Wandering Withdrawal-Times and the Racing Medication and Testing Consortium Model Rules: Time for the RMTC to get days

Clara Fenger, DVM, PhD, DACVIM; Andy Roberts, DVM; Jim Casey, DVM, MS

The ARCI Controlled Therapeutic Medication Rules have gone into effect in a number of new states, coming on line rapidly in the last few months.  The regulatory authorities have promised that providing a stringent and well defined set of uniform medication rules would make racing cleaner and safer for all participants.  Gone would be the days of supposed rampant cheating and we could all compete on a level playing field.  In fact, we have known for some time that operating outside the lines of legal and ethical competition in horse racing is extremely rare…representing only 0.015%  of horses passing through the test barn (1).  Clearly, the playing field has been quite level and well regulated for some time.  Nonetheless, it is human nature to suspect “that guy (or gal)” who is winning at a 40% clip must be using something, so we ought to all welcome the ever increasing oversight by our regulatory bodies.  Besides, even the horsemen agree that uniform rules would make racing across state lines easier.

Enter RMTC.  In an effort to produce National uniform medication rules, the RMTC has come up with a plan.  First, limit the number of medications that can be used therapeutically in race horses, and regulate them.  Have uniform National thresholds based on scientific studies which provide valid and realistic withdrawal time guidelines for trainers and veterinarians.  The Executive Director of the RMTC has suggested that adopting these rules actually reduces positive tests(2).  However, recent issues cropping up across the country seem to dramatically refute that claim.

The first uniform medication rule to be implemented across the country was to drop the acceptable phenylbutazone level from 5 µg/mL to 2 µg/mL.  Even though all of the pain relieving effect
of phenylbutazone is eliminated at the 5 µg/mL level(3), racing commissions in various jurisdictions felt that this threshold allowed levels at the time of the pre-race exam that interfered with their ability to determine if a horse was sound.  Nonetheless, at the time the change was made, the recommended withdrawal in many jurisdictions remained 2 g IV at 24 hours(4).  This, despite having data collected at the University of Florida showing that only 95% of the horses that received the original 2 g IV dose were below the regulatory threshold(5).  Which is akin to routinely giving a speeding ticket to one in 20 cars going 55 mph in a 55 mph zone.  Although the 24 hour 2g dose recommendation was continued in several states after the threshold change, the RMTC changed the dose to 9 cc (1.8 g) IV at 24 hours for the model rule, and state recommendations vary from the model rule recommendation to 1 g IV at 24 hours (KY)(6), 2 g IV at 28 (VA) or even 2 g IV at 36 hours (WV)(4).  You have no way of knowing for sure until you get back a positive test.  So much for uniformity.

Flunixin (aka Banamine®) is another example where the RMTC has been flat wrong in their withdrawal recommendations.  The manufacturer’s recommended dose is 500mg, or 10 cc to a 1,000 pound horse.  Originally the RMTC recommended that this dose be administered no closer than 24 hours pre-race(4).  Somehow, the decision was made that the cutoff for a positive test was going to be 20 ng/ml in blood(5).  This, despite the unhappy fact that when you actually read the studies, the science indicates that many 24 h post-race samples will exceed the 20 ng/ml threshold(7).  When post-race samples came up positive in droves, confirming this already-known detail, the RMTC backtracked.  In their meeting this spring at Gulfstream Park, they heard the “positives” message; their solution was to leave the sacred 20 ng/ml threshold in place but to move the withdrawal time out to 32 hours(8).

The RMTC doesn’t seem to be any more clued in with Ketoprofen.  When they set the original 10 ng/ml level, they had minimal “positives.”  So, since they couldn’t believe NO ONE was “cheating” (because there were no positive tests) with this drug, at the same Gulfstream Meeting, the RMTC reduced the threshold to 2 ng/ml(8).  Still no problem with cheating (no positive tests), so surely a further reduction is coming.  Seems like every five minutes, the RMTC and subsequently various regulators are changing a rule or a recommendation, all without real, publicly reviewable substantive scientific evidence to support their “new” position.  If you can’t dazzle the horsemen with brilliant science, baffle them with confusing and ever-changing …well you know.  Somehow, the idea of getting the facts straight with scientifically sound research before implementing rules that profoundly affect the lives of the people and horses you regulate has escaped them.

Next, Methocarbamol:  Robaxin is a mainstay of the prevention of muscle cramps (i.e. “tying up”) in training, a painful condition that plagues many racehorses and mostly fillies.  It is an important therapeutic medication to have available to horses in training.  And a rash of methocarbamol positives at Delaware Park(9) has further underscored the problems with both the RMTC studies and the implementation of changes in regulatory procedures.  Firstly, the studies were performed on only 20 horses(10), and when the results are applied across thousands of racehorses with varied management, different metabolism and under a myriad of different specific circumstances across the country, the outcomes are not so clean.  Secondly, medication interactions were apparently not taken into consideration.  The RMTC Executive Director has recently explained in great detail(11) that methocarbamol and phenylbutazone are metabolized by the same pathway in the horse and phenylbutazone is preferentially eliminated, slowing the metabolism of methocarbamol, and thereby resulting in the positive tests.   Except there is no published scientific data to support that statement(8).  And if there were, the RMTC should have been aware and done the studies to provide guidelines for the practitioners and horsemen.  Dr. Rick Sams, Director of LGC Sports Science, the lab that runs the Delaware post-race tests responded:  “While the guidelines that are in place were well thought out and researched, there will, I’m sure, be adjustments made as time goes on.(11)”  Sounds like the horsemen are guinea pigs in a high stakes game of chicken:  let’s figure out the rules as we go, and if you try to adhere to the rules and guess wrong, the penalty is harsh.  This is no way for an industry to act.  The stakes are too high for all concerned, including the horse and rider, to base medication regulations on questionable science.  

“There will, I’m sure, be adjustments made…:” not surprising when one considers the history of the RMTC threshold for Methocarbamol, which goes like this: First, RMTC commissioned a study at University of Florida using their 20 exercised horse herd and a 15 mg/kg methocarbamol dose(10)…a typically used dose(12). This study came up with a 20 ng/ml threshold and a 24 hour withdrawal time.  Unfortunately, Pennsylvania already had in place a 1 ng/ml threshold, based on studies with a REALLY low, below any clinical effect, 2.2 mg/kg dose of methocarbamol(5,12).  What to do??  Simple! Just leave the cutoff for a positive test at 1 ng/ml but arbitrarily, and without performing the necessary scientific study to back it up, move the withdrawal time out to 48 hours, and trust that it works.  If it doesn’t work out, come up with something convenient to blame, in this case apparently phenylbutazone.  At the same time tell horsemen that THEY have to move the withdrawal time out again.  The only problem is those pesky horsemen who actually got Methocarbamol positives during this “educate the regulators” “adjustment making” period.

In deflecting the blame towards a heretofore unidentified drug interaction with phenylbutazone, the RMTC is also directing attention away from the simple fact that Methocarbamol has long been known to show dose dependent kinetics.  In other words, as the dose increases, Methocarbamol is eliminated more slowly and tends to accumulate, increasing the likelihood of a positive(13).  Both the RMTC and the University of Pennsylvania studies were single IV dose studies.  We would therefore be not in the least surprised if it turns out that many of the numerous recent positives reported for Methocarbamol are more closely associated with a normal multi-dose therapeutic schedule of Methocarbamol than just with the concomitant administration of phenylbutazone.  The end result of the confusing withdrawal guidelines is to make a safe and effective therapeutic medication, Robaxin, essentially illegal and out of reach for those horses that may get muscle cramps.  

For many months preceding the adoption of the RMTC Model Rules regarding uniform medication, racing officials went around the country and were quoted in the press about the new rules regarding joint injections.  Low grade joint inflammation is an extremely common outcome of strenuous exercise, and joint injections are a useful and widely used therapeutic approach to handling this concern.  Modern human sports medicine has included the use of therapeutic joint injections for years, and studies have shown no long term ill effect from repeated injections(14).  Which fits very well with the experiences of racetrack practitioners:  Judicious joint injections are therapeutic and preserve the long term health of the athlete, not just for its racing career, but for the career that follows.  Nonetheless, the racing officials and proponents of the RMTC “driven” Uniform National Model Rule have, perhaps less than logically, insisted that veterinarians should have sufficient time after a joint injection to assess response to therapy.  They argued that horses should not be raced within 7 days of injection with a relatively quick acting corticosteroid like triamcinolone (Vetalog) or betamethasone, or 14 days of injection with a long acting corticosteroid like methylprednisolone (Depo-Medrol).  Veterinarians and horsemen have long agreed that assessing response to therapy should be part of any therapeutic intervention, but felt that the time periods set forth in the Model Rules were well beyond the time frame necessary.  Nonetheless, we were prepared to go along with it.  Unfortunately, we and other practitioners were not prepared for the outcome of the first few weeks of the new medication policy which have resulted in numerous alleged positives in at least 2 jurisdictions (IN,WV).

The uniform medication rules have put in place a 100 pg/mL blood threshold level of methylprednisolone (Depo-Medrol®), and a withdrawal of 7 days, nominally based on an RMTC sponsored report, where 100 mg was injected into a single knee(15).  And yet in the Controlled Therapeutic Medication Schedule recommendations(16), right next to the recommended 7 day withdrawal, it states that the withdrawal for 100 mg (2.5 cc) Depo-Medrol is actually 21 days…so which is it?  7 days or 21 days?  Given this uncertainty in the published guidelines, the states have varied from 10 days (IN) to 21 days (WV) for recommended withdrawal times linked to this threshold.  Faced with these ambiguities, practitioners, in an abundance of caution, have adhered doggedly to the recommended withdrawals.  And, despite this care, “cloudy” or possible positives have been coming up at a frightening rate in the first few weeks of the new rules, such as has been seen in WV(17).  It turns out, if you put the Depo-Medrol in a stifle, the clearance time is one thing.  If you put it in a hock, it is something else.  God forbid the horse moves while you inject it, because then all bets are off.   A racing official stated, off the record, that the purpose of the Depo rule was to discourage the use of Depo at all…hey wait, what happened to “so you could assess the response to therapy”?  A little deceptive to say the least.  And another, safe and effective, FDA approved therapeutic medication relegated to being essentially illegal.

To further complicate matters, Veterinarians, trainers and owners are anxiously awaiting the results of their post-race tests, which are taking an inordinate amount of time [a month or more] as a result of a laboratory backlog.  The new Uniform Model Rules mandate that a Depo Medrol positive requires purse redistribution and a fine(18).  All while the racing officials cannot even provide useful practical guidelines for withdrawal times.  As this article goes to press, even the racing commissions are unsure of their own final decision(17).  We all remember Brass Hat’s impressive effort to finish second in the 2006 Dubai World Cup.  The trainer and veterinarian tried to contact the appropriate authorities to identify the withdrawal time for methylprednisolone, and then added 5 days in order to inject the horse’s hocks well outside of those guidelines.  When the horse was disqualified for the positive test, the trainer and veterinarian protested, but to no avail.  After the trainer and veterinarian did everything possible, there was nothing that could be done: surely this can’t happen in America.

Other problems with the Controlled Therapeutic Medication Schedule (April 17, 2014), the cornerstone of the RMTC Model Rules have not yet reared their ugly heads. The recommendations on a common tying up preventative, dantrolene (Dantrium) is 48 hours.  This is based on a study performed with a single dose of 1 mg/kg, which is well below the therapeutic dose of 2-4 mg/kg(12,16).  Xylazine, a common tranquilizer, used to sedate horses for procedures, including dental work, veterinary procedures and some grooming procedures like clipping is listed as permissible at 48 hours with a published threshold level (cutoff for a positive test), but NO recommended dose and NO research paper to explain where the recommendation came from is listed(16).  Can I use the whole bottle?  Mepivacaine (Carbocaine) has a withdrawal recommendation of 72 hours, and represents a class B penalty i.e., a minimum of a 60 day suspension, loss of purse and fines (RMTC website).  And the RMTC recommendations are based on 1.5 mL of Carbocaine in a 1000 pound horse(16).  This is an amount which is below ANY usual therapeutic use of the product, which would be at least 10 mL for a Caslicks procedure or 5 -10 mL for a typical diagnostic nerve block.  So the actual RMTC recommendations appear to be at best a complete lack of understanding of how therapeutic medications are applied and at worst an intentional set up of any trainer or veterinarian who even thinks of using a therapeutically appropriate amount of mepivacaine.

This seems to be a common theme among the “permitted medication” list:  no good faith effort was made to determine how these medications are correctly and appropriately used as therapeutics before the withdrawal studies were performed or recommendations were made.  As a further matter of interest, the mepivacaine threshold is based on confidential data generated by the European Horseracing Scientific Liaison Committee [EHSLC] and therefore subject to EHSLC non-disclosure requirements apparently signed by all members of the RMTC Scientific Advisory Committee(8); so much for industry-wide transparency and independent scientific review.  Further, the cloak of secrecy does not end there:  a number of other US medications rules, such as acepromazine, albuterol, betamethasone, clenbuterol, dexamethasone, firocoxib, furosemide, isoflupredone, lidocaine, omeprazole, prednisolone, procaine penicillin and xylazine are based on secret data that has never
been subjected to independent review, and is currently unavailable to the horsemen or their racetrack vets(19). 

Drugs outside the magic “26” list of therapeutic substances are a no man’s land.  There is only one antibiotic, procaine penicillin, on the list.  States differ from 24 hours to 96 hours4 to “zero tolerance” (infinite in IN?20) on withdrawal for “sulfa drugs,” like Trimethoprim-sulfadiazine, probably the most commonly used antibiotic in horses, which is not even in the magic “26.”  Within the word “race horse” is the word “horse,” and this word is attendant with all the day to day things that might befall any animal.  In addition to scrapes and infections, a horse may get stung by an insect, necessitating an injection with an antihistamine, or scratch his cornea necessitating atropine or other therapeutic medication.  These conditions are not life threatening, but the varied therapeutic medication rules could prevent this otherwise completely healthy horse from competing, depending upon which jurisdiction you are in.  Imagine:  there are likely more than 26 over the counter medications in your bathroom medicine cabinet at home, but the most elite of athletes are prevented from benefitting from modern day sports medicine under the misnomer of “clean racing”. 

In 1900, infant mortality among humans was 30% and life expectancy was less than 50 years 21.   Much of the reason for the improvement in health of humans is the advent of modern medicine.  And yet we want to send our most precious charges, horses who have no voice for themselves, back to the dark ages.  Modern equine sports medicine is NOT a crime.  It has been developed to give the athlete the best possible quality of life and as a result to perform to the best of their abilities.  There are substances which may potentially enhance performance, and these are and should be banned.  Severe penalties should be in place and vigorously enforced.  But, folks, let’s get it right.  The rush to implement the RMTC rules has had a mountain of unintended consequences.  Shouldn’t we first and foremost get the science right, perform studies which reflect real world and appropriate uses of therapeutic medications and then establish dosage, thresholds, and withdrawal times.  Finally we should implement an appropriate phase in period allowing us to identify gaps in our scientific knowledge before imposing strict and onerous penalties.   Appears that it is the RMTC that needs to get “days.”

1. Association of Racing Commissioners International.  Drugs in US Racing – 2010:  the Facts.  2011. 
2. KAEP meeting, February 
3. Hu HH, MacAllister CG, Payton ME, Erkert RS. Evaluation of the analgesic effects of phenylbutazone administered at a high or low dosage in horses with chronic lameness J Am Vet Med Assoc. 2005 Feb 1;226(3):414-7.  4. http://www.rmtcnet.com/withdrawal_show.asp , accessed 8/12/2014
5. Summary of Medication Recommendations: Pennsylvania Horse Racing Commission Updated September 8, 2010. 6. http://www.khrc.ky.gov/Documents/24%20Therapeutic%20Medications-TB.pdf, accessed 8/12/2014
7. Sams, R.  Scientific Rationale for Establishing a Regulatory threshold for flunixin.  College of Veterinary Medicine, The Ohio State University.  2006.
8. Personal communication, Thomas Tobin 9. http://www.theracingbiz.com/2014/07/21/delaware-horsemen-concerned-positive-drug-tests/, accessed 8/12/2014
10. Rumpler MJ, Colahan P, Sams RA.  The pharmacokinetics of methocarbamol and guaifenesin after single intravenous and multiple-dose oral administration of methocarbamol in the horse. 2013 J Vet Pharm Therap 37:25-34. 11. http://www.drf.com/news/drug-combination-sets-rash-positives, accessed 8/12/2014
12. Hagyard Equine Medical Institute Formulary
13. Muir WW, Sams RA, Ashcraft S.  Pharmacologic and pharmacokinetic properties of methocarbamol in the horse. Am J Vet Res. 1984 Nov;45(11):2256-60.
14. Raynauld JP, Buckland-Wright C, Ward R, Choquette D, Haraoui B, Martel-Pelletier J, Uthman I, Khy V, Tremblay JL, Bertrand C, Pelletier JP. Safety and efficacy of long-term intraarticular steroid injections in osteoarthritis of the knee: a randomized, double-blind, placebo-controlled trial.  Arthritis Rheum. 2003 Feb;48(2):370-7.
15. Knych HK, Harrison LM, Casbeer HC, McKemie DS.  Disposition of methylprednisolone acetate in plasma, urine, and synovial fluid following intra-articular administration to exercised thoroughbred horses. 2013  J Vet Pharm Therap  37:125-132.  16. http://www.rmtcnet.com/resources/Controlled%20Therapeutic%20Medications%20April%202014.pdf, accessed 8/12/2014 17. http://www.bloodhorse.com/horse-racing/articles/86515/wv-hires-new-lab-purse-money-still-in-limbo, accessed 8/12/2014 18. http://www.rmtcnet.com/resources/RCI%20Uniform%20Classification%20Guidelines-December%202012.pdf, accessed 8/12/2014
19. http://arcicom.businesscatalyst.com/assets/arci-controlled-therapeutic-medication-schedule---version-2.1.pdf 
20. Joe Gorajec quoted during a meeting with the Indiana Standardbred horsemen on 8/12/2014 regarding the positive tests  21. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm4838a2.htm, accessed 8/12/2014

To Salix or Not to Salix

In the wake of the PETA videos, which portrayed our majestic sport in a most unflattering light, we are left reeling from the backlash.  While most of what was shown in the video was either legal (the use of Salix and thyroxine) or just edited to the extreme (video of the state veterinarian drawing a post-race blood sample for drug testing, while the commentary implied that something illicit was taking place), certainly there were things that were offensive (the non-stop stream of profane language) and things that were clearly illegal, such as forging documents for illegal workers.  The unfortunate ramifications from this video seem to be taking the form of a rallying cry against raceday medication, which, of course, means no Salix.  The clip of the track vet telling the PETA girl that Salix is performance enhancing because of the weight loss is damning.  He failed to explain the repercussions to the animal of bleeding in the lungs, how scar tissue builds up over time, impairing the horse’s long term respiratory health…or perhaps he did explain it and it just didn’t make the video.  However, if Salix is performance enhancing, oughtn’t it be banned?

  Not so fast.  The scientific paper that first suggested performance enhancement by Salix was published in 1990¹.  It showed only that geldings raced faster on furosemide with no statistically significant difference among fillies and colts.  (Meaning that any performance enhancement is negligible.)  Geldings also race longer than fillies and colts, and hence are more likely to have the effects of chronic bleeding. A previous study² showed improved performance associated with Salix, but this study was performed with known “bleeders”  so the obvious conclusion is that is that any difference in performance is exactly the difference between how well the horse would have raced had it not bled, irrespective of the furosemide (ie Salix is performance enabling).  In fact, a well designed study in 1996³ looking at horses in treadmill exercise tests showed no difference whatsoever between a horse’s exercise performance with Salix and without Salix.

 The same 1996 study mentioned above is oft quoted in the vernacular of the anti-Salix contingent, as supportive of their position.  However, the truth lies in the actual details of the study.  When calculated on a weight for weight basis, the horses had higher oxygen consumption (meaning they performed more efficiently), however, the actual oxygen consumption was unchanged.  Which is exactly what we would expect if Salix had no effect on performance, despite the change in weight.  The vet caught so ominously on video saying they run faster because they are lighter should be embarrassed, not for saying what he obviously believed, but for not carefully reading the very paper he was quoting.

What about the case for the use of Salix?  Certainly racing occurs all over the world without it, which is the primary driving argument for the naysayers.  So let’s again go to the scientific literature and investigate the facts.  A series of studies^4-11 published in 1987 carefully investigated the clinical, diagnostic and necropsy findings of a group of 26 horses retired from racing in Hong Kong.  This group of horses were almost all known bleeders.  The findings were of severe, permanent pulmonary damage.  Clearly, horses are not immune from bleeding in Hong Kong, and more importantly, bleeding was proven unequivocally to cause permanent and severe pulmonary pathology. So, what is to be done?  We look again to the published scientific literature.  The ultimate placebo controlled, cross-over study on the efficacy of furosemide was finally performed by Hinchcliff et al, in 2009¹², funded by the Jockey Club.  As a scientist who has designed and performed many studies, this was the Holy Grail of all study designs, a rare opportunity in Veterinary Science.  This paper showed beyond a shadow of a doubt that furosemide ameliorates in all and prevents in some, EIPH.  In this study, NO horses bled a grade 3 or 4 on furosemide, which answers the question of:  is this the right thing to do or not.  Clearly, yes.

 So, the scientific literature concludes that racing on Salix is beneficial to the health and welfare of the individual horse, and Salix is just as likely (or more likely) to enable normalized performance rather than enhance performance.   The states obviously came to an agreement a long time ago that, just in case it IS performance enhancing (an infinitesimally small effect, if there), we should identify horses that race on furosemide with an L in the program, in order to provide transparency to the public.  This is an effective model, and, according to the Jockey Club’s own sponsored research, should remain.  We should not aspire to the model of foreign lands, many of which have restrictive medication rules for the purpose of human food safety.  Rather than base our reactions on arguments, such as “everyone else does it,” we should rely on the facts and science to guide our future.  Should we react to the PETA video?  Yes.  Should our reaction be to eliminate raceday medication?  I think not.

 

 

1.     Sweeney CR, Soma LR, Maxson AD, Thompson JE, Holcombe SJ, Spencer PA. Effects of furosemide on the racing times of Thoroughbreds. Am J Vet Res. 1990 May;51(5):772-8.

2.     Soma LR, Laster L, Oppenlander F, Barr-Alderfer V.  Effects of furosemide on the racing times of horses with exercise-induced pulmonary hemorrhage.  Am J Vet Res. 1985 Apr;46(4):763-8.

3.     Hinchcliff KW, McKeever KH, Muir WW, Sams RA. Furosemide reduces accumulated oxygen deficit in horses during brief intense exertion. J Appl Physiol (1985). 1996 Oct;81(4):1550-4.

4.     O'Callaghan MW, Pascoe JR, Tyler WS, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. I. Clinical profile of horses. Equine Vet J. 1987 Sep;19(5):384-8.

5.     O'Callaghan MW, Pascoe JR, Tyler WS, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. II. Gross lung pathology. Equine Vet J. 1987 Sep;19(5):389-93.

6.     O'Callaghan MW, Pascoe JR, Tyler WS, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. III. Subgross findings in lungs subjected to latex perfusions of the bronchial and pulmonary arteries. Equine Vet J. 1987 Sep;19(5):394-404.

7.     O'Callaghan MW, Pascoe JR, Tyler WS, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. IV. Changes in the bronchial circulation demonstrated by C.T. scanning and microradiography. Equine Vet J. 1987 Sep;19(5):405-10.

8.     O'Callaghan MW, Pascoe JR, Tyler WS, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. V. Microscopic observations.  Equine Vet J. 1987 Sep;19(5):411-8.

9.     O'Callaghan MW, Pascoe JR, O'Brien TR, Hornof WJ, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. VI. Radiological/pathological correlations.  Equine Vet J. 1987 Sep;19(5):419-22.

10.  O'Callaghan MW, Hornof WJ, Fisher PE, Pascoe JR. Exercise-induced pulmonary haemorrhage in the horses: results of a detailed clinical, post mortem and imaging study. VII. Ventilation/perfusion scintigraphy in horses with EIPH.  Equine Vet J. 1987 Sep;19(5):423-7.

11.  O'Callaghan MW1, Pascoe JR, Tyler WS, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. VIII. Conclusions and implications.  Equine Vet J. 1987 Sep;19(5):428-34.

12.  Hinchcliff KW, Morley PS, Guthrie AJ. Efficacy of furosemide for prevention of exercise-induced pulmonary hemorrhage in Thoroughbred racehorses.  J Am Vet Med Assoc. 2009 Jul 1;235(1):76-82.

 

Eulogy for my Friends

On Sunday morning, my husband and I awoke to a conflagration in one of my barns.  The barn was already engulfed in flames and all we could do was call 911 and watch in horror as our horses and lives went up in smoke.  I have had an incredible outpouring of support from my friends and colleagues, which is strengthening during a time in which I am paralyzed with grief.  I have plenty of work to do, and need plenty of sleep, but whenever I sit to work on the computer or close my eyes, I imagine all my horses burning alive. 

 

It wasn't just a barn full of horses, or Thoroughbreds.  These were my children in some cases the third generation that has been in my family.  I hear so much negativity about the Thoroughbred and racing industry and I can't understand it, because I live this industry and it is wonderful. The greatest highs and now the lowest lows of my life have come from these incredible animals.  When you hear of a tragedy like this one, you think, how awful a bunch of animals perished.  And then the story passes on to something else.  Well, this is a eulogy for my animals.  They were not just animals, some raised to race, some raised to sell, some destined to be riding horses and some just retired: all cherished.  They deserve for the world to know that each one was an individual, and carried one veterinarian's hopes and dreams for their futures.

My first thoroughbred Broodmare, Miss Red, was in that barn.  Her first foal, a colt named Warm Courage (Howard) got loose from my help as a weanling with a chain hanging from his halter.  He freaked out, and ran around the farm, flipped over a fence and fractured his pelvis into a thousand pieces.  Two surgeons recommended euthanasia.  A third said to stall rest him for four months (after all, "you can always euthanize them later").  For over a month, you could walk into that stall and gently rock his pelvis from side to side and the bits of fractured bones made a sound like a bag of potato chips crunching. 

After four months of stall rest, he gradually made it to turnout and never took another lame step.  On the racetrack, he was a two year old workmate for a Canadian Champion, and regularly trained with good horses as a racehorse.  However, in two starts, he bled so much in his lungs that it streamed out his nose.  We turned him out for 6 months to recover.  Back then, I rode the racehorses, so when it came time for him to start back into training as a four year old, I tacked him up and rode him down to the arena on a loose rein.  He was perfect and quiet, walk, trot and canter like a seasoned show horse.  Thus he began his second career.

Howard went on to be a successful Dressage horse with my highest score on him at first level, 68.  He was a successful show hunter and jumper (3'6") on the A circuit, usually in the ribbons, and competed at Novice in eventing.  He was schooling at third level Dressage when he died, and I even bought new white breeches with the plan of starting back into my own show career this spring.  Most of his show career was with 12 and 13 year old girls.  While he had spurs in his hocks, and needed those injected occasionally, his pelvic fracture as a weanling never bothered him.  Never let anyone tell you an OTTB can't be a wonderful, talented and quiet kid's horse.  And don't give up on a pelvic fracture in a young horse, because you can always euthanize them later.  RIP Howard.

Miss Red, a Red Ransom mare,  went on to an unremarkable career as a broodmare.  During the "Tent Caterpillar Crisis"  of 2001-2002 in Kentucky, she developed pericarditis, an inflammation of the specialized membrane covering the heart.  I drained the pericardial sac, and treated her with antibiotics and anti-inflammatories and she recovered.  She went on to have a number of foals, but after they all excelled as show horses and NOT as racehorses, I decided to breed her to a Showhorse stallion in 2008 and get myself a fancy showhorse.  In the last month of pregnancy with that foal, she went into heart failure.  She was diagnosed with restrictive pericarditis, a sequela of the original pericarditis.  We nursed her along and I got my fancy showhorse (although a little small), Sweet Southern Style.  The mare's heart was fine as long as she was not pregnant, so she was retired at the age of 14.  RIP Miss Red and Sweetie.

A 23 year old Exceller mare who was a multiple graded stakes producer had been unable to have a foal for several years and the owners decided to give her up.  I took her on and got two foals out of her, before retiring her at the age of 25.  I spent the next four years of her life pampering her and nursing her through arthritis and other conditions of aging, with the help of other experts.  RIP Excedent at the age of 29.  Never thought something like this would take you.

My husband is a Thoroughbred horse trainer, but we met in graduate school.  He has a Master's Degree in Genetics.  He spends hours researching pedigrees to come up with the best matches for our broodmares.  For the first time in years, we had several commercial yearlings that we could expect a payday at the sales.  Despite the likeliness that they would go to the sale, he would watch them run and play and talk about how he hoped we could afford to keep them and put them in training when the time came, because they looked like great prospects. 

One yearling was a Proud Citizen colt out of a homebred mare.  We raced the granddam of this colt.  She won her first start and ran through her conditions easily in Kentucky, not an easy thing to do.  As a four year old, she was starting to develop marked arthritis of her hock joints:  a condition that would ultimate resolve with time, but it became difficult to keep her sound, so rather than wait out the joints to fuse, we bred her (She was a half to a Champion).  The first foal out of the mare was by Proud Citizen and was gorgeous.  He sold as a weanling for $140,000.  She went on to produce some beautiful foals, of which we raced several.  One day in the spring, when she was in foal to the stallion, Malibu Moon and had another Proud Citizen by her side, I was walking down my farm lane to feed the horses, and I heard her nickering to me.  This was not a usual thing, especially since she had a foal by her side.  I ran to her paddock to find her with a fractured cannon bone.  No, they don't just do this on the racetrack, they can do this in a paddock.  The foal by her side had a femur fracture.  I had to euthanatize them where they stood. 

We still had a filly out of the mare, whom we promptly retired from racing and bred.  Her first foal was a Flatter colt whom we sold for $160,000.  Her second is a Tiz Wonderful filly (3 yo) who is in training, and the third is a Flatter filly (2 yo) who is also in training.  The fourth was a Proud Citizen colt, as beautiful as his 3/4 brother.  RIP Proud Citizen - Saint Savior 2013. 

One of the yearlings was a Pure Prize filly out of one of our own homebred mares.  The mare, Veiled Vow, had been a hard knocking race horse, winning four of 19 starts, all in gutty fashion.  As a seven year old, she was in the lead by 5 lengths in a wide open 5 claimer (which is actually a very tough race, as many old class horses race in these), suddenly stopped, finishing third.  It was completely out of character for her.  She had torn in impressive fashion a ligament in her pastern.  While the mare's pedigree was not really strong enough to breed her in Kentucky, I looked around for someone in a different state market to give her to as a broodmare.  I could find no one I felt would take care of her, and give her the rehab needed to recover from her injury, so we decided to go ahead and breed her ourselves.  If she throws her heart, she will be a great broodmare, despite not being a producer for the commercial market.  So we found a season to Pure Prize and got a beautiful filly.  RIP Pure Prize - Veiled Vow 13.

The third yearling was the first foal out of a young mare we claimed for a broodmare.  As the industry looks to be turning around, we thought it was time to get a commercially viable mare.  She was a beautiful Successful Appeal filly that my husband was desperately hoping we could afford to race instead of sell when the time came.  RIP Successful Appeal - Miss Hanky Panky 2013.

There are always cats and dogs being dropped off in the country by people who realize that they are unable to care for them.  The local small animal clinic identifies them as "Fenger Barn Cat #x"  when I bring them in for FeLV/FIV testing.   A few months ago, a black kitten showed up and adopted us.  We named him Spooky II, since our farm is Spooky Hollow, and we always have to have a Spooky.  We kept him locked in the tack room at nights to protect him from the coyotes, who get pretty bold this time of year.  RIP Spooky II.

 

Thank you for allowing me to write a long eulogy for my friends and livelihood.  I love my farm and the business I am in, but am having a hard time seeing how I can continue in it.  I keep having to meet with adjusters and fire marshalls and walk through the burned out hull of death, and just felt like I had to express what those burnt carcasses meant to my husband and I.  I'm sure time will heal, but having a hard time right now seeing how.

Equine Protozoal Myeloencephalitis (EPM): Update on treatment

Twenty years ago when I first ventured into EPM research, the standard course of treatment was pyrimethamine (Daraprim®), a common anti-malarial drug, in combination with trimethoprim/sulfadiazine. We used a fairly low dose, and treated for only a few months. However, upon following up with some of those early cases, we discovered that this treatment was not sufficient. Researchers in Oklahoma (Clarke, 1992) found that a much higher dose of pyrimethamine is required to achieve drug levels in the cerebrospinal fluid sufficient to kill the protozoa. After these findings, we adjusted our recommendations to a combination therapy of pyrimethamine (1.0 mg/kg daily), in combination with sulfadiazine (20 mg/kg daily). It turns out that trimethoprim is not recommended, and probably should be avoided, if possible, because it is likely to add to the toxicity of the pyrimethamine, without adding to the efficacy. It's been a long time since I patented that discovery, and there are many other options available now. This disease is absolutely curable, and if you stick to a program of appropriate treatment, you will be rewarded with a healthy horse.

Treatment for EPM has since taken many turns, and hopefully, new products will continue to be added to our arsenal for this disease.

• Pyrimethamine/sulfadiazine is still the most common treatment, because compounding pharmacies have made it very affordable. This is a product which interferes with nucleotide synthesis and therefore the production of DNA. Horses require treatment for 6 to 8 months on this drug combination, and sometimes much longer. The biggest problem with this medication is that the long duration of treatment makes compliance difficult. Many horses are taken off the medication too soon, resulting in relapse of clinical signs.

Side effects are most commonly bone marrow suppression which is manifested as anemia and leukopenia (low white blood cell count). This product is not safe in the third trimester of pregnancy, resulting in foals with profound bone marrow suppression and kidney damage. A less common side effect of this product is a neurologic syndrome of ataxia and facial nerve paralysis, which is usually reversible when the drug is discontinued.

• Ponazuril (Marquis®) is marketed as a paste formulation and has been available for over ten years. The label dose is 5 mg/kg for 28 days, but the relapse rate is high (35%) with this dose. Some studies have shown a higher efficacy with 10 mg/kg (or a double dose).

Minimal side effects are seen with ponazuril, although the safety studies indicated that with extremely high doses uterine edema is seen.

• Diclazuril (Protozil®) is marketed as a daily pellet feed top dress at 1 mg/kg for 28 days. This is a difficult product to recommend, since the company's own research had only a 42% efficacy rate. We had reasonable efficacy in the 1990's when we studied a dose of 5 mg/kg, but the Protozil is very expensive at that dosing rate.
• Nitazoxanide (NTZ) was approved right after Marquis in the early 2000's, but was taken off the market when Idexx dropped their pharmaceutical line. NTZ is very effective for EPM at 25 mg/kg for the first four days and then 50 mg/kg daily for 24 days. This product is highly soluble in fat, so added fat in the form of corn or other oil improves the absorption of the product. This product is only available as the human label tablets (Alinia®).

NTZ, while highly effective, has a number of serious side effects. Much of the product is not absorbed in the small intestines, and passes to the large colon, where it can alter the normal colonic flora. The end result can be absorption of endotoxins and in some cases diarrhea. Among the effects of the endotoxemia can be laminitis or founder. While uncommon, this possible sequela should be carefully watched for in the NTZ treated horse. In most horses, the concomitant administration of oil results in improved bioavailability, which results in less drug passing to the large colon, and a lower rate of side effects.

• Decoquinate has recently been suggested as an EPM treatment in combination with levamisole as an immunomodulator (Oroquin-10®) for a 10 day course of treatment. Decoquinate is extremely inexpensive in the form of Deccox premix, a poultry coccidiostat which is added to poultry feeds to prevent coccidia. At the recommended dose of 0.5 mg decoquinate/kg, 4 g of Deccox premix is sufficient for each daily treatment. In cell cultures, decoquinate is highly effective against the rapidly dividing merozoite stage of the EPM organism. The question remains as to whether the decoquinate actually crosses the blood-brain barrier to get to the parasite. Hopefully, further investigation will add this inexpensive treatment to our arsenal.

Oroquin-10 is a new treatment and as such there is no safety data available. The primary anti-protozoal ingredient, decoquinate, is very safe at high doses in horses. Levamisole has many potential side effects in humans, and has not been studied in horses.
• Oxytetracycline is effective against many protozoa in this class. The problem with this drug is that protozoa become rapidly resistant, so it may work for a short period, but treatment doesn't result in a cure. The advantage of this drug is that it can be used intravenously, and in the case of a horse that cannot swallow oxytetracycline provides a way to get treatment into the animal.

In general, oxytetracycline is a commonly used antibiotic in horses for a myriad of conditions, and is relatively safe. In rare cases, oxytetracycline can cause diarrhea.

In addition to the anti-protozoal treatment, immunomodulators like levamisole are warranted. In addition to levamisole, there are several approved immunomodulators, including EqStim ®, Equimune ® and Zylexis ®. I investigated EqStim in the 1990s as an adjunctive treatment for EPM with pyrimethamine/sulfadiazine and found that horses on average required two months less treatment before clearing the EPM antibodies from the cerebrospinal fluid (negative CSF test). Any immunomodulator may be effective, but less is known about levamisole, so my preference is to stick with the approved products like EqStim.

Anti-inflammatory treatments are an essential adjunctive treatment for EPM. More damage is caused by the inflammation surrounding the protozoa than the protozoa themselves. This may include treatment with phenylbutazone or banamine (1.1 mg/kg 1-2 times daily for 3-7 days), as well as the addition of DMSO (1 g/kg in a 10% solution) administered either intravenously or by nasogastric tube. Corticosteroids may be used if necessary. Antiinflammatory drugs are occasionally necessary at other times during the first six weeks of treatment. Some horses actually get worse during treatment, presumably because of a reaction to the dying parasites, a condition which I termed a “treatment crisis” twenty years ago.

Important supplemental therapies are the addition of neuroprotective supplements, such as vitamin E, folic acid and thiamine.

Now that I've explained the different options, I'll tell you my personal recommendations for the treatment of an acute EPM case. I'm not interested in messing around with unproven treatments, unless I have a chronic, relapsing horse with EPM. My standard recommendation is double Marquis (10 mg/kg) for 28 days, followed by pyrimethamine/sulfadiazine for four months. Unfortunately, even with the higher dose of Marquis, some horses will relapse, making the four months of pyrimethamine/sulfa necessary.

Many of the clinical signs associated with EPM are caused by inflammation rather than the parasites themselves. Therefore, almost all of my EPM patients receive DMSO and a short course of flunixin (Banamine ®) to reduce inflammation. I also recommend daily Vitamin E and folic acid. My preference for immunostimulation is EqStim, which I use at the label recommendation of days 0, 3 and 7 and then twice monthly after the initial series.

Equine Protozoal Myeloencephalitis (EPM): Back by Popular Demand

There is no end to the requests that I get to repost my EPM website.  In response to the requests, I have revamped the site and decided to post it here.  This current installment is the introduction, and clinical signs, diagnosis and treatment will follow over the next few weeks.  Keep checking back for the next installment.

He may stumble once or twice. At first you didn't think much of it, but now it's getting worse. He's not lame, just not the same. Or your yearling colt seems to be really clumsy. He drags his hind toes, but maybe its just a stage he's going through. Maybe your trail mare is starting to be a little unsure over the terrain. Or worse, your horse is stumbling, tripping or falling, worse behind. It could be the development of a lameness, or it could be something else.  

Equine Protozoal Myeloencephalitis (EPM) is an infection of the brain or spinal cord of horses that is most commonly insidious in onset with nebulous clinical signs. However, because the organism can affect any part of the central nervous system, clinical signs can vary widely. The neurologic signs that it causes are most commonly asymmetric incoordination (ataxia), weakness and spasticity, although they may mimic almost any neurologic condition. Clinical signs among horses with EPM include a wide array of symptoms that may result from primary or secondary problems. Some of the signs cannot be distinguished from other problems, such as lameness. Airway abnormalities, such as laryngeal hemiplegia (paralyzed flaps), dorsal displacement of the soft palate (snoring), or airway noise of undetermined origin may result from protozoa infecting the nerves which innervate the throat. Apparent lameness, particularly atypical lameness or slight gait asymmetry of the rear limbs are commonly caused by EPM. Focal muscle atrophy, or even generalized muscle atrophy or loss of condition may result. Secondary signs also occur with neurologic disease. Upward fixation of the patella (locking up of the stifle) is among the most common findings among horses with neurologic disease. Another common side effect of EPM is back soreness, which can be severe. Even typical racing injuries may ultimately be caused by EPM, because horses which are uncoordinated are much more likely to "take a bad step" in racing or training. Therefore, any horse with these signs should be carefully evaluated by your veterinarian for the presence of neurologic disease.

EPM was originally identified as a fatal neurologic disease of horses by Dr. Jim Rooney in the 1960s, who saw the characteristic inflammatory lesions in the spinal cord of horses. Protozoa were first identified in the lesions of affected horses in 1974. The protozoa was identified as being similar to other members of the genus Sarcocystis by Dr. JP Dubey, a senior researcher at the USDA, who named it Sarcocystis neurona in 1990. In 1996, my research identified the opossum as the definitive host and source of infection to horses of S. neurona. Over the next several years, I worked with several pharmaceutical companies worked to develop anti-protozoal treatments.

Like other species of Sarcocystis, S. neurona has a two host life cycle. The definitive host (opossum) consumes the muscle tissue of the intermediate host (skunks, raccoons, armadillos) containing protozoal cysts. The protozoa enter the intestinal cells and undergo sexual reproduction in the intestinal cells of the definitive host, forming the infective sporocysts which are passed in the feces of the definitive host. These sporocysts are ingested by the intermediate host, where they hatch in the intestines and pass into the bloodstream. In the intermediate host (skunks, raccoons, armadillos), the protozoa undergoes asexual reproduction in the blood vessels of the liver, lungs and muscles and then encysts in the intermediate host's muscle tissue, without traveling to the central nervous system. When this tissue is eaten by the opossum, the organism undergoes sexual reproduction in the intestinal cells, and forms the infective sporocysts, which are passed in the feces. The opossum does not become sick, but may shed the parasites for months.

Horses represent an aberrant host of S. neurona. Sporocysts are ingested, but never encyst in the tissues of the horse. Instead, they migrate to the central nervous system, where they continue to undergo asexual reproduction intracellularly in neurons, without forming tissue cysts. Horses cannot transmit the organism to other horses, or even to opossums. Horses probably eat the opossum sporocysts inadvertently while eating grass, hay or grain.

In one of my research studies, I was able to reproduce the disease by feeding opossum-derived sporocysts to horses. The horses had detectable serum antibodies at about 3 weeks after infection, and all of the horses that ultimately developed EPM had spinal fluid antibodies about a week later. Those that did not develop EPM never had antibodies in the spinal fluid, even as long as 4 months later.

This disease may be preventable by some simple measures. Anything that may attract opossums into barns should be tightly covered, or put away, especially at night. This includes cat food, garbage and grain. Opossums are particularly fond of cat and dog food. Feed should not be left out at night for the morning, or even during the day to attract birds. The opossum population should be kept under control on farms and stables, where possible. Mesh wire or chain link fencing with "hot wire" around the outside may keep opossums out, since they can climb, but they do not dig. The processes of steam-crimping and pelleting grain kills off the sporocysts, so using processed grains can also decrease the exposure to EPM.

Exposure of horses to EPM occurs at an average rate of about 50%, but approaches 80-90% among some groups of horses. It is impossible to predict which exposed horses will develop fulminant disease. Some horses with active disease may be able to clear the organism without treatment. Currently, the only approach to control of EPM is early detection of incoordination, gait or other abnormalities, definitive diagnosis of the disease by cerebrospinal fluid (CSF) analysis, and appropriate treatment. The disease probably requires a minimum of two weeks and up to two years to develop from the time of exposure to the development of marked clinical signs. Exposure rates (but not disease rates) for different farms or training facilities may vary from zero to 100% of the horses at a given location. Premises with very high seroprevalence appear also to have a high prevalence of clinical disease. Most horses probably ingest the sporocysts, mount an immune response, and clear the organisms before they reach the central nervous system. Alternatively, they may be persistently infected in the central nervous system, but are able to combat the organism sufficiently to prevent the development of clinical signs. There is no "dormant" stage, and there is no "remission.".

Developmental Orthopedic Diseases and Nutrition

Long name, sounds complicated.  "Developmental Orthopedic Diseases (DODs)" sounds difficult to understand and probably doesn't apply to me.  How could it have anything to do with my horse or foal?  Fact is, in young horses, DODs are extremely common and, if not managed properly from an early age, may lead to chronic unsoundnesses in the horse as he grows.  Most importantly, many of these conditions are preventable and/or treatable with nutritional management.

What are DODs?


DODs are exactly what the name implies.  As the foal/young horse grows, abnormalities of growth cause orthopedic problems to develop.  These may show up as tendon contractures, where the knees or ankles buckle forward when the foal is standing, physitis, where inflammation and pain occur in the growth plates, or osteochondrosis (OCD), where the normal ossification of cartilage is disrupted.  All of these conditions can result in chronic lamenesses or crooked legs or both.  These are conditions that develop in young foals to yearlings and primarily during phases of rapid growth.

What Causes DODs?


Normal growth and development depends upon a delicate balance of mineral availability, vitamin cofactors, normal hormone balance, exercise and injury prevention.  The easiest method of preventing DODs is to provide proper nutrition and regular exercise.  This sounds easy, but is actually more complicated than it sounds.  There are several points to consider. 


(1)  Major minerals such as calcium and phosphorus must be present in the diet of foals and adolescent horses in a ratio of 2:1.  Imbalances in these major minerals result in abnormal growth.  While it's fairly easy to make sure that the grain fed to a horse has the right ratio of minerals (because the feed companies make them that way), hay can vary widely.  In particular, alfalfa hay can have a calcium:phosphorus ratio of anywhere from 4:1 to 8:1, making balancing the minerals in the complete diet almost impossible, unless you have the hay analyzed.


(2)  Trace minerals such as zinc and copper, as well as vitamin cofactors are key elements of enzymes that build the cartilage and convert cartilage to bone (ossification) during growth.  All of the minerals must be present within a certain range of total intake and balance, because too much of one mineral can result in deficiencies of the others.  Just a mineral block is not enough, because horses don't know when they need minerals.


(3)  Glycemic index is a term that is gradually working its way into the common vernacular.  A feed with a high glycemic index causes a spike of blood glucose and insulin in the body.  A feed with a low glycemic index is not associated with this insulin and glucose response.  The reason that this is important is that these wildly variable fluctuations in glucose and insulin contribute to the abnormal cartilage growth that results in physitis and OCD.  Therefore, low glycemic index feeds are ideal for feeding young horses.


How do I prevent DODs?


Fortunately, all this research is not just available to you and me, it is also available to the feed companies.  Therefore, most feed companies that produce horse feed, and specifically specialty feeds for growing foals and young horses provide minerals in the correct balance in their feed already.  There are only a few additional things that we need to closely watch to make sure that there are no mistakes.


(1)  Seems counterintuitive, but DON'T allow foals to eat from the mare's feed.  Mare feed is designed for high calories in order to support milk production.  The gastrointestinal tract of foals is not able to properly digest grain until at least 3 months of age.  The only thing the grain will accomplish is to produce the dreaded high glycemic response.  Foal creep feeds such as Foal Starter and Creep (Progressive Nutrition) which are milk based feeds with cooked oats or barley are designed for the intestinal tract of the foal.


(2)  Feed grain mixtures that are designed to be fed with grass hay to growing horses.  If you must feed alfalfa hay, then get it analyzed and consult the nutritionist for the feed company to have a specific grain mixture recommendation.  It is critical that the calcium:phosphorus ratio is correct for growing horses, or tendon contractures, OCDs and physitis will be inevitable.


(3)  Diet balancer mineral products are perfectly balanced in minerals for your growing horse, but the quantity may vary depending upon the age, weight and how fast the horse is growing.  Fortunately, there is almost a standard formula for these products across feed companies.  Similar products are available from most feed companies (M30, Stamm 30, Grow N Win, Purina 32); my personal favorite is Proadvantage (Progressive Nutrition).  A "unit" of balancer turns out to about a pound, or a pint volume of feed, no matter which company's product you are using.  Progressive Nutrition makes a handy chart for the horse owner to use to determine how much diet balancer you need for a growing horse in his stage of growth (http://www.prognutrition.com/pdf/GrowthChartDailyFeedPlannerLT05.pdf).

How do I treat DODs?


I've discussed how to prevent DODs, but how are they treated?  Some of the conditions are more easily treated than others.  Many physitis cases and tendon contractures respond to nutritional therapy.  These conditions are associated with rapid growth, likely because the mineral intake is imbalanced, and bone growth requires a different set of minerals than tendon or cartilage growth.  If the minerals can be properly balanced and any deficiencies corrected, synchronous growth of all the structures can be restored.

In order to restore mineral balance, I will typically feed these young horses 1/2 to 1 pound more diet balancer than the recommended quantity for their stage of growth.  If they are on alfalfa hay, it has to be discontinued and replaced with grass hay.  In suckling foals, mineral supplementation can be achieved by administering a paste or drench mineral supplement, such as Rejuvenaide (Progressive Nutrition) or Foal Aide (Buckeye Nutrition).  Again, for foals that already have a DOD showing up, I administer 15 - 25% more than the label recommendation.  Fortunately, in suckling foals, contractures will respond within just a few days to this mineral supplementation.  Physitis may take longer to respond, because the bony enlargement associated with physitis doesn't go down; it just stops getting bigger, and the foal grows into them.

If trauma or concussion is contributing to the DOD, such as can be the case with physitis, some exercise restriction is recommended.  Generally, the young horse should be restricted to a small paddock with one other buddy, so that excessive concussion from "running with the herd" is avoided.

What about non-nutritional treatments?

Physitis:  Many people advocate the use of poultice to help remove heat from inflammation of the growth plate.  This may help, but the majority of the heat and abnormal cartilage is deep within the growth plate and unaffected by the poultice.  Topical anti-inflammatory treatment with Surpass may also help, but again will only affect the superficial parts of the growth plate.  If the young horse is actually stiff or lame with the physitis, systemic anti-inflammatory medication is warranted, preferably Equioxx for 2-3 weeks.  Other anti-inflammatory drugs such as bute can predispose to stomach ulcers, so should be used with Gastrogard.

If the physitis is actually causing asymmetry of growth such that the legs are becoming crooked, then some other intervention is required.  Non-invasive therapies include trimming the feet lower on the side of the physitis to encourage growth on that side.  Shock wave therapy of the affected side may decrease the pain associated with the inflammation, increase blood flow and decrease inflammation, thereby stimulating growth of the affected side of the physis, and ultimately straightening the leg.  Some people are also advocating internal or external blistering of the affected side of the growth plate, also to increase the blood flow.

If the angular limb deformity ("crookedness") is severe, then surgery, where a screw is placed across the growth plate on the less affected side is indicated.  A screw is used to slow growth on the faster growing side of the physis and then allow the more affected side to catch up.  When the leg is straight, the screw is removed.

Contracture:  Caught early, nutritional treatment should correct most cases of contracture.  If allowed to progress, then complex splinting procedures, or even surgery, where tendons and ligaments are cut may be necessary.

OCDs:  OCDs can be prevented, but not treated with nutritional therapy.  Most researchers agree that the very beginning of OCD occurs in utero, so adequate mineral balance in the pregnant mare, and particularly in third trimester is critical.  The early signs of OCD in the young horse usually becomes evident from 8 - 12 months of age.  Treatments in this age group range from adminstration of Adequan (polysulfated glycosaminoglycans) or Legend (hyaluronic acid) to feeding calcium containing supplements.  As previously discussed, imbalanced high calcium or high phosphorus diets can cause OCDs, so additional supplementation should probably be avoided.  Shock wave therapy to stimulate blood flow to cartilage may be useful.  Platelet Rich Plasma (PRP) has also been advocated because of the growth factors that may be present in the PRP.  Equine Growth Hormone also stimulates the presence of local growth factors in cartilage that may return normal function to the cartilage.  Finally, surgery to inject corticosteroids into the lesion or remove the abnormal cartilage may be necessary.

Conclusion:


If your equine interests include foals or young horses, then developmental orthopedic diseases should be at the top of your list of concerns.  The most important factor that you can control is the nutrition.  Do not allow your foal to eat from the mare's feed tub, and provide a creep feed designed for the foal's digestive tract.  Make sure that your young horse has good quality grass hay and feed a diet balancer that is designed to be used with grass hay.  Avoid high glycemic index grains, like sweet feed until at least 2 years of age.  Allow foals to run in groups and spend at least 8 hours a days in free turnout for exercise.  Follow these simple steps to lay the foundation for a healthy and sound partnership for life.

Everything you need to know about Deworming Horses

Everyone knows how to deworm horses. You buy an inexpensive dewormer from the feed store and give it to your horse. You need to rotate the dewormer every two months to prevent resistance in the parasites. The old method of tube worming isn't used anymore since the newer dewormer compounds have become available.

Actually, recent research on parasite resistance has blown this whole concept of rotational dewormers out of the water. It turns out that (1) eliminating parasites completely from horses is neither beneficial nor desirable, and (2) our diligent rotational deworming program has not prevented resistance in equine parasites, but rather is creating super-parasites.

Historically, animals and their parasites have evolved together, reaching an “agreement” where the animal's immune system keeps the parasites under control, and the parasite agrees not to kill the host upon which it depends. By eliminating all of the parasites, the animals' immune system can go into overdrive, ultimately predisposing the horse to develop allergies, and possibly autoimmune diseases. So, in reality, a low level of parasitism functions as an “immune optimizer” for the animal. It turns out that a fecal egg count of 0-500 reflects a low level of parasitism, which is optimal for the horse, but unlikely to cause parasite related disease. Over 500 epg indicates a possibly disease causing infestation.

The more disturbing concern is the possible production of super-parasites. Resistance to every major class of dewormer has been identified.  In the case of the most common equine parasite, strongyles, eggs are passed in the feces, they are not infective to the horse. They must hatch and develop into stage 3 larvae (L3), a process which is weather dependent. They do not develop at all below 46F or over 100F, making April – November the prime time for parasite transmission in most of the United States, including Kentucky. It turns out that a solid deworming after the first hard frost in the late fall with moxidectin will take care of the parasites for the rest of the winter. Once the weather starts to break in the spring, a fecal on all the horses at a farm is indicated to determine which horses are shedding. Since 20 % of the horses shed 80% of the parasite eggs, the key is to identify those horses and treat them regularly to keep the overall worm burden on the pastures down. The 80% of horses which are low shedders should be allowed to maintain this lower worm burden, and shed eggs that are not subjected to the selection pressure of rotational dewormers. This way, only a small number of the eggs on the pasture belong to the potential “super-parasites.”

After the first spring fecals and treatment of all horses with fecal egg counts over 500 epg, the fecals should be repeated on those treated horses in 4 weeks to determine if the worms were sensitive to dewormer used. If the counts are still high, that indicates that the worms on that farm are no longer sensitive to that dewormer. This resistance is now permanent for that farm, and it is of no value for use on that farm. Worms on specific locations have been tested as long as 20 years after resistance develops, and they are still resistant on that farm. The ineffective dewormer should be permanently left out of the dewormer rotation for that farm

The pre-patent period (time from consuming the infective L3 larvae to adulthood and production of eggs in the feces) of strongyles is about 60 days, so fecals should be repeated on all the horses in 2 months. Again, any horses with 500 or lower epg counts are considered to have low level infestations and do not need to be treated. Horses with over 500 epg have high infestations and require treatment. As a rule, those horses with high egg counts will be the same horses over and over, because they lack the appropriate immunty to control the infestation on their own. Therefore, this subset of “high shedders” require a rotational deworming program. The typical rotational program for this group of horses will sound pretty familiar: Oxibendazole (Anthelcide ®), Ivermectin, and Pyrantel (Strongid ®). The reason that all the horses should not be on the rotational program is that we want to encourage the subset of parasites that can be easily controlled by the horse's own immune system, and not indiscriminately kill off that group. This is the best way to prevent the development of a super-parasite, and also allow the horses to maintain a healthy, small population of worms to properly stimulate immunity.

There are other parasites besides those that produce eggs that can be measured in the feces. Because of these groups of parasites, all the horses in a group should be dewormed twice a year with either ivermectin or moxidectin. Firstly, the large strongyles have a pre-patent period of almost 6 -9 months and the larvae can migrate through the liver, mesentary and other abdominal organs. Therefore, horses should be wormed before the eggs can be detected in the feces.

The second group of parasites that are not typically found in a fecal egg count is the tapeworms. This group of worms has a stage of its life cycle in mites that live on the pasture, and horses actually pick up the infection by eating the mites on the grass. The larvae develop into adults which attach themselves to the mucosa in the region between the ileum and cecum and can cause colic. Tapeworm eggs are not usually found in the feces because they do not float in the typical fecal lab test. In order to keep tapeworms under control, we deworm at least once a year with either praziquantel, which is found in Quest Plus ® (moxidectin with praziquantel), or Equimax ® or Zimectrin Gold ® (ivermectin with praziquantel).

Next are the bots. Bot flies lay eggs on the horses hair, commonly on the neck and inner portions of the front limbs. As the horses itch themselves with their teeth, they pick off the eggs, which hatch in the mouth and travel to the stomach. The bot larvae attach to the stomach lining, causing stomach irritation, including ulcers. Typically we control bots by keeping the bot eggs scraped off the hair to prevent ingestion and also by deworming with either ivermectin or moxidection after the first frost in the fall to eliminate the bots.

Other parasites include habronema, which contributes to summer sores (non-healing wounds on the legs), conjunctivitis and other eye lesions, and onchocerca, which causes skin and eye lesions. Since these parasites don't produce eggs in the feces, twice yearly deworming with either ivermectin or moxidection controls these parasites.

Summary of Deworming Recommendations for Adult Horses:

1. Deworm with moxidection with praziquantel (Quest Plus ®) in the fall after the first frost to eliminate encysted strongyles, bots, onchocerca, habronema and tapeworms. This should control parasites for the rest of the winter.

2. Check fecals on all horses in the group about 4 weeks after the first warm days (7 – 10 days of consistently warm days in a row). Deworm all horses with egg counts over 500 with 5 day double dose fenbendazole (Panacur ®) to eliminate migrating larvae and encysted larvae.
3. Recheck all treated horses again in 10 – 14 days to determine if the fenbendazole was effective. If yes, then the Strongyles on the farm are not resistant to fenbendazole, so it is a good product to keep in the rotation.
4. Check fecals on all horses in the group 8 weeks after the first. This allows a full cycle of infective L3 larvae picked up after the first taste of Spring maturing into adult worms which shed eggs in the feces. Any horses whose immune systems are unable to control their parasites (high shedders) will have egg counts over 500 epg, and should be dewormed with the next compound in the rotation, pyrantel pamoate (Strongid®) . Again, fecals should be checked on those that were dewormed at 10-14 days to determine if the pyrantel was effective. Again, if the parasites are not resistant, this product can be kept in the rotation. Low shedders will have low egg counts (<500 epg) at both times.
5. Now you know which horses are “high shedders” and which are “low shedders.” After the next 8 weeks, all horses should be dewormed with Ivermectin with praziquantel (Ivermectin Gold ®, Equimax ®).
6. At the next 8 week point, deworm the “high shedders” with the next product in the rotation, oxibendazole (anthelcide). Again, recheck the fecals at 10-14 days to determine if this dewormer is effective on your farm.
7. At the next 8 week point, repeat the process, this time using pyrantel again, only if it effective in your location.
8. Next, deworm with Quest Plus after the first frost.

After following this program for a year, you should have a good idea which horses are the high shedders and which are the low shedders. If you have a stable population, then, your program will be similar year after year. All horses coming into the group should be dewormed with Quest Plus before joining the herd.

Foals add a different dimension to the program. Most adults develop immunity to worms, but foals have never been exposed, so deworming is of critical importance. The first worms that foals pick up are Strongyloides (threadworms), which they actually ingest in the milk of the mare. There is some debate about whether Strongyloides causes any disease in foals. However, current recommendations are to dewormed the mares with ivermectin within 24 – 48 hours of foaling to eliminate this parasite.

The next group of parasites that are important to foals are the ascarids, or roundworms. This group is one of the biggest problems groups, because the eggs hatch in the intestines and then burrow through the tissue of the foal and migrate through the lungs. Many foals develop a cough and even pneumonia as a result of the parasites migrating through the lung tissue. For this reason, the first deworming of foals should be with a product that will eliminate most of these migrating larvae. Therefore, this early deworming at 3-4 weeks of age is with ivermectin. Those ascarids that escape the ivermectin deworming will go on to develop into adults, which can then cause generalized unthriftiness and colic. Therefore, at 8 weeks, foals should be dewormed with pyrantel.

The early deworming program in foals is designed to treat for parasites that are not mature enough to produce eggs, so fecal egg counts are not of value. However, once the foals are out to 16 weeks, they should start on the fecal egg count program. Young horses should be checked every two months until after the first frost of their yearling year, after which they join the adult program. Yearlings are still at risk for ascarids, and consequently vigilance should be maintained until they are two-year-olds.

Summary of Deworming Recommendations for Foals:

1. Deworm mares with ivermectin within 24 – 48 hours of foaling to control Strongyloides (threadworms) infections in the foals.
2. Deworm with ivermectin at 3-4 weeks of age to treat migrating larvae of ascarids (roundworms).
3. Deworm with pyrantel at 8 weeks of age.
4. Start checking fecal egg counts at 8 week intervals starting at 16 weeks of age, and use rotational dewormers of oxibendazole, and pyrantel, when counts are high. Respiratory signs without evidence of infectious disease may be associated with migrating ascarids, and may require an additional deworming with either ivermectin or double fenbendazole. Recheck fecal egg counts 10-14 days after deworming to determine if the worms are susceptible to the dewormer product you are using. If the product you are using is not effective, you need to eliminate that product from your rotation.
5. Ivermectin is indicated at the next 8 week point, similar to the adult program.
6. The terms “high shedders” and “low shedders” aren't useful in this age group, because they tend to all have high egg counts, probably because of limited immunity at this age.
7. Continue to deworm at 8 week intervals until after the first frost, when moxidectin with praziquantel (Quest Plus ®) is indicated. Always carefully estimate the foal's weight and dose exactly according to weight to avoid accidental overdose.
8. Young horses join the adult fecal egg count and deworming program 4 weeks after the first break in the weather in the spring, although most yearlings of this age have not developed sufficient immunity to control the parasites themselves, and will carry a high worm burden. This group needs to continue on the rotational deworming program, with spot checking egg counts at 10-14 days post dewormer to determine resistance among the parasites on the farm.
9. By the spring of their two-year-old year, the pattern of “high shedder” and “low shedder” emerges, and you will be able to determine which horses must remain on a high frequency rotation, and which require only ivermectin or moxidectin with praziquantel twice a year.

Management Program to keep Parasitism in Check

Management programs will also help limit parasitism in horses, and are probably a bigger part of parasite control in warm regions of the country, where you cannot count on a hard frost to “reset” the environmental parasite clock.

The most critical factor is pasture rotation. If pastures can be rested for 2 – 4 weeks at a time, the fields can be harrowed to break up the manure piles, and over a 2 – 4 week period (shorter in temperatures over 70F, longer below 70F) the strongyle eggs hatch, and the infective L3 larvae emerge. After a period of time, if they are not ingested by a susceptible host (horses), they die off, leaving the pasture strongyle free. If pastures cannot be completely rested, an alternative species, such as sheep, cattle or goats can be grazed instead, because the parasites do not cross host species lines. If horses are kept in a sufficiently small pasture, an alternative to pasture rest is manure removal. The manure can be picked up and disposed of similar to stall muck. Composting, where the internal temperature of the piles reaches and maintains 165F will also kill off the parasites. Unfortunately, very little kills off ascarid eggs, and these eggs remain viable on pasture for up to 20 years.

This is the current state of the recommendations of the parasite experts at this time in order to optimize equine health and immunity as well as prevent further resistance among the equine parasites. For specific recommendations for your area of the country, contact your veterinarian.