Search Results

​ Pasture Laminitis ​ can be a major problem for some horses, from catastrophic life threatening laminitis to lower grade separation. What does ‘pasture laminitis’ mean? ​ When we gaze out the window at our horses playing and grazing together in spring (or winter) on plenty of grass we may feel pleased to see our horses doing so well. Yet appearances may be deceiving and down the track we may find our horse’s hooves showing clear signs of separation and tenderness. ​ On top of the separation, there may be abscesses and seedy toe. The question comes to mind, why is it more likely in spring (or winter)? ​ Grass is by far the best feed for horses, with the largest range of nutrients. Not one product, in a bag or container can compete. Horses evolved on a fairly continuous intake of low fat and high fibre forage. Fibre is essential for healthy functioning of the digestive tract, it is not surprising to find horses on high grain/low fibre diets with hours between feeds are more likely to suffer from colic, ulcers and digestive upsets. All horses, even those on very heavy workloads need as much fibre in their diet as possible, and grass is an excellent source of protein, minerals and vitamins. All grass species, regardless of the quality of the soil they are grown in contain varying levels of these nutrients, without those nutrients the plants wouldn’t be able to function and survive. ​ ​ ​ ​ The ideal, able to eat grass and not be laminitic prone ​ ​ ​ Though grass (and hay) is a nutritious feed it can also be a health hazard to some horses, especially pasture improved species of grass developed to maximise growth rates in cattle. In spring, warmer temperatures and cooler nights produce a lot of new growth, timed beautifully for the higher needs of pregnant and lactating mares. This new growth can be very high in easily digestible carbohydrates called sugars and starch which in some horses, will cause insulin to rise. These horses are metabolically insulin resistant (IR), or due to high levels of gut incretins produced, have high insulin. It’s the high levels of insulin that can cause laminitis in these horses with theses metabolic conditions. The first sign of a horse not dealing well with a high sugar + starch intake can be low grade laminitis. Dr Eleanor Kellon VMD and the Equine Cushings and Insulin Resistance group, ECIR recommend sugar (ESC) + starch to be under 10%. ​ Low grade laminitis, as the name suggests, is a mild form of laminitis where the horse shows little of the symptoms associated with laminitis and is far more common than many horse owners realise. Often the horse owner is unaware of any episodes of lower grade laminitis yet the typical changes are there in the feet. If the cause is not removed then initially the horse may not show a lot of pain or discomfort in the hooves yet the hooves may undergo the following changes: ​ Horizontal ridges (rings) on the exterior of the hoof Inflammation and eventual separation of the laminae or leaf like folds in which the pedal bone is normally suspended leads to a separation of the hoof wall from the hoof. This is seen as a widening of the laminae particularly at the toe and has the effect of making the horse more susceptible to hoof abscesses. Rather than standing normally the horse will shift his weight from one foot to the other. If the hind limbs are more affected, the horse will stand with its front limbs back underneath to take more weight. Demonstrate a reluctance to step out when ridden. Reluctance to pick up feet. In time the laminitis could develop to tenderness on any surface with a strong ‘bounding’ pulse to the feet indicating increased blood flow and inflammation (heat) of the area. This chronic laminitis may then develop further with pedal bone rotation and solar penetration, known as ‘founder’. Dietary laminitis is a very complex condition, and the likelihood of any particular horse getting it from excessive sugar and starch in the diet is influenced by numerous factors: ​ Seasonal variation, with early spring grass being the big risk. New shoots of grass are higher in sugar + starch. Type of grass – legumes such as clover and lucerne being particularly rich. Grass stressed from drought or frost is higher in sugar and starch. Cold overnight temperatures can mean that the grass is very high in sugar + starch first thing in the morning. Horses that have had previous laminar disease (whether from laminitis, puncture wounds or severe sole abscesses) seem more susceptible to subsequent bouts of laminitis. Overweight IR horses can have a higher predisposition to laminitis. A horse in regular work is less likely to be affected. What actually causes the separation of the laminae that support the pedal bond is under investigation. A RIRDC study showed that high levels of the hormone insulin triggers lamellar separation. Carbohydrates like sugar and starch are broken down into glucose. As glucose rises in the blood, the pancreas secretes insulin in response to the increased glucose. Insulin enables glucose to move from the blood into cells. A large and prolonged influx of sugar and starch will cause a large and prolonged rise in insulin and this has been demonstrated to trigger separation of the lamellae in the hooves though the actual mechanism is still unknown. ​ Sugar and starch are broken down in the stomach and throughout the length of the small intestine but if a significant amount makes it to the large intestine then the delicate balance of bacteria can be upset. The large intestine becomes more acidic, potentially damaging the intestinal wall so that it becomes ‘leaky’. This acidity may cause many of the fibre fermenting bacteria to die and release toxins that pass into the bloodstream through the breaks in the wall. The toxins are thought to alter the blood circulation within the hooves, or trigger the separation of the lamellae. Another theory suggests that when the intestinal environment changes, bacteria that produces laminitis triggering factors may overwhelm others. ​ How to manage horses prone to lower grade laminitis The prevention and rehabilitation of laminitis is all about removing the cause – in this case the source of the excessive sugar and starch in the diet. To minimise the risk, regular exercise is highly effective and can make all the difference between a horse that has to be deprived of pasture and one that can handle the high sugar + starch content. Domesticated horses kept in small paddocks are at far higher risk than non domesticated horses as they would be covering large distances rather than grazing and gorging themselves in a small area with little movement. ​ Ensure your horse isn’t overweight. It isn’t clear as yet whether it’s the obesity that can reduce a horse’s ability to handle a high level of sugar + starch or the high grain and often high fat diets. At an extreme this can develop into insulin resistance where an inability to respond to insulin occurs. A greater than normal amount of insulin has to be secreted to move glucose into cells, triggering laminitis. ​ For managing horses on pasture that are susceptible to low grade laminitis it is useful to know when sugars and starch are at their highest. Generally, the safest time for horses to graze is between 3am and 10am in the morning as this is when sugars and starch are at their lowest though this won’t apply if overnight temperatures are very cold. Grass growing in the shade is safer compared to grass in full sunlight and ditto for a cloudy day compared to a day without clouds to obstruct the sun. ​ If you need to prevent horses from grazing later in the day there are two methods that can be adopted. ​ One option depending on your property is the implementation of a paddock paradise arrangement. Jaime Jackson, a hoof care practitioner in America published ‘Paddock Paradise, A Guide to Natural Horse Boarding’. The paddock paradise idea is where a laneway is fenced off around the perimeter of a paddock using electric tape or around the perimeter of the whole property. Depending on the insulin resistance of the horses, either the grass may need to be removed or their grazing may limit the grass sufficiently. Never underestimate how efficient a horse can be at nipping at the new growth, even when very short. Low sugar + starch hay could be distributed in the laneway. ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ This would entail some initial effort and expense but it would mean that the horses could graze in paddock in the morning when sugars and starch are at their lowest and then later placed in the laneway for plenty of movement which a small dirt yard cannot provide. An extra benefit is that time in the laneway means the paddocks can be rested. Another benefit is that horses kept in paddock paradise type laneway are reported to move far more than horses in paddocks. Read more about paddock paradise , an Australian example. ​ Another option is a well fitting and padded grazing muzzle. A muzzle will restrict grass intake late in the day when sugar and starch is highest but still allows drinking and socialising with other horses in the paddock. A little bit of grass can still be eaten in a muzzle. However, ensure the opening is not too small, and isn’t going to damage the teeth surface. ​ ​ ​ ​ ​ Grazing muzzle controls intake ​ ​ ​ ​ ​ ​ The worst option that cannot be recommended is locking a horse up without feed. It means the horse is prevented from moving and getting exercise, no food can lead to digestive upsets and separation from the rest of the herd is distressing. Horses tend to gorge on grass when released if locked up for a period of time. ​ Is slashing a paddock a good idea? Slashing a paddock or mowing a paddock for hay and allowing a horse to graze the new growth is asking for trouble. The best growth stage for the lowest sugar and starch is when the grass has flowered and seed is spread. If any of the grass stills has seeds this may not present a problem even though the seeds like grains are high in starch but their proportion of the grass biomass is small and soluble carbohydrates in the above ground portion of the grasses drops dramatically after the seeds are set. Unfortunately though, some horses are so sugar sensitive that even the seeds will cause harm. Many insulin resistant horses cannot tolerate any grass, let alone mature grasses. ​ Ideally, allow the grass to be grazed when mature and once eaten down to about 8 cm move the horses onto another section or paddock of mature grass. If you do need to slash to manage large areas of pasture, larger than what the horses can eat then slash and wait 2 to 3 weeks for the regrowth to reach a height of about 25 cm. The regrowth will use up a lot of the sugar and starch for growth and turn it into protein and fibre. Rotational grazing is the best way to manage your paddocks and sugar sensitive horses who can tolerate some grass. The heights given are a guide only, it will depend on the species of grass. ​ What about hay? Hay can also be very high in sugar and starch. Growing conditions, time of day when harvested and stage of growth are most important. Sugars rise through the day on a sunny day, and decrease overnight when nights are warm. Mature stands of grass are safer than young, growing grasses. This means that unstressed mature grass cut early in the morning will be safer than grass harvested late in the day. Drought or nutrient deficient stressed grass will be higher in sugar + starch. ​ Many people who own horses sensitive to high levels of sugar + starch on predominantly hay diets often like to get their hay analysed at a laboratory to find out how safe the hay is to feed. Soaking hay for up to 30 minutes in hot water, 1 hour in cold water can remove a significant amount of soluble sugar but won’t reduce the starch levels. Dr Eleanor Kellon VMD, an equine nutrition specialist in America was one of the first to be concerned about iron overload as a risk factor for insulin resistance in horses as it is in people; hence any feed or supplements with high levels of iron should be avoided. ​ Article originally published in the September – October 2009 issue of Equine Excellence magazine with the title of ‘Grass and subclinical laminitis’, updated since. ​ Further information: Links may change over time. If a link doesn’t work, search the title in your search engine. ECIR website https://www.ecirhorse.org/ Equine Cushings and Insulin Resistance discussion group. Dr Eleanor Kellon VMD oversees. https://ecir.groups.io/g/main Dr Eleanor Kellon VMD http://drkellon.com/ Jaime Jackson (2007) Paddock Paradise, A Guide to Natural Horse Boarding https://www.jaimejackson.com/ Professor Chris Pollitt https://veterinary-science.uq.edu.au/profile/2242/professor-christopher-pollitt L. R Turner, D. J Donaghy, P. A Lane and R. P Rawnsley (2007) Distribution of Water-Soluble Carbohydrate Reserves in the Stubble of Prairie Grass and Orchardgrass Plants Agron. J. 99(2):591-594 https://dl.sciencesocieties.org/publications/aj/abstracts/99/2/591 Safergrass.org with Katy Watts https://www.safergrass.org/ M Sillence, K Asplin, C Pollitt and C McGowan (2007) What Causes Equine Laminitis? RIRDC http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.577.536&rep=rep1&type=pdf raph. Click here to add your own text and edit me. It's easy. Paddock Paradise or laneway system

Home: Welcome ABOUT US Henk is a retired Bare Foot Hoof Technician I trained as a farmer and farm management at Lincoln, i have been farming all my life, and trained as a barefoot hoof trimmer to work part time of farm, this become fulltime with over 320 horses on my books. ​ Due to spinal problems, i was unable to carry on working with horses, During my trimming days i started importing horse minerals from Balanced Equine Nutrition from Australia, This morphed in to selling them online, we are now the main importer of the Balanced Equine Nutrition line in NZ, We have over 200 items on the shelf, Products related for equine health, Wormers and Drenches, Minerals, Supper Goo, VetPro products, Wound care products, Natural herb extracts from Hira Laboratories, Equine care range, Scoot boot and Accessories and much more, We also stock the Bravecto range for dogs and Dontral ​ Our mission is to supply quality products at a competitive price with quick delivery. ​ If you don't see something that you require or are after a different size of a product that we have listed, or have a product recommendation, then please feel free to message me, on hvnaturalhoofcare@gmail.com . ​ ​ Home: About Us Home: Contact GIVE US A SHOUT For general inquiries or feedback, please get in touch with us. hvnaturalhoofcare@gmail.com Submit Thanks for submitting!

Stringhalt: What to feed from a nutritional aspect. It can be devastating to discover your horse moving oddly, with the classic leg jerking. ​ Stringhalt (the Australian variety) is caused by horses grazing Flatweed (Hypochoeris radicata) though Dandelion is also implicated. It’s been theorised that a fungus associated with these plants causes damage to the peripheral nervous system but the mechanism is not clear how this happens. More recent research by MacKay et al looked at a possible toxin in the plant itself. The most obvious nerve affected is the sciatic nerve, which is the longest peripheral nerve in the horse and causes the classic leg jerking. Other nerves may also be affected, including the optic nerve, resulting in impaired vision. Depending on the severity of damage, the sciatic nerve can take approximately two years to regrow, so symptoms may persist for that length of time. ​ Number ONE: Consult your vet as diagnosis is vital. Your horse may need veterinary prescribed medication to prevent permanent damage. ​ What to feed: First step, in consultation with your vet is to remove the horse from the cause, the pasture that contains the plants that are causing Stringhalt. This is the only remedy that will prevent Stringhalt. Best approach as for any horse, of any category, whether Stringhalt affected or not is to feed a mineral balanced intake based on data (pasture or hay test, whichever is appropriate). Whether testing is possible or not, the diet should be as high in fibre as possible, 2 tablespoons of salt along with a quality mineral mix, for example Equi Horse +Se. Often magnesium is recommended to help prevent stringhalt (for example, dolomite, an inefficient magnesium source). A magnesium deficiency can produce muscle irritability, twitchiness as symptoms but magnesium is not a cause of Stringhalt or a cure. Horses outside of known Stringhalt plant areas do not develop Stringhalt. Some people say that all of Australia's grazing country is deficient in magnesium, this is not correct, it varies. Most of the pasture and hay tests I see for parts of Australia don't indicate magnesium as too low for horses though a small amount of additional magnesium can be helpful for optimising the calcium to magnesium ratio. One of the most important functions of magnesium is to control the movement of calcium along calcium channels which forms the basis for all ‘excitable’ tissue activity, including the nervous system, heart, skeletal muscle and smooth muscle in the intestinal tract, uterus, urinary tract and blood vessels. Magnesium controls the sensitivity of the calcium channel, and is also required for the production and storage of the ATP (energy) that is needed by the sodium-potassium pumps to do their job of clearing the calcium from the cell and put it back into storage sites. The symptoms of inadequate magnesium are the same as those of excessive ionised calcium. (NRCPlus, drkellon.com). A horse with Stringhalt AND a magnesium deficiency can at least be helped with additional magnesium but very important to understand, magnesium is not a cure or preventative for Stringhalt. Equi Horse, Equi Horse +Se and HoofXtra contain magnesium. Thiamine, vitamin B1 has been theorised to be able to help. An example of one of the highest natural sources is Brewer's yeast (can be around 95.2 mg/kg). Vitamin E is an important antioxidant which may help. Interesting stuff about Stringhalt: There are two types defined as Stringhalt. One is a physical clinical condition characterised by extreme, exaggerated flexion of the hindlimbs due to trauma, sometimes called classical Stringhalt. The other is called Australian Stringhalt, associated with the grazing of certain plants, including Hypochaeris radicata. ​ ​ ​ Hypochaeris radicata Flatweed ​ Horses can be diagnosed with either type of Stringhalt, either caused by trauma to nerves or the extensor tendon in the hindlimbs OR from grazing pasture that has plants that cause Australian Stringhalt. In this study it was found that plant toxins can become concentrated in plants under stress. Stringhalt outbreaks are associated with pasture that has had periods of drought and overgrazing, and in pasture that is lacking fertility. Australian Stringhalt has been diagnosed in horses not only in Australia but also in New Zealand and parts of Europe. Researchers have used the medication phenytoin to treat horses with Stringhalt, see links below. There are other medications, consult your vet for best treatment. Will a toxin binder prevent Australian Stringhalt? Unfortunately there is no evidence that supports toxin binders as an effective preventative. ​ From the RIRDC Investigation into the Cause of Australian Stringhalt “Horse owners are often advised to feed a variety of supplements to treat or prevent stringhalt. Mycotoxin binders are not uncommonly recommended (author’s observations). Our findings suggest that the practice of feeding mycotoxin (fungal toxin) binders may be unlikely to protect horses from developing AS.” Link below. ​ Further reading: Links may change over time. If a link doesn’t work, search the title in your search engine. Domange C, Casteignau A, Collignon G, Pumarola M, Priymenko N (2010) Longitudinal study of Australian Stringhalt cases in France https://www.ncbi.nlm.nih.gov/pubmed/20662969 El-Hage C (2011) Investigation into the Cause of Australian Stringhalt, RIRDC Publication No 11/127 https://www.agrifutures.com.au/wp-content/uploads/publications/11-127.pdf Huntington PJ, Jeffcott LB, Friend SC, Luff AR, Finkelstein DK, Flynn RJ (1989) Australian Stringhalt – epidemiological, clinical and neurological investigations https://www.ncbi.nlm.nih.gov/pubmed/2767028 Huntington PJ, Seneque S, Slocombe RF, Jeffcott LB, McLean A, Luff AR (1991) Use of phenytoin to treat horses with Australian Stringhalt https://www.ncbi.nlm.nih.gov/pubmed/1929987 MacKay RJ, Wyer S, Gilmour A, Kongara K, Harding DR, Clark S, Mayhew IG, Thomson CE (2013) Cytotoxic activity of extracts from Hypochaeris radicata https://www.sciencedirect.com/science/article/pii/S0041010113001803 Slocombe RF, Huntington PJ, Friend SC, Jeffcott LB, Luff AR, Finkelstein DK (1992) Pathological aspects of Australian Stringhalt https://www.ncbi.nlm.nih.gov/pubmed/1606929 Image of Flatweed sourced from WA FloraBase

EPSM/PSSM/Tying Up is characterised by painful muscle cramping when the horse is exercising, it can range from a reluctance to move to an acute episode with the horse completely seized up. ​ Equine Polysaccharide Storage Myopathy (EPSM) is a genetically programmed cause of tying up (Exertional rhabdomyolysis). The muscle pigment myoglobin causes red brown discolouration of the urine from muscle breakdown. Tying up is a symptom rather than a specific disorder. There are two categories with tying up, horses that have sporadic/isolated episodes and those that have repeated episodes. Isolated episodes are more likely to be due to management/dietary factors. Common causes include electrolyte imbalances to plain overworking of a horse to heat stroke. EPSM on the other hand is a genetic cause. ​ EPSM was first described by Dr. Beth Valentine (Oregon State University) to describe the condition in Draft horses and Polysaccharide Storage Myopathy (PSSM) was coined by Dr. Stephanie Valberg (University of Minnesota) when she first described the condition in Quarter Horses. Since then EPSM or PSSM have been found to occur in other breeds. One study documented PSSM in Warmbloods, Anglo Arabs and Andalusians. ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ Jaxon Horses with EPSM or PSSM have abnormal glycogen in their muscles. Glycogen is the storage form of glucose. In one form, the glycogen is resistant to breakdown. This is the ‘classical’ form of EPSM/PSSM. In another form of the disease, the glycogen is normal but found in abnormal locations. Drs. McCue and Valberg of Minnesota recently found a genetic mutation in horses with the classical form. This causes them to produce glycogen at a faster than normal rate. Since the enzyme systems in muscle cells prevent them from burning and forming glycogen at the same time, they likely have less glucose available for energy. It is still unknown what the root of the problem is in the other form of EPSM/PSSM, but we know that Quarter Horses with PSSM and all Draft horses have high uptake of glucose into their muscle cells, or ‘glucose hunger’. Bottom line is that there are many possible causes, end result is an energy shortage in the muscle cell that prevents it from relaxing. ​ Over time it is understandable that the terms EPSM and PSSM have become interchangeable but there are notable differences depending on breed, the studies just mentioned show Quarter Horses with PSSM are very insulin sensitive compared to other Quarter Horses whereas in Draft horses, both effected EPSM horses and non EPSM have the same high insulin sensitivity. The proportions of the types of muscle fibres matters. Draft horses have a higher percentage of type 2A muscle fibres and Quarter Horses have a higher concentration of type 2B muscle fibres. Both of these fibre types are red, ‘fast twitch’ fibres but the 2A fibres of Drafts are geared to be able to sustain a contraction for a longer period of time while 2B fibres are geared for speed. This gives the draft horse the ability to haul heavy loads and the Quarter Horse fast speed over short distances. ​ Fat can only be burned aerobically, meaning in presence of oxygen by mitochondria, the ‘powerhouses’ or energy factories of cells. No matter how much fat is available, the 2B ‘fatigable’ muscle fibres are limited in how much they can use due to the low density of mitochondria, the preferred fuel is glucose from glycogen. When glycogen runs low, the 2B muscle fibres are in big trouble, for this reason PSSM Quarter Horses are always associated with muscle damage, tying up and elevated muscle enzymes. ‘Fatigue resistant’ 2A muscle fibres have a higher capacity for aerobic metabolism than the mainly anaerobic 2B muscles. There is a higher density of mitochondria in 2A muscle fibres, the greater the number of mitochondria, the greater ability to burn fat. Draft horses are more likely to show symptoms of weakness and muscle loss and may do so without marked elevations of muscle enzymes or myoglobin, meaning it’s not necessarily a tying up issue. ​ Diagnosis and symptoms The symptoms of acute tying up can be very dramatic but acute back pain from poor saddle fit, colic and pedal bone fractures can present with similar symptoms. Horses can have darkish coloured urine which looks likes it’s stained by myoglobin but are simply dehydrated. Symptoms such as tripping can be caused poorly balanced hooves with toes too long. There is a concern that it’s being over diagnosed. Horses may display a number of the following signs: ​ Tying up Reluctance to ‘move out’ or abnormal gaits Stiff or hard muscles Muscle twitching or sensitivity Symptoms of ‘shivers’ or muscle quivering with abnormal hind leg action Unhappy attitude Kicking at nonexistent flies (muscle cramps) Resistance to holding up the hind feet Excessive sweating (muscle pain) Excessive tail swishing (muscle pain) Tires easily Subtle lameness episodes Saddle issues (sore back) Tripping A a preference for rubbing or rolling a lot Looking at belly or flanks as if colicky (muscle pain) Weakness or muscle loss Difficulty rising Bucking Muscle enzyme elevations can be measured but in Draft horses and similar breeds, there may not be any. Previously, the only diagnostic tool was a muscle biopsy to see if there is increased glycogen storage and to look at the structure of glycogen. Horses with PSSM have lower than normal numbers of mitochondria. Since mid 2008, a genetic test has been developed by Geneticist Dr. Molly McCue at the University of Minnesota, in conjunction with Dr. James Mickelson and Dr. Stephanie Valberg. ​ In Drafts, 87% of PPSM/EPSM cases have a genetic mutation for an enzyme involved in the manufacturing of glycogen. The same mutation is found in 72% of Quarter Horses. Quarter Horses and related Quarter Horse breeds may have a second mutation called the modifying gene, a positive for both mutations will have more severe signs of the disease. ​ Treatment All breeds of horse with PSSM benefit from regular exercise to improve their capacity to burn fuels with oxygen and a high fibre, grain-restricted or grain-free diet which will limit the amount of glycogen in the muscle cells. Regular exercise can increase the number of mitochondria and can even cause some muscle fibre types to switch over to aerobic capacity. The greater the number of mitochondria, the more fat can be used as a fuel. ​ Many horses diagnosed with EPSM/PSSM have been helped by changing their diet to include at least 15% fat. Supplemental fat is likely to be of more benefit to Draft than Quarter Horses because of their higher percentage of muscle fibre types that can efficiently burn fat. ​ The high fat feeding proponents say the fat gives the muscle an alternate energy source, and high fat feeding ‘trains’ muscle to rely more highly on fat. This may be so but it may be slowing down carbohydrate metabolism. ​ Horses evolved on high fermentable fibre derived from plant vegetation with less than 6% of the diet as fat. Digestion of fibre starts in the upper portion of the stomach where bacteria begin the job of fermenting sugars and starches into products that can be burned directly in the mitochondria to produce energy. The efficiency of fat digestion in horses is amazingly high, about 80 to 90%+. Since the level of fat is so low in vegetation perhaps that’s why horses need to be so efficient with absorbing fat for the essential omega-3 and omega-6 fatty acids in plants. ​ Feeding high levels of fat can come at a cost. One 2002 study found a 15.8% fat diet depressed fibre fermentation by almost 15% but the main problem for horse owners is insulin resistance(IR), especially for horses known to be ‘good doers’. Horses can develop insulin resistance and be more susceptible to laminitis (founder). Insulin resistance affects blood sugar regulation and is similar to type 2 diabetes mellitus in people. One of the triggers can be a high fat diet; fat has been used by researchers to induce a state of insulin resistance in horses. One 2005 study by Dr Nicholas Frank and others used the equivalent of just under a cup of rice bran oil and induced insulin resistance in Thoroughbreds. ​ Dr Eleanor Kellon VMD, an equine nutrition specialist recommends a different approach “I’ve lost track of how many horses suspected to have PSSM/EPSM and put on high fat diets end up with me because they get insulin resistance and laminitic. We don’t know the safe dose of fat for an insulin resistant horse, but we sure don’t want to be feeding as much fat as is already known to induce insulin resistance in a normal horse!” ​ Her approach is to limit carbohydrates and supplement with L-carnitine to assist in getting fat from body stores into the mitochondria, in conjunction with regular exercise and a mineral balanced diet. L-carnitine is a type of amino acid, necessary for moving long chain fatty acids into the mitochondria to be burned. Studies have shown that availability of free carnitine in the muscle cell influences the relative rate of burning of fat or carbohydrate. Even normal horses in training benefit from L-carnitine supplementation, showing higher metabolic efficiency during exercise. With L-carnitine supplementation, it’s been possible to greatly reduce or eliminate high fat feeding, with better results. Inside the body, L-carnitine exists either in the free, L-carnitine, form or as acetyl-L-carnitine. More recently, Dr. Kellon has been using the acetyl-L-carnitine form (ALCar) because a laboratory study has found acetyl-L-carnitine can turn on a pivotal enzyme which directs glucose into the mitochondria to be burned rather than into pathways that produce glycogen. ​ Dr. Kellon says, “Until we know more details of the biochemistry of EPSM/PSSM, it’s important to treat each case as an individual. How a horse responds to treatment depends both on the disorder and other underlying features of their metabolism. Some horses respond quite well to the high fat diet, others relapse or have a partial response. Some have complications. The L-carnitine and acetyl-l-carnitine has helped many horses improve further.” ​ If you would like to find out more about how to help your EPSM/PSSM horse or a horse that is prone to tying up, go to the EPSM-PSSM IO discussion group, run by Dr Eleanor Kellon VMD. See link below. ​ Article originally published in the April – May 2011 (Vol 32 No 6) issue of Hoofbeats magazine, updated since ​ Further reading: Links may change over time. If a link doesn’t work, search the title in your search engine. EPSM-PSSM IO discussion group https://groups.io/g/EPSM-PSSM Dr Eleanor Kellon offers equine nutrition courses, NRCPlus and Nutrition and Therapy: Genetic Basis of EPSM http://drkellon.com NRC Nutrient Requirements of Horses (2007) https://www.nap.edu/read/11653/chapter/1 Frank N, Andrews FM, Elliott SB, Lew J and Boston RC (2005) Effects of rice bran oil on plasma lipid concentrations, lipoprotein composition, and glucose dynamics in mares J. Anim. Sci. 83:2509-2518 https://academic.oup.com/jas/article-abstract/83/11/2509/4803112 Dr Beth Valentine DVM Ph.D EPSM—Muscle Disease in Draft Horses http://www.ruralheritage.com/vet_clinic/epsm.htm Thumbnail EC Stock Photo of Quarter Horse

Linseed, is it safe? Some say linseeds/flax are poisonous and should never be fed in any form and others say the opposite. The current wisdom depends on who you ask! ​ Following is a comparison of views and what the scientific studies are showing: Dr Deb Bennett (biomechanics expert) advocates flax/linseed is a poison and should never be fed yet many nutritionists like Dr Eleanor Kellon VMD, Dr Susan Evans Garlinghouse VMD and Dr David Marlin advocate linseeds/flaxseeds are fine in reasonable amounts. ​ Dr Lydia Gray VMD states clearly on her ‘Askthevetpage blog’ that feeding flax/linseed is safe. Dr Gray says feeding linseed is harmless because “a recent study confirmed that stomach acid inactivates the enzymes that interact with the cyanogenic glycosides to form cyanide (also known as prussic acid) so that is why toxicity is not observed” and advises feeding the ground up seeds soon after grinding. Links are at the bottom of the page. ​ Dr David Marlin says that “the risk of hydrogen cyanide production is very low as once the linseed reaches the stomach the low pH (acidity) prevents the breakdown of cyanohydrins to hydrogen cyanide.” Facebook 4 Nov 2019 ​ Linseed or flax (Linum usitatissimum) is the only oil seed that contains the ratio of omega-3 fatty acids (anti inflammatory) to omega-6 fatty acids (pro inflammatory) in roughly the same ratio as grass, about 4:1. Linseed oil contains roughly 58% omega-3 and 14% omega-6 fatty acids depending on the analysis. Both omega-3 and 6 fatty acids are essential in the diet, they have to come from food sources whereas the other omega fatty acids such as 9 can be manufactured by the horse. ​ What about other oils? Rice bran, sunflower seeds, canola, coconut, hemp, soybean oil and EVERY other oil are high in the pro inflammatory omega-6 compared to omega-3 fatty acids. Both coconut and sunflower seeds contain essentially zero omega-3 fatty acids. I’ve even been asked about emu oil! Definitely not suitable for feeding horses, and the processing is not great for the emus. For a comparison of some of the choices: ​ ​ ​ ​ ​ ​ ​ ​ The best oil is the one with the most alpha-linolenic acid (omega-3) vs linoleic acid (omega-6). Note that canola oil has the next best profile for omega-3 after linseed/flax but the amount is a lot less than the level of omega-6. The horse has no shortage of omega-6 fatty acids, the aim is to supplement as much omega-3 fatty acids. ​ Studies such as The Slow Discovery of the Importance of 3 Essential Fatty Acids in Human Health and The Benefits of Flaxseed explain in more detail about the benefits of omega-3 fatty acids. The study The effects of dietary N-3 and antioxidant supplementation on erythrocyte membrane fatty acid composition and fluidity in exercising horses documented the reduction in red blood cell deformity due to exercise with omega-3 fatty acid supplementation. Links at the bottom of the page. ​ Fat or oil in hays is roughly 50% of the level in fresh grass but the loss is almost entirely omega-3 as the fatty acids are heat sensitive. The curing process to turn grass into hay destroys the omega-3s. Linseed is mainly recommended as a fatty acid supplementation for horses on predominantly hay/supplementary feed diets as they miss out on the omega-3s. ​ Why is linseed a concern? The seeds contain little, to no, preformed hydrogen cyanide but hydrogen cyanide, also known as prussic acid is produced when the enzyme, linamarase comes into contact with cyanogenic glycosides that are normally kept separated in the cell vesicles. This occurs with grinding or contact with water. Linamarase breaks down cyanogenic glycosides to cyanohydrins and then to hydrogen cyanide. ​ Strains of linseed used for human consumption typically have low levels of cyanogenic glycosides. Also, hydrogen cyanide is a gas and will vaporise off the meal as it is released from hydrocyanic acid. Heat treatment of the meal to lower the moisture content will also greatly decrease it. Freshly milled linseed meal may be as high as 500 ppm according to some EU sources, but this will drop even during the oil extraction process. ​ To put the risk in perspective, cattle and pigs have been fed diets containing as much as 15% linseed by weight with no toxicity. In Plants Causing Sudden Death, it was reported that ruminants like cattle “are more susceptible to cyanide poisoning than other animals” and that “Humans, pigs, dogs, and horses that have a highly acidic stomach (pH 2-4) tend to have a reduced rate of glycoside hydrolysis and cyanide production in their digestive systems and therefore rarely suffer from cyanide poisoning of plant origin”. Dr Kellon VMD said she has never ever seen a report of cyanide poisoning from linseed in a horse. The Canadian Sweet Itch study used human grade stabilised linseed, about 450 grams/450 kg bodyweight per day and reported no issues. This page has tips for Queensland Itch remedies. ​ It has to be a personal decision by the horse owner about what they feel comfortable feeding. If not comfortable with grinding the seeds then simply use linseed oil as the cyanogenic glycosides and enzymes are not in the oil component of the seed, the oil is definitely safe. Look for cold pressed or animal grade linseeds. Cold pressed/animal grade means the oil has been squeezed out of the seeds without heating the seeds as heat can destroy the fatty acids. The oil to avoid is furniture grade linseed oil as it contains solvents to expediate the drying time when used on furniture, tool handles. A good reference to read about furniture grade linseed is at The Natural Handyman website, link below. If you buy linseed oil from a hardware, assume it’s for furniture, and toxic for horses. ​ Unprocessed oils frequently have opaque, thick yellow material in the bottom. This is lignans and other material from the linseed, rich in plant antioxidants and vitamin E. If the oil is not refrigerated there will be a rapid loss of omega-3s although there may be some protection from the natural antioxidants. ​ Boiling linseeds will destroy the omega fatty acids, if the purpose was to supplement omega-3s then boiling makes it pointless. However heating in an oven up to 150°C, ground in a blender and storing for one month was found to not degrade the omega-3 fatty acids in this study; Heat Treatment and Thirty-Day Storage Period Do Not Affect the Stability of Omega-3 Fatty Acid in Brown Flaxseed (Linum Usitatissimum) Whole Flour. ​ It has been widely believed for a long time that the seeds need to be freshly ground in a blender or coffee grinder just before feeding. At this stage there has been no studies done on how well linseeds are digested and the omega-3 fatty acids absorbed if not ground. Some people have been stating that the linseeds do not require grinding and have been feeding the seeds whole. One way to find out is to remove any seeds in the manure and place in a glass of vinegar or even milk. If a mucilage or gel forms, then the seeds haven’t been broken down properly. Another way is to observe whether a crop of linseed plants germinate in the manure though the limitations to this is that the right environmental conditions also need to be met for the seeds to germinate. Horses with compromised dentition and older horses are unlikely to benefit from whole linseeds. ​ Do you need to supplement omega-3 fatty acids? If your horses are predominantly on pasture then no, your horses are likely to be getting plentiful anti inflammatory omega-3 fatty acids from grass. If your horses have hay and any other supplementary feeds as the main forage then the answer is yes as curing hay destroys the omega-3 fatty acids. The only feed that comes out of a bag that is high in omega-3 fatty acids is linseed (flax seed) or chia seeds. ​ For insulin resistant (IR) horses, some studies have shown that supplementation with omega-3 fatty acids have demonstrated an ability to increase insulin sensitivity though more research is required with larger numbers of IR horses. The study Effects of Ω-3 (n-3) fatty acid supplementation on insulin sensitivity in horses is one example, link below. ​ Linseed vs Chia seeds Chia seeds can be fed instead of linseeds. Chia is a good source of omega-3 fatty acids though contain less per kg than linseeds and the omega-3 to omega-6 ratio is less too. It’s recommended that chia seeds do not require grinding despite being smaller than linseeds as the seed coat is softer. This is a big advantage advantage compared to linseed though unfortunately chia seeds are a lot more expensive. ​ A Effects of Ω-3 (n-3) fatty acid supplementation on insulin sensitivity in horses looked at the composition of fatty acids in flax, linseed and perilla seeds. Conversion factor for omega-3 fatty acids is roughly 1.25 depending on the cultivar. Multiply the amount of linseeds by 1.25 to get the equivalent amount of chia seeds. For example: 100 grams linseed is approximately equivalent in omega-3 fatty acids to 125 grams chia seeds. ​ Fish oil vs Linseeds There are 3 major types of the anti inflammatory omega-3 fatty acids; alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). These are essential fatty acids, they have to come from the diet for people so human studies looks at the three and how they work in our bodies. There are lots of benefits. Once eaten the body converts ALA to EPA and DHA, the two types of omega-3 fatty acids more readily used by us. Fish get their ALA from plant material and convert it to EPA and DHA. Plant based omega-6 is called linoleic acid. ​ Plant material is a rich source of ALA but does not contain preformed EPA or DHA. Since a horse’s natural diet is plant material and not fish I find it puzzling that companies are pushing fish oil which is highly unpalatable for horses unless heavily processed. The Kentucky Equine Research article (link below) is a great example of how companies push fish oil as a feed additive for horses. ​ The article above says that that the ability of horses to efficiently convert ALA to EPA and DHA is not known, and thus requires more research. ​ Whether ALA can convert efficiently into EPA or DHA or not is of lesser importance to me if a herbivore like the horse didn’t evolve on a diet that included EPA or DHA. It’s a personal choice whether to include fish in a horse’s diet. Fish oil is well established as beneficial for people which makes a lot of sense since we are omnivores. The ideal ratio of omega-3 to omega-6 fatty acids is higher in omega-6 in animals like us that are higher up in the food chain. ​ Further reading: Links may change over time. If a link doesn’t work, search the title in your search engine. Oil chart and more detailed downloadable pdf: https://www.canolainfo.org/health/canola-oil-is-healthy.php Alonzy J Linseed Oil – It’s Use and Limitations The Natural Handyman https://www.naturalhandyman.com/iip/infpai/inflin.html Dr Eleanor Kellon VMD http://drkellon.com/ Dr Lydia Gray VMD Is Flax Seed Safe to Use in Horses? https://blog.smartpakequine.com/2008/09/is-flax-seed-safe-to-use-in-horses/ Garton, GH (1960) Fatty Acid Composition of the Lipids of Pasture Grasses Nature 187:511-512 https://www.nature.com/articles/187511b0 Hess TM, Rexford J, Hansen DK, Ahrens NS, Harris M, Engle T, Ross T and Allen KG (2013) Effects of Ω-3 (n-3) fatty acid supplementation on insulin sensitivity in horses J. Equine Vet. Sci. 33:446-453 https://www.deepdyve.com/lp/elsevier/effects-of-3-n-3-fatty-acid-supplementation-on-insulin-sensitivity-in-3W2vUyuFyd Holman RT (1998) The slow discovery of the importance of 3 essential fatty acids in human health J. Nut. Feb;128(2):427S-433S https://academic.oup.com/jn/article/128/2/427S/4724041 Knight AP and Walter RG (2002) Plants Causing Sudden Death In: A Guide to Plant Poisoning of Animals in North America http://citeseerx.ist.psu.edu/viewdoc/download;jsessionid=53B006B32EDF5FFAC29E80B8D00A5544?doi=10.1.1.497.838&rep=rep1&type=pdf Portier K, De Moffarts B, Fellman N, Kirschvink N, Motta C, Letellier C, Ruelland A, Van Erckt E, Lekeux P and Coudert J. (2006) The effects of dietary N-3 and antioxidant supplementation on erythrocyte membrane fatty acid composition and fluidity in exercising horses EEP 7 Equine Vet. J 36 http://bictel.ulg.ac.be/ETD-db/collection/available/ULgetd-07232007-164244/unrestricted/EVJ.pdf Magee E. The Benefits of Flaxseed https://www.webmd.com/diet/features/benefits-of-flaxseed Morais D de C, Moraes EA, Dantas MI de S et al. (2011) Heat treatment and thirty-day storage period so not affect the stability of omega-3 fatty acid in brown flaxseed (Linum usitatissimum) whole flour. Food Nut. Sci. Jun;2(4):281-286 https://www.scirp.org/Journal/PaperInformation.aspx?paperID=5216 DHA/EPA Omega-3 Institute. Metabolism of Omega-6 and Omega-3 Fatty Acids and the Omega-6:Omega-3 Ratio http://dhaomega3.org/index.php?category=overview&title=Omega-6-to-Omega-3-Ratio Kentucky Equine Research Inc (2009) Omega-3 Fatty Acids: Consider the Source https://thehorse.com/153851/omega-3-fatty-acids-consider-the-source/ Maddock TD, Anderson VL, Lardy GP (2005) Using flax in livestock diets. NDSU Extension Service, North Dakota State University https://www.agmrc.org/media/cms/as1283_E9EE897D14437.pdf O’Neill W, McKee S, and Clarke AF (2002) Flaxseed (Linum usitatissimum) supplementation associated with reduced skin test lesional area in horses with Culicoides hypersensitivity Can. J. Vet. Res. Oct;66(4):272-277 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC227015/ Rudzińska M (2012)Lipid components of flax, perilla, and chia seeds Eur. J. Lipid Sci. Tech. Jul;114(7):794-800 https://www.researchgate.net/publication/230886089_Lipid_components_of_flax_perilla_and_chia_seeds Chart is linked to a more detailed oil chart, provided by the Canolainfo.org website.

Badly sunburnt white nose. Applying Vetpro Sunblock Powder Effects of Sun on Equine Skin The Positive Effects of Sunlight on Horses The physical positive effect of sunlight is the effect it has on the oils in the skin and that is the conversion to Vitamin D. This vitamin is fat soluble which means it can be stored by the horse. Daily exposure to light (and it doesn’t have to be bright sunlight cloudy days will work) usually provides all the Vitamin D required by the horse. The rate is improved by uncovered exposure to bright sunlight, but 5-8 hours on a cloudy day with a rug on will be sufficient. Some chemicals in fly repellents and coat conditioners will reduce the effect but these tend to be used in Summer when the sunlight is more effective. Vitamin D has two origins, D3 is a hormone that is found in animals and increases blood calcium levels. Vitamin D2 is found in plants, again from the effect of sunlight, and is ingested by the grazing horse and so is a secondary source. Note though that hay (unless it is sun cured Lucerne hay), has little Vitamin D, it needs to be provided by green pasture. Once inside the horse they both have the same physiological effect of maintaining correct blood calcium levels. Vitamin D deficiency is uncommon in New Zealand with its clear light, but can occur in stabled horses that have little or no access to light and pasture. Sometimes too frequent washing down with chemical soaps can wash away too much oil which is the prime source. When considering supplementing be aware that there is a toxic level with an upper limit of 3300 iu per day. Sunlight will never create a toxic level as the process only makes as much Vitamin D as is needed, so better to let the natural way of light produce the required amount for the horse. ​ The Negative Effects of Sun on Equine Skin The negative effects of sun on human skin is well known here in New Zealand but what about your horse. Horses with white areas, blazes legs and ears, also chestnut horses particularly their heel areas, are definitely subjected to sunburn and need protection from the UVA and UVB rays of the sun. UVA are short wave ultraviolet and UVB are long wave ultraviolet rays. Both will cause soreness, redness and discomfort but it can then progress to blistering and an oozing discharge that will need veterinary attention. However even mild sunburn that is repeated can cause damage that will create long term problems, the skin can become thick and scaling appears on the surface (known as keratosis), this in turn may transform to a squamous cell carcinoma (skin cancer). The exposure to ultraviolet light can have negative effects on the immune systems of the skin, this is why horses with white legs often tend to suffer with problems with infection like mud fever from dermatophilosis or bacterial follicitus. Once established these problems become repetitive as the horse’s ability to challenge the infections is reduced because of the lowered immune response. It is advantageous to continue use of a sun block on the legs, particularly the heel area, throughout the year. This will assist the skin to resist breaking down which is the opportunity for the germs to enter and create the problem know as mud fever. Apart from normal sunburn there is a condition called photosensitisation, it is where even lightly pigmented (not just white) skin reacts abnormally to ultraviolet light and results in photodermatitis. Triggers for this can arise from exposure to a chemical that may create the skin to be more sensitive to UV light. These can be chemical based fly sprays, some coat conditioners some dyes and some drugs such as some antibiotics and tranquilisers. Another source of photosensitisation is from some plants and weeds that are digested by the horse as they produce reactive compounds called photosensitisers or photodynamic agents which flow through to the skin and create greater sensitivity in the skin. These can be in some clovers, cow parsley, comfrey, St. John’s wort. Even contact with common buttercups can cause a localised irritation and sensitivity on the muzzle. This condition can also be seen as a side effect of severe liver damage, as a poorly functioning liver doesn’t process chlorophyll efficiently resulting in phylloerythrin in the tissues of the horse. Liver damage can have varied causes but one is the ingestion of ragwort when it has been dried such as hay cut from an infested paddock. ​ Prevention of Equine Sun Burn First of all, dealing with a healthy horse that has white skin such as muzzle and legs is relatively easy as a sunblock that is practical and long lasting will provide protection from sunburn. It is important not to wait until there are signs such as redness, but to start using it as the light levels intensify in late Spring. Attention should be paid to areas like heels which are not the most obvious points but nevertheless can become sore and irritated. Masks are useful but can slip aside unnoticed when the horse is out grazing open pasture. The masks require attachment to a halter and this is often not satisfactory as the horse can become hooked up by a halter and other horses tend to grab on to it. Long term halter wearing can result in rubs and sores. Use of human sun creams is neither practical or effective, most human creams do not block UVB rays and they just act like filters not total blocks and after a short time they are absorbed into the skin and have to be reapplied. That is not so practical for a horse who spends many hours in a sunny paddock. A block that lays on top of the skin and doesn’t get absorbed or rubbed off is the answer. Human creams were developed because they are invisible as people don’t like wearing a white cover on their faces and other areas, but of course the horse doesn’t mind what he looks like! A sticky cream is not easy to apply to horses who generally don’t like their noses being touched, and especially more so if they have been exposed to sun and are becoming sore. Vetpro have developed a powder that is a total UVA and UVB block, long lasting as it doesn’t wash off in the water trough, non-sticky and so easy to apply the horse doesn’t notice. ​ Preventing the more serious problem of Photosensitisation This requires more focussed management. As well as using a total UVA/UVB block, attention must be paid to improving the horse’s general health by providing a balanced diet with minerals, good pasture with shade. Weedy pasture and weedy hay may well be a trigger so remove weeds even excessive clover and improve the quality of the pasture. If possible provide a covered yard or a stable for the horse in the sunniest part of the day. Take care when using chemicals especially on the white or lightly pigmented areas of the horse. Any signs of sickness – liver damage- must be referred to a veterinarian.

Early signs of mud fever Very sore and established mud fever Mud Fever – Symptoms and Solutions What is Mud Fever in Horses It is not really a fever, and has several different names: greasy heel, scratches, pastern dermatitis or dermatophilosis infection. It is actually a skin infection caused by Dermatophilus congolensis, a micro-organism that is best described as a cross between a bacteria and a fungus. The organism is a normal inhabitant of the skin of horses. For an infection to occur, two predisposing factors must be present: persistent moisture on the skin, damage to the skin. It is usually found low on the legs of a horse, especially around the heels and back of the pasterns, from there it can spread up the leg. Un-pigmented skin (white socks) are more susceptible to mud fever because of the damaging effect of solar dermatitis. To read more about the negative effects of sun on your horse read our article ‘Effects of Sun on Equine Skin’. The often bare skin in the area under the back of the fetlock above the heel is quite pink and this is very susceptible especially if it had any reaction to sun during the summer months. Typically in winter the legs are often covered in wet mud, the moisture causes the skin to break down and open small cracks. It is this opening of the cause that allows the already present bug – Dermatophilus to enter through the skin which then reacts to form a scab. The constant presence of wet mud on top forms a seal which is the ideal environment for the bug to work away. Rain Scald is another name given to an infection by the same organism where the lesions are distributed over the body, neck and head, often on the back even if the horse has a cover on. The moisture from wet covers, or sweat, which is then kept covered is an ideal breeding ground for the bug. ​ What are the Symptoms of Equine Mud Fever ​ The infection is characterized by crust (scab) formation with or without swelling of the surrounding area. The crusts characteristically adhere to clumps of hair so when they are removed, the matted hairs come with them. Often the skin below is inflamed and oozes serum. There is usually a swelling of the pastern and it feels warm. The horse may or may not appear lame. Many horses move stiffly and reluctantly due to the discomfort of the sores in the skin. In severe cases where there has been no remedial action, the infection may spread up the leg causing swelling above the fetlock. At this stage a veterinarian should be called as the horse may need antibiotics and or corticosteroids . How can Mud Fever be Prevented or Treated ​ Firstly a healthy horse that is on a good well balanced diet, particularly with minerals and vitamin E supplementation, will be less susceptible. Read more on Vitamin E in our article ‘Vitamin E Supplement for Horses ’. In long wet winters prevention is not easy. Ideally the horse needs to be brought in from the paddock daily, the legs dried and cleaned and a check for any signs of skin deterioration. Washing off the mud, drying the legs thoroughly and using an antibacterial wash, particularly one containing chlorhexidine, will kill any bugs around the area. Covering the legs is not a good idea as the legs will still get wet and then you have created the ideal environment for the bug to develop. Generally, it is better not to clip the legs and leave on the feathers as these offer protection. However once an infection occurs it may be necessary to clip way the hair so you can get to the scabs and resulting wounds in order treat the area. ​ Treating Equine Mud Fever ​ Early detection and action will always produce a better result. Scabs may not always be visible under the hair but you can feel them under your fingers so make sure you run your hands over the pasterns and particularly around the heels and under the fetlock joints, the lumpy scab will be obvious then. The scabs have to be removed and the easiest and kindest way to do this is to use a gentle shampoo, preferably a fungal cleansing shampoo. Work it in to a lather which will soften the scabs. Often a towel is all that is needed to remove them, sometimes you have to pick them off. It is really important to remove all scabs even if the hair is coming off with them. Clean and dry the legs, look for signs of exudation. Use a chlorhexidine wash or cleanser as this will kill the Dermatophilous congonlensis, which lives under the scabs. The horse may be sensitive to the scab removal so go gently and reassure as if he becomes very uncomfortable he will only get more difficult to treat and then the infection can become serious. You never know when mud fever may occur so time should be spent in training the horse to accept having legs washed and dried regularly. Once the skin is clean, then basically the sores are treated as wounds and an antibiotic wound cream is the answer. Apply Equifix TTO Wound Cream – with natural Tea Tree Oil and Zinc Oxide to kill the Dermatophilus bug which is highly penetrative so the skin does not shut off the benefits such as it is very soothing, has healing properties, encourages hair growth and is known to be anti-fungal and antibiotic. Equifix TTO Wound Cream is such a cream. If the infection is casing excessive swelling, or it is above the fetlock, or the horse is clearly lame, then call the veterinarian as use of antibiotic and/or corticosteroids may be needed. Ask your local stockist for the Vetpro Mud Pack – a Grab and Go pack to have on hand ready for any signs of mud fever infection. It contains: – Equifix TTO Wound Cream – With high grade emu oil for skin irritations – Fungal Cleansing Shampoo – gently lifts scabs and relieves minor fungal and bacterial skin infections – Robinsons Activ Scrub with chlorhexidine to kill the Dermatophilus

Iron Overload by Dr Eleanor Kellon VMD Iron is absolutely essential for life. The high affinity of iron for oxygen is what makes it so useful in trapping oxygen in haemoglobin for delivery to the body tissues. ​ Iron is also incorporated in some very reactive enzyme systems. However, iron’s high affinity for oxygen and high reactivity also makes it dangerous. Free, ionised iron will react with peroxide or water in the body, ending in the creation of OH*, hydroxy radicals. OH* damages lipids/fats in cell structures and membranes, in the process generating more radicals to produce a chain reaction of destruction. ​ Iron is absorbed by binding to specific metal transporters in the small intestine, and also passively via the junctions between cells. Work in other species has shown that the volatile fatty acids produced from fibre fermentation enhance iron absorption in the colon. Because the horse is a hind gut fermenter, this likely is a significant source of iron. Iron bound to metal transporters is taken inside the intestinal cells. From there, it may be bound to blood proteins and released, or continue to accumulate and eventually be lost into the manure when the cell dies. By regulating how much iron gets released into the blood, the body has some control. However, the other pathways for absorption cannot be regulated. ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ If you ask any veterinary pathologist they will tell you that finding black, iron loaded livers at necropsy is common in horses. The colour comes from iron deposits called hemosiderin. This is so common it is considered ‘normal’. There are reports of iron causing liver disease, even death in foals, but chronic conditions related to iron overload were not recognised in horses. Iron overload in humans is usually caused genetic disorders resulting in over absorption, or diseases that require frequent transfusions. However, overload related to diet is also possible. Liver damage or liver failure does occur, but is a late stage. Earlier symptoms include fatigue, joint pain/arthritis and often metabolic syndrome/insulin resistance. ​ The same syndrome and consequences has been recognised in a variety of animal species, including several birds, black rhinoceros, tapir, lemur, and dolphin. It may also be linked to IR in other old world primates but iron overload has not been studied in them. ​ Iron overload symptoms in horses include coat changes of bleaching and red ends on dark manes and tails, often hoof issues such as laminitis and abscessing. This study linked iron status to insulin resistance (IR) in horses. Other areas for exploration to determine if there is a link with iron status include arthritis, raised liver enzymes and other issues, even Cushing’s disease because the changes seen in the brains of horses with Cushing’s are virtually identical to those seen in human brains with iron overload. There is a discussion of this and suggestions for further research in my Equine Congress paper here. ​ Diagnosis and treatment of iron overload in horses The only way to accurately diagnose iron overload is with the correct blood work. Serum iron alone is not accurate. It reflects iron in the diet but not how much is stored. Transferrin is the protein that carries iron in the blood. When transferrin and iron are both measured, the percent transferrin saturation can be calculated by dividing serum iron by transferrin and multiplying by 100. That % is useful in interpreting the third test that is needed, ferritin. Ferritin is a measure of the body’s total iron content. High ferritin can mean iron overload but chronic disease involving inflammation or infection may also elevate ferritin. ​ With true iron overload, transferrin saturation is high normal or elevated. There is currently only one laboratory in the world that can measure equine ferritin, the comparative hematology laboratory at Kansas State Veterinary Diagnostic Laboratory. [Note: The only lab in the world calibrated for horses is in America: Kansas State University. No lab in Australia is calibrated for horses.] ​ Iron overload in humans is treated by phlebotomy – blood draws. Blood letting sounds positively medieval but is a very effective way to reduce the body’s iron level because of how much iron is in red blood cells. Stored iron is then used to replace the lost red cells. It works in horses too and can have dramatic effects on IR. A case in point was a gelding with PPID (also known as Cushings) and IR that needed to have surgery to break up and remove a very large bladder stone. Despite diet and pergolide control, his insulins were always running around 120 and he was iron overloaded. The surgery took several hours and blood loss was substantial. His insulin dropped to 20 after surgery, despite a postop diet of senior feed. ​ Dr Kellon VMD ​ You can read more about iron and the role of copper and zinc supplementation to deal with iron overload in my article on minerals and coat bleaching. .hvhoofandequinehealthcareproducts.com/minerals-and-coat-bleaching ​ Further reading: Links may change over time. If a link doesn’t work, search the title in your search engine. AZA Prosimian Taxon Advisory Group (PTAG) (2003) Iron storage disease in lemurs. Working paper, PTAG meeting on iron storage disease, 29 March, St. Louis Zoo, St. Louis, Missouri. http://forageplustalk.co.uk/wp-content/uploads/2015/08/Iron-Storage-Disease-in-Leamurs.pdf Clause M and Paglia DE (2012) Iron storage disorders in captive wild mammals: The comparative evidence J. Zoo Wildl Med. 43(3):S6-18 https://www.researchgate.net/publication/233534108_Iron_storage_disorders_in_captive_wild_mammals_The_comparative_evidence Kellon E Iron status of hyperinsulinemic/insulin resistant horses http://forageplustalk.co.uk/wp-content/uploads/2015/08/IRON-STATUS-OF-HYPERINSULINEMICINSULIN-RESISTANT-HORSES.pdf Molenaar F (2005) Assessing iron storage disease in eastern black rhinoceroses (Diceros bicornis michaeli), reference ranges for iron levels and biochemistry http://www.rhinoresourcecenter.com/pdf_files/117/1175862663.pdf Nielsen B (2012) A potential link between insulin resistance and iron overload disorder in browsing rhinoceroses investigated through the use of an equine model J. Zoo Wildl Med. 43(3):S61-65 https://www.ncbi.nlm.nih.gov/pubmed/23156707 Venn-Watson et al (2012) Hemochromatosis and Fatty Liver Disease: Building Evidence for Insulin Resistance in Bottlenose Dolphins (Tursiops Truncatus) J. Zoo Wildl Med. 43(3):S35-47 https://www.researchgate.net/publication/233534111_Hemochromatosis_and_fatty_liver_disease_Building_evidence_for_insulin_resistance_in_bottlenose_dolphins_Tursiops_Truncatus Kansas State Veterinary Diagnositic Laboratory http://www.ksvdl.org/laboratories/comparative-hematology/ Anatomical drawing above of the equine liver, visceral surface sourced from here . Black iron overloaded liver

Structure Think of a tendon like a telephone cable consisting of parallel bundles of collagen fibres, arranged longitudinally (Fig 1). Cells called fibroblasts are interspersed between the collagen fibres; their job is to produce new collagen. Collagen has high tensile strength, but limited elasticity. An elastic layer of connective tissue called the paratendon surrounds the tendon, allowing it to glide freely. Where a tendon crosses over a joint a synovial sheath (tendon sheath) covers it and a supporting band called an annular ligaments help to keep the tendon in the normal position. Blood is supplied to the tendon from neighbouring muscle, bone and also from within the tendon sheath. This blood supply is limited and thus contributes to the poor healing capacity of tendons. Function Tendons connect muscle to bone. During muscular activity the force generated by the muscle is transmitted to the tendon and then to the bone, thereby initiating movement. ​ What Can Go Wrong With Tendons Tendon pathology can be grouped into two broad categories: Injury – strain e.g. bowed tendon (tendonitis) – Laceration Developmental – congenital (born with the defect) – Acquired (usually occurs following trauma) Strains are the most common cause of tendon injury and occur when a tendon is stretched beyond its capacity. This can be due to a number of reasons: Foot balance. Overly long toes predispose to injuries as the torque forces on the tendons and ligaments are increased at the start of the stride, just before the foot leaves the ground. Uneven heel lengths may also cause problems, as excess strain may be placed on one side of the leg compared to the other side. Rough ground can also cause problems for the same reasons as foot imbalances, as extra stress may be placed on certain areas of the leg. Too much fast work too early on in the training programme can cause problems. As a horse begins work, tendons, ligaments and bones become stronger in response to a gradual increase in stress. When a horse is pushed too hard too fast, its legs do not have time to adapt, consequently the tissues give way to the intense stress. Some pre-existing injuries such as navicular disease may also lead to tendon injuries as a horse has to alter its gait to avoid the pain. Overworking a tired horse can also be a risk factor. Tendons have an inherent elasticity which gives them the ability to cope with a strain. As tendons fatigue, the elasticity is lost, and they become more susceptible to stretch and strain. The faster the speed, the further the tendons are stretched and the higher the chance of injury. Strong pressure directly onto the tendon, such as an overly tight bandage can also cause injury. Tendon lacerations usually occur either as a result of a leg caught in a fence or from interference. Lacerations can extend through the entire tendon or may partially severe the tendon. It is important to realise that tendon sheaths and/or joints can be opened by laceration trauma. Tendon lacerations are difficult to treat due to their poor rate of healing and because of the large amount of tension placed on the fibres. Infection can also reduce the rate of healing, especially if the tendon sheath is involved. This is complicated by the fact that it is difficult for antibiotics to reach the tendon/tendon sheath due to the poor blood supply. Local flushing with sterile water and antibiotics is usually indicated. The lacerated tendon ends can be sutured together using a strong suture material and supported with a cast. Extensive adhesion formation (scar tissue) can occur thereby limiting the normal gliding motion of the tendon. Developmental tendon problems are classified as either congenital or acquired. Congenital deformities are present at birth, whereas acquired deformities generally develop during periods of growth. Weak flexor tendons are a relatively common condition in newborn foals, generally the hind limbs are affected. Affected foals walk on their heel bulbs with their toes pointing upwards. This condition usually resolves within a few days. Digital hyperextension is a rare condition and appears as an extreme form of weak flexor tendons. Foals walk on their pasterns. Contracted tendons (flexure deformities) can be congenital or acquired. Acquired flexural deformities occur most commonly in fast growing individuals fed on a high plane of nutrition. Pain has been implicated as a causative factor in flexural deformities. Pain results in increased tension on the flexor tendons and an altered stance, ultimately leading to flexural deformities as the young horse grows. Acquired flexural deformities occur most commonly between 3 and 8 months of age. Congenital flexural deformities can be caused by several different factors. Malpositioning within the mare’s uterus can lead to contracted tendons. Ingestion of toxins during pregnancy can also cause malformations of the tendons. Genetic factors can contribute to deformities of the tendons. Congenital flexural deformities have also been associated with an unbalanced iodine intake in the mare. ​ What to Look For Heat, swelling and pain generally indicate that inflammatory changes are occurring within the tendon. Skin wounds overlying the tendons. Severed tendon(s) can occur with very small skin wounds. Bacteria and debris can contaminate the tendon/tendon sheath leading to infection. It is important to realise that tendon rupture may occur with no skin wound due to external trauma or sudden over-stretching. Ruptured tendons cause a dramatic change in the conformation of the limb e.g. when the superficial digital flexor tendon is ruptured/severed the fetlock drops dramatically. When the digital extensor tendon is affected knuckling of the fetlock occurs. Loss of normal range of movement. ​ Diagnosis ​ Restriction of Haemorrhage Tendon fibre rupture results in haemorrhage and delivery of inflammatory cells and chemical mediators to the damaged area. This results in increased inflammation and therefore slows the healing time. You can utilise pressure bandages, cold packs or hosing to decrease the amount of haemorrhage. ​ Reduction of inflammation Cold packs, hosing and anti-inflammatory treatment (phenylbutazone, DMSO) can aid in reducing inflammation. Intermittent use of cooling techniques seems to be beneficial for 24-48 hours after injury. However, after this period, it appears to be more useful to warm the affected area as this promotes increased blood flow and hence the increased delivery of nutrients required for healing. The administration of sodium hyaluronate (e.g. ‘Hyonate’) and polysulphated glycosaminoglycans either systemically (intravenous injection) or locally can be used to aid healing by decreasing inflammation and providing supportive components (nutrients). ​ Rest It is important to rest the horse to prevent further injury. However, gentle controlled exercise (e.g. hand walking) is essential so as to create tension on the tendon(s). Tension is required for orderly healing of the tendon fibres. Turning a horse out to pasture is one of the biggest mistakes that an owner can make. The horse will be placing undue stresses on the damaged tendon(s) when it trots and canters around the paddock, this can cause irreparable damage e.g. formation of scar tissue, increasing the size of the lesion. The horse must be kept in an enclosed space where it cannot gallop around, this can be a yard or loose box. Hand walking for short periods (15 minutes) for the first month is important as it aids the healing of the tendon fibres. Exercise protocols can be devised by your veterinarian to suit the requirements of your horse. ​ Decrease wound contamination It is important to reduce the amount of contamination of open wounds. Wounds can be hosed to remove debris and bacteria. Clean bandages should also be applied to decrease further contamination of the site. ​ Support Laceration/rupture of the superficial digital flexor tendon and/or deep digital flexor tendon should be supported in flexion with a rigid device e.g. splint, cast. Conversely, laceration of the digital extensor tendon should be supported in extension. This is beneficial as it reduces the tension placed on the lacerated tendons. ​ Prevention There are many risk factors that can increase the incidence of tendon and ligament injuries. Conformation can increase the risk of developing tendonitis. Long sloping pasterns, long toes, over at the knees, and tied in at the knees can increase the forces imposed on the flexor tendons when extreme extension occurs. An important causative factor involved in tendon injuries is the physical conditioning of the horse and the tendon tissue. Resistance to injury increases as fitness improves. Tendon fibres are better able to resist weight-bearing strain overload if they well conditioned. Conditioning can be achieved by slowly introducing horses to an increase in workload. Young horses and those returning to exercise after being turned out are at an increased risk of developing tendon injuries and it is imperative that they are brought into work slowly. Unfortunately it is difficult to stop your horse getting caught up in the fence, but if you have the choice, number eight wire is a lot safer than high tensile. Number eight wire is thicker, softer and is more likely to stretch, therefore it can help to reduce the severity of the injury. Self induced trauma e.g. overreach injuries, knocking legs, are slightly harder to reduce. Protective boots are worth using on any horse that does hit himself/herself and should be used routinely on young or unbalanced horses which are more likely to knock themselves.

Is Lucerne evil? ​ Some say Lucerne hay or chaff should never be fed as the protein is too high or too rich in ??? This is an example of looking at a feed ingredient or nutrient in isolation to the rest of the diet. ​ Somewhere, somone is saying that ‘x’ feed is evil and should never be fed and often it’s lucerne. ​ The answer is no, Lucerne is not evil but there are some horses that simply don’t agree with Lucerne and it shouldn’t be fed to these horses. Horses can have a feed intolerance to any feed including Lucerne. There are some horses (fortunately rare) that can’t tolerate certain species of grass. However it is wrong to say Lucerne shouldn’t be fed to any horses. Many horses do well on a small amount of Lucerne to boost calcium and protein. No feed ingredient or nutrient is bad per se, it depends on the situation and how much is fed. The whole diet needs to be looked at and keep it all in perspective. ​ It would be unwise to only feed Lucerne (also known as Alfalfa) as the majority forage, not just because protein would far exceed needs but the main issue is the calcium to phosphorus ratio and the calcium to magnesium ratio. If there is an excessive amount of calcium in the intake, it makes it impossible to add enough phosphorus and magnesium to correct the ratios, especially the phosphorus as it is particularly unpalatable and there are limited options for supplementing phosphorus without calcium. And calcium can inhibit the uptake of phosphorus, making the situation worse. ​ However, if the diet was poor in protein and calcium – and a horse only on Oaten hay or chaff would most likely be deficient in protein and calcium, then a small quantity of Lucerne is brilliant. Protein is the most expensive nutrient to supplement, I’d much rather solve a protein need with some Lucerne than the alternative of whey powder isolate, soy bean meal or some other expensive protein additive. That’s if the horse can tolerate Lucerne, in some cases horses are intolerant to Lucerne. ​ The better approach is to think about how much protein is needed by the horse and is it being met. For example, a 450 kg mature horse in work needs about 900 grams of protein per day including roughly 39 g lysine, the essential amino acid that has to come from the diet (data from 2007 Nutrient Requirements of Horses ). The actual amount provided should exceed these amounts by a generous buffer but certainly not be less. ​ Out of more than 15000 samples (Dairy One lab) the average crude protein level of Oaten hay is 83 grams/kg. How much protein the horse is getting from the Oaten hay depends entirely on how much is eaten. If the horse was to eat 11 kg of hay (and the actual amount is anything like the average) then the horse would be getting protein needs satisfied but not by much (913 grams). If the intake was a smaller amount, say 8 kg then definitely a protein deficiency and for both amounts, essential amino acids like lysine, threonine and methionine will be too low. Balanced Equine Equine Amino can help. www.hvhoofandequinehealthcareproducts.com/product-page/balanced-equine-nutrition-equine-amino ​ A horse in work would most likely be receiving other feeds, if yes then the protein intake can be calculated by adding them all up. Hopefully this helps explain why focusing on one feed ingredient in isolation to the rest of the diet is rather unhelpful. And it matters with how much is actually fed – why % protein is silly too, something the feed manufacturers like to use for protein content. For example, 12% protein means 120 grams per kg fed. Actual protein intake depends entirely on how much is fed. ​ There are some insulin resistant/elevated insulin horses that can’t tolerate Lucerne and these horses should never be fed Lucerne. In this case, Lucerne for these horses is a risk factor for laminitis. It’s not the sugar + starch level as Lucerne is generally low but the amino acid profile may be the culprit. ​ Too much calcium in the diet from an intake where the forage is Lucerne could lead to: ​ Precipitation of calcium in the urine which could cause sediment or even stone formation. This is primarily a problem for geldings that have a narrow urethra. Bone structure may be affected but we don't know the consequences in terms of bone strength.