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Within the animal kingdom, horses are considered to be elite athletes because of their unique physiology. Since they perform at such a phenomenally high level, even the smallest change in their health can knock down their performance. These minute, often subtle effects on their health that effect performance are really challenging to detect, sometimes requiring special diagnostic tests. It is important to investigate a decline in performance right away, since it will only get worse with further athletic activities.
Common causes of poor performance are usually categorized by the body system they effect:
Clear visible symptoms that can be pinpointed to a specific body system are frequently not evident during the early stages of diseases that effect performance. Diagnosis during the early stages rests on taking a careful and precise history, detailed physical examination, and a "high-tech" evaluation of suspicious body systems.
What to Watch For
The symptoms that clue you into poor performance depend on the horse's discipline. For example:
Veterinary care should include diagnostic tests so that the specific cause(s) of poor performance can be identified and treated successfully. Because there are so many possible causes of poor performance, it is important to be logical and methodical in choosing the following examinations or diagnostic tests.
A complete physical examination and history is crucial. This may include watching the horse performing his accustomed sport, so that the veterinarian can appreciate what the owner has noted. Other tests may include:
The results of these tests will determine which of many other, more extensive diagnostic tests should be done.
Treatment of poor performance is completely dependent upon the underlying cause. Much time and money can often be saved by pursuing the cause of poor performance aggressively and early. The problems generally worsen, so watching and waiting is not a good policy. Early detection is important.
Trial or empirical treatments given without diagnostic support, often fail and costs more money in the long run.
Home care is dependent upon the cause of poor performance.
One of the most common causes of lameness in sport horses is degenerative joint disease (DJD), otherwise known as osteoarthritis. Areas that are often affected include the hocks (where it is known as bone spavin), the fetlocks, the pastern joints (where it is known as ringbone), coffin joints, and, less frequently, the carpal joints, usually called the knees by horsemen.
Degenerative joint disease, as the name implies, is a disease of wear and tear. The joints are lined by specialized tissue called hyaline cartilage that is vital to smooth joint function. This cartilage can become frayed and damaged due to the mechanical wear associated with exercise. Nasty inflammation results, which furthers the damage in a vicious cycle: damage, inflammation, damage from inflammation, more damage, and so on. The normally smooth glistening cartilage becomes eroded, exposing bone and causing pain. Horses show lameness that may respond to rest initially, but usually worsens with time. Most anyone with a knee problem can attest to the pain and recurrence of DJD.
Disease associated with the navicular bone, which resides within the hoof capsule, has shortened the athletic career of many horses. Researchers are still working hard at determining the ultimate cause of navicular disease. The accepted causes include increased pressure within the navicular bone itself and arthritis involving the navicular bone and surrounding structures such as tendons and the coffin joint surfaces. Although navicular disease has long been associated with quarter horses that possess large bodies and small feet, it is seen in most large sport horses, including racehorses and warmbloods.
Because many horses have navicular disease in both front feet, many owners do not realize that their horse is lame. Rather, they may report that the horse has developed a very short, choppy gait, a "shoulder lameness," or seems reluctant to go forward. These horses are really sore when turned on hard surfaces and actually start to limp.
Veterinarians know this disease as recurrent exertional rhabdomyolysis (RER), which literally means disintegration of muscle. It causes a painful breakdown of muscle, which is often accompanied by a high heart rate and respiratory rate, sweating, and anxiety.
RER was traditionally called Monday Morning Disease, because it was seen in draft horses who were given Sunday as a day of rest but fed the full grain ration anyways. These horses accumulated starch products over the weekend in their muscles, which rapidly broke down on Monday into lactic acid, causing them to tie up. We don't see this condition very often anymore.
We now know that RER affects all types of horses, but is most common in young fillies in training. It is seen in horses that are intermittently rested as well as in horses that are in continual work. Theories as to the cause of rhabdomyolysis include genetic defects in muscle function, carbohydrate (starch) overloading, thyroid imbalances, vitamin E and selenium deficiencies, and hormonal imbalances. The truth is that most cases are not associated with any of these causes, and the reason for the tying up is unclear.
Recently, an inherited disease, polysaccharide storage myopathy (PSSM), has been shown to be a cause of tying up in some quarter horses, draft horses, and warmbloods. Many horses are diagnosed with PSSM, but it is not certain that all of those accused of having PSSM have a genetic problem or have acquired the condition during life.
Horses with RER may show vague symptoms such as stiffness after work, a shortened stride, an odd lameness that comes and goes, stiffness and weight loss. In rare cases, this condition can cause the horses to collapse and be unable to get up on their own. Of course, this condition should not be confused with HYPP (hyperkalemic periodic paralysis), whereby horses collapse and show weakness rather than stiffness after work.
In addition to being great athletes, horses are greatly allergic. Who doesn't know a horse with hives or with heaves? An early form of respiratory disease causing poor performance stems from an allergic condition as well. In certain horses that are predisposed, allergens set up inflammation in the small airways (hence the name, inflammatory airway disease, IAD). Some of the allergens we think are particularly instrumental in causing IAD include fungal spores, bacteria and their toxins, and air pollutants. The fungal spores can come from the cleanest looking hay, so proving to someone that hay was the source is a hard sell. This inflammation smolders for a long time and is generally invisible to the even the keenest observer, until the horse slows down or can't work as hard. At this time, further diagnostic tests are pursued that reveal the problem.
In horses with IAD, there are more profound changes than just inflammation. Inflamed airways transform, becoming hyperreactive, or twitchy. Essentially, they constrict more readily and to a greater degree than do the airways in normal horses. The symptoms of constriction (bronchoconstriction) are coughing and exercise intolerance.
Because horses with allergies (IAD) have endured bouts of inflammation and constriction over and over again, their airways are also thicker due to development of excessive tissue and inflammatory secretions, and thus have a narrower lumen (passageway). The narrower airways cause a bottleneck in airflow, especially during hard work, which in turn decreases the available oxygen that is needed for work.
Because horses have an enormous respiratory reserve (the amount of excess lung not called upon during rest), the effects of IAD are often not noted until the horse is asked to exercise strenuously, breath deeply, or work at higher temperatures. This is why IAD was first recognized in racehorses. However, by the time IAD takes hold and causes the horse to slow down or a long-term cough to develop, the damage done to the lungs, while reversible, may be profound. It is absolutely imperative that IAD is recognized as early as possible, or the condition could go on to cause heaves.
The larynx or voicebox forms the passageway to the trachea (windpipe). For effective function, the larynx must be able to close while the animal is swallowing, and it must become very wide during maximal exercise to afford the greatest airflow.
Laryngeal paralysis, which is most common in horses taller than 16 hands, primarily affects the left side. For reasons that are not well understood, the nerves (the left recurrent laryngeal nerve) that serve the muscle that opens the larynx begin to die. With the decrease in stimulation of the muscle, it atrophies, and the larynx becomes paralyzed. The left side no longer opens normally, preventing the full potential of the horse to breath freely during intense exercise.
The degree of laryngeal paralysis is very minor in up to 80 percent of horses, and severe in up to 10 percent of horses. It's a problem that worsens with age, so the percentage goes up in the higher age brackets. This is one reason why older horses can't work as hard as young racehorses.
Owners may suspect that their horses have LRLN because the collapse of the larynx during inspiration causes them to make a distinctive roaring noise. In some cases, the sound is more like whistling.
LRLN is more of an aesthetic problem in horses that do not compete at maximum capacity. It is not until horses are competing in races greater than one mile, high goal polo, or upper level three-day events, that laryngeal paralysis will actually interfere with performance.
In elderly horses, the right side can get bad in addition to the left, and the larynx can collapse. These horses can no longer perform without surgical intervention.
EIPH is very common in racing thoroughbreds and standardbreds (80-90 percent of all horses in this category). However, very few horses bleed visibly (less than 5 percent).
The causes of EIPH are widely debated. One of the most accepted theories is that the pressure in the vessels of the lungs becomes so great in racing horses, that capillaries (very small blood vessels) in the lungs actually rupture.
Another theory is that horses have a low-grade blockage somewhere in their respiratory tract (nose, throat, lungs) and they need to pull air in harder. This creates a huge vacuum in the lungs with furthers explodes vessels.
Still another theory contends that a "shock wave" travels up from the weight-bearing forefeet through the chest wall to the lungs, which shake so violently that there is rupture of vessels. Of all these theories, only the first theory has a lot of support form research studies, and from the fact that lasix, which decreases vessel pressure, seems to reduce bleeding in some studies. But he debate about the cause of EIPH and the effects of lasix go on.
Although EIPH has caused great concern to many trainers, owners and spectators, and poor performance is often ascribed to EIPH, it likely does not cause poor performance except in the few horses that bleed extensively on race day. How extensive the bleeding must be to affect performance is unknown.
Horses have enormous hearts in comparison to other species, and with training, they become even larger. Intrinsic neurologic (vagal) input to the horse's heart also ensures that the horse has a low resting heart rate (32 to 44 beats per minute). This is known as having high vagal tone.
Both the size of the horse's heart and the high vagal tone contribute to the development of atrial fibrillation. In horses, atrial fibrillation is usually benign, meaning that there is no underlying cardiac disease; this is different from cats, dogs, and humans. Occasionally, horses may develop atrial fibrillation because of problems such as leaky heart valves.
With atrial fibrillation, the electrical signals that ordinarily pass from the atria, the first set of filling and pumping chambers of the heart, to the ventricles, the second set of chambers, becomes disorganized. This causes the atria to beat in a very erratic fashion.
Because the ventricles still beat normally despite the erratic signals sent to them, the heart is able to pump adequate amount of blood at rest. But the extra blood pumped in by the atria, while insignificant during rest, becomes important for the horse to perform strenuous exercise. For this reason, atrial fibrillation may go undetected for a very long time in horses that do light work, such as pleasure horses, trail horses, and show hunters. In a race horse, atrial fibrillation would be picked up very soon.
EPM is caused by a protozoal parasite that invades the neural tissues of the horse. The spinal cord is most frequently affected, but the brain may also be involved.
The parasite, Sarcocystis neurona, is thought to be passed to horses when they accidentally ingest the feces of opossums. Horses do not pass on the infection to other horses or the environment. That's because S. neurona cannot complete its life cycle in the horse, thus the horse is an accidental (incomplete), "dead end" host, in technical terms.
EPM causes a wide array of neurologic symptoms. The most commonly seen abnormalities include ataxia (lack of coordination) and muscle atrophy, especially of specific muscles in the head and tongue, as well as the gluteal and quadriceps muscles.
EPM often initially appears to be a lameness that can't be localized, which is when it becomes a cause of poor performance. With time, the disease worsens, and it is recognized as a major neurological dysfunction. Most cases of EPM are bad enough that they don't allow competition, so the symptoms are picked up at rest, but some are much more subtle. In these latter cases, it can be difficult to implicate EPM as the cause, since there is much lameness related to the muscles and bones that are more likely, and yet equally frustrating to pinpoint. Keep an open mind.
CVM causes neurologic symptoms due to problems in the neck. The bones in the neck have a deformity or instability that pinches the cord. This can happen either slowly over time due to unequal growth of the spinal cord and surrounding bones (vertebrae), or suddenly due to an up and down movement of a neck, which has unstable connections, that pinches the cord while slipping from its stable position.
Alternatively, osteochondrosis dessicans (OCD) can affect the joints in the neck bones, just as it can any joint such as a knee or hock. In this case, the OCD causes inflammation and huge calluses to build up around the bones, which later get so big that they actually pinch the spinal cord.
Horses with CVM have difficulty transmitting signals from the brain to the nerves controlling the legs, since they need to travel through the cord within the neck, which is narrowed or pinching it off.
Horses may show general incoordination, especially in the hind limbs. They may drag or catch their toes, stumble, completely knuckle, misplace their feet, sway from side to side unknowingly, or pitch out (circumduct) a leg when circled. They may also have a very stiff gait, and the owner or veterinarian may note that the toes are chipped and worn due to the abnormally stiff gait.
Although owners often report an initial traumatic incident, such as falling in the field, the fall is usually due to CVM, and the subtle signs become severe enough to be clearly recognized.
CVM is a developmental disease, and is usually recognized in young horses, especially large, rapidly growing male horses. It gets worse with development since the spinal cord is growing, but the bony canal is deformed.
Many of us know what gastric ulcers feel like. Gastric ulceration is the pitting or deep erosion of the stomach lining. It's painful, and some horses don't perform well when they have ulcers.
In nature, horses were meant to eat relatively poor quality roughage continually. Under domestication, horses are generally fed large amounts of high quality concentrates at infrequent intervals. For a horse, even 4 feedings a day constitutes infrequent intervals, unless he always has hay in front of him.
Because horses are by nature continual eaters, they also secrete gastric acid continually. When they stop eating, the acidity in their stomachs rises dramatically. It is important to note that horses that are turned out to pasture and have continual access to roughage, do not develop gastric ulceration.
Although the discovery of the bacterium, Helicobacter pylori, has been a great advance in the understanding and treatment of gastric ulceration in humans, no evidence of this bacterium has been found in horses.
Horses with gastric ulceration may show varying signs, such as poor appetite, chronic colic, poor performance, 'crabby attitude', and teeth grinding.
For Neurological Disorders
Gastroscopy (endoscopic examination of the stomach) reveals areas of reddening and erosion in the otherwise smooth, glistening surface of the stomach.
There are many potential treatments for all of the causes of poor performance. Some of the most common include:
Follow-up care depends on what your veterinarian diagnoses as the cause of poor performance. Regardless of the cause of poor performance, it is important to schedule re-evaluations as recommended by your veterinarian. A good example is to remeasure muscle enzymes in horses that have previously tied up.
It is also important to follow treatment recommendations. Do not expect overnight success. Often, specific treatments may take weeks to months to see real improvement. For example, treatment of IAD can take several weeks to months before the horse has returned to full form, and in many cases, the recognition and proper treatment can result in new lifetime marks and top performances in these horses.