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08 May


Upper respiratory infections are a significant problem across all equine industries and in the racing industry, in particular.  Studies have demonstrated considerable economic losses resulting from subclinical disease (when horses don’t look obviously sick but are performing below expectations), from acute infection (when horses have nasal discharge, a cough, and obviously need rest or a reduction in training), and from the hypersensitivity and chronic inflammatory airway disease that develops in the lungs as a result.1, 2   As there has been a sudden increase in the number of upper respiratory infections in racing stables in New Zealand over recent months, I thought now might be a good time to write something about Equine Herpes Virus.

Most frequently, outbreaks coincide with yearling sales or a change in season, as this is the time of year in which racing stables introduce new horses to their yards, many of whom will bring “colds” or upper respiratory infections with them.  Horses get “colds” just like people.  They will have a fever, runny nose, sore throat, and occasionally a cough.  Many will also appear depressed and lose their appetite.

There are a number of pathogens that cause upper respiratory infections in horses including Equine Herpes Virus, adenoviruses, rhinovirus, Equine Viral Arteritis (EVA), Streptococcus Equi Equi (Strangles), Streptococcus Equi Zooepidemicus, and Equine Influenza (EI).  (In New Zealand, so far, we haven’t had EI…touch wood…)  Equine Herpes Virus (EHV), identified over 60 years ago, remains the most common and economically significant cause of upper respiratory infections, world wide. 3,4, 5, 6, 7

There are actually nine different strains of Equine Herpes Virus, but only a few of them are clinically significant.  The most important are EHV type 1 and EHV type 4 as they produce the most virulent, easily communicable, and most costly outbreaks across equine industries, all over the world.   While EHV types 2 and 5 are ubiquitous (everywhere) and commonly cultured, the respiratory signs produced are generally mild, and they have not been demonstrated to produce serious outbreaks and economic loss.  A recent study done in New Zealand determined that 44% of individuals from a small group with nasal discharge had positive cultures for EHV type 2 and type 5 was identified in 50%.  EHV types 1 and 4 were only identified in 6% and 27%, respectively, though the small sample size and specific population tested were cited as limiting factors.  Some heathy horses also cultured positive for EHV type 2 in the study, and the author explained that there were difficulties in positively identifying EHV type 4.8  All in all, the researcher found that EHV was strongly associated with respiratory disease.  Previous studies done in New Zealand demonstrated evidence of recent EHV Types 1 or 4 infections in 72- 100% of horses and foals.9, 10

Equine Herpes Virus can be transmitted directly from horse to horse, but it can also be transmitted by droplets in the air (which can travel the length of a football field when a horse coughs). Exposure to virus particles in the environment on fences, gear, water troughs, clothing, shoes, etc. can also produce infection.

Horses of all ages are susceptible, but animals under three years of age and those under stress are most frequently affected.  This would include most weanlings, yearlings, racehorses, and horses in training of any sort. 6

Immunity from natural infection lasts for only 2 to 6 months, so the same individual can become infected more than once in a year or their lifetime.  While horses older than 5 years of age seldom show signs of illness, they often harbour the virus and provide a source of infection for the younger, more susceptible horses in the population.  Young horses, with little immunity, will almost certainly become clinically ill when exposed.   As they recover, over about 4-28 days, the virus, rather than being eradicated, enters the latent (silent) stage, sheltering in lymph nodes.6  Once the horse is under stress due to travel, training, or co-mingling at sales, the virus becomes reactivated and is shed into the environment, infecting other susceptible individuals.  Studies have shown that between 60 and 88 percent of horses may be silent carriers.6

Other Clinical Syndromes Including Abortion and Neurological Disease

Equine Herpes Virus can cause a few different types of disease syndromes including respiratory disease, abortions, and neurological problems. EHV type 4 is believed to cause the vast majority (up to 90%) of significant upper respiratory infections11  and has been identified in some abortion cases, while EHV type 1 causes the majority of abortion cases, some respiratory infections, and most of the neurological cases.6
The evidence, so far, suggests that EHV infection begins in the respiratory tract, and once the virus multiplies enough in susceptible horses, it gets into their blood stream where it produces a “viremia”.  (This just means virus in the blood.) If there is a large enough amount of virus in the blood, it gets into the central nervous system where it can damage the brain and spinal cord.  It appears that EHV-1 is the only type, or at least, the type most likely to produce neurological symptoms as it appears to be the only one that settles in central nervous tissue.12
The neurological form of EHV (Equine Herpes Myeloencephalopahy or EHM) is fairly rare, especially in Australia and New Zealand, though there is some evidence that the incidence is increasing. 13
Clinical signs often develop 8 to 12 days after a respiratory infection and begin with weakness in the hind legs and incoordination.  It can quickly progress, and within a day or two, horses will go down and be unable to get up.  In some cases, no signs of respiratory infection are obvious, and the only early indication of a problem is a fever.   Sudden weakness and death may be the first noticeable sign.

Alternatively, the viremia can allow the virus to get into the uterus.  Once there, it causes the placenta to detach and the foal to be aborted.  EHV-1 abortion was, up until the mid-80’s the most costly equine disease in North America, resulting in abortion storms that affected large percentages of mares on stud farms.  From the mid-80’s, a widespread, aggressive vaccination program was instituted, and the incidence of EHV-1 abortion was reduced by 75%.  Fortunately, in New Zealand, the incidence of abortion has been lower than in other countries.


Treatment of viral infections is difficult.  There are no really effective, economical anti-viral drugs available.  Antibiotics do not kill viruses, and can only be used to treat animals with bacterial infections.

The best way to deal with EHV infection is to prevent it.  Prevention requires a multi-faceted approach including quarantine, hygiene, and vaccination programs. Isolation of sick horses and quarantine of exposed animals and premises are useful measures, but they are not always practical at racing stables and farms. When horses attend sales or races, they are almost certain to be exposed to individuals who may not have been adequately isolated at their home stables and who may be shedding virus.  Vaccination is the most practical way to reduce the rate and severity of infections in a racing stable environment where the horse population travels and changes regularly and in the racing industry as a whole.

Vaccinating a single horse will not reliably prevent that horse from getting sick if it is exposed to an overwhelming dose of virus.14  Instead, to protect individual horses from viral infection, it is necessary to produce “herd immunity”.  The epidemiological term, herd immunity, can be explained like this.  If 100 percent of the horses on a farm are vaccinated, it is expected that 70 percent of those horses will become immune.  If 70 percent of the individuals in a population have immunity, then virus will not have enough susceptible hosts in which to multiply. This will reduce the overall viral load in the environment and reduce the viral challenge to each individual.  This will stop the transmission of virus in the herd.14

That is the long way of saying that ALL of the horses on a farm or in a population must be vaccinated to prevent respiratory infection from being transmitted from horse to horse and therefore to protect individual horses.

A vaccinated horse may still get sick if it is exposed to an overwhelming viral challenge at the races or during shipping.  They may be exposed to a sick horse or placed in a stall where a sick horse has been. Vaccination, however, will ensure that the horse will not get as sick and will recover faster than if not vaccinated. 15

Vaccinate all young horses frequently and older horses regularly, particularly if there is an outbreak.  Use a modified live vaccine containing EHV 1 and 4, if possible.  If horses have never been vaccinated for EHV before, 1 to 2 booster shots are recommended at 4-6 week intervals after the first dose.  Foals should have their first dose at 4 months of age.  Since immunity only lasts 12 weeks, one EHV 1+4 vaccine should be given every 3 months for optimal protection and for young horses in higher risk environments (racehorses in training would fall into this group), though the minimum recommendation is every 6 months.11,16,17

Vaccinate pregnant brood mares at 5, 7, and 9 months of gestation with an inactivated vaccine that contains only EHV-1, preferably at high antigenic levels.  Pneumabort K, which is available in New Zealand, and Prodigy are two brands to consider.

There is very little evidence that vaccination can specifically prevent the neurological form of the disease, but recent studies have found that modified live vaccines can reduce the “viremia” and this may reduce the likelihood that the central nervous system of the horse will be affected.18

It has been noted that EHV types 1 and 4 are fairly consistent and antigenically stable,19 so unlike influenza viruses that mutate regularly, the same strains of EHV 1 and 4 remain basically unchanged over many years.  The implication of this is that vaccines need not be adjusted annually or for each outbreak to be effective.

It is important to understand that once horses are affected with Equine Herpes Virus, they can continue to be carriers for life.  At times of stress, they may begin to spread the virus around in their environment and infect susceptible horses around them. As a result, it is worthwhile to vaccinate young horses regularly to reduce the likelihood that they will become infected and then become silent carriers, even if there are no reports of a serious outbreak.


1.    Viel, 2009. A New Understanding of Equine Inflammatory Airway Disease, OVMA Conference Proceedings, 2009.
2.    Bailey, 1988. Wastage in the Australian Thoroughbred Industry)
3.    Allen, GP, 2002. Epidemic Disease Caused by Equine Herpesvirus-1: Recommendations for Prevention and Control, Equine Veterinary Education, 2002.
4.    Bryans, JT & Allen, GP. 1989. Herpes Viral Diseases of the Horse, Herpesvirus Diseases of Cattle, Horses and Pigs, edited by Wittman, G.
5.    Crabb, BS. & Studdert, MJ, 1995. Equine 86 Herpesviruses 4 (Equine Rhinopneumonitis Virus and 1 Equine Abortion Virus,  Advances in Virus Research, 45, 153–190.
6.    Allen GP, JH Kydd, JD Slater and KC Smith. Equid Herpesvirus 1 and Equid herpesvirus 4 infections. Infectious Diseases of Livestock, (Ed.) JAW Coetzer and RC Tustin. Oxford Press (Cape Town), Chapter 76, pp 829-859, 2004.
7.    Ostlund, EN, 1993. The Equine hHerpesviruses. Veterinary Clinics of North America, Equine Practice, 9, 283–294.
8.    McBrearty, Thesis, 2011.
9.    Dunowska, M, Wilks, R, Studdert, MJ, and Meers J, 2002. Equine Respiratory Viruses in Foals in New Zealand, NZVJ, 50, 140-147.
10.    Dunowska, M, Wilks, R, Studdert, MJ, and Meers J, 2002. Viruses associated with outbreaks of equine respiratory disease in NZ, NZVJ, 50, 132-139.
11.    Townsend, H and Morley, P, 1992.  Western College of Veterinary Medicine, Department of Large Animal Internal Medicine, lecture notes.
12.    Allen GP, JH Kydd, JD Slater and KC Smith. Equid Herpesvirus 1 and Equid herpesvirus 4 infections. Infectious Diseases of Livestock, (Ed.) JAW Coetzer and RC Tustin. Oxford Press (Cape Town), Chapter 76, pp 829-859, 2004. 13.
13.    D.P. Lunn et al – EHV-1 Consensus Statement J Vet Intern Med 2009;23:450–461
14.    Iverson, J, 1992. Western College of Veterinary Medicine, Department of Veterinary Epidemiology, Lecture Notes.
15.    Patel, JR, Foldi J, Bateman H, Williams J, Didlick, S, Stark R.   Equid Herpesvirus (EHV1) Live Vaccine Strain C147:  Efficacy Against Respiratory Diseases Following EHV Types 1 and 4 Challenges.  Veterinary Microbiology vol 92, Issues 1-2, 20 March 2003, pg 1-17.
16.    Hines, M.  Department of Veterinary Clinical Services, Washington State University,  Recommended Vaccinations for Washington Horses, 2001.
17.    AAEP website, 2001.
18.    University of California Davis School of Veterinary Medicine,  EHV-1 Vaccination Fact Sheet.
19.    Allen, GP & Bryans, JT, 1986. Molecular Epizootiology, Pathogenesis, and Prophylaxis of Equine Herpesvirus-1 Infections. Progress in Veterinary Microbiology and Immunology, 2, 78–144.
20.    Perkins, NR, Reid, SW, And Morris, RS, 2004. Profiling The New Zealand Thoroughbred Racing Industry, NZ Veterinary Journal 53, 69-76.

08 May


Does It Have the Right Stuff and Is the Balance Right?

When reading labels, it is important to consider all aspects of the nutrient composition, including, completeness, balance, form, and dose.  Then you can compare the composition to the nutrient requirements of your horse.


Metabolism is quite complex, requiring a broad range of essential nutrients to function optimally.  You can’t just feed two or three nutrients and hope to support performance, recovery, health, and metabolism.  A lot of one nutrient doesn’t make up for deficiencies in another.  If you ran out of food in your house and tried to just live on a big bag of salt, you wouldn’t last long.


The balance between nutrients is equally important.  Some nutrients are required for the uptake and function of other nutrients. (These supportive and cooperative nutrients are called co-factors.) Too much or too little of one nutrient may result in deficiencies or toxicities of other nutrients.  Imbalances, therefore, can adversely affect health, performance, and recovery. At a minimum, imbalances in a feed or supplement can render a product ineffective.

For instance, vitamin C is required for the absorption of iron from the gut.  Without vitamin C, iron passes straight through the gut and out in the faeces.  Vitamin E, on the other hand, has a negative interaction with iron.  It binds with iron and reduces its absorption, causing much of it to be wasted. So, in order for horses to use dietary iron effectively, it must be administered with vitamin C and without vitamin E.  Iron balance is also closely related to Zinc, Manganese, Cobalt, and Copper.

Common Feed Ratios

Ca:P 1-2:1
Zn:Mn 0.7-1.1
Zn:Cu 3-4:1
Fe:Cu 4:1

B vitamins are known to work better when administered in optimal balance with each other.  They act in concert in many metabolic pathways important in energy production, red blood cell production, coat and skin condition, nerve cell function, and appetite.  Giving a bigger dose of one B vitamin may not produce improvements in health or performance if the entire range of B vitamins is not supplied in optimal balance.

Amino acids are another good example of how nutrient balance is important.  That is a topic I will discuss further in READING LABELS PART 4 – about evaluating feeds, but in the meanwhile, read the article written by Dr. J. Stewart that we posted on our blog about top-line.  In that article, Jenny explains how the balance of amino acids in a feed is as important as the amount of protein.  Imbalances in amino acids limit the amount of protein in a feed that is usable in the horse to produce proteins and muscle cells, and the wasted amino acids, that can’t be used for protein synthesis, create a load on kidneys, elevate body temperature, and elevate heart rates.


Bioavailability refers to how absorbable and usable nutrients are.  While this is partly related to the composition and balance of nutrients in a product, the term is most frequently applied to the form each nutrient is provided in.

Some forms are more easily absorbed and used than others.  The trace element Chromium, for example, exists in several different forms.  The form of chromium found in a chrome bumper on a car is not very digestible at all, but the form incorporated into yeasts is very easily absorbed and then used by cells.  Minerals including Calcium, Magnesium, Iron, Cobalt, Copper, Zinc, Selenium, and Manganese can all be provided in a variety of forms, each of which have differences in their bioavailability.  In general, inorganic forms of nutrients are less well used than organic forms, though that is not always a reliable rule.  Zinc Oxide is one of the most bioavailable forms of Zinc, whereas Zinc Chelate forms a big molecule that remains quite inert.  In most cases, though, minerals provided as gluconates, lactates, and amino acid or protein complexes are well used.

When reading labels, you should note whether the amount of the ingredient or the amount of the active molecule is listed.  For instance, Iron Bioplex (iron is bound to amino acids or protein) contains only about 10% iron.   If a label says a product contains 400mg of iron per dose, that would mean that a dose contains about 4000mg of Iron Bioplex yielding 400mg of very well absorbed and used iron.  If the label says a product contains 400mg of Iron Bioplex per dose, then it really only has 40mg of iron.  Make sure that you read those details carefully when reading labels and comparing products.

So that’s part 2 done!

To recap Reading Labels – Parts 1 and 2 on Supplements

From Part 1:  If labels are easy to understand so that you can tell, at a glance, what you are giving your horse, then the manufacturer is probably proud of their formulation and believe it will stand up to scrutiny. If you have to perform too many calculations to figure out what you are giving, there is a fair chance that the formulation isn’t great. In any case, take the time to do the math and make sure you are comparing apples before picking the cheapest or prettiest product on the shelf.

From Part 2:  When reading labels, it is important to consider all aspects of the nutrient composition, including balance, form, and dose, in relation to the nutrient requirements of your horse.

Make sure you read the third instalment of this Reading Labels Blog Reading Labels Part 3 – Product Quality Management. This looks at the quality of ingredients and manufacture.

08 May


Are You Comparing Apples with Apples?

(After working on this for more than an hour and barely scratching the surface, I suddenly realized that this will end up a very long (and boring) blog entry, indeed, so maybe I’ll try to do this in a series of smaller bite-sized chunks.  For now, I’m going to start with supplements. I think they will be easier to sort out.  If you want to know more about feeds, keep checking back.  I’ll eventually finish this…I hope.)

With the tremendous range of feeds and supplements available, how do you even begin to select the right ones for the horses in your stable?

Do you mostly rely on testimonials from friends, feed merchants, or sales reps from the feed/supplement companies themselves?  If so, you are not alone. The most common questions I am asked, by the horsemen I meet, from all around the world, relate to comparing feeds or feed supplements.  I get a lot of,  “hey doc, a rep from a supplement/feed company came the other day and told me about one of their products.  They said it was the best ever… but they all say that.  What do you think of it?  Should I feed it to my horses?”

If you have ever wanted to ask those questions, read on.  I’ll try to give you some tools to sort out the wheat from the chaff.  Just like the horsemen who ask me about new products they have come across, I can’t always answer those questions immediately.  I have to follow a process to objectively evaluate them.  I’ll get to that next.

To begin with, so you feel better about your state of confusion when looking at supplements, here is my experience with the same thing.  (…and keep in mind, I am a veterinarian, and I studied nutrition in university before starting veterinary school.)

Back in 1999-2000 or so, I started looking at oral pastes and powders as a practical, economical alternative to the more invasive and expensive pre-race treatments I used to give my patients.

(My “loaded amino acid jug” was a Duphalyte or Amino Plus with 30cc’s CaCo Copper, 10cc’s Hemo 15, and 10cc Hippiron, with or without vitamin B12 and vitamin C, given iv along with folic acid given im.  Some of my clients liked to have their horses tubed with electrolytes and given Co-Forta injections instead).

In order to find one, or a couple of pastes in combination, that I could recommend to my clients, I looked at lots of supplements…practically all that were available in 2000, in fact.  I found a huge number of products listing different combinations of nutrients that were:

  • included in different forms (For example, Calcium could be provided as Calcium carbonate, Tri-calcium phosphate, or Calcium gluconate), and
  • quantified with different units of measure (mg/kg, %, ppm, to name only a few).
  • Then, they were to be given in different doses.

The most confusing paste I found listed contents in terms of parts per million (ppm), percentages, and mg/kg.  Then, the syringe was in pounds and the recommended dose in ounces. OMG!!!  Clear as mud!!!  What I was beginning to wonder, was that if some companies don’t actually want you to know how much or little of each nutrient is in their product.  Standing in the feed store, it was nearly impossible to do all of the mental gymnastics required to evaluate and compare the products available. So, I did what you must do if you want to fairly compare apples to apples rather than apples to oranges.

  •  I made a list of label information and recommended feeding rates.

Then, before I could really compare supplements, I had to go home with my lists of label information, sit down with a calculator or spreadsheet (…and a wine…or a latte…), look up conversion factors, and look up nutrient requirements.

Here is a link to my basic spread sheet that you are welcome to copy rather than typing all the nutrients into your own.


(If you just fill in the quantities and units as well as the dosage found on the label, the spread sheet should calculate the contents per dose for you.  If you come across units not covered in my spread sheet, please read on and try and understand how to convert units yourself.  If the math is just too off-putting for you, contact us at Pro-Dosa, and we will be happy to do the conversions for you and add them to my spread sheet for everyone else’s benefit.)

  • Enter or write down the contents as listed on the label, including the units.

Are the quantities listed in micrograms (mcg or ug), milligrams (mg), grams (g), kilograms (kg), parts per million (ppm), percentages (%), international units (iu), or 1000-international units (kiu or IU)?  Are those quantities listed per kg, pound,or dose of the product in question?

Here’s an example.

In this example, Arginine is listed as                                                                                                                                  0.31%, Iron is 3500 ppm, VitaminB12 is 1013mcg/lb, and Thiamine is 992mg/lb.  (…No, it doesn’t make much sense to me either…Yes, stop now and go get that glass of wine!)  Here’s where we will start to make some sense of this stuff.

You will need to convert all the units to milligrams per gram (mg/g) or whatever units you understand.  (In NZ, we use the metric system.)  I generally convert everything to mg/g, as I have entered the nutrient requirements into my spread sheet in milligrams (mg) (more on that later), and the dose of product you will give your horse will mostly be measured in grams (g).  You can use the conversion factors here or google each nutrient.

A percentage, as you know, is a number out of 100, so a percentage is the same as an amount in milligrams per 100 milligrams or the amount in grams per 100 grams or the amount in peaches per 100 peaches.  Make sense?  Then, there are 1000 milligrams (mg) per gram (g), so we have to multiply the amount per 100 mg by 10 to get the amount per gram.

Conversion Factor For Percentages to mg/g

% X 10 = mg/g

OK, in this example, Arginine is listed as 0.31% so that means there is 0.31mg per 100 mg.  We multiply this by 10 to get 3.1mg of Arginine per gram of paste.

Parts per million (ppm), using the peach analogy, is the amount in peaches per 1 million peaches.  So that is the same as the amount in micrograms per gram.  There are 1000 micrograms (mcg) per 1 milligram, and there are 1000 milligrams in a gram, so there are 1 million micrograms in a gram.  Anything listed in ppm, therefore, can automatically written instead as mcg/g.  We, of course, are working towards having everything in mg/g, so divide the amount in ppm by 1000 to get the amount in mg/g.

In this example, the Iron is listed as 3500ppm.  That’s the same as 3500 mcg/g.  If we divide by 1000 to get mg/g, there is suddenly only 3.5mg/g.  That doesn’t sound like nearly as much.

Conversion Factor for Parts Per Million (ppm) to mg/g

ppm divided by 1000 = mg/g

Now, on to the vitamins in this example…

As we learned before, there are 1000 micrograms (mcg) per 1 milligram.  Divide the amount in micrograms by 1000 to convert to mg.  In this example, Vitamin B12 is actually 1.013mg/lb.  Easy!

Conversion Factor for micrograms (mcg) to mg

1000 mcg per mg
amount in mcg divided by 1000 = amount per mg

Whoa!  Not so fast.  That’s 1.013 milligrams per pound.  Now I didn’t grow up with the imperial system, so I had to think about that one.  There are 2.2 pounds per kilogram, and there are 1000 grams in each kilogram.  First multiply by 2.2 to find out how many milligrams are in a kilogram (1.013 x 2.2 = 2.23mg per kilogram) and then divide by 1000 to find out how many mg are in a gram.  It turns out, there are 0.00223 mg/g.

Conversion Factor for Kilograms (kg) to Grams (g)

1000 grams per kg
Amount in a kg divided by 1000 = amount per g


Conversion Factor for Milligrams per Pound to mg/g

mg/lb X 2.2 and divide by 1000 = mg/g
or……. mg/lb X 0.0022 = mg/g

Thiamine (Vitamin B1) is already in mg…thank you very much!! However, it is also listed per pound, so as we learned above, multiply by 2.2 and divide by 1000.  You can fill in Thiamine on your spreadsheet as 2.18mg/g.

You can then just repeat this process for everything listed on the label.

There are a few conversions that I haven’t included here.  International Units (iu) are frequently used as a unit of measure for vitamins, medications, hormones, and other biologically active substances.  These are different for every form of vitamin as they include a measurement of effectiveness or biological activity.   I have to look the conversion factors up every time I have to use them, and the best place to find them is on Google.   So you don’t have to, here are a few of the main ones.

Vitamin A (as Retinol) 0.3 mcg 300mg
Vitamin A (as Beta-carotene) 3.6 mcg 3600mg
Vitamin C 50 mcg 5000mg
Vitamin D 0.025 mcg 25mg
Vitamin E 0.67 mcg 670mg
  • Convert the contents per kg, L, g, oz, or pound to the content per dose.

If you have converted the contents to mg/g and the dose is in grams, just multiply your quantity in mg/g by the dose.  If you have converted to mg/kg, then multiply your quantity by the dose and divide by 1000.  (There are 1000 grams per kg).

We have already calculated the contents in mg per g, so we just have to work out how many grams are in our dose and multiply by that number.  In this example, there are 68 grams (1 full syringe) per dose.

Arginine = 3.1mg/g x 68 g = 210.8mg per dose syringe
Iron = 3.5mg/g x 68 g = 238 mg per dose syringe
Vitamin B12 = 0.00223mg/g x 68g = 0.152 mg per dose syringe
Vitamin B1 (Thiamine) = 2.18mg/g x 68g = 148.24mg per dose syringe

Conversion for mg/g to Contents of a Dose

amount in mg/g X grams in a dose

  • Write down the nutrient requirements for your particular horse, at the specific level of work and stress they are under. In my spread sheet, I have included the requirements for a 450 kg horse in intense work.  Those requirements will work fine for a Standardbred at 400-450 kg, a flat racehorse at 500-550 kg, or a sport horse at 550-600kg, but you can look up the precise requirements that pertain to your horse.  National Research Council (NRC) is the best resource, but you can check out our Blog, Google, nutrition books, or ask an expert (nutritionist, veterinarian, etc).
  • Compare the contents per dose that you calculated to the nutrient requirements you looked up just now.

Your average horse needs about 400mg Iron per day and there is 238mg in this dose.  That’s not bad.

Doses of thiamine required to support nerve cell function are 1000mg upwards, so the 148mg in this fall a bit short.


While that seems complicated, it is really the only way to do it.  If you do it a few times and get comfortable with converting units and doing the basic mathematics, and if you have some of the basic nutrient requirements committed to memory, then you can do a rough comparison in a feed store.

Quick and Dirty Method

Most commonly, companies based in countries that use the metric system list their contents in mg/kg.  Divide the contents by 1000 to get to mg/g and multiply by the dose.

For example, we will use a dose of 50g, As there are 1000 grams in a kilogram, then your 50mL dose has about 1/20th of the contents on the label (50/1000 is about 1/20th).  You can just divide the quantity on the label by 20 to get a rough idea of what is in a dose and then compare that to what you remember of the requirements.

If the label is more complicated, then I do the calculations for one nutrient and then figure out what to multiply or divide the label quantities by to get what is in a dose.  Then I apply that factor to all of the nutrients.  Easy!

In our example, nutrients listed as percentages can be multiplied by 680.  In your spread sheet, you can multiply the column of percentages by 680 and the results are half done.

In general, divide nutrients listed in ppm by 1000 and then multiply by the dose in grams.

In our example, the nutrients listed as ppm can be divided by 1000 and multiplied by 68…or just multiply by .068.  (68 divided by 1000).

The nutrients listed as mg/lb can be multiplied by the dose and 2.2 and then divided by 1000 or just multiplied by 0.15.

The hard part is done.  You can now easily compare the quantities in any product with nutrient requirements and see for yourself if each product in questions measures up and which ones looks to be the best.  To really make a fair comparison, though, you will still have to learn something about what nutrients to look for and why they must be in optimal doses; neither too much nor too little.

Next, you must consider the composition and balance of nutrients in the product, so once you have recovered from the mathematical ordeal, make sure you read Part 2 of our Reading Labels series.

08 May

To get the most out of this article, you really need the pictures that go along with it.  Please download the PDF version here.  EQUINE CONFORMATION – WHAT IS CORRECT? 

Definition:  Conformation refers to the shape, dimensions, and proportions of a horse, created by its musculoskeletal structure.

Wider Definition:  A more holistic definition considers the implications of form for dynamic function as well.

Beauty is in the eye of the beholder.  The assessment of conformation is subjective, and different people will have different preferences, tolerances, and intolerances.  In addition, different breeds and horses with different jobs to do may be compared to slightly different ideal conformation standards.  For our purposes today, we will mostly talk about racehorses, and Standardbreds in particular.  We will talk about the most common conformation flaws and why some might be quite tolerable in the Standardbred racehorse and why others aren’t.  As many racehorses will be evaluated and selected as foals or yearlings, I will also try to touch on a few developmental features of conformation.

When selecting yearlings at a sale, what we would really like to know is which individuals have the X-factor that will make them great racehorses.  That, unfortunately, is an intangible factor that we have no measure for.  Instead, we try to choose individuals that are likely to stand up to the physical stress of training.  At least, we try to reduce the list of yearlings with bloodlines we are keen on, by eliminating the horses with significant conformational flaws that will predispose them to injury and reduce the likelihood they will ever make it to the races.

Overall and the Body Proportions:

When you look through references on judging conformation, you will find a variety of “standard” measurements recommended for evaluating the overall shape of horses.  Some suggest that the length of the head, neck, shoulder, back, and hip should be equal; others say that the height of the horse at the wither and the length, from point of shoulder to point of buttock, should be equal; and still others say that the shoulder, body, and hip should be of equal lengths.  In general, these are reasonable rules of thumb to follow as they are all about overall good balance, and horses that depart significantly from these proportions are unattractive and may have difficulties with some types of work.

There are recommended proportions for heads and for the relationship between the size of the head and the length of the neck, but I’m sure we have all known pretty decent Standardbreds with roman noses or relatively long heads that would be considered poor specimens by these measurements.  On the whole, if the horse has to be a riding horse that must engage the hind quarters and lighten the front end for jumping or dressage, a big head makes that more difficult and it could be considered a flaw.  For Standardbreds, it probably doesn’t affect balance and performance to the same extent, and whether these proportions are considered a flaw or not largely comes down to personal preference.  In fact, the only conformational flaws of the head I worry about involve the eyes and mouth.  Horses with narrow foreheads and small eyes can have some difficulty seeing, and parrot mouthed horses (where the upper jaw protrudes beyond the lower jaw) or monkey mouthed horses (where the lower jaw is longer) will have more dental issues than average that must be looked after regularly.  The neck shouldn’t be too short as it is important for balance, but a slightly longer neck isn’t a disaster, so long as it is not set on too low, shifting weight bearing towards the front and loading joints in front legs.  In running quarter horses, researchers found correlation between longer necks and an increased incidence of knee chips.  Jumpers, on the other hand, need a relatively long neck for balance over jumps.

The shoulder should be relatively sloping, forming an angle of 45 degrees or so with the ground.  A more vertical shoulder often goes hand in hand with a shorter humerus and a lower neck set.  The upshot of all of this is a shorter stride.

It is also worth noting that the pastern angle, when viewed from the side, is generally the same as the slope of the shoulder.  An overly sloping shoulder, therefore, often comes along with a long, sloping pastern, low heels, and a whole host of problems associated with that.  This reminds me of the song…the hip bones connected to the thigh bone, the thigh bones connected to the leg bones…and so on.

For most breeds, a short back is considered ideal, and one standard suggests that the shoulder, back, and hip should all be of equal length.  In the picture with the grey horse above, the three sections, while similar, are not quite the same.  If the back was really the same length as the shoulder, it would really be too short, in fact.  Horses with very short backs may be predisposed to interference problems.  Horses with long backs, in contrast, are susceptible to injury due to weakness.

The croup in some breeds should be relatively flat, and in others, a moderately sloping croup is ideal as it allows for easier engagement of the hindquarters.  A very sloping croup or a very flat croup are not ideal in Standardbreds, as both conformations limit the power generated by the hindquarters.  Arabians shown at halter have quite flat croups, while Arabian flat race horses look like slightly smaller thoroughbreds with moderately sloping croups and well developed hind quarters.

Feet and Legs:

While “ideal” body conformation varies quite significantly for horses of different breeds and purposes, standards for legs and feet apply quite uniformly across breeds. While not many horses are perfect specimens, those that come closer to the ideal, generally have the right biomechanics for correct and athletic movement.  They will suffer the least abnormal forces on feet, legs, and body; hopefully preserving soundness and health during training and racing.  In this section, I’m going to address the significance of conformation flaws while discussing normal conformation to help you to decide which flaws you might tolerate and which you really shouldn’t.

Front legs:

When a horse, standing square, is viewed from the side, a plumb line, dropped from the top of the leg along the middle of the forearm (elbow joint), should fall straight through the middle of the knee (carpus), down the back of the cannon bone, pass through the middle of the fetlock, through the back of the heel bulbs, and end up on the ground just behind the heels.  If the knee falls to the front of middle, the conformation is referred to as buck-kneed or over-at-the-knee, and if the knee falls more to the back of the midline, then the conformation is referred to as back-at-the-knee.

The back-at-the-knee conformation is an interesting one.  Depending on the breed and work a horse does, it may or may not be significant. You could well imagine that horses with a back-at-the-knee conformation would be a greater risk for fracture, or at least lameness, as the joint appears to be partially hyperextended, even when at rest.  Interestingly enough, research says that for most breeds, unless the flaw is severe, there is little impact on the incidence of chip fractures or lameness.  This may be because the back-at the knee conformation is created when the top row of bones in the knee is set slightly back of the bottom row.   In the normal horse, these rows of bones are arranged so that the front faces are lined up with each other.  Some evidence does exist of increased incidence of lameness in racehorses, but it isn’t the same for all types.  Thoroughbreds and trotters appear to have a bigger problem with slight back-at-the-knee conformation than pacers do. A slightly back-at-the-knee conformation is pretty common in Standardbreds, and if the shoeing is right, pacers, at least, can generally be managed.  (Research has demonstrated an increase in carpal chips and synovitis in horses with long toes in combinations with a slight back-at-the-knee conformation.)  In more significant cases though, it should be avoided for any racehorse.

The over-at-the-knee conformation in young racehorses is associated with a reduction in risk for carpal chips, but the incidence of tendonitis is clearly increased.  Bowed tendons are best avoided, and any conformation that predisposes a horse to this injury is best avoided.  In older jumping horses (steeplechasers, show jumpers, and eventers), the over-at-the-knee conformation can be acquired and this acquired form does not appear to be correlated with lameness or instability, despite all appearances.

A narrowing of the leg, just below the knee, is the feature of the tied-in-below-the-knee conformation.  For some reason that is not obvious to me, researchers have found this problem to be of bigger concern in pacers than trotters.  Again, there appears to be some correlation with increased incidence of tendonitis, so I think it is best avoided in racehorses of any type.

When viewed from the front, a plumb line dropped from the point of the shoulder should bisect the forearm, knee, cannon, fetlock, and foot.  Deviations indicate a conformation flaw.

Toe in and toe out conformations both place extra stress on the fetlocks and coffin joints.  The toe in conformation places the stress on the outside of the joints, and the toe out conformation places extra stress on the inside.

The toed in conformation results in a paddling gait in which the foot swings outward while the toed out conformation results in winging-in, with the toe at risk of contacting the other front leg. The toed out conformation, therefore, is a very undesirable one in Standardbreds as they will be at greater risk for hitting a knee or splint.

Normal – moves in a straight line
Base Wide – feet move forward in inward arcs
Splayed Foot – “toed out” feet move forward in larger inward arcs
Base Narrow – feet move forward in outward arcs
Pigeon Toed – feet move forward in larger outward arcs

The toed in conformation often goes hand in hand with offset knees.  This conformation is associated with increased incidence of synovitis and capsulitis in the fetlocks and coffin joints, and the greater the offset, the greater the incidence of problems in the lower joints.

When the lower limb deviates outwards from the midline, the conformation is sometimes referred to as knock-kneed.  It is actually an angular limb deformity called a Valgus deviation.  The opposite condition in which the lower limb deviates inwards, is correctly termed a Varus deviation.

The valgus deformity is common at birth, but most foals straighten up within a few days.  Those that don’t can be corrected with a surgery that slows the rate of growth on the inside of the leg and increases it at the outside.

You would guess, by looking at the valgus deformity, that additional stress would be put on the inside of the lower limb, and you would also probably expect some knee problems to go along with this.  Oddly enough, research has demonstrated the opposite.  The incidence of carpitis and fractures actually decreases in Thoroughbreds with a valgus deformity.

Pastern angle and foot conformation are closely related to one another, so we will discuss these together.  The angle of the foot should be the same as the angle of the pastern.  Both will be fairly similar to the angle of the shoulder, though not necessarily exactly the same.

Generally, a foot angle of 50 degrees or so would be considered ideal for front feet.  With a foot and pastern angle of 50ish, the pastern will be neither too short and upright, which would place extra stress on the fetlock, pastern, and coffin joints, nor too long and sloping, which will place extra stress on the coffin joint, pastern, fetlock, knee, and the flexor tendons. From a soundness perspective, I would rather a horse be slightly more upright than have long, sloping pasterns that place the foot way in front of the leg.  This conformation frequently results in crushed and underrun heels, and maintaining a healthy foot will be an ongoing battle.  The long pastern/long toe/low heel conformation has been associated with an increased incidence of front leg fractures in general, and carpal chips in particular.  While more upright pasterns are associated with an increased incidence of fetlock chips, it is a very slight increase that I think is a better risk to take.

Hind Legs:

To evaluate conformation of the hind legs when viewed from behind, imagine a plumb line dropped from the point of the rump.  It should run down the middle of the hock and bisect the canon and foot.  If the hocks deviate to the outside of the line, the horse is considered to be bow-legged, and if the hocks deviate to the inside, they are called cow-hocked.  In fact, few horses are dead straight behind. The majority have a very slightly cow-hocked conformation.  If either deviation is significant, it should be avoided.

The hind legs should also be viewed from the side, and you must take care to ensure that they are standing up square, with either the canon bone vertical or the point of the hock lined up under the point of the rump.  A plumb line dropped from the point of the rump should run just behind the point of the hock and run straight down the back of the flexor tendons.  Horses that stand too straight behind, post-legged, will have the plumb-line fall behind the leg, and a sickle-hocked horse, with too much angulation through their hind joints, will stand out behind the plumb line.

Some diagrams will show two additional conformations; camped under and camped out.  These are not really different conformations but are, instead, positions.  If a sickle-hocked horse stands with the point of the hock under the point of the rump, then the cannon bone will slope forwards.  This is the usual depiction of the “sickle-hock” conformation.  If that same horse stands up with the canon bone vertical, then they stand camped-out behind.  The post-legged horse, in contrast, generally stands camped-under.

Post legged horses do not have enough angulation through their joints.  These horses are predisposed to stifle and hock problems, and they are generally weak behind.  They are unable to engage their hind ends sufficiently, and they should be avoided for jumping.

The sickle-hocked conformation is reasonably common in Standardbreds, and it has been associated with speed in some families.  Sickle-hocked horses are predisposed to hock joint problems and curbs.  From a soundness perspective, significantly sickle-hocked individuals should be avoided.

Dr. James R. Rooney wrote some very interesting text books about the biomechanics of lameness that are worth reading if you would like to know more about how form affects function and dysfunction.  He explained that the sickle-hock conformation allowes horses to get underneath themselves and use their hind quarters for more power.  As a result, draft horses should be slightly sickle-hocked, and so should be old-time Standardbreds who pulled heavier carts and drivers and who were required to race multiple heats in a single day, but were not required to pace or trot as fast as horses must now.  As Standardbreds have had to go faster and faster, a straighter hind leg conformation has been selected for.  I’m not convinced the straighter hind leg conformation is necessarily related to more speed, but it certainly helps horse stay sound enough to race successfully for a longer term.  If sickle-hocks allow a horse to generate more power behind, then they should also provide for more speed.  Soundness would certainly suffer, though, and lameness will almost always reduce speed in the end.

Conformation Changes from Birth:

Researchers have found that only 13% of foals can be considered to have straight legs during their first 10 days of life, however, only a few require any sort of intervention to help them to straighten up.  The deviations notable at this early stage in life include angular limb deformities and rotation of limbs, mostly to the outside.  After the first few days, weaknesses begin to correct, and many of these legs begin to straighten up.  Rotational abnormalities of from the elbows start to straighten as pectoral muscles develop.

Between two weeks and 6 months of age, valgus deformities are improved as is a toed-out conformation.  The base wide stance also corrects.  Varus deviations, toed-in conformations, and offset knees can worsen, however.

By the yearling sales, leg conformation is permanent.  The stage of growth, however, can mean the the croup is higher and yearlings can look poorly balanced.  I would generally expect that Standardbred yearlings who have narrow chests and who toe out will have major interference problems, but many Thoroughbred trainers will overlook these flaws, believing that yearlings will straighten out as the pectoral muscles continue to develop with training and growth.


While there will always been exceptional creatures who become champions despite dreadful legs, most will break down before they can distinguish themselves on the racetrack.  It is an integral part of a horse trainer’s job, therefore, to select horses for purchase that will stand up to training and racing.  To do this successfully, they must become students of conformation; learning how to evaluate it, how it affects function, and how it might lead to dysfunction.

For more information, I would recommend reading Dr James R Rooney’s books, “The Lame Horse” and “The Biomechanics of Lameness”.  It can be hard going if you aren’t fond of physics, but I think his books are fascinating.  Dr W. McIlwraith wrote an article, “Conformation and Musculoskeletal Problems in the Racehorse” that is also worth a read as it talks about development of foals and the incidence of injury relating to conformation.  Kobluk, C. N.; Robinson, R. A.; Gordon, B. J.; Clanton, C. J.; Trent, A. M.; Ames, T. R. have written “The Effect of Conformation and Shoeing: a Cohort Study of 95 Thoroughbred Racehorses”.  This is about feet and their affect on lameness

08 May

Twenty years ago, stomach ulcers in horses were not a commonly reported problem and veterinary texts listed them only as an infrequent finding in sick foals. Today, they are reported to occur in anywhere between 60 and 90% of standardbred racehorses and 50 to 60% of show ponies, stabled yearlings, eventing and dressage horses. The only group of adult horses free of ulcers are those on pasture 24 hours a day.

Pastured horses have a very different diet to stabled horses – and diet has been shown to contribute to ulcers. Under natural conditions, horses graze for around 16 hours per day. The stomach has adapted to a constant intake of grass by constantly secreting acid (for around 45 minutes per hour). The acid is buffered by saliva, which is produced during chewing and has a very high content of bicarbonate and mucus. The number of chewing movements and the amount of saliva produced varies with the type of feed. One kilogram of hay requires over 3000 chewing movements and results in the production of over four litres of saliva. One kilogram of grain requires only one third as much chewing and yields only two litres of saliva. The sign of an acid stomach is chewing of bedding, wood etc – the chewing process stimulates the flow of saliva, which in turn lowers stomach acid levels and the horse feels more comfortable – a bit like chewing an antacid tablet.

Stabled horses spend an average of four hours a day eating – compared to 16 hours for pastured horses. When chewing time and hence saliva production are reduced, stomach acid levels rise, increasing the risk of ulcers. High acid levels are a result of modern feeding practices: the amount of roughage, feeding frequency and type of feed have profound effects on stomach acidity. If the stomach sits empty for a prolonged period, the acid is not buffered by the food and saliva and the stomach will empty less frequently, allowing the acid fluid to remain in contact with the lining.

When feed is eaten rapidly, less saliva is produced and the sudden flow of a large volume of feed into the stomach causes a rapid increase in acid secretion. Both grains and pelleted feeds have been associated with increased risk. High grain diets favour bacterial growth and fermentation in the stomach. There is an increase in the number of bacteria that produce lactic acid and gas. Acid secretion increases in response to pelleted feed because pellets are eaten rapidly. Both weanling and adult horses consume pellets faster than they eat traditional grain diets.

Simply changing from pasture to hay and confining a horse to a stall can cause ulcers. Because hay is drier and coarser than grass, it can damage the lining of the stomach. Soaking hay for 6 hours will soften it and also reduce dust and airborne particles that irritate the respiratory system. In addition, any alterations in intestinal function may also be associated with stomach ulcers.  Insufficient blood flow due to worms can cause death of gut lining cells, resulting in slowing ulcer healing.

The most reliable way to produce ulcers in a horse is to provide insufficient roughage or to fast them. Multiple studies have demonstrated that periods as short as 12 hours without feed can result in low grade stomach irritation. Even beginning an exercise program results in more acid secretion by the stomach – making the provision of adequate roughage even more critical for the standardbred entering training.

Phenylbutazone or other anti-inflammatory drugs can also cause ulcers. The risk increases with long term use but can occur even after a single high dose. Phenylbutazone (bute) especially has an extremely low margin of safety and should only be used under veterinary supervision. A high salt intake can irritate or worsen pre-existing ulcers. To avoid excessive irritation, ensure that electrolyte intake matches need and give the daily dose with food.

Signs of stomach ulcers include poor performance, loss of appetite, poor condition and mild colic.  With the exception of mild colic, these symptoms can also be found in horses with a developing lameness, subclinical tying-up, a gut upset, electrolyte imbalances, sand ingestion and enteroliths.  However, loss of appetite for grain, signs of mild pain after eating, teeth grinding, salivation and belching are characteristic signs of stomach ulcers. While horses with a nervous temperament are thought to be more prone to ulcers, it is more likely that discomfort from stomach ulcers makes horses agitated and restless.

Horses with severe ulcerations and clinical symptom require treatment for at least 3 weeks. Around 20% of horses do not respond in that time and may need a different pharmaceutical or a spell. Horses with ulcers have notoriously poor appetites and may not have been eating all their medication if it was in the feed.  If dosed with it, poor technique could also lead to loss of some medication.  There is also a widespread problem with horses being given inadequate doses or not being dosed frequently enough, in attempts to save on the cost.

As few as 3% of moderate to severe ulcers heal without treatment in horses kept under conditions that predispose to ulcers. The only treatment that is 100% effective is to turn the horse out on pasture. Bear in mind also that the combination of poor appetite and alterations in gut pH, have negative effects that drugs cannot correct and supportive therapies, such as probiotics, should be considered. Even with improved appetite and weight gain, there can be a persistent mild dehydration, which can respond to combined probiotic/amino acid/electrolyte. Gamma oryzanol has been shown experimentally to have a protective effect on ulcer formation in several species, particularly ulcers induced by stress or fasting.

For less severe symptoms, and after the initial drug treatment, there are far less expensive therapies for continued treatment and prevention. Good results have been obtained with probiotics, gamma oryzanol, fermentation products, yeasts and digestive enzymes. These actives can be very effective in improving appetite, correcting diarrhoea and promoting weight gain. Some horses with ulcer-like symptoms that do not respond to anti-ulcer supplements respond extremely well to probiotics. In addition, under the guidance of your veterinarian, consider a special worming program for immature worm stages and for tapeworms.

In addition, not all gut symptoms are caused by ulcers and it is essential to have a veterinary assessment to rule out other causes of reduced appetite, weight loss and discomfort. Following a clinical and/or endoscopic examination, the various ulcer treatment options can be assessed.  Because of the major drawbacks of treatment –  cost, contravention of the Rules of Racing and recurrence of ulcers once treatment stops – long-term prevention with gamma oryzanol or another protectant, is advisable. Preventatives and treatments include good quality aloe vera juice, chlorophyll, gelatin kaolin, apple pectin, aluminum and calcium-based antacids, however, long-term use of compounds containing aluminium has been associated with toxicity.

The following feeding management practices can reduce the risk of ulcer formation:

  • Avoid prolonged periods of fasting – ulcers have been shown to develop within 10-12 hours when horses have no access to feed – ensure roughage available at all times
  • Feed on the ground – horses chew and swallow more efficiently when their heads are down and the throat extended. Feeding above the ground also results in abnormal movement of the lower jaw and unnatural patterns of chewing and teeth wear.
  • Feed frequent small meals – optimum is 4 times a day and not more than 2 kg of grain per feed.
  • Use steam-extruded grains and feeds which have been processed in such a way that eating is slower, resulting in more chewing, increased saliva production and higher saliva bicarbonate levels.
  • Deworm regularly with the correct compound.
  • Include probiotics and protectants such as gamma oryzanol in the daily diet.

By Dr. Jenny Stewart  BVSc BSc PhD MRCVS
Equine veterinarian and Consultant Nutritionist

07 May


Equine Herpes Virus

Equine Herpes Virus is the most common cause of upper respiratory infections.

Clinical signs of EHV infection include a fever, runny nose, runny eyes, cough, sores in the nose, depression, loss of appetite, and swelling in the legs.

EHV can occasionally cause a neurological disease characterised by various degrees of weakness, inability to get up or stand, and even death.

EHV is also a cause of abortion in mares.

There are several different types of EHV. Type 4 causes most of the respiratory disease; type 1 causes virtually all of the abortion and some of the respiratory disease; and many types can cause the nervous system symptoms.

Vaccinate all horses except pregnant broodmares with a modified live EHV-1+4 vaccine (Duvaxyn) every three months to maintain good immunity.

At a minimum, vaccinate every 6 months. Vaccinate pregnant mares at 5, 7, and 9 months of gestation with a killed EHV-1 vaccine (Pneumabort K +1B) to prevent abortion.


Tetanus causes “lock jaw” and death

Tetanus is caused by a clostridial bacteria that lives in the soil

It infects animals with deep wounds

Vaccinate in the neck muscles once a year or if animal gets a deep wound.

Do not use the vaccine that combines strangles with tetanus. You will get a much higher rate of site reaction.


Strangles is caused by a bacteria, Streptococcus Equi

It is characterised by swollen, abscessed lymph nodes, thick green nasal discharge, difficult breathing, and even death in severe cases

“Bastard strangles” involves abscesses in the chest, abdomen, or legs. These abscesses may remain for months causing severe weight loss and ill health for extended periods of time. When they eventually rupture, the animal may die.

Vaccinate in the large muscles at the back of the back legs if possible as this reduces the possibility and severity of site reactions.

Repeat every 6 months for good protection.

As this vaccine has a higher rate of reaction, many people choose to vaccinate only when there is an outbreak of the disease in the area.

A Strangles vaccine is less likely to cause a reaction if it is given alone rather than in combination with any other disease antigen in the same vaccine.

A new intra-nasal vaccine (Pinnacle) has become available in New Zealand. This has been used for several years in North America and is effective while eliminating the site reactions that were common with the injectable versions.

07 May

Protein features frequently in discussions on feeding, nutrition and performance. Alternately feared and revered, it is part of the bigger picture of conditioning/nutritional protocols that result in specific changes in body composition and performance.

The word protein comes from the Greek word ‘protos’, meaning ‘first’, because protein is the primary basic constituent of all living cells. It makes up 3/4 of the dry weight of most living cells and is involved in the formation of hormones, enzymes, antibodies and many other functions essential to life.Protein is a collection of amino acids tied together. Once the protein is consumed and digested the amino acid chains breakdown into single amino acids. To appreciate how much the racehorse depends on receiving the correct amino acids in the diet, is to be aware of how dynamic the equine system is. Every second the bone marrow makes millions of red blood cells; every four days the blood platelets and most of the lining of the gastrointestinal tract are replaced; every 10 days, most of the white blood cells are replaced and the number of muscle cells repaired or created in horses that are training and racing is huge. In addition, necessary for muscle growth and repair, strong tendons, optimal energy metabolism, increasing bone density, joint health, hoof wall thickness and greater overall soundness is the interaction of vitamins and minerals with amino acids.The horse requires a precise number and balance of amino acids. Essential amino acids cannot be synthesized by the horses system and are so-called, because it is essential that they receive them every day in the feed. The exclusion or a deficiency of even one essential amino acid from the diet will reduce total body protein synthesis. In horses where everyday maintenance is necessary and improvement with training is required, the creation of new cells is a priority. If just one amino acid in the profile is missing the creation of new cells stops.

Horses receive amino acids from the protein in both concentrates and hay. Every protein source has a different combination of amino acids. Some combinations are very good and some not so good. For this reason, the total protein of horse feed is a worthless term, unless you know the amino acid profile. For example, the feed tag might say 14% crude protein, but to the horse, if all the amino acids are not supplied, it may be only 8 or 9% usable protein. The more unusable protein the horse consumes the more he has to excrete. The feeding of unusable protein stresses the horse’s system. Excess protein can contribute to higher heart and respiratory rates, increased sweating and dehydration.

While some studies have concluded that the racing standardbred does not need additional protein, they do not take into account the quality of the protein. Poor quality protein in terms of amino acid profile, can contribute to the gradual weakening of supportive tissues, bone loss, muscle atrophy and the weakening of blood vessel walls that eventually lead to bleeding or breakdown. What is important is that the horse receives the amino acids that it needs in the correct amounts, readily digested and absorbed.

Over the centuries, horsemen and women have ground, cracked, crushed, boiled, dry-extruded and pelleted feeds for horses. They have done this to increase the digestibility of the feed and to decrease the risk of grain overload, a major player in colic, diarrhoea and laminitis. However, all amino acids have a different melting point and many of these older methods of grain processing result in damage to the amino acids and little improvement in digestibility. Soybeans and processed grain by products must go through some sort of heat process. This heat can destroy the most important essential amino acids. Feeds such as brewers grain are almost always heated at a very high temperature. This heat process destroys many valuable amino acids and makes the feed unbalanced, preventing the horse from getting the full value of the feed protein and taxing the liver and kidneys in excreting all the out of balance and, therefore, unusable amino acids.

The most recent advance in preparing feeds for horses is steam-extrusion. Whereas essential amino acid losses of up to 50% have been measured during dry-extrusion, losses during steam-extrusion are less than 5% and digestibility of the feed increases to over 90%. The application of steam-extrusion and the provision of high levels of essential amino acids in the correct balance are fundamental. Protein in general should never be fed in excess to any horse and neither should there be an overload of protein types that are poorly digested or that the horse cannot use. Essential amino acid deficiencies can occur even if diets containing excess protein and deficiencies cannot be corrected by feeding more of it, if it is not correctly profiled.

The second, separate issue is restoring protein balance after hard work or racing and encouraging the building of lean muscle mass. During hard training and racing, standardbreds damage muscle tissue as a result of the production of high levels of lactic acid and exertion. Muscle must be repaired rapidly to maintain improvement, prepare for the next training session and minimise delayed muscle soreness and stiffness. While in training or before and after racing, dietary programs must be chosen with care to facilitate quick recovery. Hard work causes a decrease in protein production that continues for a few hours after exercise has ceased. Protein in muscle is extensively broken down during exercise and this process serves a number of functions, but it is during recovery that the protein will be working hardest, repairing and building the rips and tears that occur during training.

No matter how balanced the diet is beforehand, exercise naturally causes a disruption. During exercise muscles use fuel at a very high rate and this is a catabolic process, i.e. it involves the breakdown and utilization of body reserves.  However, we are able to switch the catabolic environment into an anabolic (ie, a building of body tissues and reserves) environment after work by supplying the proper tools. Feeds chosen must contain protein that is profiled properly for amino acids, along with minerals, vitamins, fat and carbohydrates.

Nutrition is a powerful tool when used properly.  To the extent that we focus on the challenging bigger picture of conditioning/nutritional support protocol, the horse can harmonise the multiple systems necessary to reach genetic potential. High quality protein in terms of amino acid profile and availability is essential for maximum performance of the Standardbred racehorse.

07 May

Peak performance depends on the supply of energy to drive and fuel the working muscles. Providing almost three times as much energy as oats on a weight basis, oil offers many advantages in terms of energy efficiency. For both digestive and metabolic efficiency, oil is superior to grains and protein. In fact, the efficiency of ATP synthesis (i.e. the currency of energy), is around 39% for oil and 20% for carbohydrates.

In addition, calmness, as measured by spontaneous activity and reactivity (spook tests), is lower when diets are fortified with oil. Oil-enriched diets reduce the amount of metabolic heat generation, both at rest and during exercise and for the racing standardbred, this reduction in heat load can provide a competitive edge. The lower heat load lessens the need for sweating, reducing fluid loss during exercise. Studies have traditionally shown that oil-enriched diets affect working muscles by increasing oxygen uptake, increasing fatty acid utilization, sparing muscle glycogen during low intensity exercise and increasing glucose availability during intense sprinting exercise. Fat supplementation also reduces heat production, improves hydration and perhaps most importantly, improves the power : weight ratio.

Overdoing oil can result in decreased glycogen stores in the muscle, meaning the horse could “hit the wall” sooner, or have nothing left at the end. However, this does not happen until oil comprises more than 8-10% of the total diet – including hay, chaff and concentrate. So, for a 450kg horse eating 10kg of feed, oil intake would have to exceed 800-1000ml a day before there was any interference with muscle glycogen.

However, not all oils are created or utilized equally. Cold pressed oils are far healthier than solvent-extracted oils. Cold-pressed canola contains vitamin E, Coenzyme Q10, lipoic acid, omega-3 essential fatty acids and other very potent natural antioxidants. Without the addition of EPA and DHA, up to 10 times more oil is required to achieve the same levels of omega 3 activity, so for both ourselves and for hard-working horses, it is important to check that EPA and DHA are present in the oil. The maximum benefits from oil occur after two to three months, so it is best to introduce oil-enriched feeds and Omega 3 supplementation early in the program. This will allow sufficient time for metabolic adaptation to occur and ensure that the benefits of fat supplementation are realized when they are needed most.

The ratio of muscle to body fat affects the power to weight ratio – so when we want topline in a racing standardbred, we must use the combination of work and diet that will promote muscle building and not fat deposition. Just as occurs in humans, the finer details of the diet affect body composition. In addition to the type and intensity of exercise, the amount of muscle development is determined by the amino acid composition of the feed protein. Soybean meal, lupins and lucerne are well known as good sources of protein and this is because they are high in lysine.

Lysine and methionine are just two of the essential amino acids that make up protein. Just as branched chain amino acids have been found to be important in horses, on-going equine nutrition research has shown that other amino acids, including threonine are important for muscle building. Regardless of the percentage of protein in the feed, if there is not enough of each amino acid a limit will be put on muscle development and the horse will lay down cover (fat) instead of muscle.

But even if the feed contains good levels of lysine and other essential amino acids, for several reasons, they may not be available to the horse. Some feed processing techniques, such as dry-extrusion, rely on high temperatures and shearing forces which can damage lysine and other amino acids. Steam-extrusion includes moisture in the cooking process and losses are negligible and digestibility increases to over 90%.

As well as a sound daily nutrition program, strategic timing of meals pre- and post work can impact profoundly on the development of muscle power. Muscles consume vast amounts of anti-oxidants and essential amino acids during work and at the microscopic level, small strains, rips and tears occur. Correct composition and timing of feeding can take advantage of the window of opportunity created by the raised hormone levels and increased blood supply that accompany exercise. To be effective and hasten muscle recovery, the concentrate must provide anti-oxidants, amino acids and be consumed no more than two hours before or one hour after work.

The effectiveness of the diet is measured in terms of metabolic efficiency, i.e. the maximum output with the minimum production of undesirable products such as manure, acid and heat. To increase power for work, diets need to be designed to influence muscle fuel levels. But the feed chosen also influences the power : weight ratio (ratio of muscle to fat), thermoregulation (heat production and hydration) and mental attitude – all of which impact on performance and fatigue.

07 May

It has been reported that about 90% of poor performance cases can be attributed to lameness, either clinical (obvious lameness) or sub-clinical (lameness not readily visible under normal exam conditions).

It is logical that noticeable lameness causes horses to perform below their potential, but sub-clinical lameness can be an even greater problem.  Clinical lameness can be quickly recognised, investigated, and corrected.  In horses with sub-clinical lameness, however, the disease process remains undetected and untreated.  It is allowed to progress, resulting in irreversible damage to the structure of joints, secondary lameness, muscle pain, behaviour problems, impaired performance and economic losses.

Early diagnosis and intervention can stop minor problems from deteriorating, preserving long term soundness and maximising performance.

Most of my clients present every horse in their stable, on a regular basis, for physical exams.  This enables the identification of subtle or sub-clinical problems.

Clinical Lameness

A horse is clinically lame if it has a visible limp or asymmetric gait.  It will try to lift its weight off the sore leg and place more weight on the sound legs.  A “head-nod” results.  (When the sore front leg hits the ground, the horse lifts its head up to shift weight to the back legs and off the sore front leg.  When the sound front leg hits the ground, the head nods down, loading that leg excessively.)  Sometimes, when a horse is very lame in a hind leg, the horse will nod its head down to shift weight onto the front legs and off of the hind legs. Sometimes, a horse with a sore hind leg will lift its pelvis higher on the lame side (called a hip-hike).

Lameness is only visible (clinical) when one leg is relatively more painful than the opposite leg.  Both legs can be sore, but as long as the pain is unequal, the horse will protect the more sore side and the head nod will be evident.  There are various degrees of clinical lameness ranging from an inconsistent or almost imperceptible limp to an inability to bear any weight at all on the affected leg.

Sub-Clinical Lameness

Sub-clinical lameness is lameness that you can not see under normal conditions.  Bilateral lameness, lameness in all four legs, and lameness that only manifests under extreme stress or speed is sub-clinical.

Bilateral lameness is often unapparent.  If a horse’s legs are equally sore, he will not favour one and will not limp.  Instead, he will shorten his stride, develop back or muscle pain, perform and below expectations. This could include the following:- “stopping” in the last part of a race, refusing jumps, making mistakes of stride in dressage tests, tie up, blowing after working, having a longer than normal recovery, or developing behaviour problems such as pulling, bucking, and rearing. Many horses just develop a poor attitude to work. “Bleeding” or Exercise Induced Pulmonary Haemorrhage and dorsal displacement of the soft palate (“flipping the palate”) are common presenting complaints.

Some lameness only shows up at high speed or under extreme stress such as in the last part of a race.  Some will manifest only with a rider or doing particular movements like flying changes or lateral work.  Some will appear on a lunge line or on particularly hard, soft, or irregular or unstable footing.  Some only present in the cart and not in-hand. Once again, these lameness cases are often presented for performance and behaviour problems, back, or other muscle pain.

Lameness in My Practice

In my practice, the majority of horses presented for lameness or performance problems have one or more of the following:

  1. Foot pain including sole bruises, abscesses and, corns
  2. Arthritis (joint inflammation)
  3. Tendonitis (a bowed tendon) or
  4.  Suspensory Desmitis.

Bowed tendons and suspensory desmitis present as clinical lameness and there is obvious pain, heat, and swelling.

By far, the most common sub-clinical lameness or performance problems involve joint and foot pain.  In many cases these conditions are both present.


Arthritis is a term that means “joint inflammation” (arth-joint, itis – inflammation).   Inflammation occurs in joints when they are placed under stress in excess of what they have adapted for.  This stress can be sudden and severe (stepping in a hole, taking a bad step on poor footing, or some other accident), or it can be repetitive and low grade (wear and tear).

Horses are designed for eating grass and running away from the occasional predator.  They are designed to land flat on their feet, load bones and joints evenly from side to side, and break over the middle of their toes. Unfortunately, not many horses have perfect conformation, perfect hoof balance, or work on perfect footing so stress is not distributed evenly.  They are not born readily adapted for repeatedly pulling a sulky or carrying a rider around a track at top speed or over jumps.  The idea behind training is to gradually increase the stress on a horse causing them to adapt to the work we expect them to do.  In short, training a young horse or training a more mature horse down to race after a spell is constantly placing their joints under stress they have not adapted to. Therefore, inflammation occurs on an on-going basis in most horses in training.

Joints are made up of the ends of two or more bones which are covered with cartilage and joined together by the joint capsule.  The joint capsule is lined by the synovial membrane.  This membrane is very important as it produces the synovial fluid (joint fluid) that lubricates, protects and nourishes the joint cartilage.  In a healthy joint, synovial fluid is thick like syrup.  It is replaced every 24 hours or so on an on-going basis.

Inflammation in joints begins with synovitis and capsulitis. In synovitis and capsulitis, enzymes are produced that breakdown joint fluid, making it thin and watery.  It no longer lubricates and protects the joint properly.  With a lack of nourishment and lubrication, the cartilage surface of the joint becomes abraded.  Over a more extended period of time, the sub-chondral bone (bone underneath the cartilage in the joint) begins to change.

Over time, then, synovitis and capsulitis will progress to sub-chondral bone disease and osteoarthritis.  This entire process is referred to as arthritis or degenerative joint disease (DJD).  X-rays only show bone, so relatively advanced DJD is the first stage that is reliably visible on radiographs.

It is much better to identify and treat joint problems before they are visible on radiograph. If inflammation is stopped, the synovial membrane will make new fluid that will remain thick and sticky.  If the breakdown of synovial fluid is the only damage that has occurred, a completely normal joint environment will be restored.  If the cartilage surface has been damaged, some treatments can provide repair, and a normal joint can be created.  Once bone has changed, however, it cannot be reversed.  Thick, healthy joint fluid will stop rough bones from rubbing together in the joint, and DJD will be arrested, but a truly normal joint cannot be restored.


Since the primary goal of therapy is to stop inflammation and to stop the progression of degenerative joint disease, the treatment of choice in most cases is intra-articular cortisone.  Cortisones are very effective anti-inflammatories, and remain the treatment of choice in human medicine for intra-articular therapy.

There are several different types of cortisone that can be used in joints.  Controlled studies have shown that all cortisones reduce inflammation and that most improve the health of joint cartilage. Triamcinolone (Vetalog, Kenalog, or Kenacort), Isoflupredone (Predef 2X), and Betamethasone (Celestone Soluspan) have all been shown to be safe or beneficial for joint cartilage. Methyl Prednisolone (Depo-Medrol or Vetacortyl) is likely safe in low doses, but can impair the healing of joint cartilage if given too frequently or in large amounts. Triamcinolone has been anecdotally linked to laminitis, but the relationship has not been confirmed.  It has never been caused in healthy horses at normal doses and has not been caused experimentally using doses up to six times those commonly used.

NSAIDS like Phenylbutazone (Bute) and Banamine tend to kill pain better than they reduce inflammation in joints, so they are not a sufficient treatment in most cases.

Once inflammation is resolved and DJD is arrested, the second goal of therapy is to restore a normal joint environment.  Hyaluronic acid (HA) is a building block for thick joint fluid, so supplementation may be useful.  HA can be administered directly into a joint, however, it does not work very well if there is a great deal of inflammation present and it is generally used in joints along with cortisone.    Studies have shown that IV HA (Hyonate or Legend) is as useful as intra-articular treatments, and recent research indicates that oral administration of HA may be helpful.

If cartilage damage has already occurred, then it can be beneficial to treat horses with a product that can stimulate joint repair or provide the building blocks for cartilage repair.  Adequan, Glucosamine Sulphate, and Pentosan may be used for this purpose.  Glucosamine Sulphate supplementation increases the body’s production of hyaluronic acid as well.

Additional medications are available to treat arthritis including some homeopathic treatments that reduce inflammation and stimulate joint healing.  The homeopathic medications I mainly use are Traumeel and Zeel.

Finally, the third goal of therapy is to prevent reoccurrence of lameness.  Adequan, Glucosamine, or Pentosan can be given regularly to reduce inflammation and repair cartilage.  They can keep inflammation at bay in sound horses in training, and they can increase the interval between joint injections in horses with lameness problems.  Optimal shoeing and good footing are of utmost importance, and adjustments to the training regimen may be helpful in some cases.


  1. The products of inflammation are enzymes that damage the joint.
  2. Early diagnosis and treatment will preserve normal joint structure and function maximizing long term soundness and performance.
  3. The first goal of therapy is to stop inflammation and, therefore, to stop the progression of degenerative joint disease.
  4. The second goal of therapy is to restore the most normal joint environment possible.
  5. The third goal of therapy is to prevent re-occurrence of the problem.

Dr.Corinne Hills

07 May


Tying up (Exertional Rhabdomyolysis) is a common cause of poor performance in racehorses and performance horses of all types.  It is a syndrome with a variety of causes, but always involves the breakdown of muscle cells which in turn causes a serious, easily recognisable clinical condition involving muscle stiffness, pain and a reluctance to move.  Sub-clinically, it can cause poor race performance or may present as a lameness problem.

I did up a basic outline of the condition and its treatments about 15 years ago for one particular client and one particular horse.  Since then, I have sent the information out to countless others, and they have in turn passed it on.  I have been told by many people who have read this that it was helpful to them, so here it is. Please keep in mind that this is my own interpretation of the papers I have read, cases I have seen, and thoughts on the subject from other veterinarians and horsemen.  Your own veterinarian may or may not agree.  Some of the information is well documented and widely published.  Some is not.  I have not referenced any of this as I did not originally prepare the paper for general review, but only for individual clients with specific horses.  I hope it gives you something to think about, but please consult with your veterinarian regarding your own particular situation.

Clinical Signs of Tying Up

  • Shaking, sweating, stiffness, reluctance to move
  • Can look like a colic or laminitis
  • Poor performance in races or competition
  • Dark urine

Diagnosis of Tying Up

Clinical Signs
As Above

Blood Test
The muscle enzymes, Creatine Kinase (CK) and Aspartate Transaminase (AST) (and LDH in some places) are checked in serum samples (red topped blood collection tube).
CK is an enzyme that goes up quickly and down quickly (It starts to go up in a couple of hours and peaks in about 24 hours).  AST is an enzyme that goes up slowly and down slowly (It goes up in a day and back down in a week).
If CK is elevated and AST is normal, the muscle cell damage has occurred in the last few hours.  The AST has just not had a chance to rise yet.  If the AST is high and the CK is normal, that indicates that a tie-up is resolving.  The CK has gone back down to normal, but the AST has not yet had enough time to recover.  If a tie-up is on-going, both the CK and AST would remain elevated

Causes of Tying Up (or predisposing factors)

A)   Lactic Acid Damage – lactic acid is a product of the metabolism that occurs in muscle cells when they are reaching the end of a race, or when a lot of energy is stored in muscle cells and then burned off quickly

  • Too much feed or soluble carbohydrate in the feed
  • Not enough work
  • Lameness – lame horses move differently to protect sore areas.  This makes certain muscles work much harder as well as inefficiently.  This results in greater lactic acid accumulation and muscle cell damage

B)  Calcium Insufficiency – calcium is important for the normal contraction of muscle cells.  In some horses, that mechanism requires more calcium than average (apparently this is more common in exceptionally good horses)

C)  Hypothyroidism – the thyroid gland doesn’t work as well as it should, and the horse is deficient in thyroid hormone.  A blood test can identify hypothyroidism

D)  Exposure to a Virus – recently, I have noticed in the literature references to tying-up in relation to exposure to Equine Herpes Virus (Rhinopneumonitis).  I don’t know the mechanism behind this, but will update this at some point when I do.

E)  Muscle cells not properly Hydrated (not bathed in enough fluid)

  • Dehydrated (HCT or PCV above about 0.45 or 45%)
  • Not enough electrolytes or an imbalance in electrolytes or minerals
  • Fillies and mares lose more electrolytes in their urine (especially when they are in heat) compared with geldings and stallions.

Treatment of Tying Up:

A)  Reduce Muscle Enzymes in Blood

  1. Administer additional electrolytes (1 cup) and salt (handful) with water (2-3 litres) via stomach tube.  This will cause the horse to drink more water and produce more urine.  This will help to clear the high levels of muscle enzymes while protecting the kidneys (which can be damaged by myoglobin which is released when muscle cells are damaged)
  2. Anti-inflammatory
  • Tube with Dimethyl sulfoxide (DMSO) – 1 cup or 250 ml this has a 7 day withdrawal, ½ cup or 125 ml has a 4 day withdrawal (you can put 110mL in an IV electrolyte jug) this is a great anti-inflammatory and will help get the muscle enzymes back to normal
  • Give Phenylbutazone (Bute) for the first day or so (7 day withdrawal for iv)
  • Give Dexamethasone – 50 mg IV.  This is a steroidal anti-inflammatory where as Phenylbutazone (Bute) is a non-steroidal.  This means that they work by different mechanisms, so their effects will be additive.  Also, Dexamethasone may help decrease the GGT.  If GGT is much over 20-30, horses will not race well.  This is really an indicator of stress, and I don’t really know the mechanism by which it affects racing performance, but it certainly can indicate poor performance.    For some reason, the metabolites of DMSO (the things it is broken down to by the body) can result in a higher GGT.  This does not appear to be related to impaired race performance.  I don’t have a good scientific understanding of this.  Maybe I will add a discussion of GGT to this someday…

Prevention of Tying Up:

  1. Anatest – 5cc IM every 2weeks – this messes up the hormonal cycle in fillies, so they shouldn’t lose so many electrolytes in their urine.  I don’t have any idea why progesterone (in Regumate) doesn’t work as well for this, but it doesn’t seem to.  In New Zealand, you cannot use Anatest, so you must make do with progesterone.  Hydroxy-P 500 is no longer allowed in NZ either.
  2. Electrolytes – increase daily electrolyte supplementation in feed – try doubling recommended levels.  This will ensure that the horse has sufficient electrolytes available.  They will urinate out the excess anyway, but will keep what they need.  Also, a small handful of regular table salt each day will increase water consumption.  Dunstan “all-you-need” contains about 3-10 times the electrolytes contained in most feeds.  Switching your concentrated feed to Dunstan “all-you-need” will provide all the electrolytes you require.
  3. Chromium – chromium has many effects, but for racehorses, its best effects are on muscle cells.  Chromium ensures that muscle cells are bathed in more fluid and electrolytes.  It protects muscle cells from lactic acid accumulation and the damage that results from it.  (i.e. finish races better with decreased lactic acid at the end, and prevents tying up)  It also acts as a natural anabolic, causing the horse to put on more muscle than fat.  It makes insulin work better, so anything insulin is involved in will be affected by chromium (I.e. it helps boost the immune system).  Only certain forms of chromium are useful, and the one from Nutritech (Altech), Biochrome, is the best.  It is in a form that can be absorbed and used by cells well.  It is also very safe.
    Read the label on the tub.  You will need to use four times the label dose for the first two weeks, then you can cut it back to about two to three times.  That means you could feed 8 scoops (20g) every day for the next two weeks.  Then, feed 4-6 scoops daily after that.  Dunstan “all-you-need” contains Chromium.
  4. Vitamin E/ Selenium – generally, selenium is included in supplements as sodium selenite.  This is an inorganic form, and some horses are not able to absorb it or use it that well.  If you are continuing to have problems, you can feed a yeast-based selenium.  It is in an organic form that cells can easily absorb and use.  It is put out by Nutritech (Altech) as well.  Dunstan “all-you-need” contains yeast based selenium from Altech.
  5. Keep your horse sound – have a lameness exam done, treat the significant problems, and treat with glucosamine regularly to repair any damage present in joints and to prevent the reoccurrence of problems.
  6. Calcium Supplementation – feed skim milk powder regularly.  It is in a good form for absorption.  The balance between calcium, magnesium, and phosphorus is important too.
  7. Baking Soda – you can feed baking soda so long as you stop a good 24 hours before racing.  Check with your veterinarian about the dose and when to stop.
  8. Traumeel – may be useful about an hour or two before training.  It is a good muscle anti-inflammatory as is herbal so it has no withdrawal time (but you are not supposed to give it on raceday, anyway).  Give it orally.
  9. Feed High Fat, Low Soluble Carbohydrate Diet – This is the most important way to prevent tying up.  The way you feed your horse is the most vital factor.  A really good study was done on quarter horses and thoroughbreds several years ago.  It showed that if you fed horses on a high calorie diet they were more likely to tie up than if you fed them a low calorie diet.  Obviously!  It also showed that WHAT you fed affected the incidence of tie-up.  If you fed a high calorie diet that was low in soluble carbohydrate and high in fat, you had a low incidence of tying up, while a high calorie diet that was high in soluble carbohydrates caused a lot of tying up.  Soluble carbohydrates are grains like oats and barley.  Insoluble carbohydrates are hays, grass etc.  In New Zealand, a great feed to try is Dunstan “all-you-need”.  In North America, a good feed to try is Purina’s Competitive Edge.  Both are high fat, low soluble carbohydrate, fully extruded feeds.  Feed them with free choice, quality hay or grass.  Dunstan “all-you-need” has the added benefits of MSM.  This is a derivative of DMSO, a great anti-oxidant and useful in the management of lameness, as well.
  10. Don’t feed them if they are not working – if you are giving your horse a day off, cut out the grain part of the ration.  Contrary to popular belief, they will not starve to death if they do not get grain on Sunday if they are not working.  They will survive quite nicely on hay or grass.  If you are feeding Dunstan “all-you-need”, you can feed them as normally as it is low enough in soluble carbohydrate.
  11. Relax – Since nervous horses are prone to tying-up, it can be useful to treat with various things that relax the horse.  Ensure they are receiving adequate B vitamins—especially B1 (Thiamine).  Some amino acids are helpful with this as well.  Treatments like Modecate can be helpful (it is a human anti-psychotic drug that is in the same class as Acepromazine but acts for 3 months at a time).  As the FEI withholding time has increased to 90 days, Modecate is less useful.  In some racing jurisdictions, the withholding time is as little as 7 days, though, so check your local restrictions.

Dr. Corinne Hills, DVM
Equine Veterinarian & Nutritional Consultant