jarisch-Herxheimer reaction which has been observed in Lyme Disease in humans [16]. The fact that changes in behaviour are not more appreciated by trainers seems odd, particularly in view of the fact that they should be obvious to any reasonably competent observer. One former extremely successful trainer, for example, said that he was unaware of any behavioural problems in his string despite the fact that the vast majority of his sales consignment had demonstrated antics odd enough to be mentioned in "Timeform". However, David Whited, a well respected and experienced rider in the Mid-West over many years, was certain of some relationship between erratic behaviour and unexplained form loss in his last years of riding and Darrell Vienna, a long time successful West-Coast trainer seems certain of a similar scenario concerning E.P.M. It would be interesting to have access to the sequence of events towards the end of Vincent O'Brien's magnificent career - it seems simplistic to put the deterioration in the stable’s fortunes down to anno domini, or to an unidentified virus. It was obvious in a T.V.documentary on the new Ballydoyle regime that several horses wore various forms of restraint not normally associated with racehorses, which might suggest that behavioural irregularities are a problem there. The fact that they do produce a few very good horses each year doesn’t mean it’s all plain sailing – they have literally several dozens of potentially top class animals. Henry Cecil, Guy Harwood and Peter Walwyn all suffered devastating deterioration in their results. Possibly these trainers were doubly hampered, not only by their animals' being effected, but by their own confidence being shattered when they could no longer predict their horses’ performances with any accuracy. Those trainers who are more or less guessing anyway might be less disturbed! Some unusually able, or extremely resilient, racehorses may probably cope with these infections, even though they might display some quirks, purely because they are not obliged to be trained to their limit in order to achieve some success. On Stage* ,Provideo* and Fayruz* may have been cases in point as they all displayed some odd characteristics which had to be accomodated. It is worth noting that Timeless Times[USA]*, a not outstandingly talented but very healthy horse, had no difficulty in replicating the perceived impossible feats of Provideo[USA] *, who was definitely more able. Possibly the great success shown by some Classic
  • 11. Systemic Disease and Loss of Performance in the Racehorse disappointments when reverting to the much easier field of sprint racing also demonstrates this point. It could also explain why a less "severe " trainer might in practice be less aware of the syndrome than one who adopted stringent methods with a view to getting the most out of his charges. Even though it is very unlikely that an infected horse will either achieve a high standard or hold his form consistently over an arduous campaign, both those shortcomings are widely accepted as being the norm. Set Fast The "tying up syndrome" seemed to be common in what I would now regard as having been infected animals, although they might go through periods of responding normally to exercise. In most cases attacks were not excused by excessive or unprepared [ Monday morning] exercise. There were several cases of horses becoming very agitated after exercise with what seemed like spasmodic colic. Some of these had resolved themselves within minutes, even before the vet arrived, and there may, with the benefit of hindsight, have been some confusion between these and true setfast cases. Both the colicky ones and the tied-up ones invariably fitted into a Lyme Disease pattern in other ways. Lyme Disease's reputation as "the great imitator" in humans arose from the wide variety of it’s manifestations . Feet Mild laminitis is not uncommon in suspect Lyme horses. It is not feed related. In many cases it is probably not even diagnosed. It may be a factor in the “mystery shifting lameness” scenario which commonly occurs. Their feet often show cherry red around the white line when being shod. This is unlikely to be reported unless the farrier has been specifically instructed to remark on it, and has been assured that it is not about to be regarded as his fault. White feet will often show severe reddening in wall. [Similar looking marks can regularly be seen in the cleaned and polished horns of cattle at agricultural shows - presumably they don't all bang their horns about to the extent that they bruise them severely. Stockmen seem to be no more interested than are the horseshoers, in fact most don't seem to have even noticed!]. Black feet on horses which have shown other, unconnected, signs of being “wrong” will very often show white marks on wall. Given that white horn is never supposed to occur beneath a whole coloured hairline, this might possibly indicate the aftermath of the bleeding that would have shown up as red in the walls of white feet. These marks can be taken as an indication that there is, or has been, some challenge to the horse’s system. In his 1892 publication “How to train the racehorse” Col. Warburton states {p.19] that the feet of prospective yearling purchases Bill O’Gorman Page 11/26
  • 12. should “be free of rings and streaks, which are sure indicators of disease”. Concave walls and poor quality horn [often requiring glueshoes and rebuilding with equilox], lowering of soles, contraction of heels and loss of integrity of bars are regularly seen in horses with unspecified unsoundness, even though many of these horses do not appear laminitic in their stance or action. Because lameness is often not specific in these animals they are sometimes referred to as shouldery or jarred-up. There is often immediate improvement even in the action of moderately unsound horses without overt signs of foot disease when they are put on isoxuprine, supposedly a specific for laminitis. Horses which appear "thin soled" in that they are ultra- sensitive to stones improve more with isoxuprine than with pads under their shoes, which would also appear to indicate a minor laminitis, rather than bona-fide thin soles. The 1997 Keeneland September sale seemed to include a high [possibly 20 -30%] number of horses showing white on what should have been a black foot - it would be interesting to know whether this was indicative of an outbreak of some systemic disease and indeed whether those horses, on the whole, performed as well as previous crops. I bought two, out of two, E.P.M.s from this sale. Although there was no white on their feet at that time both soon developed hind gait irregularities. One of them was a useful horse called River Times, the other absolutely failed to maintain early promise. Some indication of whether the eventual racing class of those horses was comparable to other years would have been more interesting. The 1999 sale also seemed to include many examples, although again no- one appeared to remark on it.[2003 U.K. yearling sales had a very high number of horses with white hairs in their coat. Nothing to do with this but interesting how few people had noticed until their attention was drawn to it. It had been very dry for a long time - sunburn??] Discoloured feet do seem to be much more common on both sides of the Atlantic in recent years, but there still seems little interest when it is pointed out to vets or blacksmiths other than to say "interesting", or perhaps, "must have taken too much toe off". The latter is not a problem with most racehorse shoers and is most unlikely to be the only explanation; it patently cannot be the explanation when the marks occur high on the wall. As previously remarked, the white marks could be loss of pigmentation following an unsuspected laminitic episode which would have shown up as red on a white foot. 2004 updateto above Engenvall [17] found, as had the AHT, that there was little evidence
  • 13. Systemic Disease and Loss of Performance in the Racehorse to confirm what was widely perceived [in Sweden] as a connection between vague or non-specific clinical signs and exposure to BB and granulocytic Ehrlichia. There was found to be some correlation in the specific case of non-septic arthritis of the coffin joint, they dismissed this however as probably a spurious effect. 2004 update Filly vetted for USA purchase - William Huntingdon said that prospective trainer R. McAnally was paranoid about white marks on dark feet. To be clarified. 2005 update to above Daily Mail Good Health section 12/4/05 - "Nails with what seem to be several splinters underneath are not always hat they appear to be. A condition called subacute bacterial endocardtis- an infection of the heart and blood - can cause tiny "splinter haemorrhages" under the nails. This occurs because the infection causes bacteria to enter the bloodstream, which causes the tiny capillaries under the nails to bleed. Co-ordination Loss of co-ordination is possibly the most serious and certainly the most recognised symptom of E.P.M. It is certainly a factor in Lyme Disease, if to a lesser extent. Many infected horses display a tendency to stumble, particularly at the trot, and to suffer from interference problems, usually brushing, scalping or speedy cut type injuries behind when galloping. Naturally there will often be no sign of the hind leg injuries until speed is increased, however the problem often worsens and interference occurs even at slower speed. This might indicate the flaring-up of latent infection under stress of increased training. Once interfering has begun the problem has proved difficult to resolve by shoeing. However cases of stumbling, speedy cutting and scalping have virtually disappeared now that everything goes on a prolonged course of antibiotics before serious training commences. 2004 updates 1 Blood Horse 3/1/04 Article on Michael Gill, Eclipse award winning owner with a very large claiming stable said that “ beginning in 2002 Gill began giving all his horses daily treatment for EPM, which is the number one cause of respiratory problems in horses. Gill theorises the presence of EPM antibodies can lead to respiratory problems such as flipped palate. That is why myectomy surgeries, which cost $500 each, are performed on all his horses” etc. Horses claimed by the stable are widely perceived to move up to a remarkable degree which begs the question - is the improvement because of the treatment of general malaise or is the EPM treatment merely a Bill O’Gorman Page 13/26
  • 14. smokescreen?! Emma says that Richard Galpin has all USA yearlings etc treated whilst in quarantine for export to UK - he would be one of the few with the wit to have read and absorbed the Gill article! Until comparatively recently any proprietary “tonics” are likely to have contained arsenic; their regular use may have had some effect in controlling various systemic infections in racehorses in the past. 2 Dr. Sarah McCracken by e-mail “..when I was getting ready to use Baycox [toltazuril] on my own horse with EPM a few years ago their [ manufacturer] Bayer's scientist/vet said that some harness trainers were seeing improvements in off-form horses that travelled with a particular gait, [she thought from memory wide behind], but that did not [apparently] have EPM He attributed this to changes in cecal flora, but perhaps they were on to something else”. “The New Care and Training of the Trotter and Pacer”, as mentioned earlier [11], advises the culling of horses unable to establish their gait and on p. 591 it also remarks that "when all else checks out normally, a decrease in tail tone seems to be a finding fairly consistent with E.P.M. ....". The checking of tail tone is probably an example of how easily the inherited lore of horsemen has been lost in the last decades. Although the tail test is still practised, few probably realise its possible significance. Galvayne [18] states "Stringhalt is a nervous disease ... it is very frequent in some parts of Australia and South Africa ... in Australia I frequently heard some such remark as the following: "I shall not put my horse in this or that paddock [of thousands of acres], or it will be sure to get Stringhalt." Although recognising that stringhalt is a completely different subject it is certainly the case that historically certain locations have been recognised as detrimental to herd health. Although the cause illness, lameness, abortion and so on was unknown for centuries, it has often proved to be the herbal or mineral toxicity of specific sites. Logically there is no reason to suppose that vectors for various diseases are not present in certain studs and stables. The inmates of these premises will never do as well as they should until the problem is addressed. Colonel F. MacCabe [19], trainer of Epsom Derby winner Orby, specifically implicates ticks and spirochetes in epidemics of “relapsing fever” or “Dublin fever” in both humans and animals almost a century ago. This illness is apparently easily confused with Lyme Disease. Given the similarities
  • 15. Systemic Disease and Loss of Performance in the Racehorse between the two syndromes, the involvement of the tick and spirochete in the latter should have been suspected sooner. In fact, those credited with the discovery a new disease based on an outbreak of arthritis-like symptoms in young people in the town of Lyme Connecticut should probably have diagnosed a variant of Relapsing Fever from the start! Heels and girths We had a serious and very long standing problem with sore heels, invariably [with the benefit of hindsight] in males and on forelegs, which refused to heal starting from about 1984. This problem had a tendency to spread to or to occur on girths of yearlings if they got a chafe. The fillies too were at risk of infected girths if they sustained broken skin. No-one remarked that the fillies never got a sore heel in front simply because they didn’t urine-splash themselves! This heel infection had proved impossible to resolve by any topical treatment, although it was contained by liberal application of Dermobion cream. It had sometimes cleared up spontaneously in horses that had been gelded or had received sustained antibiotic treatment for other reasons – even that didn’t wake anyone up to the fact that the problem was internal rather than external to the horse. Routine treatment with antibiotics for six weeks on first arrival has resolved the problem, and re-infection of the sore area through urine which carried the infection is the [now] obvious explanation. Rodent urine and bird droppings are likely to play a part in the disease becoming firmly established in premises [20] [21]. Urine splashing is proven to be effective in spreading the disease in cattle, and the urine/oral route is proven effective between cattle and mice [22] [23]. An unnamed investigator in England stated that “spirochetes were constantly present in every case of canker of the foot and "greasy heels” examined by him [24]. Blistering of the muzzle which was occasionally seen, and which was variously diagnosed [including by an expert from the AHT] as “sunburn” or “blister beetle from American hay”, probably resulted from the same cause. With the benefit of hindsight the infection could easily be as viable in saliva as in urine, and because many racehorses do have minor cuts in their mouths, bridles may also have spread the disease amongst untreated animals. Update to above, 2002. We have had sore heel problem this year in horses which had been treated. Probably Lyme if present had been eliminated based on previous experience so possibly very resistant bacterial infection following the prolonged low intensity antibiotic treatment; also had some fracture lame ones among older ones with no wound or broken skin which responded to injected antibiotics, which might point to an unusually aggressive infection? Probably rethink routine extended treatment unless Bill O’Gorman Page 15/26
  • 16. there are some temperament signs of Lyme because we might be creating a less resistant horse? More likely just a very aggressive infection; Look Away Now and Red Vintage – no other manifestations and no recurrance. 2003 update one or two heels again amongst the breeze-up horses; quite easily resolved by keeping them covered and treating with dermobion + honey [heat and mix] there has been quite a bit in the papers about honey killing "Golden Staff" in hospitals. These may be simply resilient infections rather than Lyme disease; they are on the polytrack a lot so their heels are never really clean. 2005 – Stopped making Dermobion! Infected broodmares The urine-oral route of infection is proven to be possible in cattle[22]. This would explain the strong impression that the produce of certain stud-farms are extremely likely to show signs of infection. The offspring of infected mares seem very likely to emulate their dams, and are likely to be compromised as runners. The spirochete is capable of multiplication and development in the presence of it’s host’s antibodies [26], which raises the question of whether re-infection is likely to occur. It may also be simplistic to say that windsuckers, box-walkers and crib-biters, for example, merely imitate their mothers when in fact they may well simply be exhibiting the same symptoms of an inherited neurological disease. Obviously some experimentation will be necessary to determine the optimum timing, nature and duration of antibiotic treatment in a situation where the subjects are being retained for breeding, however the sooner the problem is addressed the sooner it might be resolved. The fact that Trimediazine apparently proved to be so successful in the resolution of the syndrome, despite not being recognised as a specific against spirochetes, might suggest that [a] either this opinion of the efficacy of the drug should be reviewed or that [b] in spite of the positive tests for Lyme Disease, the actual problem was in fact some other infection known to respond to this treatment. In either event further investigation is required. Stallion involvement It would be interesting, although politically sensitive, to investigate thoroughly whether an infected stallion meant possible infected offspring - in other diseases that could be the case and the spirochete has, in Australia, been found in a stallion's semen [27]. There seems no more more logical reason for a stallion being an influence for bad temper because of genetics than because of his health status. Unpleasant though this might sound to a stud, it would actually be sensible to discreetly address the possibility and to treat all stallions as a matter of course. Such action is well worth considering on the grounds that "if a good bull is half
  • 17. Systemic Disease and Loss of Performance in the Racehorse the herd - a bad bull is all the herd!" Red God, Aureole, Ribot, and Pinza and Nasrullah, to name a few, have all been regarded as sires which could get talented but temperamentally flawed offspring. Laser Light combined the influences of Red God and Aureole with predictable results, however we had several Laser Light’s that could really run had their "temperament" not got the better of them. Superlative* and Imp Society[USA}, from personal experience, would have been very successful sires if the offspring could have been trained to their full potential. There may be many others – perhaps even Montjeu as mentioned above. Given that the infectious agent seems to be relatively easily destroyed before being transferred in urine there seems no reason to suppose that control of the spread of the disease in semen should prove any more difficult. Prior, perhaps the greatest authority on the Thoroughbred, remarked that Friar Marcus "appears to have transmitted a tendency to windsucking and cribbiting...which cropped up even to the second and third generation" [28]. Temperature Many infected horses exhibit a slight [101.5] temperature most of the time. Normally quiet and friendly horses may look extremely sour when approached in the stable - they look like the proverbial "bear with a sore head". Some horses may be severely compromised in their proven racing performance with little more than this slight temperature visible as a symptom, however B.S.E. cattle, for example, may show little more than head-pressing as a symptom in the early stages. Obviously horses showing such slight symptoms are unlikely to be identified as having a serious problem. That is particularly true if they go wrong before anyone has been able to make an educated judgement of their ability. Hundreds of animals may soldier on at a level many pounds below their potential; that does not mean that there is nothing wrong with them, but simply that no-one suspects their true capability. Due to the increased numbers of low-level handicaps such animals might easily be regarded as relatively successful. Many low grade performers might, as Michael Gill theorises, respond well to aggressive antibiotic therapy, particularly if they are not showing any other signs such as lameness or ill-temper. Tame Deer was a prime example of this type of horse; although his feet also seemed sore no connection was at that time made between that and consistently running a very slight fever. In fact he was the first one in the yard tested for Lyme Disease at Neil Steven’s suggestion; he was then three. As a result of a positive test, ten days treatment with oxytetracycline was reccommended but little change was noted in his condition and he eventually won as a four year old at a low level. In March as a two year old he is recorded as working with decent old Bill O’Gorman Page 17/26
  • 18. horses which were currently running well, and was regarded as possessed of some natural talent. A similar case was Gold Trail* who always showed the same slight temperature and sour expression and was slightly “off” in his action although no structural or soft tissue injury was discovered. He had looked to be potentially very useful when he worked, in February as a two year old, with an old horse, completing the last three furlongs 13, 12, and 12 seconds. His only two runs were acceptable in that he was placed in maidens behind subsequent Group winners, however he never seemed "right in himself"; he was sold without further racing for export, and proved extremely unsuccessful. Had such horses joined the stable two or three years later they would almost certainly have responded to a constant broad spectrum antibiotic. Muscle, lack of Seeming inability to build muscle as normal with gradually increasing workload is common in these horses. Burgess [22] found that 10% of serum-antibody positive horses had chronic unexplained weight loss] Horses which fail to build up across their loins and their hindquarters despite eating well should be regarded with suspicion, especially if this resolves itself for no apparent reason following anti-biotic treatment for some unrelated problem such as a wound or castration. An explanation along the lines that a horse had really built up since he became a gelding might be offered, however one of the prime reasons for cutting is to reduce body mass! In fact many of these symptoms may suddenly cease due to therapy for apparently unrelated problems. Stables which routinely treat every minor setback with antibiotics might be inadverantly protecting themselves whilst those trying to “do the right thing” by developing some natural immunity to various illnesses may ironically be allowing various systemic diseases to run riot. Obviously some strains of disease are likely, over the last twenty five years, to have become more resistant to antibiotics. There are now at least seven tick species infected with borrelia burgdorferi [30]. Complete or Partial Loss of Ability and/or Unwillingness to Train There was a marked tendency for an unusually high percentage of horses from the three studs to come to an absolute and sudden halt in their athletic progress. This did not seem explicable in normal training terms. They often changed quite abruptly from normal racing prospects to almost completely useless. The deterioration tended to be permanent, although some of them raced reasonably well at a much lower level than looked probable based on their early work. For example, they frequently progressed normally through
  • 19. Systemic Disease and Loss of Performance in the Racehorse the “2 minute rate”, then 28 second quarters, on down to a sub-50 second half mile perfectly happily. If a horse suddenly becomes unable to get out of his own way at that stage then there is something wrong! It may be difficult to spot exactly where the reversal takes place if there is no record of the preliminary work times, however it should be obvious if steady planned progress does suddenly reverse itself. Despite being given a break to recover their strength the most severely effected of these horses appeared so painfully slow and deliberate in their action that it seemed inconceivable that they had ever shown any promise at all. If this had happened once or twice it might be attributed to a mistake in the original evaluation, however regular misjudgements are most unlikely in any proven two year old producing stable unless there has been some major change in circumstances. Moonstrike[USA]* for example was asked a severe question before his debut with a horse which was currently running to a rating of 100. He easily won his trial with the last four furlongs in 45 seconds and change, but was well beaten in a maiden race. He was subsequently continually and largely inexplicably lame on various legs, he had poor feet and an erratic temperament. He won two small races for us and then he ran at a fairly low level for various trainers until he was six. Repeated body scans had proved unenlightening at two and three years although he did win two small races during this period. His achievement of a rating of 105 as an old horse was widely regarded as something of a revelation, everyone in the meantime having naturally accepted that he truly was a 75 rated horse. That work before he ran had indicated that 105 was likely to be well within his capabilities. In the worst cases, or possibly in the case of horses whose maximum potential was limited to begin with, it appears that their central nervous system can no longer instruct their limbs to work efficiently enough to produce any degree of speed. Some of these horses tend to develop a deliberate rolling gallop as soon as they are expected to quicken, even if their earlier training had shown every indication of normal stride patterns. The prognosis for these particular individuals is grim even at the lowest level. Many of them, even if they don't refuse to train, become obviously upset at being asked to do something which is no longer within their capability. Possibly a similar syndrome applies to dispraxic children. Whether anything more specific than the increased workload triggers the deterioration is unclear, but it is very clear that without treatment the prognosis for getting back to a level which had originally seemed a realistic aim is extremely poor. Firmament* in 1982 was an isolated earlier case in point; this big unraced horse was easily following On Stage in his work at Bill O’Gorman Page 19/26
  • 20. the time when the latter ran second in the Prix Morny. Although apparently doing this work well within himself he quite suddenly became a confirmed jibber and developed a dysfunctional gait. From being a potentially top class horse he died a maiden point to pointer. In the 1990s this scenario became a regularly recurring one, although in most cases the expectations held of the animals were rarely so high initially. Some of the less severely compromised were able to win due to Emma’s careful "rating" of them in their races, which enabled them to maintain their most efficient stride pattern - any sudden call for extra effort would lead to disastrous loss of momentum. There has been a tradition of "Not Trained On" in racing, as a coverall explanation for complete loss of form at three years, in horses which had already established a level of ability as two-year-olds. The fact that some horses may recover some level of competence at four years might indicate the sporadic nature of some systemic challenge. The likelihood of regaining their best form is slight. However owner/trainer expectations, to say nothing of handicap ratings, will tend to reduce during the period in the wilderness. Obviously when there is a general acceptance, however illogical, of the "hasn't trained on" theory, there is little incentive to rock the boat by searching for puffs of smoke from the grassy knoll! Brondesbury* may have been a case in point as long ago as 1983 . After breaking the track record at Ascot as a 2 y.o. he was coughing. It then proved impossible to get him back to form; in fact at three he was physically a pale shadow of what he looked like at two especially as regards muscle tone. He kept giving the odd cough [which is not in fact unusual in itself], and there was a theory that he may have been carrying a lungworm infection due to the sheep grazing Cedar Tree - which was the first one to become a regular supplier to the stable. This suspicion was never confirmed by faecal sample and the blood picture could conceivably have indicated other parasites [such as spirochetes] rather than lungworm . There was a horse more recently, Prodigious, who also indicated a parasitic burden in his blood, and exhibited every downside of Lyme infection, including, which is not invariably the case, a strong positive blood test. One of the worst cases, in that he exhibited several different manifestations of the syndrome, was Reformed Imp. He was sent to the A.H.T. for pre and post mortem examination which proved inconclusive. This animal was originally tested positive for Lyme but his readings reduced to a negative score after treatment; however there was no improvement in his demeanour despite his being cut and having an enormous amount of trouble taken with him. Being by Imp Society[U.S.A.] both he and Prodigious may have inherited something else from their sire apart from Lyme disease.
  • 21. Systemic Disease and Loss of Performance in the Racehorse Mac's Imp [USA]*, like Brondesbury *, showed nothing at 3 years, and he too never looked well as a three year old. He proved generally unhealthy during his stud career and hedied suddenly; he too was by Imp Society[USA] and his offspring demonstrated more of his ill-temper than his speed. Imp Society [USA] himself was termed by the stud farm in America a " workman's compensation horse " i.e. not easy to work with. We had great difficulty with two others by him, Retiring Imp[USA]* and Society Times [USA], which both refused to train at all having clearly demonstrated ability to at least Listed Race standard in their early work. Retiring Imp[USA] did in fact win a Graded Stake in Italy eventually after being operated on for his wind, which probably involved some antibiotic therapy, however we got him back eventually and any improvement had evaporated!. Superpower* was unlucky not to win a major race on his first 3 year old start but subsequently showed little approaching his two year old ability; at stud he failed to get anything approaching his own racing ability. His sire Superlative was very likely carrying something throughout his racing career, because although he was pretty successful I don’t think he ever did anything like he was capable of – he could give Raami or Reesh 21 lbs in the morning. At stud he was responsible for a high proportion of very disappointing runners, although they almost invariably showed great promise. Both his son Superpower* and Imp Society’s son Mac's Imp]USA]* were extremely tricky to deal with at exercise as two year olds. Why did they cope at a very high level at two and subsequently go to pieces at three? If we had not appreciated their potential early would they have just sunk without trace even at two as being too much trouble to bother with? In fact, had we been aware at that time that they probably were infected with something rather than being purely awkward customers, would we have achieved so much with them [they were both Group 1 winners]? On the other hand, had anyone shown any interest in the fairly meticulous reports that were made to owners, breeders and vets we might have got on top of things and had two champion older sprinters which may have gone on to be successful sires! As with so many aspects of the horse business everyone's face is saved by the fact that we'll never know. The widespread acceptance of a number of traditional "explanations" of form-loss, such as poor jockeyship, in season, wrong ground, too much weight, spread a plate, track turned wrong way, swallowed tongue, etc., to say nothing of coveralls such as "the virus" and "they aren't machines", does not encourage the serious pursuit of more realistic causes of disaster. However the thoroughbred is a far more resilient animal, if properly prepared and in good health, than is generally perceived and, assuming he is Bill O’Gorman Page 21/26
  • 22. running in a grade where he belongs, he should perform with reasonable consistency. Obviously it is not in the interest of trainers to over-emphasise this point. The present regime which is almost completely geared to lowly rated handicappers, most of which are running off a mark which there were no races for 30 years ago, has filled the sport with unsuspected and unsuspecting under achievers, both human and equine Lameness, Unexplained and Shifting There is a tendency to lameness, both front and rear, which may have no obvious explanation. These horses often show very little clue as to the cause of lameness even on very sophisticated investigation. For example several of those which were transformed by isoxsuprene and or glueshoes had not been diagnosed as lame in their feet by nerve blocking – although they felt footsore to ride. Also the usual confusion, of course, exists as to whether hind lameness is caused by compensation for a problem in front - not a popular concept with the legion of "back specialists" that have sprung up in recent years! Mimicced Tendon Strain These occurrences can be quite bizarre, and can appear exactly like a strained tendon, although the exercise immediately preceding the discovery may have been such that a tendon injury is very unlikely. There seems to be a tendency for this to occur in horses whose dams showed distinct signs of being affected by various odd symptoms when in training [that is, with the benefit of hindsight; at the time those fillies were thought to be suffering from the universal ill - a virus]. Rassam*, Chloe's Anchor, Pacific Rose, Red Tower, Alabama Girl*, Echo, Wild Palm [The first five got false tendon strains and the last two appeared to have sprained suspensories]. There was no reason for them to have sustained any damage from their exercise on the day in question, they were never lame and obviously as it transpired had NOT suffered any injury. The first four were all out of mares trained here which exhibited unusual manifestations either in their own racing careers and /or in their other offspring, but we had no first hand experience of the dams of the last three]. See [31]. Obsessive Behaviour The babyish habit of chewing and sucking of reins and headcollars and repeated "yappy" or "calfish" behaviour when being saddled or groomed is quite common in infected horses [11]. Box walking and scraping of litter are also unusually frequent. The litter scraping can be sporadic, and there seems little hope of much success when severe episodes are going on although some progress may be possible during lulls. Some of
  • 23. Systemic Disease and Loss of Performance in the Racehorse these horses that display extremely neurotic or irritable behaviour improve markedly when exercised in blinkers, which might indicate that their eyes may in some way be a factor. Many of them also seem to cope better under an extremely fixed and rather light training regime, which might also be said to apply to children with learning difficulties. This obviously causes problems with trying to push fitness thresholds, but may account for many undiagnosed cases in yards with less strenuous training programmes and “institutionalised “ horses. Diagnosis of poor or irritable behaviour might also be complicated by lads reporting to the trainer that horses jig-jogging and fretting are “well in themselves”! Virtually all the intake from the Cedar Tree were extremely "ignorant", their yearlings were sent home without even being broken on one occasion! This was originally attributed [including Ron Boss who received the rejects] to the poor handling of the young stock. Although their manners did leave a lot to be desired, it seems likely that there was a deeper problem, and that in fact the rough handling which they did receive may have been as much due to their poor behaviour as vice-versa! All these symptoms have a tendency to fluctuate. They often decrease if the horse is taken out of strong work, however they almost invariably return if the horse is hard trained unless a course of antibiotics has been administered. An effective treatment may actually in many cases have been administered for some unrelated problem. The occasional dramatic and immediate good results which are sometimes attributed to castration may be for this reason as it seems reasonable to expect any improvement based on hormonal changes to take some time. Now that the testing regime allows, it may be desirable to keep some badly behaved horses on constant treatment to enable them to be trained to best advantage. This may not be ideal, however it can only be regarded as the lesser of two evils – and that the results of sustained antibiotic treatment in rehabilitating some very badly behaved horses have been far more dramatic than even those obtained with A.C.P. it must demonstrate that these suggestions have some merit. *Since writing this I have been made aware of a paper published in 1998 [33] which describes a reform in obsessive behaviour supposedly initiated by a concentrated diet to occur in animals fed non-therapeutic levels of virginiamycin in the form of Founderguard. It seems unlikely that any such trial would have been launched unless appreciable numbers of those animals which were treated with Founderguard for laminitis had also showed behavioural abnormalities, which had been markedly reduced on treatment with the product. This might tend to reinforce some of the thoughts above, Bill O’Gorman Page 23/26
  • 24. and the matter is worthy of further investigation. *July 2000 update to above There was a report in The Daily Express[?] on the dramatic improvement in autistic children treated with antibiotics. Dr Sydney Finegold University of California and Dr. Richard Sandler of Rush- Presbyterian-St. Luke’s Medical Centre in Chicago quoted as being initially impressed with results. *2004 update to above Blood Horse Health Watch [31/1/0] included a report from the Centre for equine health at U. Ca. Davis that Fluphenazine is a viable treatment for horses with head shaking syndrome. [34] Loss of Horseman's Awareness of Normal Parameters Over the Last Several Decades. Since the motor engine took over the transport of the world the general awareness of how horses behave has fallen rapidly, although some degree of revival is taking place with the "Horse Whisperer" culture now in vogue. However, as in any movement capable of commercial exploitation, there is a lot of showmanship wrapped around the basic horse knowledge and it may be some time before many people currently professionally involved with horses realise to what degree they have failed to recognise just how much simple common sense can achieve with many horses. If the capability of a normal healthy Thoroughbred were better appreciated, then it might be easier to recognise those animals which are compromised – but then again many trainers would lose all their horses! The widely repeated feeling that "horses are much less tough than formerly was the case " is a comforting thought for many, in that it pre-supposes frequent failure to deliver results and thus effectively exonerates trainers, and breeders, from blame ! C. 1999/03 Bill O’Gorman Seven Springs, Newmarket, CB8 7JQ
  • 25. Systemic Disease and Loss of Performance in the Racehorse Bibliography 1: Infection in Wisconsin horses and cows. Burgess and Patrican 1987. 2:Tizard 1982. 3:Burgess, Gordon-Fitzpatrick and Mattison; Abstract, Proceedings 5th Int. Conf. Eq. Inf. Dis. 1987. 4:Herzer, Wilske and Preac-Mursic; Klin Wochenschr 64[5] 206/ 11 1 1986. And Magnarelli, Anderson and Barbour; J.Infect. Dis 154[2]: 366 8 1986. 5: Blood Horse Magazine, Health Watch 31/1/04 6:Baird, Gillies, Bone and Miscampell; Brit. Vet. Med. Jour. 1989 299 836/7. 7:Blood Horse Magazine Health Watch 27/9/03. 8:Ditto 7/2/04. 9: Ditto 10/4/04. 10: New Scientist October 1998. 11: New care and Training of the Trotter and Pacer; U.S. Trotting Ass. Pub. 1996. 12: Pachner “ B.B. in the nervous system; the new great imitator” Ann. N.Y. Acad. Sci. 1989; 539 56/64. 13: Burgess, Mattison “Encephalitis ass. With B.B. in a horse” J. Am. Vet. Ass. 1987; 191 1475/58. 14: Eq. Vet.m Jour. 1996 28 [1] 84/8. 15: Lyme Borreleosis; J.E. Palmer V.M.D. 1995. 16: J.A. Moore Cutis 1987; 34, 397/8. 17: Engervall et al. Preventitive Vet. Med. 49[2001] 191-28 18: Sidney Galvayne; Twentieth Century Book of the Horse, 1905; pp 277/8. 19: Col. F. MacCabe; Horsemastership, 1911; p.50. 20: Bosler and Sculze; Zbl. Bakt. Mikrb. Hyg. [A] 1986: 263: 40/44. 21: MacNeil, Hinshaw and Kissling; J. Bact. 57:191/206 1949. 22: Burgess; B.B. infection in Wisconsin horses and cows; Annals N.Y. Acad.Sci. 23:Burgess and Patrican; Am. Journ. Trop. Med. Hyg. 36[2]: 402/7. 24: Methods of Vet. Microbiology, Cornstock Pub. Ass. P. 506. 25 see 22 26: Barbour and Garon; Ann. N.Y. Acad. Sci. 1988: 539:144/53. 27: Osbornne and Bain; Austral. Vet. Journ.37 !90/1 1961. Thoroughbred Record 1942, Family Characteristics, Prior. 29: see 22. 30: Sonenshine 1991. Bill O’Gorman Page 25/26
  • 26. 31: Illustration, Eq. Vet. Journ. 1996 28 [1[ 84-88 Fig.1. 32; See 11; p.147. 33: Rowe et al. Eq. Vet. Journ. 1998 30 [2] 139/43. 38: Blood Horse Magazine, Health Watch 31/1/04. 38: Healthnotes, Mail on Sunday, You Mag. 14/1/07. Lifetime total [1969/1998] of about 530 2yos, 352 2yo runners, 1687 starts, 152 2yo winners [43%of runners, about 66% of total]. Won 304 2yo races, 18% 0f starts, 85% 2yo races won per 2yo runner]. From 1977 until 1990 333 2yos, 234 2yo runners, 1163 starts, 116 2yo winners [50% of runners 70% of total]. Won 259 2yo races, 22% of starts, 110% 2yo races won per 2yo runner!