Written By Barbara O’Brien
All photography© 2011-2012, Barbara O’Brien
Written By Barbara O’Brien
All photography© 2011-2012, Barbara O’Brien
Written By Dr. Kris Hiney
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.
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.
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.
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.
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.
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.
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.
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.
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 tendons. 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.
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 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?
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