By Dr Peter Huntington, Kentucky Equine Research, Inc.
What is OCD, Wobbler Syndrome – and how does the weight of your broodmare affect your chances of getting her into foal or having a foal with crooked legs?
Australian veterinary expert, Peter Huntington examines the ways in which your feed program can influence the soundness of your foals…
f you really can’t figure out the problem it must be the feed! Many of us in the nutrition and feed manufacturing business have felt the frustration of having our formulas and our feed blamed for a myriad of problems on the horse stud and in the stable.
Many people engaged in the production of horses, attribute miraculous healing and preventative qualities to feed and or feeding management. This is all too easy to understand as the easiest change to make in response to a problem is to change the feed.
The old saying goes, ‘if it ain’t broke don’t fix it’. It seems that the second part of the saying is: ‘If it is broke, fix it’. Even if you don’t know what’s ‘broke’ by changing the feed!
Certainly much of the overall success of a stud, training centre or racing stable can be attributed to accurate feeding programs and good feed management systems. This alone is why we as feed manufacturers and horse nutritionists have jobs.
However to attribute all or a majority of the problems on a stud to nutrition is foolish. It is the purpose of this article to try to identify areas of production that are nutrition responsive and to try to explain the manner in which nutrition may be related to various problems that exist on the stud or in the stable.
Obviously time and space do not permit a thorough discussion of all of the various problems that may have a nutritional variable but I will try to discuss some of the more important ones. The problems and conditions below are still only a partial list of the problems that may have a nutritional origin or the manner in which nutrition is thought to influence productivity on the horse operation.
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Very Poor
· Very suncken rump
· Deep cavity under tail
· Skin tight over the bones
· Very prominent backbone and pelvis
· Marked ewe neck - Poor
· Sunken rump · Cavity under tail
· Ribs easily visible·
Prominent backbone & croup· Ewe neck – narrow and slack
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Moderate
· Flat rump either side of backbone
· Ribs just visible
· Narrow but firm neck
· Backbone well covered
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Good
· Rounded rump
· Ribs just covered but easily felt
· No crest, firm neck
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Fat
· Rump well rounded
· Gutter along back
· Ribs and pelvis hard to feel
· Slight crest
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Very Fat
· Very bulging rump
· Deep gutter along back
· Ribs buried
· Marked crest
· Folds & lumps of fat
Nutrition and the Broodmare
It is a common occurrence for people to erroneously attribute many fertility problems in the brood mare to vitamin deficiencies and to neglect to consider the single most important nutritional variable in reproductive efficiency -Energy Balance. More progress can be made in terms of increasing conception rates by ensuring appropriate body condition than by using any other nutritional tool. This is not to say that meeting vitamin, mineral and protein requirements is not important but from a practical standpoint energy balance tends to be more a concern. There is really no reason to assume that any specie of animal is designed to conceive, carry a pregnancy to term and re-breed while in a negative energy balance. It is surprising that energy intake should be a major problem as it is really one of the easiest nutrients to assess. Broodmares should be kept in reasonable condition throughout the year. I ask clients to try to practice what I would refer to as straight line broodmare nutrition. By this I mean that an optimum condition should be established for each mare and appropriate adjustments made in the feeding program to maintain this condition. This means that coming in to the last trimester of pregnancy the mare should begin receiving more feed in preparation for lactation and that during lactation, feed intake should be increased to support the production of milk without excessive loss of body condition.
During the final half of lactation, the energy intake of the mare should be adjusted depending on condition at that point in time and on forage availability, again in hopes of maintaining optimum condition. Once a foal is weaned and the mare ‘dries up’, an assessment of condition should be made and this period should be used to adjust the mare’s condition back to optimal. This means that for the heavy milking mare that has gone through a tough lactation, we may want to continue to feed her at pre-weaning levels of feed intake and allow her to gain condition, and for the mare that is fat we may want to not feed at all and allow her to meet needs on good quality pasture alone.
Work at Texas A&M University shows that mares that are a little too fat are far more reproductively efficient than are mares that are too thin.
For barren and maiden mares, the plane of nutrition should be increased as the mares come into the breeding season. It makes good sense to increase nutrient intake when mares are put under lights so that an increase in condition is achieved at the same time as an increase in day length.
The use of artificial lighting is a common practice in the thoroughbred breeding world to advance the time of cycling and ovulation in early spring. Mares are placed under 16 hours of light at the start of July and this can advance the onset of ‘normal’ cycling and ovulation by 6 weeks. These mares can then be bred in early September for an early August foal.This practice is referred to as nutritional flushing and from experience is effective in shortening the transitional period and increasing conception rates. This practice, done on mares to be bred in September and October would mimic what would occur in nature, when the spring flush of grass would result in mares increasing in body fat stores.
If we are limited to one practice to increase conception rates in mares it would be ‘suturing’ or ‘caslicking’ the mare.
However, poor conformation of the external genitalia of the mare is often as much a function of body condition as anything else. Thin mares are especially more prone to sunken vulvas that are apt to result in fecal contamination or wind sucking (pneumovagina).
Especially in older mares, adding body weight may improve conformation and hence reproductive performance.
One unfortunate consequence of having your mare too fat is an increased risk of having a foal with bent legs (Angular Limb Deformities). Another problem is that the mare may go away to stud and lose weight which will make her less reproductively efficient. Remember brood mares don’t have to look like show horses.
Another nutrient that I am always looking at in terms of reproduction is selenium. Maylin, at Cornell reported that mares receiving inadequate selenium were much more prone to reproductive problems than were mares receiving adequate selenium. I try to ensure that selenium intake in the
mare is from 2 -3 mg/day. Many pastures, hays, grains, prepared feeds do not contain enough selenium and you must add a supplement such as EQUIVIT NUTREQUIN (since my company, Kentucky Equine Research manufactures the Equivit range, I am obviously comfortable about recommending their products, but there are of course, others in the market place with similar qualities).
One vital area of mare nutrition is late pregnancy. Deficiencies of calcium, phosphorus, copper and zinc at this time can cause DOD (see below) in the foal or weanling.
It is vital that your late pregnant mare has a balanced diet, but the consequences of an unbalanced diet may not be evident until the foal is a weanling or yearling.
Developmental Orthopedic Disease
Developmental orthopedic disease (DOD), also referred to in some circles as metabolic bone disease, consists not of a singular but of several related disorders affecting the young horse during the critical developmental stage. Included in the disease are: Epiphysitis (Physitis), OCD (OC), OCD Dissecans (OCD), Wobbler Syndrome and acquired flexural deformity.
At the outset it must be understood that all of these conditions are multifactorial in cause and are for the most part, a related set of diseases. Furthermore, it is important that one realize that there is a strong genetic component which must not be disregarded. Whether the genetic component is a specific gene, or several genes that do not behave in a normal fashion, or simply as a result of selection pressure for one trait that resulted in the increase in the incidence of the problem, is not well understood. The genetic relationship has been shown in several breeds of horse in Europe and the USA including Standardbreds, Thoroughbreds and Warmbloods.
Certainly it is known that faster growing, earlier maturing, larger horses exhibit a greater tendency toward the disease than do their slower growing, smaller counterparts. The selection for early and rapid growth along with speed has seemed to bring with it an increased tendency to develop DOD and a greater need for understanding the problem.
In other species, the problem has been diminished by eliminating offending individuals from the gene pool and from the standpoint of the purist this is not a bad idea. However, this approach is not feasible in most horse breeds. Those breeds that have put selection pressure on elimination of the problem have had some success yet this is the exception rather than the rule.
The solution to the problem rests in an understanding of the possible causes, a realization of the genetic component and the establishment of management and feeding techniques that minimize the expression of these potentially catastrophic disease states.
Physitis
Actually the term epiphysitis is in itself a misnomer. The condition should more appropriately be referred to as physitis or metaphysitis. Defined simply, physitis is an inflammation of the physis(epiphyseal plate) which exist as centers of ossification or growth in the bones of all of the mammalian species. Epiphyseal plates are found both at the proximal and distal ends of all of the long bones and are the means by which longitudinal growth occurs. The epiphyseal cartilage is dynamic and new cartilage is being formed as old cartilage cells are converted to bone.
Physitis occurs when the cartilage growth plates become inflamed or when normal maturation of cartilage to form bone is disrupted. Although any growth plate can be affected, the most common sites are above the fetlock in weanlings and above the knee in yearlings.
The ‘lesion’ appears as a bony enlargement at the level of the metaphysis and is more frequently seen on the inside rather than outside of the joint.
Physitis may be accompanied by palpable amounts of heat in the affected areas and in some cases by lameness, though many young horses show varying degrees of clinical physitis without exhibiting lameness. Causes of physitis include but are not limited to:
* Angular Limb Deformity
* Very Rapid Growth
* Nutritional Deficiencies in diet of late pregnant mare or young horse
* Injury
* Nutrient excess
* Nutrient Imbalance
* Concussional damage
* Genetic predisposition
* Conformational abnormalities
* overweight young horses
One must be sure to understand those changes in joint architecture that are normal and distinguish between normal changes and physitis that is potentially threatening to development. It is entirely possible that subtle changes in the shape of joints is in the realm of what is normal in the developmental process and should not be misconstrued to be a real threat.
It is also possible that some mild physitis is a normal process or at least that what some people might be calling physitis is not outside the normal range of what is acceptable. Treatment of physitis is varied depending on the severity and the cause, (if one can be determined). In most instances it is advisable to reduce caloric intake such that the rate of growth of the affected horse is slowed. One of the most critical errors that is commonly made is to slow growth excessively and not only reduce the intake of energy but also of other nutrients critical to bone growth. You should try to continue to meet the horse’s requirement for protein, minerals and vitamins rather than to simply quit feeding the affected horse.
One of the ways in which this can be nicely done is by utilizing a protein, vitamin, mineral supplement fed at approximately 1 kg per day. eg EQUIVIT ALL PHASE PELLET (once again there are obviously other products on the market that will do the job, the critical fact is that a suitable supplement should supply 25-30% protein, 30 g calcium, 15-20 g phosphorus, 150 mg copper, 400 mg zinc, 300 mg manganese and other trace minerals and vitamins.
In addition to this ‘supplement’, good quality hay and chaff should be offered freely. Once feed intake has been reduced, a professional assessment of the diet should be obtained. Nutrients of critical concern in doing a ration evaluation for young horses include: protein, calcium, phosphorus, copper and zinc.
If an evaluation reveals a deficiency in a particular mineral you can adjust the feed inatke, use a new feed, add a different supplement or use the correct amount of a supplement for your situation. Calcium can be added from limestone
and dicalcium phosphate can supply calcium and phosphorus, but trace minerals need to be supplied in a fortified feed or supplement. The current practice of adding copper sulphate is dangerous and likely to be ineffective as a means of getting copper into the horse. Copper sulphate can be irritant to the horse’s mouth and the daily copper requirement will be fulfilled by less than a gram of copper sulphate. It is difficult to accurately feed that small a quantity, let alone know if the horse eats it. Often copper deficiencies are matched by zinc, manganese, iodine and selenium as well. Use copper sulphate in the water to control algae, but stick to the proven methods to supplement a deficient diet.
If, after evaluation of the ration, one can find no nutritional reason for the problem, then other causes of the problem should be considered such as angular limb deformities, conformation and so on.
Even if the ration appears to be balanced in all respects it is probably best to proceed conservatively in terms of feeding rates until the problem is resolved. Many times it seems that mild physitis goes away in 60 days if it is treated and two months if it is not.
In the final analysis it is not particularly alarming to see some inflammation of the physes just prior to closure. The major concern about physitis is that it may be the visual indicator that a more serious metabolic problem such as OCD exists.
It may be that the cause of the problem is a mineral deficiency in the diet of the late pregnant mare. Recent research in New Zealand using mares that were entirely fed on pasture has shown that failure to supplement copper and zinc in late pregnancy led to an increased incidence of physitis and other DOD in weanlings. As far as the foal is concerned, nutrition in late pregnancy is vital.
Osteochondrosis (OCD)
One of the more serious aspects of the DOD complex is OCD. Unlike physitis, OCD may result in a debilitating lameness in many instances reducing or eliminating any chance of an athletic career. Many horses have had their working life shortened with arthritis or chips that is related to OCD damage in joints as a young horse. OCD is a disorder involving the maturation of cartilage in the growth of the bone. There is a failure of the calcification of cartilage that occurs during normal growth of long bones. This leaves a plug of retained cartilage in normal subchondral bone and results in the separation of cartilage from the underlying bone resulting in the formation of subchondral cysts, chips and cartilaginous flaps.
Some OCD may not be clinically obvious until later in life when wear and tear results in signs of arthritis. In other cases a weanling or yearling will have a swollen joint and they may be lame.
The diagnosis is made by taking X-rays and it is most frequently seen in the fetlock, hock and stifle joints. Surgery can be used with varying degrees of success, but some horses respond to confinement and medical treatments.
A number of causes of OCD have been proposed, yet the specific cause is far from understood. It is difficult to determine if indeed the incidence of the problem has increased or if the condition is being diagnosed more frequently due to superior radiographic techniques and equipment.
With respect to the trace mineral theory, careful balancing of rations containing liberal concentrations of copper and zinc have resulted in only a slight reduction in the occurrence of OCD, emphasizing the multifactorial cause of the problem. However remember to supplement the pregnant mare as well as the foal.
Other factors currently under consideration include low calcium and high phosphorus intake, high calcium intake in mares and abnormal hormonal responses to normal or excessive carbohydrate intake. Some young horses may be insensitive to insulin and have an excessive insulin response to grain. This is thought to have an indirect negative impact on cartilage maturation into bone. Contrary to popular belief, high protein does not cause OCD or other DOD conditions.
Exercise is an important preventative factor and Dutch research has shown that forced exercise reduced the incidence of OCD dramatically when horses were fed a risky diet. You should avoid confining foals, weanlings and yearlings as confinement weakens bones and damage may occur when they go back in the paddock.
If they need to be confined for more than a few days provide a graded return to unrestricted exercise, or exercise the horse by walking or lunging. We do not need to box young horses to avoid poor weather and they should be in the paddock as much as possible. Make sure paddocks are large enough to allow babies enough room to run around, however don’t allow youngsters to exercise to the point of exhaustion.
Rapid growth creates an increased risk of OCD and this has recently been documented in research by KER. In this study weanlings with hock and stifle OCD were larger than unaffected foals of the same age, whilst some cases of OCD in fetlocks were small foals that grew rapidly to catch up. It is best to try and avoid growth spurts and rapidly growing or fat foals should be weaned early.
It is likely that genetic, nutritional, environmental and endocrine components contribute to the etiology and to obtain a decrease in incidence all must be considered.
Until the cause of OCD is better elucidated it is appropriate to take a conservative approach to the nutritional management of affected populations of horses. Rations should be designed that meet, but do not significantly exceed the horse’s requirements for all nutrients, with specific emphasis on copper, zinc, manganese, calcium and phosphorus.
Once formulated the ration should be fed in a manner that results in moderate rather than maximum growth rates and maximizes the forage rather than the grain part of the diet. Young horses should not be allowed to get fat and ideally you should be able to see some ribs and certainly feel them easily.
I recommend you feed no more than 1% of body weight as grain or concentrates to young horses which equates to approximately 1/2 kg per month of age until 6 months of age then level off the grain increase.
Many Warmbloods do not need this much grain and a reduction in intake of a prepared feed may create a diet that meets energy and protein needs for growth but is deficient in minerals. In this instance you need to add extra minerals from a supplement or balancer pellet.
Many feed companies and veterinarians offer diet formulation advice to breeders and a number use the Kentucky Equine Research ration evaluation program Microsteed. This program allows you to customise a diet to your farm and situation and allow adjustments to be made for changes in growth or season. A horseman’s version of this program is available for individual breeders to use from Kentucky Equine Research, 112B Martin St, Brighton, 3186 at a cost of $25.
Wobbler Syndrome
One of the earliest accounts of the wobbler syndrome was written in 1939 by members of the Department of Veterinary Science at the University of Kentucky. They described 47 cases which had occurred in central Kentucky between 1937 and 1939. Cases occurred particularly among Thoroughbreds and Saddlebreds, breeds which have long necks. Foals around weaning developed a lack of coordination in the hindlimbs, which progressed to include the forelimbs, eventually causing the animal to stumble and fall. Well grown weanling and yearling colts seemed particularly prone, with three colts affected to every one filly. As a result of necropsy studies, it was suggested the condition was related to abnormalities of the vertebrae of the neck, which caused damage to the spinal cord.
These observations were confirmed some 20 years later by Dr. James Rooney, also from the University of Kentucky, who identified more precisely the sites and nature of the lesions in the cervical vertebrae. Rooney suggested the overgrowth of the articular processes on which vertebrae move upon each other causes distortion and narrowing of the spinal canal and results in pressure and damage to the cord.
The most frequent sites of lesions are between cervical vertebrae C3 and C7, although the presence of lesions does not always result in clinical signs of wobbler disease. When the neck is flexed, the lesions may cause pressure to be exerted on the spinal cord.
Clinical signs associated with wobblers may be related to other causes including trauma, parasitic infection of the spinal cord, and infection with equine herpes virus.
In terms of prognosis it is therefore important to differentiate and establish an accurate diagnosis. Currently a true wobbler – the condition of which has recently been given the name cervical vertebral malformation (CVM) – is confirmed by taking X-rays of the neck region.
To do this, the horse must receive a general anaesthetic so that a technique known as myelography can be performed. This involves the injection into the spinal canal of a contrast fluid so that the space between the cord and the surrounding bony mass of the vertebra can be readily visualized. Narrowing of this space due to lesions of CVM can then be located.
The procedure is not without its hazards and should only be undertaken by those who are experienced with the technique and its interpretation.
Two types of lesions have been identified. The first typically affects horses from 4 to 12 months of age and occurs most frequently between vertebrae C3(cervical vertebrae #3) and C4, and C4 and C5 It causes pinching of the cord only when the neck is flexed.
The second affects horses between 12 and 36 months of age and occurs between vertebrae C5 and C6, and C6 and C7. Compression of the spinal cord is not relieved or exacerbated by flexion or extension in this region. Injury to the cord results from pressure which interferes with blood flow, causing damage to the cells comprising the cord. It is this injury which results in signs of incoordination, the severity of which are related to the extent and site of damage.
In the young horse destined to become a wobbler, OCD intervenes, allowing cartilage within the vertebra to develop in the absence of bone formation. The blood supply becomes inadequate leading to death of the surrounding tissue and the subsequent development of chronic joint lesions between the cervical vertebrae.
What triggers these pathological changes at this critical growing period is still a matter of considerable debate. The initial suggestion that wobbler syndrome was an inherited condition linked to certain families has not been proven, although genetic influence has not been eliminated. By breeding two wobbler parents it has not been possible to increase the incidence of wobblers in their offspring. It was noted, however, that the incidence of other bone deformities eg OCD was dramatically increased.
It is interesting to compare the development of similar bone lesions, including spinal deformities in other species, particularly in poultry and pigs, both of which have been subjected to intensive genetic selection and high planes of nutrition to improve growth rate and feed conversion. It is apparent that within these populations, genetic selection has contributed to an overall increase in skeletal problems.
A similar situation may well have evolved in the Thoroughbred and Warmblood, with the current commercial incentive to produce a well-grown but nevertheless skeletally immature weanling or yearling.
Foals and yearlings which receive a diet high in protein and energy have a critical demand for the correct balance of vitamins and minerals. This feeding level occurs at a time when the skeleton is still not capable of bearing increased muscle mass, nor is it able to respond to the strains and pressures imposed upon it. As a consequence, lesions of OCD may develop, causing CVM.
The prognosis for a wobbler has always been poor because of the progressive nature of the condition. However, within the last ten years a number of wobblers have been treated surgically. It has been reported that clinical improvement does occur in some cases but there is still considerable concern as to whether such animals should be allowed to participate in athletic competition. An alternative but less dramatic approach is to try to eliminate factors which might promote the wobbler condition, primarily by reducing the level of nutrition in the young horse.
Treatment of the ‘suspect’ horses includes complete stall rest and a level of energy and protein intake only slightly in excess of maintenance requirements. Minerals are retained at normal levels. Horses on this program can be neurologically normal after completion of the treatment regime and by late in their two-year old year have achieved growth similar to that of their contemporaries.
Acquired Flexural Deformities
Acquired flexural deformities, also acquired contracted flexor tendons, appear frequently as a sequel to DOD. Rapidly growing horses that are erect in their pasterns are at most risk. The exact cause and an effective treatment remain elusive. Reducing growth rate, bandaging, surgery and tetracycline therapy have all been tried with varying degrees of success. The incidence of acquired contractures is high among horses that have been on a restricted diet and are then fed more liberally, a trend observed among horses in a number of countries.
Conclusion
The commercial requirements of rapid growth and development in young horses has led to an increase in the incidence of DOD in many breeds. These problems may be short or long term and may have no impact on athletic potential or ruin a horse’s future. DOD has a number of potential causes and it is often difficult to identify a cause. Nutrition is only one factor, but it is often the easiest to control. Feeding a balanced diet will reduce but not eliminate the risk of DOD and breeders need to carefully consider genetics, growth rates, condition, exercise and environment in the quest to control DOD in their young horses.