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.
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.
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.
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.
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, 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.
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