Horse Articles

  • Vitamin E

    Written By Dr. Kris Hiney

    We have already discussed two of the fat soluble vitamins in a horse’s diet. This month we continue with a closer look at vitamin E, a vitamin which is commonly supplemented to horses for a variety of reasons.  It is often used for aging horses, horses which have muscle disorders and horses which undergo strenuous exercise.  But how do you know if your own horse needs more vitamin E in its diet?

    First, let’s explore the role of vitamin E in your horse’s body.  Vitamin E occurs in a variety of forms (both tocopherols and tocotrienols).  Of these, there are then four subgroups, α, γ, β and δ. While γ is the most common in the natural diet, the alpha form is the most potent in activity, the most supplemented and the subject of most studies.   In their natural diet, horses receive the most vitamin E as γ tocopherol from growing forages or harvested forage that was cut at an immature state.  As the plant ages, vitamin E decreases in content.  Vitamin E concentration also decays over time in harvested forages, as much as 50% over one month.  Therefore, older hays which have been stored for some time will have little activity.  If you also feed non-processed concentrates  to your horse (such as oats, barley, corn etc.) they will also be low in vitamin E. However, most commercial equine feeds will be supplemented vitamin E, usually as α tocopherol acetate.   It can be provided as either natural α tocopherol or synthetic, with natural forms having 36% more biological activity than synthetic.  The natural form has been shown to increase plasma α tocopherol concenrations greater than its synthetic counterpart but both are effective supplements.

    (This is the structure of alpha tocopherol.)

    Despite its form, vitamin E’s function is most frequently thought of as an anti-oxidant.  Vitamin E can work to eliminate free radicals which are formed through the incomplete oxidation of oxygen or other molecules.  During normal metabolism some amount of free radicals are always formed.  However, stress, work, aging, poor nutrition etc can increase the amount of free radicals in the body.  These are essentially molecules which are missing an electron, making  them highly reactive.   This is an unstable condition and the free radical can remove electrons from other cell components, such as lipids, cell membranes etc.  Vitamin E, along with other anti-oxidants donates an electron to the free radical, thus stabilizing it and preventing further damage.  One oxidized, vitamin E itself must be reduced back to its active form.  This is usually accomplished through the action of other anti-oxidants in the body such as ascorbic acid or glutathione peroxidase.  As the cells of the immune system have a high amount of polyunsaturated fatty acids which are quite susceptible to damage by free radicals, vitamin E plays a vital role in the optimization of the immune system.  Furthermore, vitamin E plays a role in reproduction, gene transcription and platelet aggregation.

    (Traditional concentrates such as just corn and oats may be relatively low in vitamin E content.)

    Currently, vitamin E is recommended to be fed to maintenance horses and breeding horses at 1 IU/kg of body weight (not sure if your horse is a maintenance horse, see Energy Requirements).  Growing horses  and lactating mares are suggested to need more vitamin E in their diet, at double the rate of maintenance horses or 2 IU/kg body weight.  Vitamin E intake for the working horse may need to be a bit higher.  While the current recommendation for working horses is 1.8 IU/kg body weight for moderate work and 2 IU per kg body weight for heavy work, many research studies have provided Vitamin E at higher levels.  Supplementation rates from 150-250 IU/kg DM, 300 IU /kg DM or even as high as 11.1 IU kg/body weight (in a simulated endurance race) have been found to be necessary to maintain blood and muscle concentration of vitamin E in more rigorously exercised horses.  To make these values seem more familiar, if we assume we are feeding a 500 kg horse 2% of its body weight, than the range of vitamin E would be between 1500 – 5500 IU of vitamin E per day in these studies.

    Therefore, Vitamin E is often part of the suggested management protocols for horses which are heavily exercising or may have muscle disorders. In fact, in a study looking at endurance horses and supplementation of Vitamin E, the authors were unable to create a control group as no riders were willing to not supplement their horses!  However,i t has been difficult to prove the effectiveness of supplementation for the enhancement of the horse’s health.  In exercised horses receiving 300 IU/kg DM of vitamin E compared to 80 IU/kg DM, or no supplementation of vitamin E, the higher rate of supplementation did increase the muscle concentration of vitamin E.  However, it did not affect the indicators of oxidative stress in the muscle following a submaximal exercise test.  Perhaps a difference would have been observed with a more aggressive exercise regimen.  More recently, horses supplemented at a rate of 3000 IU per day of vitamin E compared to 80 IU/kg DM, underwent a training protocol.  The anti-oxidant capacity of all the horses increased following training, which is a natural adaptation to exercise.  There were no differences in reduced or oxidized glutathione peroxidase at rest, or total glutathione peroxidase.  However after a standard exercise test, the horses receiving 3000 IU vitamin E did have more reduced gluthathione peroxidase, suggesting a greater anti-oxidant capacity. Horses exercised to fatigue following 8 weeks of supplementation of 3000 IU of vitamin E had less muscle oxidation as measured by myofibril carbonylation( a measure of protein oxidation).

    (Heavily exercised horses may need more vitamin E in their diet than maintenance horses or lightly worked horses.)
    Determining if your horse has a vitamin E deficiency may not be as straight forward as taking a blood sample.  It has been shown that the concentration of vitamin E in the horse’s blood  varies irrespective of diet.  In one study, the variation within an individual horse in a 72 hr period would have shown the same horse as more than adequate in vitamin E, to marginal as well as deficient.  Therefore, it may be more important to look at your feeding regimen and the feedstuffs your horse consumes to determine whether or not they may have a deficiency.  The diet your horse is on may also affect his vitamin E needs.  Vitamin E is protective against the peroxidation of lipids in the body, especially the polyunsaturated fatty acids.  Horses which consume diets higher in PUFAs, which is certainly recommended in many cases, may increase the need for anti-oxidants in the body to prevent lipid perodixation.  Thankfully, many sources of PUFAs may be higher in vitamin E content.

    If your horse is older, they may also be a candidate for vitamin E supplementation.  As horses’ age, their body systems may not function at the same level seen in their younger years.  As in people, the immune system of our aged horses may begin to fail.  When horses over 20 years of age were vaccinated for influenza, they were unable to mount the same immune response as their younger counterparts.  Therefore, older horses may be prime candidates for supplements which are known to complement the immune system.  In older horses fed vitamin E at 15 IU/kg of body weight, the bacterial killing ability of specific immune cells was increased, along with an increase in some, but not all, of the specific types of immunoglobins (or antibody).  However, in this study, the horses were previously on a marginally deficient amount of vitamin E. Therefore, it is not known whether it was the correction of the deficiency or the over supplementation that yielded positive effects.
    Horses are fairly tolerant of relatively high amounts of vitamin E in the diet.  The upper range of vitamin E intake has been set at 1,000 IU/kg of DM. To think of this in more common terms, we will do a brief example using an 1100 lb horse that consumes 2% of its body weight.  Thus this horse would typically consume 22 lbs of feed per day.  We will convert this to kg to look at our total amount of vitamin E the horse should ever safely consume.  22 lbs of feed is equivalent to 10 kg of feed. Thus, the upper range of safe intake of vitamin E is 10,000 IU per day for a 500 kg horse.

    However, vitamin E should not be used without caution.  In human medicine supplementation of vitamin E has not always yielded positive results, and if fact can actually enhance the disease state.  In humans undergoing heavy exercise, vitamin E supplementation actually decreased some of the positive adaptations to exercise.  In addition, heavy supplementation has been actually linked to mortality. As always, supplementation is never the answer for a properly balanced diet.   Overzealous  supplementation may actually work against your horse’s health!  But if your horse is older, more heavily worked or has added poly-unsaturated fatty acids in its diet, you might want to examine your diet for its Vitamin E content.

    Next month we will finish our discussion of the fat soluble vitamins with vitamin K.

  • HOW TO MAKE YOUR HORSE SMARTER

    Written By Walt Friedrich

    Feral horses are smart horses. Living in a vast geography, they know where all the water holes are, where to find the best grass, where the mountain lions hang out. Very smart, indeed – but it’s all built around feral living. The feral has much, much more learning to do before he’s capable of routine, daily life with humans – yet the domestic horses we live with and enjoy, same species, identical animals – seem much smarter by comparison. But not really – it’s just that they’ve had opportunity to further develop their minds. It’s said that the human brain is capable of so much more than it typically uses. Same thing with horses. The domestics just give us a clue about what’s possible – and their thinking powers can be quite surprising.

    To illustrate: Gail was riding her horse, Rocky, on a pleasant cross-country outing one warm summer day. Off in the distance, an interesting rock formation covered with wildflowers attracted Gail, and so she had Rocky leave the trail and walk through the brush toward it. The brush got thicker and thicker as Rocky plowed on, until he found himself unable to continue, with his legs tightly tangled in brush and vines. He was struggling to proceed, unsuccessfully, when Gail stopped him and asked him to stand still. She dismounted to examine the situation, saw that it was hopeless to plod through, and so she took out the small garden shears from her riding kit and calmly snipped away the entrapping vines, then led Rocky away from that patch of brush. Rocky followed her, calmly, and when clear, she remounted, patted his neck to tell him what a good, smart boy he was, and continued her ride.

    Many horses, in that situation, might have panicked, thrown Gail, hurt themselves in the process. But Rocky understood that Gail will help him out of any difficult situation; he kept his cool and allowed her to do so. He showed far broader comprehension of unusual circumstances than would a herd-raised horse without human experience. But what made Rocky capable of controlling panic so well? Why is he so smart?

    A horse’s lifetime is one of continuous learning. The two basic learning environments are his herd and the geography in which he resides. We’ll examine both, but first, let’s have a look at what happens between his ears, that makes it all possible -- the controlling factors that set the parameters for how he perceives and copes with those social conditions.

    Learning by developing his cognition:

    How he develops mentally is strongly influenced by what he views his physical limitations to be, what are his likes and dislikes, and does he know when he needs help, for example. But -- and this is tricky – we’re talking about understanding self-awareness in an animal, a challenging subject that’s difficult to define for even humans, about whom we do know something. It must be considered as the foundation on which knowledge is based because everything we see and understand is observed from a totally personalized standpoint. It seems unlikely that the relationship we humans have with our horses, as with our dogs, could exist if animals act only out of instinct. As we shall discuss, horses shape their behavior to fit the herd’s requirements; there seems to be some evidence, perhaps only intuitive, that they would do likewise in the company of humans. And it works both ways – a positive environment elicits positive attitude, and negative elicits negative.

    Learning from the herd:

    We know that the group environment is a highly influential factor in developing cognition. How smart a horse becomes is defined by the circumstances into which he is born and in which he develops – and it is a continuing process. Every event he experiences contributes to his fund of knowledge, and thus his intelligence. It follows, as studies confirm, that youngsters develop best in a herd environment, where its members have established complex interrelationships among themselves. The youngster comes to understand hierarchy, and that he must comport himself accordingly. But herd dynamics is much more than an unwritten rulebook – it’s also a blueprint for comfortable and safe living within a broad society, and to participate, he must learn it. The importance of the social environment cannot be overstressed. If you and I were to learn only at our mother’s knee until we were adults, we would be quite ill-prepared to exist in a society of people who developed within the broad panoply of school, playmates, close friends, neighbors, society in general. Likewise, a foal, growing up in such a group environment, will be far better prepared to cope with life’s events than one who knows only his mother and perhaps a few others during his developmental years.

    Not only does the foal learn the dynamics of living with his mother, he also learns the relative position of  every member of the herd toward himself, his mother and each other. Processing this data and understanding it, then living within it, develops his social intelligence so that he can quickly and efficiently continue the process going forward. Most importantly, this mental development forms the foundation for his ability to “fit in”, without unwarranted fear or anxiety, in new and different social situations. That means joining a new herd, for example, when he changes homes; it means handling show environments, joining strange horses in group rides, training experiences, and especially events with humans – as witness Rocky’s performance when tangled in the vines.

    Learning from the environment:

    Since a horse is such a physical animal and he lives in a primarily physical world, that physical environment is a major teaching aid in his mental development. It is the violin from which the music emanates. The objective is to allow the horse as great a range of experience as possible, with the understanding that the most threatening thing for many horses is, simply, change. But constant changeless environments set the horse up to react badly when change does occur. He learns to deal with changes by experiencing changes. Developing his experiences and thus his intelligence is squarely in our bailiwick. Keep him bottled up and we can expect him to be frightened of anything unfamiliar. But keep him in a complex social group and manage his terrain to promote frequent learning, and he will develop the ability to operate intelligently within his environment no matter how dynamic.

    Jaime Jackson recognized that a plain vanilla environment is a boring place, for domestic horse as well as human. He also understood horses’ need for constant movement in order to maintain physical condition. He developed the concept of the Paddock Paradise, a whole new way for the average person with a bit of land and a drive to practice optimal husbandry, to create a stimulating world for her horses, for their health and deep contentment. The difference between Jackson's approach and the usual fenced acreage is like the difference between an animal safari park and a zoo with barred cages. Creating physical, social, even emotional environments in which animals can believe they're in their primordial setup, yields fascinating results when applied to horses.

    Here's how Pasture Paradise works: instead of housing our horses in rectangular fields where they just stand in one spot and eat, an additional "inside" fence is added to create a "track" system. The track shape and width can vary - the narrower the track the more the horses will move. The topography can be changed quickly and easily, rock piles, sandy areas and water locations added. Hay can be piled in different locations within the track every day. The electric fencing can be moved to change the pathways, also allowing grazed areas to recover before being grazed again. The more innovative and creative our management methods become the more likely it is that we can create a real harmony between the needs of the horse and the space he lives in. It’s easy to change around, and it all can be done quite cheaply and quickly using electric fencing. It’s well worth the effort when you see how much happier and healthier he becomes. Horses adapt to such an extent that they look forward to changes in the route, watching while modifications take place. Once a change is complete they move into it without any need for pressure.

    The sum of the parts:

    The foal raised within the herd, an environment of diverse and interesting activity, builds a great deal of knowledge that influences his relationships, personality,  decisions and actions into and through his own adulthood – it makes him a “smarter” horse, very much better prepared for your teaching and training when he joins you as your equine partner. And when he is your partner, allow his natural intelligence to continue to develop in an environment of diverse and interesting activity. The more he learns, the greater his capacity to learn still more, and the greater will be your own pleasure and safety. It’s one of the best investments you can make.

  • Vitamin D

    Written By Dr. Kris Hiney

    Last month we began a discussion of what we currently know about the vitamin requirements in horses.  Unfortunately, the actual vitamin requirements for a particular horse are often hard to define.  Most vitamin requirements represent the amount needed in the horse’s diet to prevent the classic deficiency symptoms.  However, as stated previously, that may not be the same as the amount required for optimum health, well-being, or even performance.  It is certainly possible that the vitamin requirements for the horse might also alter with their stage of life, work load and management.  With this in mind, we will continue our vitamin discussion with the fat soluble vitamin D and what we currently know.

    Most individuals with some nutritional knowledge are familiar with vitamin D’s role in calcium absorption, and that it is synthesized  by the skin when exposed to sunlight.   However, the various precursors of vitamin D, and its active and inactive forms may be less familiar.  To provide some background, vitamin D is actually a steroid hormone.   Horses consume  vitamin D naturally from plants in the form of ergocalciferol, or vitamin D2.   In manufactured diets, vitamin D is typically supplemented in the form of vitamin D3, or cholecalciferol. Horses also synthesize D3  from skin exposure to ultraviolet light, through the conversion of  7-dehydrocholesterol into cholecalciferol.  Dietary  ergocalciferol and cholecalciferol are absorbed out of the small intestine and where it is converted to 25, hydroxycholcalciferol in the liver, or calcidiol.  Calcidiol is the compound that is typically used as an indicator of vitamin D status, as it closely reflects both dietary intake and skin synthesis.  However, horses do differ in the concentration of calcidiol in the blood in comparison to other animals, as it is much lower. All of the forms listed above represent inactive forms of the vitamin. One more reaction must take place in the kidney  before vitamin D is in its active form of the vitamin: 1,25- dihydroxycholecalciferol, or calcitriol. This final reaction is actually tightly regulated according to body needs.  More calcidiol will be converted to this active form, calcitriol, when needed.

    Activated vitamin D directly acts to regulate the amount of calcium and phosphorous circulating in the blood.  It can act to increase the amount of calcium in the body by increasing its rate of absorption out of the small intestine, and increasing reabsorption by the kidney.    Vitamin D promotes mineralization of the skeleton through its regulation of calcium, and deficiencies of vitamin D result in osteomalacia.   In young animals and humans, this is referred to as rickets.  While the function of calcium regulation is commonly known,  vitamin D is actually involved in the normal function of a variety of tissues.  Beyond bone health, vitamin D also has a role in in cell growth and tissue differentiation.  Vitamin D receptors have been found in all cell types in the body, emphasizing its much wider role in the physiology of the body.

    In human nutrition, vitamin D and its role in other body functions, particularly immune function, has been more fully explored than in any of our animal species.   Macrophages, large immune cells capable of engulfing pathogens, produce calcitriol locally.  Here vitamin D is used as a cytokine , or a substance released in response to the presence of an antigen, which acts as a cellular mediator and enhances the immune response.  In humans, low vitamin D status has been linked to cardiovascular disease, auto immune disorders, neoplasias, infectious disease and even psychiatric disease.  Of the autoimmune diseases linked to vitamin D deficiency, these include type I diabetes mellitus, Crohn’s disease, rheumatoid arthritis and multiple sclerosis.  Indeed many cancers have also been linked to hypo-vitamin D status.   However, with this said, large scale studies have been inconclusive, yielding conflicting results.    Recently,  supplementation of vitamin D in controlled studies was found to be ineffective in preventing the common cold or upper respiratory infections.  However, the possibility exists that some of the diseases listed above may actually result in the destruction of vitamin D rather than being caused by its deficiency.   It is interesting that here in the US, the only legal claim which can be made in regards to vitamin D supplementation is that it can reduce the risk of osteoporosis, yet in the European Union, products can also state that vitamin D helps with normal function of the immune system, and normal inflammatory response.

    Most work in animals has really only centered on bone metabolism and calcium homeostasis, which is not surprising as the link to overall health and human nutrition is somewhat new.  Human nutritionists have now recognized that the amount of vitamin D needed to prevent rickets is inadequate to maintain other vital functions.  However, remember that random supplementation is never advised, and results in humans can never be directly extrapolated to animals in general, let alone horses specifically.   In addition, over-supplementation is never recommended.  While vitamin D toxicity is unlikely, it has occurred experimentally.  Vitamin D toxicity is marked by calcification of the soft tissues, and can be fatal.  Interestingly, it is actually used in lethal doses in baits as a rodenticide, when combined with calcium.

    So what does all of this mean for your horse?   It has been shown repeatedly that vitamin D in the blood is higher in the summer than the winter, which would certainly make sense as the sun is the principle source of vitamin D for most horses. Most management systems where the horse is regularly pastured or turned out  where it is exposed to sunlight will be sufficient to provide enough vitamin D.  However, many performance horses are stalled almost continuously, even more so in the winter.  For these horses, it is important that they do receive a feed which contains vitamin D. In the past, the vitamin D requirements of the horse have been stated to be 300 IU of vitamin D per 100 lbs.  Currently, the requirement is 6.6 IU/kg bwt for horses not exposed to sunlight, with the exception of growing horses.  Growing horses requirements are stated to be much higher, 22.2, 17.4, 15.9 and 13.7 IU/kg bwt for horses from 0-6, 7-12, 13-18 and 19-24 months respectively.  This is due to the need to form bone properly as the animal grows.  To provide a quick example, a 650 lb horse who is 15 months old would require:

    650 lbs converted to kg-  295 kg * 15.9 IU/kg bwt = 4698 IU of vitamin D per day.

    Next month will discuss the role of vitamin E and its  various effects on the health of your horse.

  • Get Ready For A Spring Tack Sale: Find Cash In Your Tack Box

    Find Cash In Your Tack Box:  Get Ready For A Spring Tack Sale

    Nearly every 4-H horse club and many breed and show organizations now sponsor spring tack sales or swaps.
    “For horse owners these tack sales can bring in some extra cash and they’re also an incentive to clean out tack boxes and tack rooms,” says Laurie Cerny, editor and publisher of www.good-horsekeeping.com.  “If you’re not using it, or if it doesn’t fit – whether it’s tack or show clothing, it should go.” 

    Cerny warns against keeping tack and apparel for sentimental reasons.  “These things get dated in a couple of years, so keeping a show halter from your retired showmanship horse is probably not a good idea.”  She added, “When tack and show clothing are still in style, and if these things are in good shape, you should be able to get at least 50-60 percent of what you paid for it new.  Years down the road you might be lucky to even find a buyer for it.”

    Here are some tips for selling items at an upcoming tack sale:

    • Clean tack and wash and press clothing, blankets, and other soft goods.

    • Get your items gathered and organized at least a week before the sale.

    • Mark sale tags with the size and price of the item.  Either purchase tags from an office supply store, or make your own – using small squares of paper.  These can be stapled to the clothing tag (located in the collar of a shirt or in the waist band on a pair of pants), or around the browband, cheek piece, etc. of a halter or bridle.  Self-adhesive labels should only be used on items where they have a solid surface for adhering to - like on the shank of a bit, or on the cover of a book.

    • Use rubber bands or string to tie together reins and other strap items like lead ropes and lunge lings.

    • For large ticket items (like saddles, show halters/bridles, chaps, etc.) make take-away cards for potential buyers that have the item, price, and your phone number on them.  These cards can be really helpful at large tack sales - where shoppers may want to look around first, but then forget where your table is at, etc.  It also gives them a way to contact you after the sale – should you still have the item and they still want to buy it.

    • Take at least $20 to make change with (13 singles, one five, and two dollars in quarters).

    • Use a fanny pack as a moneybox.  This way your change and the money you take in are always on you.  Have a separate location to keep checks and to put large bills and extra cash once you start to make sales.

    • Take a variety of bags.  Buyers really appreciate having something to carry their purchases in.

    • Arrive to the sale location early and be ready at least 15 minutes before the start of the sale.  There’s nothing worse than trying to set up while people are shopping your table.

    • Think height when it comes to organizing your table.  Take a couple of milk crates (or similar containers) to set on your table.  These will give you more display space, and will give buyers somewhere else to look besides your table.
     

  • Vitamin A

    Written By Dr. Kris Hiney

    This month we will begin a series examining the function of vitamins in the health and well-being of horses.  We will also discuss natural sources of vitamins which occur in the horse’s normal feed, as well as different forms which are offered in supplements.  Finally, we will look at the latest research on vitamins in equine nutrition.  Unfortunately, there is a paucity of information regarding vitamin requirements in the equine.  While recommended  intakes have been established for vitamins A, D, E, thiamin and riboflavin, all others essentially fall into the category of educated guesses.  Often equine nutritionists must rely on published information in other species, and extrapolate that to the equine.  These suppositions may or may not be valid, but often allow the only approach available.

     

    (If we were feeding these two hays, you would most likely need to supplement your horse with vitamin A if you were feeding the discolored hay.)

    We will begin with a discussion of the fat soluble vitamins in a horse’s diet, in particular vitamin A.  The fat soluble vitamins will be absorbed out of the gut of the horse along with the lipid component of the diet.  While that may seem odd considering that horses naturally consume a very low amount of lipid in an all forage diet, remember that plant cells do contain waxes, sterols and other compounds that are soluble in ether.   Even hay will typically contain around 2-3% crude fat on a DM basis.

    While many of us know these fat soluble vitamins as their familiar names of vitamin A, D, E and K, we may not be as familiar with their scientific nomenclature.    Vitamin A falls into the sub group of trans-retinols.  Vitamin A, or retinol, serves a host of functions in the body, far beyond the traditional role of assisting in night vision.  Vitamin A is also involved in gene expression, reproduction, embryological development and immune function.  Metabolically, retinol can be converted to either retinal or irreversibly to retinoic acid.  While retinal plays a role in vision, retinoic acid is more active in epithelial cells health, anti-oxidant function  and gene expression.  As retinol cannot be stored by itself in the body, it is stored in animal tissues as retinyl palmitate, or retinol linked by an ester bond to palmitic acid.  In supplements, vitamin A typically is provided as retinyl-acetate or retinyl palmitate.  In the intestine, retinyl  palmitate is cleaved to just retinol.  In the natural equine diet, horses primarily receive vitamin A as carotenoids,  which are precursors to vitamin A synthesis in the body.   The functional carotenoids include alpha, beta and gamma carotene, as well as beta cryptoxanthin.  Of these beta carotene provides the highest vitamin A activity.   Beta carotene is cleaved into two, to form retinal.  The rate of conversion of beta carotene to vitamin A is actually dependent on vitamin A status, and will decrease if vitamin A intake is sufficient.    Thus, no direct conversion ratio is actually appropriate, as the individual animal’s vitamin status alters its conversion rate.  Additionally, as beta carotene intake increases, the rate of conversion to vitamin A may decrease, at least has been proved to do so in other species.  Beta carotene is thus considered a very safe form of supplementation, as no toxicities have been linked to beta carotene consumption.  Animals will decrease the conversion to vitamin A, thus avoiding toxicities.

    With that said, we can attempt to generalize the biological activity of the different forms of vitamin A.  For instance, .3 micrograms of all trans-retinol is equivalent to 1 IU, or international unit, of vitamin A.  In the conversion of beta carotene to vitamin A, differing values are used for equine diets.  Original estimates were 400 IU of vitamin A are created for every mg of beta carotene consumed.  However, beta-carotene may have a different conversion  rate between life stages of the equine.  In brood mares, an estimate of 555 IU for every mg of beta carotene is used, while it is presumed to be only 333 IU of vitamin A per mg of beta carotene in growing horses.  While this conversion data is actually extrapolated from studies in rats, it does appear to be reflected in horses.   Mares kept on the same pastures as yearlings had higher serum retinol concentrations than the yearlings, while the yearlings had higher serum beta carotene concentrations.  This does indicate that the mares were more efficient in converting beta carotene to retinol.

    Natural sources of vitamin A are higher in fresh, growing forages, and are associated with the bright green color in hay.  Many horse owners associate the bright color of corn with a substantial amount of vitamin A, but it actuality it contains only about 6 mg/kg of DM of beta carotene.  Concentrations of beta carotene in hay can range as much as only 30 mg/kg of DM to as much as 380 mg/kg of beta carotene.   Thus, corn, is typically much lower in beta carotene activity than hay.  Typically, the content of beta carotene is reflected in the quality of the hay.  What we typically call low quality hay, that of excessive maturity, lengthy storage, rain damaged, sun exposure etc. will be potentially deficient in vitamin A.  The type of the hay also influences vitamin A content.  Legume hays not only have higher concentrations of vitamin A, but it may be more available as well.    We can do a quick calculation using an intermediate conversion number of 400 IU of Vitamin A/mg of beta carotene and the range of beta carotene seen in hays.  Per kg, forage can vary from 1200 IU of vitamin A per kg, to as much as 152,000 IU per kg of hay.  The requirement for vitamin A for a maintenance horse is recommended to be 30 IU/kg of bwt. Thus our 500 kg horse is would need 15,000 IU per day.  Assuming he was eating 2% of his body weight in a low vitamin A forage (typically mature  ), he would be receiving only 12,000 IU per day, which would be short of his requirement. Horses which were fed a low quality forage with no grain supplementation were depleted of their vitamin A stores within two months.  Comparatively, horses which had access to pasture at the same time experienced no change in vitamin A.  Therefore, horses on fresh pasture, or more brightly colored forage would easily meet his vitamin A requirement and should need little supplementation.  A horse eating a high quality forage may actually be receiving the equivalent of 1,520,000 IU of vitamin A!  While this may seem excessive, remember, the horse will essentially decrease the rate of vitamin A synthesis from the beta carotene in the diet.

     

    (Despite its bright appearance, corn offers relatively little beta carotene compared to forages)

    Many horse owners are also interested in the synthetic vitamin A which may be found in feeds, and how that compares with the natural carotenoids.  A water soluble, synthetic beta carotene was not able to support vitamin A status to the similar extent seen in naturally occurring beta carotenoids, or in comparison to retinyl palmitate.  This may be similar to trials even in humans, where water soluble supplements were not as beneficial as fat soluble.  However, an alternative synthetic beta carotene source was able to increase blood concentrations in of beta carotene in the horse.  Thus subtle differences in chemical composition may be key.  Retinyl esters, or retinol attached  by an ester bond to either short chain or long chain fatty acids, are also used in equine diets.  Again, these represent the similar form to how retinol is found in the actual animals body.  Due to their increased stability both retinyl acetate and retinyl palmitate have been used in feeds which allow for longer storage.  If we look at these two sourced, retinyl acetate offers .344 micrograms for each  IU while .550 micrograms of retinyl palmitate is needed for 1 IU of vitamin A.

     

    (Retinyl palmitate.  The storage form of retinol in animal tissues, as well as a common supplement in animal feeds.)

    So how much vitamin A should a horse consume? The original information provided concerning vitamin A requirements was obtained as the concentration needed to prevent the classical deficiency diseases. Deficiencies of vitamin A are actually quite hard to produce, at least as the classical symptoms of vitamin A deficiency diseases are known.  These include night blindness, hair loss, and ataxia.  Certainly as has been stated before, as the content of beta carotene decreases in the diet, the animal may adapt to becoming more sensitive to absorption and assimilation into the body.  Furthermore, as vitamin A is a fat soluble vitamin, it can be stored in the liver and in adipose tissue, and mobilized to support peripheral tissues when the diet is insufficient.  Growing and exercising horses are recommended to receive 45 IU /kg bwt, while pregnant and lactating mares require 60 IU/kg bwt.   However, there may be a difference between the amount of vitamins in the diet to prevent deficiency diseases, compared to what is optimal for overall health and well-being.   It has been suggested that broodmares can benefit by receiving 400-500 mg per day of beta carotene in late gestation and early lactation.  This is truly the area of future research, establishing how much should be fed to offer health benefits without exceeding either the safety margin, or simply wasting money as no additional response can be seen.  Certainly fat soluble vitamins should be considered more carefully as they are also more likely to cause toxicities, as they can be stored in association with lipid, while water soluble vitamins fed in excess are typically excreted more rapidly.  Many horse owners may reach for supplements too often, with little regard to actual dietary concentrations.  Over-supplementation of vitamin A has actually been linked to developmental disorders in young horses.  However, no direct information is available to state at which exact level vitamin A can interfere with proper bone development.

    So what is the bottom line for vitamin A?  If your horse is grazing fresh growing pastures or consuming high quality, bright green hay, it is probably more than adequate in vitamin A. However, if your hay is of lower quality, or your horse does not have access to pasture, you should consider a supplement or a grain that is fortified with vitamin A. If you are concerned with toxicities, remember that beta carotene is by far a safer choice.  Perhaps some time in the future we will have better information as to what values are optimal for growth, reproduction or performance.

  • Keys to Preventing Laminitis

    Written By Dr. Kris Hiney

    In previous articles we have discussed some of the key strategies in preventing laminitis in the equine.  Many of these have centered on grazing strategies which limit the horse’s access to pastures high in fructan content.  Remember that fructans are carbohydrates which are enzymatically unable to be digested in the small intestine of the horse.  These fructans pass into the hindgut of the horse where they are fermented by the microbial population, specifically gram positive bacteria. The production of certain organic acids and amines enhance the permeability of the gut wall allowing these and other endotoxins to enter the bloodstream of the horse and ultimately effect  the circulation to the digit.  However, it is not practical to simply right off all horses’ ability to graze.  Rather, we should try and identify those individuals which may have a susceptibility to fructan content in the grass.  With this month’s article, we will try to identify which individuals may be at risk, and other strategies that may be employed to reduce your horse’s risk.

    While the outward appearance of your horse may give you an indication to whether they are susceptible to laminitis (See Carbohydrates III: Metabolic Syndrome), there may be more to it than just which horses are overweight.  There certainly appears to be a genetic link to laminitis, with pony breeds leading the list of susceptible horses.  Their comparatively thrifty genotype may make their utilization of carbohydrates and insulin sensitivity differ from breeds which typically do not possess these characteristics. For example, thoroughbreds, which typically have the reputation for being “harder keepers” do not experience the same rate of laminitis.  However, the lifestyle and management of thoroughbreds may differ significantly enough to partially explain the decreased incidence of laminitis.  Even within ponies, there does appear to be a decided link to genetics.  In a study examining the pedigrees of an inbred herd of ponies, 37% of these ponies had experienced laminitic episodes.  Of those, half had at least one parent which had also experienced laminitis.  Even in controlled research trials which attempt to examine the effects of various carbohydrate loads on horses, wide variability exists between individuals. This leads to the supposition that individual variation, thus genetics, is at play.  Thus, if you aware of your horse’s pedigree and know of relatives which have experienced laminitis, you might want to manage your own horse more carefully.  Perhaps some day the genes which make a horse more susceptible to laminitis will be identified, and we can use genetic tests in developing management protocols.

    As mentioned previously, development of obesity and insulin resistance certainly predisposes the horse to laminitis.  One theory behind the development of laminitis in the insulin resistant horse is the glucose deprivation model.  When a horse becomes insulin resistant, more and more insulin release is needed to elicit a normal tissue response.  In essence, the tissues become “desensitized” to insulin.  One of the key roles of insulin in the body is to allow cellular uptake of glucose.  Due to the polarity of glucose, it cannot freely enter the cell without the presence of specialized protein transporters. Glut 4 is a protein transporter which is located internally in the cell until insulin binds to the cell membrane.  Binding of insulin to the receptor causes a cascade of intracellular reactions to occur and initiates the translocation of Glut-4 to the cell membrane.  The insulin insensitivity may result in Glut 4 no longer moving to the cellular membrane, and the inability of glucose to enter into the lamellar tissue of the foot, thereby starving it of glucose.  A recent study looked at the presence of different glucose transporters  found in skeletal muscle, the coronary band and lamellar tissue.  Glut-4 is the insulin dependent transporter found primarily within muscle, while Glut 1 is found in other tissues which have non-insulin dependent uptake of glucose, such as the brain.  While Glut 4 was heavily expressed in skeletal muscle, only Glut 1 was found within hoof tissues of both normal and insulin resistant ponies.    Therefore, glucose uptake in the hoof is thought to be insulin independent  and glucose deprivation within the hoof is unlikely to be the cause behind laminitis.  However, in a subsequent study, laminitis was induced in normal healthy ponies using a hyperinsulinemia-euglycemia clamp technique.   In this model, insulin is infused into the ponies at a constant rate, while glucose is infused at a sufficient rate to maintain euglycemia, or normal blood glucose levels.   Therefore, it is not an absence of glucose which causes laminitis, but perhaps the sustained levels of insulin or other hormones which causes this disorder.  This would certainly support the observation of the increased laminitis risk to the insulin resistant horse which suffers from hyperinsulinemia.

    If owners wish to try and avoid the development of insulin resistance, the diet the horse receives may be critical.  Diets which avoid high amounts of sugars and starches, and have a low glycemic response, result in less insulin release.  For horses which still need a significant amount of calories, diets which are fat and fiber based and properly formulated, rather than those which provide a higher glucose or insulinemic response, may prevent the development of insulin resistance.   Certainly just monitoring body condition in the horse may be the easiest way to avoid insulin resistance.  Although if you ask any horse owner if that is easy you may get a different response!  In addition, horses which receive regular exercise seem to be fairly protective against laminitis.  However, it is difficult to know whether the exercise regimen aids in increasing insulin sensitivity, or is simply protective against obesity.

    Many horse owners wonder if there is a magic pill or supplement that they can provide their horse in order to prevent laminitis.   One approach is to reduce the gram positive, lactate producing bacteria which prefer to ferment sugars and fructans.  Antibiotics are commonly used in the livestock industry in order to promote growth by shifting the microbial population within the gut. Some antibiotics select against gram positive bacteria, thus have been studied in the horse as a way to prevent laminitis.  While this may work, the use of anti-biotics in livestock for growth promotion has been banned in the Europe Union over concerns of anti-biotic resistance.  Similarly many in the United States have followed suit, searching for other ways to influence growth and increase immune status.  The use of probiotics and prebiotics may influence the gut microflora in favor of less potentially problem causing bacteria.  Ironically enough, short chain fructo-oligosaccharides have been demonstrated to improve insulin sensitivity, if not glucose levels, in obese horses.   However, none of these methods have been proven to prevent laminitis.  I would caution individuals to monitor diet, grazing patterns, and body condition first, before relying on supplements to prevent laminitis.

  • How to Sell through Your posts on Social Media

    Written By Randi Thompson, Founder of the Award-Winning “How to Market Your Horse Business” website

    Welcome to the fourth and final article in my series, “Marketing Your Horse Business through Social Media.” Here’s a quick recap of Parts 1-3:  In Part 1 we explored how having a presence on social media can benefit your offline, “real world” horse business. Part 2 focused on developing a content strategy that becomes the foundation for all your online marketing. And in part 3, I covered my magic “Rule of Three” and introduced how to use your comments to create relationships and attract those who are looking for what you have to offer. Now in Part 4, we’ll go even deeper into how to use your posts to promote what you have to offer as you continue to build your network.

    How to Market Your Horse Business with the Posts You Share

    Marketing on Social Media is all about how we use our posts to “talk” to other people. Each post you share is an investment in your business and future success. By connecting with other people in your field, you will become a part of a network that will continue to expose you to more people who are looking for what you have to offer.

    How to get Other People Talking

    One of the best ways to get people to exchange comments, and to start “talking” with you is to respond to one of their posts first. Take your time and choose the posts of people you want to know better, or posts that a lot of people are already talking on.  Join in that conversation and see if you can get people to respond to what you have to say. Imagine you are talking with a group of friends, how would you keep the conversation going? One way to get people talking is by asking questions.  You can use open questions to everyone, or ask direct questions to whoever you want.  Once the people in a community begin to respond to your posts, you will know that you have established yourself as a valued and welcome member. You will feel like you are a part of that community. That is when you can start letting people know what you have to offer with a “sales post.”
    If you are not a part of the community you are sharing your “sales post” in, no one wants to hear from you and your posts will be ignored.  In fact, you will be seen as a spammer and your post may be deleted and you banned.

    Here are two important rules to understand about a “sales post”

    1) Never try to sell through your posts or comments. Comments are for building relationships and interacting. Your “sales posts” should direct people to your website or sales page.

    2) The Golden 90/10 Rule of Sales Posts. 90% of all the content (what you share) in your posts should be information that people might need, find valuable or enjoy. Only about 10% of your posts should promote what you offer.

    Crafting Your “Sales Posts”

    There are basically two ways to sell, or share what you have to offer, through your posts.  One way is by responding to another person’s comments on a post.  For example, you might be reading a post about an issue that someone is having.  It just happens that you have the perfect solution with your product or service.  Rather than trying to sell that person through a comment reply, you should contact them off the page first. If you can’t do that, then gently suggest that you might have a solution that could help them and ask them to contact you.

    The second way to sell what you have to offer is by starting a new post,  your “sales post” Here’s a technique that you can use that works very well.  It does not sound or look like a sales pitch.

    *Start with a good photo that will catch people’s attention.
    *Introduce yourself with a friendly greeting: something as simple as “Hi, Everyone” or “nice to see you” will work.
    * Share a few benefits people will receive through your product or service. This should be only a few sentences so it’s not spammy! You can also ask questions that lead back to your product or service as being the solution.  This is the area you will be using to get people to “talking” to you on your post.
    * Invite people to find out more by clicking on your link below the comment.
    * Add your first name and tag your link with your website URL so people will begin to associate your name with your business. If your comments are interesting enough, they will go to your business page to see what you’re all about.

    What about the Follow-Through?

    Sometimes people are so focused on sharing their “sales posts” in as many places as they can that they forget to notice if anyone is responding to the posts they have left. This makes them look very unprofessional. You need to be very aware (and thankful) when someone takes the time to “talk” to you on any of your posts.  Those comments are worth their weight in gold. Make sure you always respond to any comments that people make on your posts.  Also, make sure that you “Like” any comments that other people add to the posts you’ve shared.

    Social Media: It’s Easy, Fun and It Works!

    Following the recommendations I’ve made in this “Marketing through Social Media” series can help you enter the Social Media world for the first time or improve on what you’ve already tried. You’ll find that your interactions and the relationships you build will help expand your business and open doors to new markets.

    With a little practice, you will begin to enjoy social media and all the benefits it will bring to you and your business. Be patient with your process and join us at: https://www.facebook.com/howtomarketyourhorsebusiness

  • Laminitis In The Equine

    Written By Dr. Kris Hiney

    Earlier we posted an article on the typical causes of laminitis and some feeding strategies that may help in preventing laminitis (Feeding Horses for the Prevention and Management of Laminitis).  We also discussed how we might approach feeding a horse which has already experienced  laminitis.  This month we will begin to delve deeper into the causative factors of laminitis and how to prevent its development.

    Remember that laminitis is actually a systemic disease, with just the symptoms being visualized within the hoof.  Some insult to the horse’s system creates an alteration in circulation, ultimately leading to tissue damage of the sensitive laminae.   This period of time, referred to as the development phase or prodromal phase, includes the actual insult prior to the development of symptoms.    It is thought to be due to some change within the vasculature, that leads to ischemia, or lack of blood flow to the digit.  Whether it is a lack of nutrients or oxygen due to the decreased blood flow, tissue damage or death results.  This initial insult is then followed by the acute phase of laminitis.

    In the acute phase, blood flow returns to the foot, typically at an increased rate, as this is the body’s normal response to tissue injury.  Even this reperfusion response can cause tissue damage.  This is when the owner now recognizes the development of symptoms. The horse will appear very stiff and reluctant to move, and may even lie down.  A particular stance may be assumed by the horse as he appears to rock back on the hindquarters and place the forefeet forwards in order to limit weight bearing.  Due to the pain and anxiety the horse is experiencing, his heart rate and respiration rate may both be elevated.  Finally, the owner may even be able to detect an increase in temperature of the hoof wall and a bounding or throbbing digital pulse. 

    If permanent changes to the architecture of the foot occur, whether in PIII displacement, permanent changes to the normal lamellar architecture of hyperkeritization of the hoof wall, the horse has entered into the chronic phase. These horses are typically more susceptible to recurrent episodes of laminitis.  Diet restrictions and specialized hoof care are typically required to allow the horse to lead a comfortable life (Feeding Horses for the Prevention and Management of Laminitis).

    Obviously laminitis can be a devastating disease for the owner, and most would strive to prevent the disease, rather than address a symptomatic horse.  If we look more closely at the causative factors in these alterations to circulation of the horse’s digit, we may be able to do a better job at identifying horses at risk.

    We will begin with a review of pasture associated laminitis, which has been addressed in previous articles (Feeding Horses for the Prevention and Management of Laminitis and Carbohydrates III: Metabolic Syndrome).  Remember that pastures grow more rapidly at certain times of the year, and may store their energy as different types of polysaccharides depending on the species of the plant.  Frequently fructans are noted as the culprit in causing laminitis. Fructans are found in greater quantities in cool season grasses, as well as during periods where photosynthesis is favored over plant growth. As fructans contain beta bonds, which are not digested enzymatically by the equine small intestine, they pass through the tract and arrive at the large intestine where they then undergo bacterial fermentation.   Other types of carbohydrates may act similarly, including sugars and starches which escape the small intestine undigested (the classic carbohydrate overload model of the horse in the grain bin), as well as other types of carbohydrates that may be rapidly fermented (pectins, resistant starches etc). (For more information on carbohydrates, please revisit Carbohydrates: Definitions and Relationship to Equine Diseases.)


    In this first model of carbohydrate/rapidly fermentable fiber overload, too much of this rapidly fermentable material reaches the hindgut of the horse. These feedstuffs favor the proliferation of a particular bacterial population.  These bacteria produce more lactate as their excretory waste.  Excess lactate production lowers the pH of the hindgut which allows the mucosal cell wall to become permeable. In addition, too low of a pH stresses the bacteria causing them to either die or release endotoxins. Furthermore, altering the bacteria’s environment also changes their metabolism, releasing vasoactive amines into the hindgut.  As the gut wall becomes more permeable, these toxins and amines are able to cross the mucosal wall and enter the bloodstream of the horse, where they then can exert their effects at the level of the hoof.


    Horses which need to be restricted from pasture typically include ponies, as they are highly susceptible to laminitis.  In addition, any horse that has a history of laminitis, or has been diagnosed with PPID (pituitary pars intermedia disfunction)(Carbohydrates III: Metabolic Syndrome) should be grazed with care.  Horses with elevated insulin levels, or insulin resistant horses, also have a greater sensitivity to pasture associated laminitis, due to the influence of insulin on the vasculature of the horse.  Hyperinslulinemia increases the production of endothelin-1, and down regulates the production of nitric oxide.  A decrease in nitric oxide production has been linked to an elevation of homocysteine.  Incidentally, elevations in blood homocysteine are also linked to heart disease in humans. There has even been a suggestion, although with no scientific data to support this theory, that excessive supplementation of sulfur amino acids to horses with insulin resistance is unwarranted.  Typically sulfur amino acids (ie methionine) are included in hoof supplements, and homocysteine originates from methionine metabolism.   To further confuse the issue, it does appear that individuals are more susceptible to this disease, even if they are the same age, sex, breed and are managed the same as non-effected individuals.

    Obviously preventative measures aimed at reducing carbohydrate related laminitis issues center on diet management.  Certainly it is not practical or even advisable to state that all horses must be kept away from pastures.  However, knowledge of which horses are susceptible to pasture associated laminitis is key.  Once these individuals are identified, they should be placed on a principally harvested forage diet.  The forage chosen should have very little rapidly fermentable material.  However, horse’s which do not have these susceptibilities can continue to be managed with relative ease.

    Next month we will continue to discuss laminitis at a more detailed tissue level, and address further strategies to limit your horse’s chances of acquiring this disease.

  • Yellow Flies (or And I Thought The Humidity Was Bad!)

    Written By Julia Dake

    I start this tale by saying that I am new to riding in the South. I have ridden many miles in the Sierra, the redwoods and along the coast of California. But I have returned to the land of my girlhood recently and found the riding to be very different. The sandy wide trails, the ancient oaks covered in Spanish moss and the very flatness of the land are all new to me. One of my first trail rides in the south began with the guide telling me “If you come across an alligator on the trail, don’t ride over it”. I thought to myself; You have to tell people this?! Add in the humidity and the afternoon thunderstorms and it couldn’t be any different from the trails I’ve ridden in the West.

    The weekend is going to be warm. For some reason, I think that North Carolina is going to be cooler after all it is NORTH Carolina. It might be a nice treat to get out of the city and have some quiet time. Mom and I head to the barn. Yes my 70 year old, very arthritic mom is going with me. I hook up the rig. Mom offers to help but retracts when I give her 'the look'. I bathe my gelding, Dakota. I get him and his food loaded and off we go. The truck is running great, Dakota is quiet, Dru (my dog) is asleep and mom is happily reading the road signs. I have directions from the internet. It’s a pretty straightforward trip, mostly freeway until we get to the campground turn off.

    Everything is going smoothly but not for long. An accident closes I-95 to one lane. We lose twenty to thirty minutes but that’s okay because I have directions from the internet. And it’s a pretty straightforward trip.

    Past the accident, slowly, and we are on our way once again. We haul down the freeway, me, mom, my dog and the horse. The campground is near the tiny teeny tiny town of Everwild (the name has been changed to protect everyone) and I have mistakenly asked the amazing internet for directions to the town and not the campground. Unfortunately, I don’t know this…yet.

    Mom, who has been reading every sign for the last 100 miles on the road STOPS....and I sail at 60 miles per hour past the turn. In truth she did say I needed to slow down. We turn around three miles later because the rig is 35 ft long and, even with a gooseneck trailer, I prefer a football field when I have to turn around. We get back to the original turn and turn the wrong way.

    Quickly, we are in the little town with no place to turn around. We roll through the ‘main’ street and I notice that pretty much everyone owns a pit bull. Dru is slunk down in the seat. He’s met pit bulls before and these look like they mean business. At least I don’t hear the theme from ‘Deliverance’ strumming in the background. Mom keeps telling me that we are going the wrong way. How does she know?

    Finally in the spirit of women, I call the camp ground. The lady is very helpful but in giving directions feels it is necessary to give the entire history of the inhabitants of Everwild. I mutter ‘huh huh’ while trying to keep the directions straight.

    We get turned around, again. And carefully following the directions from the owner of the campground, we find the place at last. It’s lovely. Quiet. The stalls are small but okay. I get everything settled but we are missing a lot of needed items in the rig and mom doesn’t have a clue where anything is. The rig is too small for anyone other than me and one other person who is agile and can move quickly. That lets mom out. Let’s add the dog to the mix. Getting a good picture?

    It’s HOT and HUMID. I have to run the A/C the entire night. It sounds like the Starship Enterprise is landing on the roof of the living quarters. Mom, under a blanket and a minus 40 degree sleeping bag, is a frozen Popsicle in the morning. I suppose it was a blessing that the dog felt the need to sleep with her. Bless him.

    In the morning (six a.m. because there is no point trying to sleep with the Enterprise hovering just over head) I feed and water the horse. Mom makes coffee. I pull out the awning and set up the TV so she can watch while I am riding.

    I get my gelding ready. I am going to ride early because of the heat and humidity. Unbeknownst to me there is another thing I haven't considered. Bugs.

    A couple of nice men (one deaf and the other in his 80s; "I got a lot of health problems you know") ask me to ride with them. Why not? I've never been here and it might be safer. After a long lecture about something called a 'yellow fly' we start down the trail toward the forest. Being from California the lecture means nothing to me but being raised politely I listen and nod. I’ve hauled a long way and not just to sit in camp!

    We ride about a mile on an asphalt road. I don’t like it because it’s hard on the horses’ feet but hey...the forest is up just ahead. I can almost feel the coolness against my skin. We ride into the beautiful, verdant forest (I am sighing softly right about now) and get swarmed, SWARMED, by yellow flies. Biting and buzzing down my shirt, in my hair, my mouth, my ears and they bite leaving quarter sized welts when they do! They bite my horse. They buzz his ears. He is getting crazy, stomping and bucking. Dakota rarely misbehaves but this is something else. NOW the lecture about ‘yallah flies’ means something.

    One of the gentlemen I am riding with comes up next to me and hands me a slender tree branch. “Use this to brush them yallah flies off yah horse". I have now discovered an essential piece of gear while riding the Carolinas; a small branch with the leaves on the end. Dakota found some relief as I rode along brushing his ears and face and all other reachable parts of his body. Pleasure trail riding. Yeah right.

    Finally, I give up. Forty minutes into the ride I turn around. Anyone who knows me knows that is NOT something I do. The Granite Stair Case at Echo Summit didn't cause me to turn around....but bugs...biting stinging bugs...that’s it. I tell the gentlemen I am riding with that I am returning to camp. They also turned around. I’m not the only one who finds these flies too much.

    I ride back into camp and start stripping the gear of my gelding. No yellow flies so he stands quietly. My mom comes out of the rig. I can hear the question before she speaks.

    “We’re outta here.” I don’t hike. I don’t swim. I don’t catch sun in a lounge chair. I ride and if I can’t ride I’m leaving. It sounds petulant but it’s one of the little truths about me that I won’t hide.

    I pack the camp up in forty minutes. That has to be a record. Mom is in the truck with the dog, the horse is loaded and I haul on down the road nearly turning right when I should have turned left but mom-mom (I don’t own a Tom-Tom) caught that one before we had to hunt for a church parking lot to turn around in and we are on the road. Interstate 95 south toward Charleston. The weather is cool. In the south, in the summer that is usually a bad sign.

    We roll down the freeway. Mom is quiet and I am happily following a motorhome that is going my perfect speed. I get lulled into a kind of hypnosis, following the sway of the coach in front of me. I’m humming and thinking about yellow flies, the cost of diesel and going to work on Monday when my mom quietly mentions, “This is our exit right here.”

    Now when my mom says “right here” she means right here. It’s a good thing that gelding of mine stands up in the trailer with his feet spread because the exit to I-26 came up quickly. I nearly missed it and would be in Florida by now still following the motorhome. But I make the turn. I don’t know what possessed me not to go on to the next exit but when my mom said ‘right here’; I turn.

    I hear my mother gasping as I make the turn and head south toward Charleston. Tires squeal. I make a mental note to have the brakes checked on the rig. At least they aren’t smoking. This time.

    I relax my grip on the steering wheel. What more can happen? Through my windshield, ahead in the distance is the blackest, meanest thunderstorm on the planet straddling the freeway. Will this fun filled weekend never end?!

    It sits over the interstate; a monster waiting and like a moth to the flame I haul myself, my mother, my dog and a 35 foot aluminum lightening rod toward it. The storm is right over head. The lightening strikes and crashes at the same instant. I am IN a lightening storm. Mom is trying to comfort the dog. He is shivering and his teeth are chattering. Mom is, with the same words, comforting me. I've slowed to twenty mph with my flashers on. I’m thinking about pulling over even though I know better when twenty feet off the right front of my truck, lightening strikes a pine tree and it explodes. Dru now wants in my lap! I want in my mom’s lap!!!! Dakota is hopping around in the trailer. The air is hot and every hair in the rig is on end. Mom later tells me I was talking a mile a minute and white as a sheet. She also mentions that I might want to unclench my jaw.

    We make it to the barn. I unload. Unhook. Take care of Dakota. We drive home. The sun is shining. The next day is Sunday. I watch NASCAR and paint cabinets in the kitchen for my mother. I don't complain. I'm just happy there are no yellow flies at my mother’s house.

    Yippee Ti Yo!

  • EQUINE THRUSH – WHAT IT IS AND HOW TO DEAL WITH IT

    Written By Walt Friedrich

    It is a condition – or more precisely, an infection – in the hoof. It is not a disease. Its elimination has been the goal of massive efforts to develop the ultimate product, as witness the vast variety of thrush-busting products on tack shop shelves. All of them do sell, and each of them probably does reduce and control the infection in some hooves – but there are a couple problems: one is that a given product may clear things up for some horses, but seems ineffective for others. And secondly, many of those hooves whose thrush does get controlled end up with a re-infection a couple months later.  Right up front, the problem is not a simple one.

    Just what is this elusive infection, anyway?

    Well, that’s part of the problem. The term “thrush” gets hung on just about every hoof ache or pain that comes along, but it is not necessarily just one type of microbe that’s responsible. There are enough bad guys to fill a Post Office bulletin board, including yeasts, bacteria, and fungi! The most common of the “usual suspects” is a yeast named Candida albicans, a nasty little creature, and very difficult to eliminate. In addition to albicans, there are a number of other species within the genus Candida that are known to cause human and equine infections. And to add some complication, a bacterium called fusobacterium necrophorum is also commonly held responsible for many “thrush” infections, PLUS numerous fungi in the line-up as well. The invading army that causes “thrush” can have many mercenaries, and it is asking a great deal of any one treatment to go out there and kill ‘em all.

    As if that’s not complex enough, yeasts and fungi exist in both “live” and spore form. Consider the spore to be an “egg”, containing the microbe, which “hatches” when environmental conditions are favorable. Killing an army of microscopic fungi may be doable, but the spores they leave behind are virtually bullet-proof; they patiently wait for those favorable conditions to return, at which time they “hatch” and re-form a brand-new army!

    Tackling the problem…then back to the drawing board

    So here are we, one day, observing our horse three-legged lame, perhaps, with a gooey, stinky mess exuding from a frog. “Aha,” we think, “this is thrush and I’m gonna get rid of it.” Of course, we don’t know what organism or organisms are responsible, so we ask the guy in the tack shop for the best of the thrush killers, we buy it, then take it home and have at it. Sure enough, after a few applications, things appear to getting better, the frog is healing, the goo and the smell are gone, and our horse is happy – until a few weeks later, when we see a rerun of the problem developing. The spores have hatched and have started to party again, plus some new neighbors from the stall floor have joined them, and we’re ready to return to the tack shop to look for a newer and better anti-thrush miracle cure.

    More about these nasty little critters

    One of the basics we know is that we can be dealing with two entirely different entities, here – aerobes and anaerobes. Aerobes live and breathe even as do you and I, which means they need air to survive, which makes them relatively accessible to our attacks. That opens the field to most of the on-the-shelf products that we wipe on or spray on. These are the easiest to apply, and when they work, our job is easier.

    The anaerobes are quite another story. They cannot live in air, consequently, when without a host, they exist in spore form, sort-of in a state of suspended animation. But those spores, along with their aerobic cousins, cover the stall floor and walls, even the very dirt we walk on, even our own shoes! It takes two things for an infection to hit a hoof: the hoof needs to be standing amid the microbes (that’s a “gimme” – if he’s in the stall, he’s standing amid them, and standing anywhere in mud or feces, it’s like he’s put out the welcome mat for infection), and the hoof needs to have some “outside doors” open – any tiny lesion on the bottom of a foot will do. Both microbes and spores get jammed into the lesion, where they get sealed in when the horse stands or walks in mud. The living microbes are already at work, and when the spores realize that there’s no air, it’s warm, it’s moist, they burst forth and join the party.

    How to fight back

    Now we start to see the complexity of fighting “thrush”. Topical treatments work on aerobes because we can get at them. But not so for the anaerobes. Living in an airless environment means they are buried deep in the tissues, hard for us to reach. A new approach is called for; soaking those feet in the appropriate microbe-killer long enough for the medication to soak in and do its job. A 30-minute soak in apple cider vinegar or dilute chlorine dioxide (Oxine or White Lightning, for example) will do the job on the microbes, but not their spores. For that, soaking in a product designed to kill spores is needed. There are several on the market, but the most effective may be CleanTrax, available on-line – it will kill aerobes, anaerobes, and spores.

    So when you can see deterioration of the frog, and/or smell a real stink on those hooves, the “enemy” is obviously present and you can deal with it. But the real trick in dealing with it is to catch it early, before much damage has been done, and for that, some preventive measures are called for. When thoroughly cleaned, the entire bottom of the hoof is in clear view – difficult for undesirable microbes to hide. Consider forming the habit of thorough picking and wire-brushing the hoof bottom clean, a quick scrub with Dawn Detergent, every day, then spraying the entire surface with a microbe-killer; keep the foot off-ground for fifteen or twenty seconds to allow some penetration of the spray. Two very useful sprays are colloidal silver (silver ions are believed to destroy key enzyme systems in the cell membranes of these pathogens), and Usnea (a symbiosis [one organism living on another] of a fungus and an alga, used for its antibiotic and antifungal properties). Both are available on-line: consider the colloidal silver brand, “Silvetrasol”, about $20 for a spray bottle, and Usnea Tincture, about $10 for four oz., available from Essential Wholesale & Labs, among others. Mix Usnea 50-50 with water and spray daily, but Silvestrasol once a week.

    Preventive medicine

    Spraying is a quick and easy preventive procedure – but take it a step further and disinfect any crevices you see. For example, a healthy hoof has no crevices or clefts (the commissures don’t count), but a potential problem will show up as a cleft developing in the center of the heel of the frog. It will usually be just a slit, but if you can insert the metal tip of your hoof pick into it to any depth at all, it’s a problem in development. Left untreated, that cleft will develop into a crevice that’s as deep as your pick’s tip is long – or deeper. That means trouble is coming, and you should take countermeasures right away. Such clefts are well-protected hidey-holes for thrush-causing microbes to start their damaging work. The trick is to deposit some microbe-killer directly into the bottom of that cleft, and to do that you need a special, inexpensive, syringe (no needle). Your vet can probably provide you with one; it has a long, flexible tip that allows you to get it into tight quarters. An alternative is to buy the product, “ToMorrow”, from your local Agway, Tractor Supply, or equivalent. ToMorrow contains medication useful in treating mastitis in cow udders, hence its long, flexible tip. You can use it to deposit a pea-sized glob of medication at the very bottom of a frog cleft. You can use the mastitis treatment cream itself in frog clefts, but a better alternative is to empty the syringe, and then refill it with a 50-50 mixture of Triple Antibiotic Cream and Clotrimazole, both available on your druggist’s shelves. TA Cream is effective in combating Athlete’s Foot – a fungus infection – and Clotrimazole is a powerful treatment, especially useful in combating thrush. Added bonus is the cost for one ToMorrow syringe is only about two bucks.

    The outlook is positive

    And so, with all this, we’ve not yet crossed home plate – but we’re on third, waiting for the base hit that lets us score. We have a pretty good idea what causes the thrush condition. We have not yet found the silver bullet – but we’re getting closer. The thrush condition in horses is actually quite similar to the human version, and when we are able to nail it completely in humans, we should have it licked in horses, too. Meantime, we do have means to control it and make our equine partners more comfortable while we’re at it. It’s so insidious that it can slide in under the radar and our problem becomes repair rather than prevention; but to prevent takes vigilance and some effort on our part. So for our horses’ sake, keep the stalls clean, keep the floors cleared of feces, keep them clear of mud, keep that pick and wire brush close at hand and use them daily. Catch it early!

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