A Tale of Two Mares

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Written By Barbara O’Brien

All photography© 2011-2012, Barbara O’Brien

My most recent horse rescues are two lovely Morgan mares that came from a Pennsylvania horse auction widely known to be attended by large-scale slaughter brokers. Fortunately, a sales broker who works with the group Forever Morgans, purchased them. Forever Morgans’ mission is to find good homes for horses that would have most likely ended up on a slaughter truck.
The first mare, Laurel, arrived in the summer of 2011. She was a 16 year old mare that had been an Amish carthorse. When she arrived, she still had on a full set of driving shoes, which we quickly pulled to let her just be a horse. Although, she had a lovely temperament, she didn’t really understand being a pet. She didn’t know what apples or carrots were and did not understand why we would just come into the pasture and brush her for no particular reason. It took awhile but she soon began to realize that she had a new life here, full of lazy days in the pasture with lots of treats and kind words.
In December of 2011 we rescued, again through Forever Morgans, a 17 year old mare we call Ivy. She had had some success in the show world and then had been sold to the Amish to be a carthorse and broodmare. She had been run trough the auction with her six month old filly who was sold separately and unfortunately did not make it. She was a flashy big bay with a graceful long neck and big expressive eyes. When I rode her, it felt like I was going like a freight train, but her trot was as smooth as silk. Remembering her early life as a show horse, she was appreciative of the treats and good food and lots of love so she settled quickly into her new life with us.
The winter of 2012 was mild here in Wisconsin and passed without a fight. Laurel did well all winter. With her heavy winter coat, and 24/7 access to hay she gained weight quickly and was looking good. But, no matter how much grain and hay I fed Ivy she did not seem to be gaining as quickly I would have liked.
Even though she was ribby, I noticed her belly getting wider and wider. It was then I suspected that she may be pregnant, but no… that couldn’t be. She was sold as open (not bred) so she couldn’t be pregnant… could she? So I increased her feed just in case and kept an eye on her to see how she progressed.
I guess I shouldn’t have been surprised when on April 1st, I noticed the first signs of eminent foaling. She was all bagged up, meaning her udder was developing in order to nurse a foal. I was happy and excited. We had not had a foal around for years. How fun to have a surprise one and most likely a purebred Morgan at that! I prepared a stall for her and began the waiting game.
After many restless nights spent checking on her every few hours, on April 10 she had a beautiful, healthy bay colt. As a firm believer in imprinting newborn foals (the practice of familiarizing a newborn foal with humans) I spent the next few hours carefully touching every part of his silky soft body and tiny little hooves.
Ivy proved to be an excellent mother and it was evident that she had done this many times before. She was calm and let me handle the foal with no sign of nervousness or stress. We decided to name the foal Quincy, as it seemed to suit the friendly colt’s exuberant personality.
Laurel, who was in the paddock with Ivy all along, proved to be an excellent auntie. She gave Ivy plenty of space with the foal but stayed near enough to make her and Quincy feel safe as part of a herd. When Quincy was a little older he naturally, as colts do, began to pester Laurel. She, being the good-natured mare that she was, would gently reprimand him and teach him important horse manners.
One morning when Quincy was about a month old, I was surprised to find Laurel missing. Ivy and Quincy greeted me like usual, but Laurel was nowhere to be found. There had been a thunderstorm the night before and I checked the fence to see if she was frightened by something and ran off but it was working just fine. It was then I found her behind the barn. She was covered in mud and in obvious pain. She grunted and rolled and I knew right away we were dealing with a bad case of colic. Horses cannot burp or release excess gas through their mouths and so whenever they get a stomachache or a blockage it needs to go through their whole system. I called the vet and then went back and got Laurel up and began to walk her. Walking helps get their systems moving again. There was nothing to do now but wait.
When our vet, Dr. Tom, arrived he treated her with medication to ease her pain and help her muscles relax. We also tubed her with mineral oil to ease her digestion. We were instructed to keep an eye on her and see if her symptoms and her pain subsided. Laurel’s condition turned out to be what was most likely torsion colic or a twisted gut, a much more serious case, where part of the gut gets twisted, like a kink in a garden hose. We planned on giving her the night to allow the mineral oil to work but when I went to check on her about 8:00 that evening she was thrashing in her stall. My heart sank as I realized Laurel was not going to recover, and it became clear to me what I had to do. I called Dr. Tom and asked him to come out and put her down, as she was suffering and I knew she wasn’t gong to recover. I went back out and led her out onto the grass to wait for Dr. Tom. It was then I let out a short sob, which startled Laurel and even in her pain she leaned her head into me as if to say are you ok? Her attention made me cry even harder. She was finding it hard to walk so I just stood with her, and a moment later she lay down in the cool spring grass. She was breathing heavily as I knelt down and stroked her head. “You can go now,” I said. “You can go.” With that, Laurel looked at me one last time, her eyes soft and warm. She heaved a last big sigh, and then she was gone. I wept while I petted her, not wanting to leave her, but I knew I must Tell Dr. Tom that he did not have to come after all. I finally went inside, thinking how courteous she was, saving Tom a trip in the dark night and me an additional vet bill.
The next morning, I let Ivy and Quincy out into the paddock. They quickly realized that Laurel was gone. Ivy called for her but after awhile, she went back to eating her hay.
I noticed Laurel’s grooming kit with the extra soft brush for her face and the empty hook where I hung her halter and I began to cry again for my poor mare. As all animal lovers can attest, it is never easy to lose the one you love.
While I openly wept for my beautiful mare, I tried to console myself that Laurel had a good life here. There was always food, there was always pasture, there was no work or a harsh smack from a whip, and there was plenty of attention from children, who were only too happy to brush her coat and comb her mane. I had to tell myself that at least we did what we could for her and both our lives were better for having found each other.
At that moment, I felt something come up behind me and nibble on my shirt. It was little Quincy, trying to get my attention. He jumped and snorted as I turned and then came up to me again, cheerfully demanding to be scratched and fussed over.
Hey, I’m still here. He seemed to be saying. You still have me to love. And that is just what I am going to do.

Equine Carbohydrate Disorders, Part 1: Definitions and Relationship to Equine Diseases

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Written By Dr. Kris Hiney
Equine disorders related to carbohydrate consumption have received much attention by owners and researchers alike, as of late. This has resulted in almost a mistrust or fear of feeding horses carbohydrates.  But in reality, almost all of the horse’s calories come from carbohydrates – there is no way to avoid them in the horse’s diet. What one must do is understand all of the forms in which CHO (carbohydrates) are found, identify horses at risk for CHO disorders and select the appropriate feeds to keep them healthy.
To begin, carbodydrates are simply molecules composed of carbon, hydrogen and water. Monosaccharides are single units of sugars which vary slightly in their structure.  Common monosccahrides in the horse’s diet consist of glucose, galactose, fructose, mannose, arbinose and xylose. While these monosaccharides are not normally found in their single form in plants, they are joined together to make  longer polysaccharides. However, monosaccharides are produced through  enzymatic digestion by the horse.  Disaccahrides, then, are just two sugar units linked together. Common disaccharides include lactose (found in mare’s milk and is formed by glucose and galactose linked together) and maltose (two glucose units linked together).
Figure 1. Glucose and galactose. The two structures only differ by the location of the hydroxyl group on the left side of the structure.
Oligosaccharides are longer chains of a variety of monosaccharides linked together, typically between three and ten sugar units.  The primary oligosaccharides in the horse’s diet are stachyose, raffinose and fructo-oligosaccharides (FOS).  FOS have received attention in animal nutrition as a way to supply pre-biotics to the animal. Pre-biotics are often oligosaccharides which are resistant to digestion in the foregut of the horse but are digested by bacteria in the hindgut. These supply a source of nutrition which supports the growth of beneficial bacteria and perhaps reduces the population of disease causing – or “pathogenic” – bacteria. In fact they are looked at as an alternative to feeding antibiotics in livestock. FOS are believed to alter the pH of the colon to a more favorable environment for the most productive bacteria. Mannose specific oligosaccharides are also thought to reduce the adherence of pathogenic bacteria to the epithelium of the gut wall. In yearling horses, feeding FOS reduced fecal pH and increased the production of volatile fatty acids from the hind gut. FOS supplementation also decreased the incidence of diarrhea when fed to foals. It has also been shown to have a protective effect on the development of foal diarrhea when fed to their dams. However, it is not known if that was an indirect effect passed through the milk, or if the foals simply ingested some of their dams’ feed containing the supplement. While feeding oligosaccharides does not appear to have an immune boosting effect that has been suggested in other species, it does appear to have beneficial effects on gut health in the equine. Horses receiving FOS and challenged with a large barley meal had less lactobacilli in their colon compared to controls. Thus FOS may help prevent GI disturbances due to diet changes or CHO overload.
Fructooligosaccharides also belong to the category of carbohydrates labeled as fructans.  Fructans are polysaccharides which have multiple fructose units. Inulin is also classified  as a  fructan. Many horse owners have heard of fructans as a risk factor for pasture associated laminitis. A sudden increase in fructans in the diet can alter the microbial population in the hindgut which may then subsequently lead to the development of laminitis. Fructan concentrations in grasses vary with both season and time of day.  Fructans and other starch concentrations are highest in the spring, lowest in the summer and intermediate in the fall. During the day, the process of photosynthesis results in the highest concentrations of fructans in the afternoon with sometimes half or less in the morning or evening hours.
Other CHO include longer chains of sugar units and are known as polysaccharides. Most commonly we think of starches and fibers as the common polysaccharides in the equine diet. Starch occurs in either linear form known as amylose or branched form, amylopectin.  It is composed of only glucose linked by bonds that can be enzymatically digested by the horse. In contrast, cellulose is also a straight chain of glucose but is linked by a different type of bond , a beta bond, which must be broken by microbes. Fermentation of this fiber fraction results in formation of volatile fatty acids which are metabolized by the horse to produce energy. Pectin and hemicelluloses are also common polysaccharides found in the equine diet.
Figure 2. Amylose is a chain of glucose units linked by alpha bond.
Figure 3. Cellulose is a similar chain of glucose units, but linked by beta bonds instead, making it indigestible by mammals.
Those CHO linked with alpha bonds can be digested in the foregut, allowing the monosaccharides to be absorbed intact. In contrast, cellulose, hemicelluloses, pectin, raffinose and stachyose, which contain beta bonds, will all need to undergo microbial fermentation to provide energy to the horse.   Hemicellulose, compared to cellulose, is a mixture of arabinose, xylose, glucose , mannose and galactose. Pectin is made up of beta linked galacturonic acid, arabinose and galactose. Pectin and hemi-cellolose are more rapidly fermented than cellulose and increase the digestibility of the feed if present in a greater proportion.
Now that we know what different types of carbohydrates exist in the horse’s diet, let’s look more closely at some differences that occur in forages. Typically, forages should always make up the bulk of the horse’s diet. They are made up of structural CHO which make up the cell wall as well as some indigestible lignin.  The plant cell wall is made of cellulose, hemicelluloses and pectin. Forages also have non-structural CHO or NSC in the cell content, though certainly not as much as concentrates. The NSC is a mixture of monosaccharides (glucose, fructose, etc.) and disaccharides as well as starch and fructans.
If we compare common forages, cool season grasses are made up of primarily cellulose, then hemi-celluose and the fairly small amounts of pectin. Cool season grasses include Kentucky Bluegrass, orchard grass, fescues and ryegrass.  Legumes, which are typically high in digestible energy are relatively higher in pectin. Legumes would include alfalfa, clover, lespedeza and peanuts. Warm season grasses grow and mature more rapidly and have much more cell wall/kg DM and thus much more fiber. Warm season grasses include Bermuda grass, switchgrasses, and bluestem. Therefore warm season grasses at a later stage of maturity may be ideal for horses with carbohydrate sensitivities. In general, there is a higher proportion of cell content in a younger, or more immature plant. This makes grasses or hays harvested at an earlier stage more digestible.
Interestingly, the storage form of CHO in legumes and warm season grasses is primarily starch, while cool season grasses prefer to store energy in the form of fructans with much less starch. There is also a limit to how much starch the chloroplasts of warm season grasses and legumes can contain, yet there is no limit to fructan accumulation. Fructan also accumulates more to the base of the plant and more so in the stem than in the leaf. Cool temperatures and droughts (which typically don’t go together) may also increase the fructan production by the plant. Anything that promotes photosynthesis but retards growth ends up increasing NSC (lots of light with cool temperatures).   Therefore, be especially careful to observe growing conditions, especially if the horses are consuming cool season grasses and have carbohydrate sensitivities.

Minimizing the Stress of Weaning

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Written By Dr. Kris Hiney

The fall season is here and with it often comes the time for weaning our foals. Many successful weaning strategies exist but it is important for the manager to choose the optimal one for their facilities and management style. These decisions are important and can affect the growth, well being and even the future behavior of your foal.
When is it appropriate to wean?
Foals can be weaned at any age provided their proper nutrition and socialization skills are ensured. Foals whose dam’s may die at birth are obviously “weaned” from their dam at an extremely young age. While it is preferable to find a willing nurse mare, and it is even possible to induce lactation in a non-pregnant mare, many owners choose to put the foal on a liquid diet of formula designed to match the mare’s own milk.  Specialized milk replacer, goat’s milk and supplemented cow’s milk can all be used successfully.  Prior to doing so, it is important to ensure that the foal has received adequate amounts of high quality colostrum, as the proteins found in the milk replacer may block the later absorption of immunoglobins from colostrum. Colostrum content quickly decreases in post-partum mares and should have been harvested within the first three hours post parturition of the donor mare.
Orphaned foals must be fed frequently , initially from a bottle, but can then be taught to drink from a pail, similar to calves. Initially the foal should be fed at 5-10% of its body weight in the first day, and then increase to 20-25% of its body weight by day 10. Solid feeds can be introduced early, as the foal would typically begin to ingest feed in imitation of its dam after only one week of being born. Milk replacer pellets are available, and can help supplement the foals’ initial liquid diet.   Foals can be weaned from this liquid diet by 10-12 weeks of age. Most importantly, some sort of companion should be found for the foal. Often orphan foals develop undesirable behaviors as they have no guidance from a mature horse as to what constitutes appropriate social behavior. Typically, orphaned foals view humans as their peers, which may result in some rather inappropriate rough play!
With the exception of extremely early loss of the dam for a variety of reasons (death, injury, sales, etc.) most managers choose to wean foals between three and six months of age. In the feral state, foals typically are self weaned by 35 weeks of age or between eight and nine months. At five months all foals spend 50-70% of their day consuming solid feed, compared to about 2% of the day suckling. Mare’s milk production also begins to drop off by three months of age, at which time foals are consuming a high percentage of natural feeds through grazing, hay or concentrates.  It is advantageous to introduce the foal to the feeds it will be consuming post-weaning to ensure an easier and more stress-free transition. This will also help prevent fluctuations in growth rates that may place the foal at risk for developing developmental disorders.
After insuring that the proper diet is being fed (see previously related articles concerning protein, energy and minerals for growth), the management system used is important to consider. Foals weaned in isolation (such as confined in a box stall) show more incidences of stereotypies (such as weaving, cribbing and wood chewing) and are more vigilant (less time standing relaxed) than foals weaned in pairs. Foals weaned in stalls also show more abnormal behaviors such as stall licking, kicking, rearing and pawing than weanlings weaned in a paddock. Even horses stabled for the first time as two year olds exhibited much less aberrant behavior and were more relaxed when stalled in pairs versus singularly.
Therefore the ideal management system would wean the foals with a counter-part, rather than in isolation. For example, at our facility we wean the foals by removing the dams, with foals remaining in the same pasture and with the same herd mates with which they have been raised. This results in very little stress (at least as exhibited by vocalizations and seeking of their dam) which is frequently resolved within two days post weaning.   Even in this system we wean in pairs, whether or not this actually relieves stress for the weanling. If raising only one foal, it is advisable to seek out an older quiet pasture mate, or even to find another youngster to raise with it. Many horse owners find themselves in a similar situation and may be willing to board another weanling or send theirs as a companion.
Alternative strategies include gradual weaning, in which the mare and foal are separated, but are allowed all behaviors except nursing. Typically this is done over a fence that the foal simply cannot nurse through. After one week, the mare is removed completely. Foals weaned in this manner, exhibit less stress and have lower levels of cortisol (a stress hormone) than foals which are weaned abruptly. However, these foals are no different than abruptly-weaned foals after two weeks. The advantages to this system may simply be a lessened possibility for injury or disease.
Weaning stress may also make the foal more susceptible to diseases. Because of this, be sure that the foal is in good health prior to weaning (we typically have vaccinated the foal and ensured a high immune status prior to weaning) and there are no undo stressors. For instance, plan the time of weaning for when the climate is not too adverse (either too hot or too cold/wet).   Because the mare and foal may show high stress and try to re-unite, check that the facilities used for weaning are extremely safe. Expect that maiden or younger mares may exhibit a longer period of time in which they still call for or seek out their foals. Halter breaking is not advisable right at the time of weaning either, as the foal is already stressed and more reactive. Ideally foals are handled from birth, which can lessen the stress of procedures often introduced at this time (vaccinations, deworming, farrier care, etc).
Care of the mare is simple, with usually a decrease in ration quality or quantity from that received as a lactating mare. Although her udder will fill initially, it is important to not milk the mare, as this will only further stimulate lactation. The udder should become soft within a week of weaning.   She can then be returned to her pre-foal life, whether that is as a riding horse, a gestating mare, or simply a mare of leisure.

By thinking through the weaning system and the safety and nutritional needs of both mare and foal, the stress of “growing up” for the foal can be greatly minimized.

Developmental Orthopedic Diseases: Part 2, Can They be Prevented?

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Written By Dr. Kris Hiney

Now that we are aware of the potential problems of the skeletal system of the foal, we will address some management techniques that may aid in preventing their occurrence. These include dietary management of the mare and foal, exercise needs, controlling growth rate and even selection of appropriate breeding stock.

Size and growth rate

One of the commonalties amongst all developmental orthopedic diseases (DOD) includes the size and growth rate of the foal. Obviously the larger the foal, the more stress which will be placed on the limbs simply due to weight. Bigger and more rapidly growing foals have been repeatedly shown to be at more risk for DODs. Body size is inherently a genetic issue, while growth rate can be modulated by the owner. If you are breeding for larger foals, more caution should be taken with their diet to ensure a more moderate rate of growth. This includes avoiding sudden changes in rate of growth. One way to limit changes in growth rate is to avoid ad libitum feeding or to avoid stress placed on the foal. Stresses may include environmental (weather dependent) or social stress, such as weaning. One method to manage stress of weaning in foals is to creep feed foals prior to weaning to accustom them to consuming concentrates. Also, the manner in which the foal is weaned can reduce their stress. Babies weaned in isolation exhibit more stress behaviors than foals weaned with a pasture-mate. Try to keep their environment as close as possible to what they experienced prior to weaning.

Exercise

The amount of exercise the foal receives can also influence the development of DOD. Excessive trauma to the joint through overwork can influence development of osteochondrosis (OC) as well as restriction of exercise. So what exercise program is correct for a foal? Foals in adequate pasture size typically spend their time sleeping, nursing, following their dam, and playing in short bursts of activity with other foals. Foals without peers may spend less time playing. Similarly if they are confined to too small of a space they exhibit less play behavior. In addition, if their environment is too small with no novel objects or activities, foals tend to be less active. At the furthest extreme would be foals and young horses confined to stalls without access to voluntary exercise. The best advice for proper bone development in the young foal is to provide adequate pasture space to allow them to run and play on their own. How do you know your pasture is big enough? Simple observation will tell you if your foals are playing. If the foals just stand around, or if you have a single foal with no playmates, they may not have the stimulus to run and play.

Diet

Many nutritional causes of DOD have been proposed with very few providing direct causative relationships in a research setting. However, that may be due to a lack of combining the correct causative factors in this multifactorial disease. Perhaps the foals used in the studies need to have a genetic predisposition for DOD, and then must be exposed to the right management conditions to initiate the disease process. However, the most commonly proposed theories include excess energy, mineral imbalances, and inadequate protein. One of the proposed theories in the development of DOD is feeding of excessive non-structural carbohydrates to growing horses. These feedstuffs (think traditional cereal grains like corn) cause a more rapid increase in blood glucose post feeding versus feeds containing more fiber. Higher levels of blood glucose increase insulin levels in the young horse, which may have a cascade of metabolic consequences down to the level of cartilage maturation. While it has been shown repeatedly that feeding high concentrate diets alters the glucose/insulin response and reduces insulin sensitivity, the direct causative relationship to DODs has not been established. The most important guideline appears to be to avoid unregulated feeding of concentrates. High protein diets have also fallen under the radar of causing DOD, but this has not been able to be shown in a research setting.

Mineral nutrition has probably seen the greatest attention related to DODs. To begin with the simplest, imbalances of deficiencies of calcium (Ca) and phosphorus (P) can clearly lead to abnormalities of bone development. (Please see the articles about calcium and phosphorous in my series, Minerals for Horses, for more details.) However, just because foals are fed adequate amounts of Ca and P in the correct ratios does not guarantee they will be free from abnormalities.

Another mineral which has received much attention is copper. One of the original studies which pointed to deficiencies of Cu causing OC in foals unfortunately also allowed deficient levels of Ca and P to be fed to the foals, thus making it difficult to point to only one cause. Later studies found highly contradictive results and have not offered any protective benefits to feeding supplemental copper. Taken all together, the most promising results of supplementing copper have been seen when providing copper to the dam in late gestation, or in supplementing copper to promote the repair of OC lesions.

Trauma

Included in the list of “just bad luck”, trauma may also result in a DOD. Young horses have a great propensity to get themselves into trouble. They can get kicked by a pasture mate, run into a stationary object (believe me I’ve seen it), or even tumble head over heels for no great reason other than they are still learning their balance. While not much prevention can occur here, at least try to ensure that no overly aggressive horses are housed with young stock, and that dangerous obstacles are not in the pasture. For example, I’ve seen weanlings during a running fit run headlong into an automatic waterer, somersault over the top, and, luckily, continue on their way. If you raise foals, always expect some sort of trauma to arise. Just try to ensure their environment is as safe as possible.

Genetics

Unfortunately, the genetics of your foal may be the single largest contributing factor to DOD. Many recent studies have found numerous markers across a number of chromosomes that have been linked to OC. While this sheds some interesting new light on the problem, it is also difficult to select against. Compared to a single point mutation like HYPP, horses cannot be identified as simple carriers of the gene for the disease. Screening for potential carriers of OC would be costly and ineffective. However, that does not mean the breeder has little recourse. If your mare has consistently produced foals with OC, one of two things may be true: one, your management program may be inadequate or, two, she may have a genetic likelihood to produce these types of foals. You can often hear rumblings in the horse community about certain stallions which also tend to throw a lot of foals with OC. Perhaps these are individuals we should select against. However, the amount of research currently being conducted on the genetic link to OC does provide some promise that we may be able to limit this disorder in the future.

Taken all together, the best plan for avoiding DOD may be, first, to select genetically healthy individuals to breed, and, second, foals should be managed with attention to diet and exercise until they are two years of age. Many causes of DOD may be unavoidable, but hopefully with proper care and management, one can produce a healthy normal adult.

Next month we begin talking about the usage of fat in the equine diet, and how it may be able to improve the health or performance of your horse.

 

Developmental Orthopedic Diseases: Part 1, What are they and why do they occur?

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Written By Dr. Kris Hiney

Developmental orthopedic diseases are a serious concern for the equine breeder.  All of the hard work and preparation of selecting the right match between mare and stallion, the hours put into proper mare care, culminates hopefully in the arrival of a sound, healthy foal.  All of this excitement and hope can be ruined if your foal ends up having skeletal abnormalities which may jeopardize his future success.  With this article we will explore some of the many causative factors of this spectrum of disorders and what you may be able to do to prevent or reduce the likelihood of their occurrence.

First of all, developmental orthopedic diseases, or DOD, is actually a generic term for a host of disorders.  Simply put, anything which is an abnormality of the horses’ skeletal system during its formative years can be classified as a DOD. The most commonly occurring maladies are angular limb deformities, flexural limb deformities, osteochondrosis and physitis.

Angular limb deformities

Angular limb deformities are very common in all breeds of foals. These can include either an inward deviation of the joints (varus) or outward deviation of the joints (valgus).  Most commonly these deviations are seen in the knee, hock and fetlock joints. The foal can have one or more joints affected, and can also vary quite widely in the severity of the condition.  The causes of this condition vary; with some the manager can address, while others are due to random chance.   Both premature and dismature foals very commonly have angular limb deformities due to the lack of strength in supporting structures, or the failure of complete ossification of the cuboidal bones (small bones of the knee and hock).  The causative factors of these conditions may be an infection or inflammation of the placenta or uterus, twinning, and severe stress in the mare.  Development of angular limb deformities post foaling is due to a difference in the growth rate across the inside and outside of the growth plate.  In essence, the difference in speed in bone development causes the bone to veer to one side or the other.  This can be due to a variety of factors including dietary imbalances or environmental factors, as well as genetics.

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Premature foals are those born before 320 days of age, while dismature foals may be of a normal gestational age but are weak, small and appear unready to have been born.  These foals are typically thin, are slow to stand, have poor suckle reflex, can chill rapidly and are marked by fine silky hair coats and soft ears and lips.  These foals will require a high level of assistance in their care, but with proper supportive care and a lot of time and effort, can continue on to lead normal lives.

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If your foal does have angular limb deformities, there are actually many therapeutic management techniques used to help straighten the limb.  They range from quite simple to the complex and expensive, usually depending on the severity of the deviation.  Conservative techniques involve stall rest in order to prevent uneven loading of the foal’s developing legs.  The foal may be bandaged or splinted, or the hoof can be trimmed or glue-on extensions can be used to help straighten the limb.  For example if the foal has a valgus deformity in in its knee (the lower leg will sweep outwards), the outside hoof wall is lowered, or a glue on extension is placed on the inside of the hoof.  Often dramatic improvements are seen with these simple techniques.  If the limb deviation is more severe, and budgets allow, corrective surgery may be required.  These include periosteal stripping, or placing screws, staples or wires across the growth plate.  The goal of periosteal stripping (removing a section of the periosteum, or membrane covering the bone) is to accelerate growth of the side of the bone growing too slowly. Typically this procedure is done in young foals.  Alternatively, transphyseal bridging is used to slow down the rate of growth on the side of the bone with too fast a growth rate.  However, before deciding on which management technique is the correct one for your foal, be sure to consult with your veterinarian.  Mismanagement can acerbate the problem, and it is also possible to overcorrect the foal, and end up with a deviation in the opposite direction!

Flexural limb deformities

Flexural limb deformities are more commonly referred to as contracted Glue on shoe extension can correct contracted tendonstendons.  Foals can either be born with flexural limb deformities, or they may develop later in life.  Foals born with flexural limb deformities may be due to poor positioning in the uterus, toxicities, genetics or infections in utero.  If the condition is mild, foals can recover typically with just restricted exercise.  Foals should be allowed some exercise either in a paddock or by hand walking for short periods of time.  Additionally, the veterinarian may choose to use oxytetracycline to help relax tendons in more severely affected foals.  Some foals may require splints or casts to help in straightening the limb.  However, this should only be done with a veterinarian’s  supervision as  it is quite easy for the foal to develop pressure sores and may be painful.  Acquired flexural limb deformities can be due to traumatic injuries which cause the foal to protect the limb and not bear full weight on it.  The reduced stretching of the tendons with normal loading results in tendon contracture.  They can also be due to a discrepancy in the growth rate between the flexural tendons and the long bones.  It can also be completely normal to see young horses having temporary periods of being over at the knees.  If the foal is showing signs of being over at the knees, the rate of growth should be modulated and caloric intake should be reduced.

Physistis

Physitis or inflammation of the growth plate is usually seen at the distal end of the radius or tibia, or within the distal end of the cannon bone.  It is seen as puffiness in the affected joint and may be associated with heat and swelling.  Physitis is typically seen in foals on too high of a plane of nutrition, or in foals being fed for rapid growth.  If the foal is still nursing, the mare may actually be contributing to the development of physitis.  Some mares are simply better milkers than others.  Suggested management techniques may be to discontinue any creep feeding of the foal, or do not allow them access to the mare’s feed.  In addition, the foal may be muzzled periodically to decrease his milk intake, or the foal may be weaned and put on a less calorie-rich diet.

Osteochondrosis

Osteochondrosis or OC is caused by a failure of the endochondral bone (the bone underlying the cartilage) to properly ossify.  Bone growth occurs first with the growth of cartilage which is then replaced by bone. If this fails to happen, essentially the bone has a weakened area underlying the cartilage.   It can cause further development of bone cysts or osteochondrosis dissecans (OCD). While these terms are often used interchangeably, OCD refers to a flap of cartilage displacing away from the joint surface.  Causes of OC in young horses are quite diverse and include dietary mismanagement, traumatic injuries, inadequate or excessive exercise, genetics, toxicities, body size, and growth rate.

Osteochondrosis: Is it the end of the world?

One of the interesting things about this disorder is how frequently it may actually appear in the equine population.  Many figures are given, with some stating that 20-25% of European foals will develop an OC (Barnevald and van Weeren), while others have found an incidence of 32% in Hanoverian Warmbloods.  However, in the latter study, there was no correlation between radiographic findings of OC and lameness. Indeed, in a recent study of Dutch Warmblood horses presented for a pre-purchase exam, 44.3% of clinically sound horses were found to have OC lesions  (Voss).  Therefore, even if your foal has radiographic evidence of lesions, unless accompanied by joint effusion or lameness or presenting as fragmentation within the joint, it may never represent a soundness issue.

Next month we will look at what we can do to try and prevent our foals from acquiring any of these development orthopedic diseases.

Voss, N.J. 2008. Incidence of osteochondrosis (dissecans) in Dutch Warmblood horses presented for pre-purchase exams.  Irish Veterinary Journal. 61:1)

 

 

What is the difference between premature and dismature?