Search Our Website

E.O.T.R.H. (Equine Odontoclastic Tooth Resorption and Hypercementosis) is a disease process of the incisor and canine teeth mostly seen in older horses. For reasons unknown, the body begins to resorb the bone and surrounding gum tissue. With increased loss, pockets will form causing feed to accumulate between the teeth and a subsequent infection occurs. The infection can further destroy the bone along with ligaments holding the teeth in place. Cementum (the hard covering of a horse’s tooth) proliferates near the gum line causing the incisors to take on a characteristic rounded and overgrown appearance. This disease process can be painful and cause the horse to become reluctant to eat. E.O.T.R.H. can be treated with partial or full removal of the incisor teeth. Many clients wonder, “How will my horse eat without front teeth?” But horses tend to do well and typically go back to normal feed within 24 hours after the procedure. Steinbeck Peninsula Equine Clinics Surgery Director and dental specialist Dr. Nick Carlson routinely performs this surgery and explains, “By the time the disease has progressed enough to warrant complete incisor removal, the horse has likely already adapted to using their tongue and cheeks to graze and chew.” This procedure can be done in the hospital and usually only requires a 1-night stay. The extractions are done with the horse standing, using intravenous sedation and local anesthesia. The horse is typically fed a wet pelleted mash that evening and begins back on normal feed the following day. Owners have reported significant improvements in behavior following extraction, such as increased energy, brightened attitude, eagerness to eat, and lessened facial sensitivity. If you believe your horse might be experiencing this or any other dental problem, please call to schedule an appointment with a member of our team.

Neurological form of Equine Herpesvirus-1 — Important information about EHV and EHM from the CEH Horse Report, a publication of the UC Davis Center for Equine Health, UC Davis School of Veterinary Medicine.

In this video, Dr. Amanda Hedges shows you how to administer liquid medications, supplements and dewormers with a syringe. (Be sure to turn up your sound!) Related resources you may also be interested in: British Equine Veterinary Association (BEVA): Don’t Break Your Vet - Worry-free Deworming McKee-Pownall Equine Services: How To Give Oral Medications

In this video, Dr. Nora Grenager shows you how to take your horse's vital signs. (Be sure to turn up your sound!) Related resources you may also be interested in: “Emergency Horse Care” (PDF) “Emergency First Aid on the Trail” (PDF) Steinbeck Peninsula Equine Clinics Emergency Services

By Matt Durham, DVM Published in Bay Area Equestrian Network June 2008 Horse owners have probably all experienced “heart” in a favorite horse, that indefinable quality that makes certain horses stand out. In the article The Equine Heart: Part 1, we examined the remarkable abilities of the equine heart, and its role in making horses superior athletes. In this article, we will examine some of the more common cardiac problems found in horses. How the Heart Works (the boring part) Horses, like all other mammals, have a four-chambered heart. The circuit can be divided into left and right portions. Blood is collected from the body into the right atrium, which acts as a reservoir to prime the main pump, the ventricle. From the atrium, the blood is pumped into the right ventricle, and from the right ventricle, the blood is pumped through the lungs where carbon dioxide (CO2) is removed and oxygen (O2) is added. This oxygenated blood then continues back to the heart into the left atrium, and follows a similar course through the left ventricle. The left ventricle is the most muscular portion of the heart, having to pump blood throughout the entire body via the aorta. Blood is delivered to muscle, brain, and other organs, which then extract O2 and add the waste product CO2 back in. The unoxygenated blood then returns to the right heart via the vena cava, and the cycle is started again. The atria and ventricles are composed of a type of muscle somewhat different from skeletal muscle. Cardiac muscular contraction is initiated by electrical impulses. The heart has a built-in pacemaker called the sino-atrial (SA) node, living at the top of the heart, which governs heart rate and rhythm under most circumstances. The SA node sends its impulse out in a wave across the atria, causing muscular contraction in a similar downward-moving wave, pushing blood downward into the ventricles. Once the electrical impulse reaches the bottom of the atria, the atrio-ventricular (AV) node is triggered, which sends an electrical impulse through the bundle of His, which carries the impulse down to the bottom of the heart. During this time, muscle tissue is bypassed. At the bottom of the heart, the Purkinje fibers carry the electrical impulse in an upward direction, causing the individual muscle fibers to contract in a coordinated upward wave towards the openings of the “great vessels” at the top of the heart (the aorta in the left ventricle and the pulmonary artery in the right ventricle). The cardiac cycle is divided into two cycles: diastole, where the right and left atria contract, and systole, where the right and left ventricles contract. Valves are present between the atria and ventricles, and between the ventricles and the “great vessels” to prevent significant backflow. The valves are flexible flaps of tissue which are pushed out of the way by forward flow of blood. When back pressure starts to develop, the valves start to push back, but are held in place by connective tissue bands called chordae tendinae, thereby sealing the valve opening and preventing backflow. The left atrio-ventricular valve is called the mitral valve, and the right one is called the tricuspid valve. The valves associated with the great vessels are the aortic valve on the left and the pulmonic valve on the right. Evaluation of the heart (the slightly less boring part) One of the simplest and most effective tools for evaluating the heart is the stethoscope. The heart gives important clues as to its function through its heart sounds. There are two main heart sounds that can usually be heard in the normal horse, which correspond with the closure of the valves. With the stethoscope under the left elbow (further forward than you might think), a lub-dub sound is heard, with a longer pause between dub and the following lub. The lub corresponds to mitral and tricuspid valve closure, while the dub corresponds to pulmonic and aortic valve closure. A normal cycle would sound like: lub-dub……… lub-dub……… lub-dub……… lub-dub. In between the lub-dub sounds is systole, the period when the ventricles are contracting. The longer pause, between dub and the following lub, is diastole, when the atria contract to refill the ventricles. Each lub-dub accounts for a full cardiac cycle, or one beat. Typical heart rates in resting adult horses are between 32 and 40 beats per minute. (Count the number of beats for 15 seconds and multiply by 4) Exercise and anxiety are common causes for elevations in heart rate, while pain and cardiac problems can also cause elevations. The heart rate will stay elevated in horses with pain or cardiac disease, while the rate will come back to normal in the nervous or recently exercised horse. The heart rhythm in horses is typically stable, meaning that each beat occurs at a predictable interval. By tapping your foot to each beat while counting, deviations from the expected rhythm can be detected. A heart murmur is an abnormal sound caused by turbulent blood flow. The murmur itself is not a disease, but is merely a physical finding. Most murmurs are associated with turbulence created from leaking valves. Turbulent blood flow can sometimes be created in normal highly fit horses, causing a ‘physiologic flow’ murmur. During a cardiac examination, the lungs sounds are also evaluated, since certain heart disease conditions can lead to a buildup of fluid in the lungs. Palpation of pulses can be useful in counting the heart rate without a stethoscope, and in evaluating the strength and character of ventricular contraction. Electrocardiography (ECG or EKG) works by detecting and mapping out the electrical flow patterns throughout the cardiac cycle. A normal ECG traces atrial contraction (P-wave), ventricular contraction (QRS waves), and re-polarization (T wave) in a uniform cycle. Deviations in the shape of a wave, distance between waves, or lack of certain waves give important information about the function of the heart. Normal ECG from a horse: This horse has normal 2-part (bifid) P-waves (blue arrows), QRS complexes (red arrows), and T-waves (black arrows). The use of ultrasound to visualize the physical structures of the heart is called echocardiography. Echocardiography provides a dynamic image, which allows for evaluation of the valve structures, quality of movement of the ventricles, and chamber size throughout the cardiac cycle. Normal measurements of the different cardiac structures have been well documented. Abnormal measurements help to define what problems are present, and the degree to which the heart is affected. A useful tool in echocardiography is Doppler ultrasonography (like the Doppler radar shown by weather reporters), which shows direction, volume, and speed of fluid movement. This helps in detecting abnormal blood flow patterns, particularly with leaking valves. Doppler ultrasonography can also measure the speed of blood flow, which can help to determine the severity of a leak. Visual mapping of blood flow patterns and measurements of flow rate help to define the character and severity of the leak. Color Doppler echocardiographic image of the left atrium (purple outline) and left ventricle (white outline) during systole in a horse with moderate to severe mitral regurgitation. The red /blue/green area represents turbulent backflow of blood from the ventricle through the mitral valve (which sits at the junction of white and purple), causing enlargement of the atrium. During systole, there should be no flow through the mitral valve. (Image obtained from the left side of the horse.) Congenital Heart Problems A congenital problem is a problem present at birth. The normal fetal heart is very different from the adult heart. If problems occur during the transitional stages from fetal to adult circulation, certain openings between structures that are normal in the fetus can persist. Other congenital problems occur early in fetal development, causing abnormalities that are not normal under any circumstances. Congenital problems occur fairly infrequently in horses when compared with dogs. By far the most common congenital heart problem in the horse is a ventricular septal defect (VSD). In this condition, an opening is present between right and left ventricles. The right ventricle works under low pressure, since there is little resistance to blood flow through the lungs. The left ventricle works under high pressure, since the kidneys require high pressure to function properly and the large volume of muscle and other tissue leads to resistance to flow. This pressure difference leads to blood flow from the left ventricle into the right ventricle. Horses with VSDs are often smaller than expected, and may be poor athletes. Coarse sounding murmurs heard during systole are typically found on both sides of horses with a VSD, usually louder on the right. Depending on the size of the defect, some affected horses can perform well, while others are at high risk for developing congestive heart failure. Normal heart rate and rhythm are typically seen with smaller defects, while larger defects may be accompanied by elevations in heart rate, abnormal rhythms, visual pulsations in the jugular veins, and/or other abnormalities. Monitoring the heart with echocardiography is helpful in guiding medical treatment options and prognosis. Many other congenital abnormalities have been described in horses, including Tetralogy of Fallot, atrial septal defects, and patent ductus arteriosus, among others, but all are rare in occurrence. In humans and dogs, abnormally small (stenotic) valve openings are relatively common congenital conditions, but these too are rarely seen in horses. Developmental Cardiac Problems Developmental diseases are, as the name implies, not present at birth, but occur later in life. The most common developmental diseases in horses involve the valves. Leaky aortic and mitral valves are the most common, with the tricuspid valve affected less commonly, and the pulmonic valve rarely affected. Abnormalities in rhythm are somewhat less common, as are aneurysms and pericarditis. Myocarditis, which is common in humans, is uncommon in horses. Valvular Disease Slowly progressive scarring of the valve margins is relatively common in older horses in the aortic and mitral valves, which can lead to poorly functioning valves and variable degrees of leaking. Tearing in the valve leaflets, buckling of the leaflets, or ruptured chordae tendinae lead to improperly functioning valves as well. Rarely, bacterial infections can occur on or near the valves, which can severely affect cardiac function, and can be life threatening. Leaking of the aortic valve (aortic regurgitation) is common in older horses, and is often tolerated well. The backflow causes an overload in volume in the left ventricle, but in early stages the ventricle does a good job of adapting. Murmurs are present during diastole (after the ‘dub’), present on both sides, but louder on the left. The murmur can sometimes have a ‘divebomber’ sound, which likely occurs from vibrations of the aortic valve leaflets. Long term aortic regurgitation can lead to stretching of the ventricle and the mitral valve opening, which can cause leaking in this valve as well. Leaking of the mitral valve (mitral regurgitation) is also relatively common. The backflow causes the left atrium to enlarge, which causes a backup of blood into the pulmonary vein. Murmurs are during systole (between ‘lub’ and ‘dub’), and are heard on the left side of the horse. Most mitral valve leaks can be tolerated well if the onset is slow, allowing the lungs to compensate for the increase in blood pressure. Sudden-onset mitral valve leaks, such as with ruptured chordae tendinae, are more difficult for the body to handle, because sudden backflow causes a sudden pressure increase in the lungs, which causes fluid to leak into the air sacs of the lung. In this situation, the outcome is usually poor, while small or slowly progressing leaks can often be managed medically. Leaking of the tricuspid valve (tricuspid regurgitation) occurs less commonly and is typically well tolerated by horses. Backflow can sometimes be seen as prominent jugular pulses, prominence in other blood vessels, or edema in the legs or abdomen. Murmurs are during systole (between ‘lub’ and ‘dub’), and are heard on the right side of the horse. Leaks in the tricuspid valve are most commonly caused by enlargement of the inside of the right ventricle, which can happen from resistance through the lungs in chronic respiratory conditions or mitral valve regurgitation. The right ventricle can also be enlarged in certain athletic disciplines such as in the sustained aerobic effort of Standardbred racehorses. Tricuspid regurgitation is more common in athletic humans as well. Aneurysm Aortic root aneurysm is a very rare, but serious condition. The typical aneurysm is an abnormal bulging of the aorta, which is at risk of rupturing. This can lead to collapse or sudden death, usually when the horse is exercising. Aneurysms in the blood vessels leading to the intestines can be caused by the parasite Strongylus vulgaris (large strongyle), but this is easily prevented by proper de-worming practices. Myocarditis Damaged or inflamed heart muscle (myocarditis), usually occurs in horses as a result of certain viral infections or toxins. Monensin is a feed additive found in some cattle feeds, which is extremely toxic to horses. Oleander, Yew, and avocado branches and leaves are among other plants that are cardiotoxic to horses. Very rarely, coronary artery disease leading to myocarditis can be caused by infections within the heart. Cholesterol plaques, which cause coronary artery disease in humans, are not seen in horses. While myocarditis is rare in horses, coronary artery disease is the leading cause of death in humans. Arrhythmias Abnormal cardiac rhythms, or arrhythmias, are uncommon in horses. Second-degree AV block is common in horses, but is almost always considered normal. In this rhythm, the horse’s heart actually skips a beat. The SA node sends its signal, but the AV node decides that the heart is functioning efficiently, and does not send the signal through for one beat. In the normal situation, only one beat is skipped, and the normal rhythm is resumed. This sounds like: lub-dub……… lub-dub……… (pause)……… lub-dub……… lub-dub. If keeping rhythm by tapping your foot, you should detect a gap when you expect a beat, but then find the following beat with one more foot tap. Atrial fibrillation occurs when the normal wave of electrical impulses that moves across the atria is broken up into many random waves, moving in different directions at the same time in an uncoordinated manner. This causes the atria to contract in a random uncoordinated manner, and does not provide the AV node with a reliable signal. The rhythm of the ventricles must be taken over by the AV node, which usually does not create a predictable rhythm. This typically sounds something like: lub-dub.. lub-dub………………… lub-dub……… lub-dub… lub-dub……………… lub-dub in an unpredictable pattern. ECG findings are characteristic, exhibiting no P waves, but an undulating baseline (f-waves), and random distribution of otherwise normal QRS complexes. ECG of a horse in atrial fibrillation. Note random distribution of QRS complexes (red arrows) with no associated P-waves and the presence of an undulating baseline (‘f-waves’, blue brackets) Electrolyte abnormalities, particularly low potassium and/or magnesium levels may predispose a horse to atrial fibrillation. Enlargement of the atria, most commonly from mitral regurgitation, also increases risk. Echocardiography should be performed to help define any underlying problems. Horses with severe cardiac enlargement or longstanding atrial fibrillation are less likely to be able to convert to a normal rhythm, and if they do convert, may revert back into atrial fibrillation. Typical treatment is with quinidine sulfate administered through a stomach tube or, in horses with a very short history of atrial fibrillation, injectable quinidine gluconate is used. Recently, electric conversion of atrial fibrillation has been performed. Atrial premature contractions are relatively common, while ventricular premature contractions are relatively rare. Both of these conditions occur when there is localized myocarditis. The conditions can sometimes be differentiated by carefully listening to rhythm abnormalities, but definitive diagnosis is made with an ECG. Both conditions require a period of rest and anti-inflammatory medications, as well as investigation into any underlying causes of disease. Ventricular tachycardia and ventricular fibrillation are rare and generally are associated with serious underlying disease processes. Management of Horses with Cardiac Disease (a little good news) Depending on the severity and type of abnormality, most common heart conditions in horses are manageable. In fact, most horses can compete effectively in all but the most rigorous events with mild to moderate valvular problems. Horses with valvular disease should be evaluated periodically with a thorough physical examination and echocardiography to monitor progression of disease. Horses with mild to moderate valvular disease often benefit from exercise. The amount of exercise should be tailored to the individual horse, based on age, fitness, degree of cardiac dysfunction, and soundness. Depending on the type of disease present, horses may need to be maintained on daily medications. Enalapril and furosemide (Lasix), with or without digoxin, are common choices for treatment of ongoing conditions. The use of these medications in some horses may delay the progression of cardiac disease, and can often alleviate some of the clinical signs seen in moderately affected horses. Severely affected horses may improve somewhat, but typically have a poor prognosis even with aggressive treatment. Insignificant aortic and mitral regurgitation are commonly found cardiac problems, typically with only a subtle murmur, and no other abnormal findings on a physical examination. In these mildly affected horses, medical therapy is not necessary, but the murmur should be monitored at each examination for signs of progression. Final Word Horses are remarkably athletic creatures, in large part due to their incredible hearts. Fortunately, significant heart disease is uncommon in these amazing creatures, allowing us to enjoy our equine friends for many years. We are enriched by their company, we marvel at their physical abilities, and we always remember that special horse with lots of “heart.”

By Matt Durham, DVM Published in Bay Area Equestrian Network September 2007 Without a doubt, one of the most awe-inspiring things about our equine companions is their remarkable athleticism. Their sheer power, grace, and refinement of movement have captivated the imagination of people throughout history. But beyond the sinew and muscle and bone of these intricate machines is a power plant unequalled in any other creature: the equine heart. In some ways, the job of the heart is really quite simple: it is mainly just a pump. Blood must be moved from one area of the body to another. What makes the equine heart so remarkable is its adaptability and efficiency in doing this job under different conditions. The Role of Blood Blood must circulate throughout the body for many reasons. The most obvious is the delivery of oxygen (O2) from the lungs to the tissues, and carbon dioxide (CO2) back from the tissues to the lungs. Blood also transports nutrients and by-products to and from the intestines and other internal organs. Additionally, blood works in the same way that radiator fluid works in a car, carrying heat away from the power source to an area of cooling. Muscles (like a car engine) convert fuel into movement. The car engine and muscle both produce waste heat which must be removed to prevent overheating of the system. The main radiator in the horse is the skin, followed by the lungs. A Smart Pump The equine heart has many ways of adapting to differing demands. Cardiac output is the measure of blood pumped per minute. Cardiac output is calculated by multiplying the heart rate by the amount of blood pumped with each beat, termed stroke volume. Stroke volume is close to one quart of blood per heartbeat. So, a horse with a heart rate of 40 beats per minute pumps 40 quarts of blood (10 gallons) every minute. The average resting heart rate in an athletic horse is typically between 32-40 beats per minute, while maximum heart rate at a full gallop can exceed 240 beats per minute. In humans, the typical athlete has a resting rate in the 50-60 beats per minute range, with a maximum heart rate of about 220. Besides increasing the rate, the heart muscle increases the amount of contraction (increasing the stroke volume) when requirements increase, pumping out the maximum volume possible. Obviously, a lower cardiac output is required at rest than at maximum exercise levels. The heart limits the amount of energy expended in three main ways. First, the heart rate is decreased. Second, the amount of contraction of the heart muscle is decreased, pumping out only part of the volume of blood in the heart, (decreasing stroke volume). Third, the heart can skip a beat allowing the heart to rest. This change in heart rhythm is called 2nd degree AV block, which is normal in horses, and is occasionally seen in human athletes. Racing Arabians, Thoroughbreds, and Quarter Horses A critical difference exists between horses of different disciplines in terms of cardiac requirements. Compare the Arabian, Thoroughbred and Quarter Horse to Olympic marathon, middle distance runners and sprinters. From one group to the next, we see a shift from extreme endurance to prolonged strength to raw power. The difference in these groups comes from the difference in muscle type. The ‘slow twitch’ or Type I muscle fiber produces less power, but can continue to work for extended periods. The Arabian horse has primarily Type I fibers, which can utilize fat and sugars in the presence of oxygen for sustained moderately fast-paced aerobic exercise. Below about 140 beats per minute, most endurance horses can deliver all the oxygen their bodies require. Above this heart rate, termed the lactate threshold, the horse’s muscle must start exercising anaerobically. Anaerobic exercise uses faster-produced and shorter-lived fuel from sugars, and produces lactate. Excessive lactate production can lead to fatigue and even muscle damage. An endurance horse exercising below its individual lactate threshold will recover rapidly and be able to sustain for the longer distances because it is exercising aerobically. The Thoroughbred racehorse has a mixture of Type I and Type IIa or ‘intermediate twitch’ fibers. Type IIa fibers produce more power than Type I fibers, and rely on sugars for fuel. The larger more efficient hearts of Thoroughbreds allow for the type IIa fibers to use oxygen at a high rate for a longer period of time. The more efficient the heart, the more aerobic use of sugars can be maintained, pushing off fatigue. The Quarter Horse has mostly type IIb or ‘fast twitch’ fibers. Type IIb fibers produce the most power, but rely on unsustainable anaerobic exercise. A sprinting Quarter Horse can accelerate more rapidly than any other horse, with speeds clocked at around 50 miles per hour. But this maximum rate can not be sustained beyond a half mile. Because the racing Quarter Horse relies on anaerobic exercise during this sprint, heart size is not as large as in Thoroughbreds. The Sedentary Steer, the Cross-Country Skier, and the Racehorse In an interesting study, the horse was compared to the steer to show differences in ability to sustain exercise. Among the striking differences were vast differences in lung capacity and heart size. Comparing animals of the same weight, researchers found the lung and heart volumes to be twice as large in the horse. Researchers use the term VO2max to measure the oxygen carrying potential in different individuals on a per weight basis. An elite cross-country skier had the highest measured VO2max in a human of about 96mL/kg/min, while measurements almost twice as high may be reached in the Thoroughbred racehorse. In cattle, VO2max is more in the 30-40mL/kg/min range. Conditioning As in humans, the ability of the heart to function efficiently relies on exercise. Increasing the strength of heart muscle improves the stroke volume, which allows the heart rate to decrease at rest. Heart Size Of all equine athletes, Thoroughbred racehorses have the largest and most efficient hearts. Part of this is genetic, and part is from their rigorous training. Typical heart weights are in the 10-12 pound range. Phar Lap, the famous New Zealand-born racehorse, had a heart that weighed 14 pounds. The heart of Secretariat was believed to be even larger. (The autopsy performed on Secretariat was incomplete, so some have suggested that some of the enlargement could have been from common age-related heart problems.) The size of the Thoroughbred heart has been watched closely, and is believed to be influenced most by the X chromosome. The ‘X-factor’ is a horse-picking system based on this, which contends that heart size can be predicted genetically, and that larger heart size means better performance. While heart size is an important factor in performance, other factors are obviously critical as well, so relying on the ‘X-factor’ alone is dubious. Size also can increase with disease. Hearts which become overly enlarged are actually less efficient, whether in humans or horses. It is common for older horses to have leaky valves, which can eventually lead to congestive heart failure, where the heart enlarges well beyond that of the fittest racehorse. (This topic is discussed further in The Equine Heart Part 2: Common Cardiac Disease.)

By Nora Grenager, VMD Updated in 2020 (originally published in Bay Area Equestrian Network September 2006) The two main endocrinologic concerns in horses are equine Cushing’s disease (also known as pituitary pars intermedia dysfunction) and equine metabolic syndrome (also known as “insulin dysregulation” or, formerly, “insulin resistance”). These disorders are increasing in prevalence as our equine population is better cared for and living longer, and improved diagnostics are available. There are two main similarities between these conditions: 1) insulin dysregulation, and 2) the potentially devastating possibility of laminitis. While it is an area of much research, there are numerous theories as to why these horses are predisposed to laminitis, and it is beyond the scope of this article to discuss them all. However, laminitis is likely related to insulin dysregulation, which is a reduced ability of the body to respond appropriately to insulin released by the pancreas after eating a meal. It is important to understand the signs of insulin dysregulation and be able to effectively manage these horses to decrease the risk of laminitis. Equine Cushing’s Disease The cause of equine Cushing’s disease is a benign tumor, likely caused by oxidative stress, in a part of the horse’s brain called the pituitary gland. It is not a typical neoplastic tumor, rather a lack of regulation of hormone secretion due to alterations in local factors in that region of the brain. This alteration (namely, a decrease in local dopamine production) leads to unregulated hormone secretion by the pituitary gland, enlarging this area such that it forms a tumor. This tumor secretes a variety of hormones, including one called adrenocorticotropic hormone (ACTH) that causes the adrenal gland (in the abdomen) to release increased amounts of steroid (cortisol). Other secreted hormones include α-MSH, POMC, and β-endorphin. The increased levels of these circulating hormones cause the typical clinical signs, including: a long, wavy hair coat that does not completely shed out; abnormal fat distribution, such as a cresty neck or fat pads above the tailhead; weight loss, especially over the ribs; muscle loss, along the top line or leading to a pot belly; recurrent laminitis; lethargy and exercise intolerance; increased sweating, increased water intake and urination; and immune system suppression or recurrent infections. Many horses with Cushing’s disease also have chronic insulin dysregulation. The most common clinical signs are the abnormal, long hair coat (called “hirsutism”) and chronic laminitis. However, it is important to remember that horses with milder disease can have milder signs, and a long haircoat may not be seen in all horses with Cushing’s. Equine Cushing’s disease is more common in older horses (in their late teens to 20s), but can be seen in horses as young as 7 years old. There are some breeds that seem to be more predisposed, and ponies also seem to be predisposed to the condition. Definitive diagnosis of equine Cushing’s disease can be challenging. It is relatively easy to diagnose in an older horse with more severe disease and typical clinical signs, such as a long hair coat and laminitis. In these cases, in which the horse has the typical clinical signs of equine Cushing’s disease, diagnostic tests are sometimes skipped because the signs are so suggestive. Remember, though, that having lab values to monitor is very helpful so testing should be done when possible. Yet sometimes a “diagnostic therapeutic” challenge is used, in which we try treating a horse for 30-60 days and monitor the response; the treatment for Cushing’s (pergolide) is so effective and safe that we have our answer if the horse improves on medication. There are several tests available. The difficulty with all the available tests is that they can be negative in horses with early Cushing’s disease; thus, if the index of suspicion is very high, we may still opt to treat the horse even if the test is negative. The first recommended test is measurement of the resting levels of ACTH, one of the hormones that is overproduced by the tumor in the pituitary. This test requires one blood sample. While it is fairly accurate, it still can have false negatives (i.e., about 30% of the time horse with Cushing’s disease has a negative test result). If the resting ACTH levels are normal, the next recommended test is called the thyrotropin releasing hormone stimulation test (the TRH stim test). This test is slightly more sensitive (i.e., more likely to correctly diagnose the horse with Cushing’s), but requires two blood samples, taken 10 minutes apart, and intravenous administration of TRH. The test is very safe but is obviously a bit more expensive than just measuring the resting ACTH once. The dexamethasone suppression test is another test that is slowly falling out of favor as the ACTH testing has been shown to be more reliable. This test requires two veterinary visits: at the first visit, blood is drawn to measure the cortisol level and a dose of dexamethasone is given. At the second visit, about a day later, blood is drawn to again measure the cortisol level. The test relies on a normal endocrine negative feedback loop. In a normal horse, a dose of dexamethasone (steroid) suppresses the pituitary gland, telling the gland that it is unnecessary to make more cortisol (steroid made by the body) because some has just been given. Therefore the second sampled blood level of cortisol is very low in a normal horse. In a horse with Cushing’s, the tumor in the pituitary gland results in production of cortisol no matter what levels of steroid are in the body, so it does not respond to the dexamethasone the veterinarian administers; therefore the second level of cortisol is not significantly different from the first, pre-dexamethasone, level. This test can also have false positive or false negative results. There are two potential drawbacks: first, it necessitates two visits from your veterinarian, which increases cost. Second, it involves the administration of steroid to a horse that is already possibly predisposed to laminitis. Therefore there is a very low risk of precipitating a bout of laminitis. Most practitioners feel, however, that the benefits of knowing the test results often outweigh the risks. It has recently been shown that the tests for equine Cushing’s disease are even more sensitive in the late summer/early fall (i.e., mid-August through mid-October); therefore, veterinarians may recommend testing at that time. A variety of other tests exist, and there is ongoing research to develop even more sensitive and specific ways to diagnose equine Cushing’s disease in those horses in which the diagnosis is difficult. The astute reader may be asking why we do not just measure cortisol levels, since the overproduction of that hormone is a hallmark of the disease. Unfortunately, the daily variations in cortisol levels render this measurement useless. Evaluation for insulin dysregulation should always be performed with with tests for Cushing’s disease since many horses with Cushing’s have concurrent insulin dysregulation. Discussion on the diagnosis of insulin dysregulation is in the following section. Treatment is advocated because of the possibly devastating effects of laminitis and immune suppression. Fortunately, there is a highly effective specific treatment for equine Cushing’s disease called “pergolide.” Pergolide acts like dopamine and works on the pituitary gland to prevent the release of excess hormones from the tumor. It is given as a tablet once daily for the rest of the horse’s life. Most of the time a beneficial response is seen in 4–6 weeks, but sometimes the dose needs to be increased or decreased. Pergolide has virtually no known side effects in horses at appropriate dosing levels; some horses will become mildly inappetant when the medication is first started. The appetite returns in these horses when they are started on a lower dose and it is gradually increased. Often bloodwork is repeated to help monitor response to treatment, and generally the response to treatment is easily seen. The trade name for pergolide is “Prascend®”—while there are compounded versions of pergolide that are less expensive, they are considerably less reliable and effective, so in the long run end up costing more for less effect. Several other drugs (such as cyproheptadine and trilostane) have been used to treat equine Cushing’s disease, but none have been shown to have the efficacy of pergolide. Occasionally one of those drugs is added to pergolide treatment in severe cases that need additional therapeutic help. Many nutritional or herbal supplements are also available (often including magnesium and chromium or chasteberry), and may have variable efficacy; however, none have been proven to be safe and effective. Often these horses also have insulin dysfunction, so treatment for that will be similar to what is described in the next section. The proper treatment of Cushing’s disease with pergolide eventually alleviates many of the signs of insulin dysregulation since the underlying cause is being treated. In addition to daily medication, some feed and management changes should be considered. These horses need regular farrier care, good dental care (immune suppression and older age make them prone to dental problems and secondary sinus infections), routine preventive veterinary care including fecal egg counts, and good quality feed. Some horses may need to be clipped to help prevent hyperthermia. High starch/sugar feeds should be avoided in the horses that have insulin dysregulation to help minimize fluctuations in glucose levels. More about nutrition for horses with insulin dysregulation is written in the following section on metabolic syndrome. Horses with Cushing’s that do not have documented insulin dysregulation but suffer from weight loss will have different dietary needs. Equine Metabolic Syndrome Equine Metabolic Syndrome is defined as chronic insulin dysregulation, obesity or abnormal fat distribution (e.g., a cresty neck; fat pads over the tailhead, eyes, and withers), and increased risk of laminitis in horses that do not have equine Cushing’s disease. This is a relatively newly recognized condition, and there is a lot of ongoing research about this disorder and our understanding of it continues to grow. Horses with this condition tend to be younger than horses with Cushing’s disease. These horses have documented insulin dysregulation and sometimes have increased circulating fat levels. Example of horse with metabolic syndrome. Note the cresty neck and excess fat by the tailhead. The cause of metabolic syndrome is not fully understood, but several theories are being closely considered. First, obesity leads to insulin dysregulation (much like people with Type II diabetes). Second, insulin dysregulation develops secondary to abnormal nutritional usage in genetically predisposed animals. Third, fat cells can be metabolically and hormonally active and alter insulin usage in a peripheral Cushinoid-type syndrome. It is logical to think that horses with metabolic syndrome will perhaps transition into equine Cushing’s disease as they age; however, this has not been proven. There are several ways to test for insulin dysregulation associated with metabolic syndrome (and for horses with Cushing’s disease). The most basic, first-line, test is to measure resting fasting glucose and insulin concentrations first thing in the morning before breakfast. Basically, a normal horse should have low insulin levels when glucose levels are normal. A horse with insulin dysregulation has increased levels of insulin (to try to make up for tissue resistance to it). The second, slightly more sensitive, test for insulin dysregulation involves administering a specific amount of light Karo syrup, then testing the blood a specific amount of time later (approximately 1 hour) to monitor the response. A third, more involved, test is the combined glucose-insulin test (CGIT), which is used when insulin dysregulation is suspected but the first two test results are normal. The CGIT involves placing an intravenous catheter, administering glucose and insulin, and measuring the body’s response to this at multiple time points. There is no one specific treatment available for equine metabolic syndrome regardless of whether it is definitively diagnosed or not. Treatment focuses on the management of the insulin dysregulation, including reducing the horse’s weight, dietary management, and increasing exercise. The most important goal of dietary management is to restrict the amount of soluble carbohydrates (often called “nonstructural carbohydrates”) in the feed, because they alter the insulin levels the most. Grazing should be discussed with your veterinarian and many owners use grazing muzzles or dry lots; however, it is not recommended to lock the horse in a stall. Hay can be analyzed (your vet can direct you to a company that will do this) for its soluble carbohydrate content; it is worth doing this if you purchase large amounts of hay at a time. Some types of grass hay have fairly low soluble carbohydrates, and should be fed at 1.5 to 2% of body weight, as directed by your veterinarian. Oat hay should be avoided. If the horse’s hay intake is tapered down to 1% of its body weight and it is still having difficulty losing weight, soaking the hay is a way to further decrease the soluble carbohydrates. It should be soaked in warm water for 20 minutes, or cold water for 60 minutes, immediately prior to feeding. A vitamin/mineral supplement should be fed, and if additional calories are needed they should be provided by sources high in fat and protein, rather than carbohydrates, such as corn oil or rice bran. Sweet feeds, apples, carrots, and high sugar treats should be minimized or, more often, completely removed from the diet. Most feed companies also make low-carbohydrate feeds specifically designed for horses with insulin dysregulation. Unless a horse is currently dealing with a bout of laminitis, increasing exercise is essential to reducing body fat. Some studies have shown that increased exercise also might help improve tissue insulin sensitivity. If a horse is on a good exercise program with a proper diet and still not losing weight, or is in a current bout of laminitis, thyroid hormone supplementation may be recommended by your veterinarian to improve insulin sensitivity. Many horses with insulin dysregulation used to be incorrectly categorized as “hypothyroid.” Further research has shown that very few horses are actually hypothyroid, however many horses with insulin resistance can have low measurable levels of thyroid hormone. However, their thyroid glands are working fine, and the insulin resistance is the main issue. In spite of this, supplementing with thyroid hormone can help boost the metabolism, improve insulin sensitivity, and get a horse to start losing weight. The thyroid hormone is typically given once daily for a couple of months and then tapered down and discontinued. A drug used to treat insulin resistance in humans, called “metformin,” is also used in horses with severe insulin dysregulation. It is typically given 30 minutes prior to feeding and can only be used for a few weeks at a time. Many other medications taken from the human medical field have also been evaluated and tried though many are cost prohibitive in the majority of cases at this time. Also, just as with equine Cushing’s disease, there are many herbal supplements advocated to treat equine metabolic syndrome. Again, there is little proof of efficacy or safety of these treatments, though anecdotally there are some that are beneficial. If you are concerned that your horse has signs of either metabolic syndrome or equine Cushing’s disease, set up an appointment with your veterinarian for an examination and discussion. It is not always easy to distinguish between these two conditions, and they can often be concurrent. Early recognition is critical to provide your horse with the best care and prevent the potentially devastating disease of laminitis. Ideally, endocrine testing would be part of the annual physical exam in all horses.

By Timothy G. Eastman, DVM, DACVS, MPVM Published in Bay Area Equestrian Network May 2006 The coffin bone is the primary bone within the horse’s foot (Figure 1). The hoof capsule encases this bone like a body in a coffin, hence the name coffin bone. The laminae within the foot are the soft tissue structures that firmly attach the coffin bone to the hoof wall. Laminitis, in its simplest terms, is inflammation of the laminae that attach the coffin bone to the hoof capsule. This inflammation decreases blood flow to the area of the laminar attachments. Local alterations in blood flow may be the result of a variety of systemic illnesses, such as grain overload, colic, retained placenta, etc. Oftentimes this disease is triggered by unknown causes. Whatever the source of the disease, laminitis usually causes crippling pain in horses and is potentially devastating to horse owners. In some instances, the laminar attachments become so compromised that the coffin bone and hoof capsule actually separate from each other (Figure 2). If the normal pull of the deep digital flexor tendon exceeds the strength of the remaining laminar attachments, the bone may rotate downward away from the hoof wall. Veterinarians consider the disease chronic if rotation occurs or if the condition lasts for more than several days. Affected horses often appear as if they are “walking on eggshells”, hold their feet camped out in front, shift weight frequently, and are reluctant to turn. Most treatments for laminitis focus on improving blood flow to the foot, alleviating the pain associated with this condition, halting disease progression, and reestablishing a functional relationship between the coffin bone and hoof wall. Veterinarians often use vaso-dilating agents such as acepromazine, isoxsuprine, pentoxyphyline, and nitroglycerin in hopes of improving blood flow. Phenylbutazone (Bute) commonly relieves pain and decreases inflammation in laminitic horses. A variety of recommended shoeing and trimming techniques attempt to decrease the amount of tension on the coffin bone and redistribute pressure on the hoof’s weight-bearing surfaces. If one shoeing method was consistently successful, it would dominate as the therapy of choice. However, as there are a multitude of ways to shoe a laminitic horse, people need to be open to the experience and expertise of their farrier and veterinarian. There are at least a dozen different shoeing programs that can be successful in horses with laminitis. A healthy relationship between your farrier and veterinarian is never more important. In spite of extensive research, numerous approaches to treating horses with laminitis are sometimes frustrating and unrewarding. A multi-factorial condition, laminitis involves several body systems and prevents a single treatment regimen from becoming universally accepted or effective. Our understanding of this disease is expanding rapidly thanks to the efforts of researchers around the world. A complete overview of laminitis is beyond the scope of this paper but we would like to discuss several recent advances in the management of this disease. Radiographs should always be taken of horses with laminitis. Not only are they useful in establishing the diagnosis, they also help determine the chances of a successful outcome and are very useful in guiding farriers through the therapeutic shoeing. Recently, many practices have coupled their radiographs with computer software to get very accurate representations of the angles of the bones of the feet (Figure 3). These programs are of tremendous value in assisting your farrier to determine how much toe and heel to remove, where the breakover should be, and potentially what type of shoe to apply. Radiographs also help identify whether or not “gas pockets” are present along the toe which could need to be addressed. These gas pockets are generated by necrotic tissue in the foot which oftentimes becomes infected. These are the horses that are frequently managed with a dorsal hoof wall resection which simply removes the dead tissue and prevents infection from becoming established. Special radiographs that use a dye which is injected into the vasculature of the foot called venograms are useful in determining an individual horse’s prognosis and being done by more and more practices. Some specialists feel that if bloodflow to the toe is reduced by approximately 30% or more, the chances of survival are very slim. A venogram is obtained by placing a tourniquet around the ankle (for just a few minutes) and injecting a large volume of dye into a vessel below the tourniquet and quickly taking a radiograph (figure 4). The Christmas Tree like pattern of dye highlights the blood supply. When cases of laminitis do not respond to conventional medical therapy and therapeutic shoeing, another alternative is to have a surgery called a Deep Digital Flexor Tenotomy performed. The surgery involves transecting the deep digital flexor tendon which is the main flexor tendon in the horse. While it sounds severe, this procedure relieves tension at the source of the pain and generally makes horses more comfortable in several days. The tendon ultimately reattaches in approximately 4 months which is frequently ample time for a qualified farrier to drastically improve the health of the foot. With this procedure, farriers can often accomplish improvement in the angles of laminitic horse’s feet that would have otherwise been impossible. This procedure can be done under anesthesia or in the standing patient and is a relatively low cost procedure with minimal risk in these patients. The prognosis for horses with laminitis is very hard to predict. Severity of the radiographs doesn’t always correlate well with the amount of lameness seen clinically. The best way to guarantee the highest level of success is to assemble a team of experts including your farrier, veterinarian, and potentially trainer all communicating well and working towards the same common goal. While we are a long way off from a full understanding of the disease, advances in management of Laminitis are occurring at a steady pace.

By Matt Durham, DVM Published in Bay Area Equestrian Network September 2007 (Also described as: intermittent upward fixation of the patella (IUFP), upward fixation of the patella (UFP), ‘stifled,’ catching stifles, locked stifles, sticky kneecaps…) Horses, as we all know, have many special abilities. Among the less dramatic, but no less important, of these abilities is their ability to sleep standing up. Horses have a complex system called the passive stay apparatus that allows them to do this while using minimal muscular effort. One of the keys to this system is the ability to lock the kneecap (patella) in place, which keeps the stifle extended. Normally, the horse can lock and unlock the patella with no resistance. Horses affected with delayed patellar release (DLP) have an alteration to their hind limb movement that can affect performance. Anatomy Without the passive stay apparatus, the quadriceps muscle would be in constant use. Figure 1 shows the alignment of a normal stifle, which is analogous to the human knee. Figure 1: Skeletal anatomy showing femur (red arrow), patella (black arrow), and Tibia (blue arrow) Imagine standing with your knees bent at this angle and trying to relax, or even rest one leg the way a horse does. We would fatigue very quickly in this position. Humans minimize muscular effort at rest by bringing our knees back so that the thigh and shin are in a straight line. This takes minimal muscular effort to maintain, and allows the downward forces to travel straight through the bony column. Horses have three ligaments connecting the patella to the tibia (shin bone), while humans and most other species have one ligament right in front. The end of the femur (thigh bone) in horses and in humans has a smooth, cartilage covered, pulley-shaped structure at the lower end where the patella glides. This structure is called the trochlea (which means ‘pulley’ in Latin). In horses, the groove and the ridges are fairly pronounced (Figure 2) when compared with other species, which is part of the reason why patellar luxation (where the patella slips out of the trochlear groove to the side) is not common in horses except the miniature horse. The top of the medial trochlear ridge in the horse is very pronounced, giving the patella a place to latch on. Figure 2: Trochlea of femur in horse (left) and dog (right), showing large medial trochlear ridge in horse The medial patellar ligament is connected to the patella with a flexible extension called the parapatellar fibrocartilage. This is the portion that actually ‘locks’ onto the prominent medial trochlear ridge of the femur. (Figure 3) Figure 3: Front view of stifle joint parapatellar fibrocartilage patella medial patellar ligament attachment of biceps femoris medial trochlear ridge lateral patellar ligament middle patellar ligament In the normal situation, the patella is pulled up by the quadriceps and to the side by the biceps femoris muscle, allowing the patella to move instantaneously off of the medial ridge. (Figure 4) In affected horses, there is some degree of hesitation as the patella moves off of the ridge. This can be subtle, to the point where it is difficult to detect. It can be extreme, where the stifle becomes locked and the horse is unable to flex the leg at all. Far more commonly, the condition is somewhere in between, where there is some degree of notable hesitation. Affected horses show signs more significantly at the start of exercise, and in milder cases may move completely normally once warmed up. Common signs include stumbling in the hind end (which can lead to stumbling in the front end and occasionally falling). This feels as though one of the rear ‘corners’ drops out from under the rider. Horses may have difficulty cantering in one or both leads, and often have very awkward canter-trot and canter-walk transitions. Horses may become hesitant performing jobs that they had previously performed with ease. Figure 4: Muscles of stifle, showing upward pull from quadriceps (blue arrow), and sideways pull of biceps femoris (red arrows) This gait abnormality is caused by a mechanical abnormality with varying degrees of pain. In contrast, the gait abnormalities seen with bone spavin or ringbone are primarily caused by pain. Horses with only a mechanical component will not respond to anti-inflammatories, and do not ‘block out’ with nerve blocks or joint blocks. If a horse does have a pain component, it is important to determine whether the stifle is the entire source of pain, a partial contributor, or non-painful. The Chicken or the Egg Horses with delayed patellar release often have lameness originating from the hind limb. Delayed patellar release itself can lead to lameness in the stifle: the increased friction of the patella against the trochlea of the femur can cause joint inflammation, and the patellar ligaments are sometimes strained. The joint inflammation can be treated, but unless the delayed patellar release is resolved, the lameness component will continue to resurface as a problem. It is also common to have a lameness problem somewhere else in the limb, such as the hocks, which can be a contributing factor in the development of delayed patellar release. Because there can be a mixture of factors occurring at the same time, it can sometimes be difficult to determine which is the ‘chicken’ and which is the ‘egg.’ In these cases, treatment directed at several areas may be necessary to resolve the issues. Causes Upright conformation (Figure 5) through the stifle is an important risk factor. This causes the patella to sit higher above the trochlea, and for the prominent medial trochlear ridge to be directed somewhat more forward instead of mainly upward. Overlong patellar ligaments have also been blamed, with the possibility of strain and repeated stretching as a potential risk factor. Decreased muscle tone in the quadriceps muscles is known to be a factor. The other muscle that is important for patellar function is the biceps femoris, which helps to pull the patella to the side, releasing it from the trochlea. Lack of fitness is often blamed as the cause. While unfit horses are definitely at risk, it is also not uncommon to see very fit horses affected. However, these fit horses often have what could be considered a hidden fitness issue: decreased or altered range of motion in the hind limb. Horses with an altered range of motion probably do not develop normal coordinated movement in the quadriceps and biceps femoris muscles. Contributing Factors Lack of fitness: This includes rapidly growing horses that have not developed the muscling and coordination to fit their bodies yet. Retired and other sedentary horses comprise another group at risk. Horses in lay-up for an injury will sometimes develop delayed patellar release as they are starting back into work. The common thread is decreased muscle tone. Concurrent lameness: Horses with lameness issues, particularly originating in the hind end and/or back, may develop delayed patellar release. Horses with sore hocks, for example, often have an altered range of motion, sparing their hind ends. This limited effort from the hind end probably causes deconditioning in the quadriceps and biceps femoris muscles. Neurologic disease: Wobblers and horses with other causes of neurologic disease can be affected. Neurologic disease can contribute directly and indirectly to delayed patellar release. If the nerve supply to the quadriceps or biceps femoris is affected, there is a direct effect on patellar release. Neurologic horses often lose overall muscle tone and coordination as well.Training factors- Fatigue is thought to contribute to delayed patellar release, particularly in young horses. Horses that use the hind end heavily, such as in cutting and dressage, particularly if in heavy training, may become fatigued. Fatigue may lead to uncoordinated movement. These are the classic horses that do not fall into the ‘unfit’ category. Some believe that these horses may be affected because of stretching of the patellar ligaments. Horses with jobs that limit motion may also be affected. Western pleasure horses are often trained without doing any significant extended trot. This limited range of motion can contribute to delayed patellar release. Keeping the horse in an ‘inverted’ or ‘hollowed out’ position during exercise are also thought to lead to poor patellar function. Mechanical factors: Hind foot balance is an often-overlooked factor. Horses with a long toe/ low heel conformation in the hind feet have an altered footflight: stride length does not tend to be affected, but the forward part of the stride is exaggerated and the back part of the stride is limited. These horses tend to overreach or forge, and tend to stumble. This alteration of range of motion probably changes the development in the quadriceps and biceps femoris muscles. Horses with this conformation often have a bullnosed appearance to the foot. When viewing the horse from the side, imagine a line following the coronary band of the hind foot up to the front leg of the horse. This line should hit around the chestnut of the front limb. In affected horses, this line will hit closer to the elbow or even back to the girth area. Some horses, when standing squarely on hard footing may be seen to have their heels slightly off of the ground. Some horses appear to have normal foot conformation when viewed from the side. Figure 6: X-ray image of the hind foot in a horse with delayed patellar release, showing very low heels, a bullnosed appearance to the front of the foot, lack of contact in the heels, and negative P3 angle. X-rays of the hind foot (fFigure 6) can define the angulation of the coffin bone most precisely, and can be used to measure sole depth. Often, this can be corrected through trimming alone. At times, if sole depth at the toe is minimal, wedges can be used. OCD: Osteochondrosis in the stifle can affect the gliding surface of the patella. Osteochondrosis dissecans (OCD) is a condition where the cartilage and underlying bone on the surface of certain joints develops abnormally. The trochlear ridges of the femur and sometimes the patella itself can be affected in the stifle. Diagnosis In severely affected horses, diagnosis is obvious: the hind leg gets completely stuck in extension. Far more commonly, the patella is not completely locked, but hesitates in release, causing a gait abnormality that varies from barely perceptible to relatively obvious. While observing the horse at rest, rocking the hind end from side to side causes the stifle to engage and disengage. Affected horses have a snapping movement to the patella that can be seen, felt, and occasionally even heard as a ‘clunk’ as it snaps back into place. While watching the horse in movement, affected horses tend to have a mechanical movement in the hind end at the walk. Some will drag the hind toes. Some affected horses move well at the trot, although there is sometimes an exaggerated snapping movement that can be seen along the Achilles’ tendon at the attachment to the hock. Some affected horses may prefer the trot to the canter. The canter may be affected in one or both leads, and may appear awkward or mechanical. Canter-trot and canter-walk transitions are often very awkward in affected horses. Because delayed patellar release is primarily a mechanical issue, nerve blocks and joint blocks typically do not change the patellar function. However, lameness is often present, so it is important to determine the source(s) of lameness, whether the lameness is a cause or a result of delayed patellar release. X-rays of the stifle are helpful to rule out OCD and other bony abnormalities in the stifle. Radiographs of the hind feet are also useful to measure angles if low heels are a potential contributing factor. Ultrasound can be useful in evaluating the patellar ligaments and other soft tissue structures of the stifle, including subtle OCD lesions not visible on x-rays. Treatment Conditioning: In some horses, resolution of delayed patellar release can be as simple as improving fitness level. This is often effective in horses that are obviously out of shape. Conditioning exercises are important for all affected horses, but exercise alone may be inadequate to resolve the issue in many horses. Helpful exercises include extended trot, trotting up hills, trotting over poles, and (with the right horse and a Western saddle) dragging objects such as hay bales or railroad ties. Resolution of underlying issues: When possible, underlying lameness issues should be resolved. Similarly, horses with neurologic disease will typically improve if the neurologic disease is treatable. Horses with low heel angles should have their balance corrected. Hormone injections: A series of injections of estrone sulfate (similar to estrogen) can be used to treat the condition. Estrogen causes relaxation of ligaments. One theory is that these injections relax some of the pelvic ligaments, altering the angulation of the pelvis and stifle. Another theory is that the patellar ligaments themselves relax. In some horses, this can be a very effective treatment. Disadvantages include the need for repeated injections and hormonal behavioral changes, particularly in mares. Internal blistering: Injections of Iodine in oil in the medial patellar ligament or the medial and middle patellar ligaments can be an effective treatment. Medial patellar ligament transection: In this procedure, the medial patellar ligament is cut all the way through. This procedure has fallen from favor with most veterinarians because of the potential for development of arthritis in the joint and/or fragmentation in the patella due to rotation of the patella relative to the trochlea. This is the treatment of last resort for most veterinarians, reserved for those rare severely affected horses that become completely locked and do not resolve with other treatments. Medial patellar ligament splitting: In this newer procedure, instead of cutting through the ligament, multiple very small incisions are made into the ligament parallel to the fibers. This procedure is considered much safer for the joint than complete transection. This procedure was initially only done under general anesthesia, but some veterinarians prefer to perform the procedure with the horse standing under sedation. Joint therapy: Because many horses develop inflammatory joint disease from the increased friction in the joint, treatment for joint disease can be helpful. As with other joint issues, there are many levels of treatment. Because the inflammation is often not arising from the cartilage, but with the tissue that produces the joint fluid, IV hyaluronic acid (Legend®) can be effective, particularly in mildly affected horses. Joint fluid in an inflamed joint becomes watery, and is a less effective lubricant. Horses with lameness originating from the stifle may benefit from injections into the joint itself. The use of nutraceuticals may also be of some benefit. One Clinic’s Approach to Treatment At our clinic, the typical approach to treatment for a horse with delayed patellar release is to define as many risk factors as possible, including underlying lameness, neurologic, or shoeing issues, and attempt to remedy these. Depending on the severity, some horses may do well with conditioning exercises once the underlying issues are resolved. Horses affected more significantly will be started on intravenous Legend® and sometimes intramuscular Adequan®. Horses with stifle lameness may also receive stifle injections. We have moved away from hormone therapy and iodine injections, in favor of the patellar ligament splitting procedure, which we feel is very safe and very effective. We prefer to perform the procedure with the horse standing. Arthroscopic surgery is typically recommended for horses with OCD lesions. Conclusion Although delayed patellar release is a relatively common cause of decreased performance in horses, most cases can be treated effectively, allowing horses to return to full performance. Image sources: Figures 1, 2 (left), 3, & 4: Sisson and Grossman’s Anatomy of the Domestic Animals Figure 2 (right): Michigan State University School of Veterinary Medicine Figures 5 & 6: Steinbeck Country Equine Clinic

By Nora Grenager, VMD Published in Bay Area Equestrian Network September 2006 Strangles is a highly contagious respiratory disease of horses caused by the bacteria Streptococcus equi subspecies equi. The disease was initially given this name because it can cause abscesses of the lymph nodes in the throatlatch region, which if severely enlarged can compress the airway and suffocate the horse. If strangles is suspected on a farm, all horses at that location should be divided into three groups: infected horses with clinical signs, horses that have no clinical signs but may have been exposed to the bacteria or to a sick horse, and horses without clinical signs who have not been exposed. Rectal temperature should be taken daily of all horses on the property (or at least those that have been exposed). Transmission can be direct (horse-to-horse nose contact) or indirect (shared housing, shared water or feed containers, shared equipment, and people). Infected horses typically get a fever 3- 14 days after exposure to the bacteria. This is followed by a large amount of mucopurulent (yellow-white snot) nasal discharge and painful swelling of the submandibular and retropharyngeal lymph nodes. Affected horses may be depressed, lethargic, have a sore throat, and be reluctant to eat. The lymph nodes will enlarge and eventually rupture, draining creamy yellow-white pus. Horses typically feel better once the lymph nodes have ruptured. Culture of nasal swabs or abscess material is the best way to diagnose strangles. Cultures are diagnostic approximately 70% of the time. Another test called the polymerase chain reaction (PCR) is rapid and very sensitive at detecting bacteria, but cannot distinguish between live and dead bacteria. Serology (blood samples to detect the horse’s antibody levels to the bacteria) can be helpful but often necessitates two samples taken two weeks apart to confirm current infection. Multiple horses on a property with the typical clinical signs is also Abscessed submandibular lymph nodes Nasal discharge in horse with strangles suggestive of a strangles outbreak and should be treated as such. If Strangles is suspected on a farm, all horses at that location should be divided into three groups: infected horses with clinical signs, horses that have no clinical signs but may have been exposed to the bacteria or to a sick horse, and horses without clinical signs who have not been exposed. Rectal temperature should be taken daily of all horses on the property (or at least those that have been exposed). Horses that have clinical signs of enlarged lymph nodes should generally be treated with supportive care aimed at enhancing lymph node abscess maturation and drainage. Antibiotics are not typically recommended because they just delay, not prevent, the abscess maturation. It is best to use a hot pack or topical drawing agent to promote maturation of the abscess until it opens and drains on its own. Sometimes if the abscess is mature (has a soft center), drainage can be surgically performed by a veterinarian. Once the abscess is open, it should be flushed once or twice daily with a dilute antiseptic solution until there is no more drainage. Horses may be given anti-inflammtory medications such as Banamine or bute to help reduce fever and any pain. Horses without clinical signs that develop a fever (if their temperature has been monitored daily) may be given antibiotics for 5-10 days (veterinarian-dependent) to prevent lymph node abscessation. They can also be treated with anti-inflammatories like the horses in the previous group. These horses will remain susceptible to reinfection after the antibiotic therapy is discontinued. If strangles is suspected or diagnosed on a farm, a plan should immediately be implemented to prevent spread of infection. Every situation is unique and requires the veterinarian and barn manager/owners to develop the best quarantine and treatment plan for that location. Movement of all horses on and off the property should be stopped. Horses should be segregated according to the three previously mentioned categories (sick, exposed but not sick, not exposed and not sick) with no mixing of equipment (especially water troughs) or people between the three groups. All horses should have their rectal temperatures taken once daily to identify any new infections as early as possible. Ideally recovering horses should have 3 negative cultures or PCR samples prior to being considered noninfectious but this is often not economically practical. It is not entirely clear how long the bacteria can live in the environment, but most veterinarians recommend quarantining infected pastures or stalls for 4 weeks. Equipment can be cleaned with a dilute bleach (1:10) solution. Up to 10% of horses can become carriers of strangles and shed infectious organisms, even without clinical signs. Most often these horses are harboring the Strep. equi bacteria in their guttural pouches. This infection can be a result of a retropharyngeal lymph node abscessation into the guttural pouch. It is easiest to diagnose a guttural pouch infection by endoscopically visualizing the guttural pouches. Your veterinarian may be able to perform endoscopy at the farm, but often it will need to be done at a referral facility. It is also possible to lavage the guttural pouch and collect the fluid for culture or PCR. This is a useful way to monitor a horse with a diagnosed guttural pouch infection. Preventing strangles is obviously preferable to dealing with an outbreak but it can be difficult. When possible, a horse being brought to a new location should be isolated Culturette for 3 weeks to evaluate for any clinical signs. This is sometimes not feasible given that horses often mingle with other horses at events. Horses that have had the disease usually develop a good natural immunity for up to 5 years. Vaccination and good biosecurity are ways to prevent outbreaks. Two basic types of vaccine exist; both require a booster at 2-4 weeks, and both should be given once a year. There are an intramuscular vaccine and an intranasal vaccine. The intranasal vaccine is generally associated with better immunity and less adverse side effects. It is best to talk with your veterinarian about whether your horse should be vaccinated, and with which vaccine. As with most diseases, vaccination decreases the severity and duration of clinical signs, but does not completely prevent the disease. Vaccine reactions are rare but include purpura hemorrhagica and guttural pouch empyema (discussed later). Some horses may get a mild strain of the disease with fever and lethargy following vaccination. The vaccine manufacturers recommend not vaccinating horses in the face of an outbreak unless there has been no possible exposure. This, however, should be tailored to each specific situation. Most horses that get strangles need rest and supportive therapy but recover from the disease without complication. However up to 20% of horses can have complications such as guttural pouch empyema (infection), “bastard strangles,” or purpura hemorrhagica. Guttural pouch empyema can be treated with an indwelling catheter lavage system, guttural pouch antibiotics, and systemic antibiotics. Occasionally the pus can become dried out and form little concretions called “chondroids,” which may need to be removed surgically. Horses should be quarantined while being treated for guttural pouch empyema. The only way to definitively prove that the infection is cleared is three negative guttural pouch cultures at weekly intervals. Bastard strangles is when an abscess forms in a lymph node at a distant site such as the lung, abdomen, liver, spleen, kidneys, or brain. These infections have varying clinical signs depending on the location, and can be difficult to diagnose. There is a blood test (for “SeM-specific antibody titer”) that can be useful. These infections are hard to treat and require long-term antibiotics and sometimes even surgery. Normal guttural pouch Guttural pouch with chondroids and indwelling catheter. Purpura hemorrhagica is an immune-mediated vasculitis, which means the horse’s blood vessels are compromised by immune complexes secondary to the bacteria. The compromised blood vessels lead to edema (swelling of the limbs and belly), petechiation of the mucous membranes (spotty gums), and fever all of variable severity. This is uncommon but can be a very serious complication requiring intensive treatment with a guarded prognosis. Strangles is considered one of the three most significant respiratory diseases of horses. Because it is so highly contagious, and horses are a very mobile population, achieving prevention and control can be difficult. It is important to be aware of the typical clinical signs and discuss vaccination of horses at risk with your veterinarian.

By Nora Grenager, VMD Published in Bay Area Equestrian Network May 2009 Nasal discharge can vary in significance, from being innocuous to being indicative of a serious problem. It is important to have an understanding about which types of nasal discharge signify a problem worthy of an immediate call to your veterinarian, and how best to describe the discharge to your veterinarian. It is essential to note that if your horse is having difficulty breathing, making any noise while breathing, has feed material coming from the nose, or is very ill, you need to call your veterinarian immediately. The respiratory tract can be divided into upper and lower parts; upper includes the nasal passages, paranasal sinuses, guttural pouches (air-filled outpouchings of the Eustachian tubes unique to horses), pharynx (area where the entrance to trachea and esophagus meet at the larynx (voice box) at the back of the nasal passage and mouth), and upper trachea. The lower respiratory tract includes the lower trachea and lungs. There are many different types of nasal discharge. Defining some of the characteristics can help you better describe it to your veterinarian, who will use this information, along with the exam, to discern the cause. Discharge can be serous (clear, watery), mucoid (yellow and mucous-like), purulent (green-yellow, thick, looks like pus), sanguineous (bloody), or contain feed material and saliva. Nasal discharge can be unilateral (only ever from one nostril) or bilateral (has come from both nostrils at some point in time), which helps identify the source of the discharge. Discharge that is unilateral typically comes from the nasal passage, the sinus, or occasionally the guttural pouch. Discharge that is bilateral can arise from the guttural pouches, the pharynx, or the lower respiratory tract (trachea and lungs). Discharge can be constant or intermittent or only associated with certain activities like eating or exercise. Discharge can be acute in onset (within hours to a couple days) or chronic (lasting more than 2-3 days). Nasal discharge may be the only clinical sign (symptom) or there may be other clinical signs such as ocular discharge, enlarged lymph nodes (which is nonspecific and present with many types of nasal discharge), fever, cough, facial deformity, abnormal noise when breathing or exercising, exercise intolerance or poor performance, poor appetite, difficulty eating, lethargy, or weight loss. Sometimes nasal discharge can have a foul odor, which can be specific to certain types of bacterial infections, tissue damage, or sinus infections secondary to tooth root infections. There are other historical factors that are important in helping diagnose a cause of nasal discharge. Does only one horse have clinical signs and nasal discharge or do many horses at the stable have clinical signs? Has the horse recently been to a show or clinic or been exposed to new horses in the barn? Have there been any recent management changes, travel, or other illnesses? When and for what has the horse been vaccinated? How old is the horse? A typical workup for nasal discharge will include a complete history and physical examination, and may include a rebreathing lung examination, blood work, nasal swab evaluation, upper airway endoscopy, skull radiographs (x-rays), thoracic ultrasound or radiographs, and possibly sampling of the guttural pouch or airway for laboratory evaluation. The physical examination will probably include taking the rectal temperature, heart rate, evaluation for facial swelling, symmetry of the airflow from the nostrils, breathing depth and rate, palpation of lymph nodes, and possibly sinus percussion. Since we cannot ask your horse to take a deep breath to hear the lungs better, a rebreathing exam involves briefly placing a bag over the horse’s nose to encourage deeper breathing so lung sounds can be heard better. Blood work would be useful to identify infection, inflammation, or other systemic disease. A nasal swab can be evaluated at the laboratory for some of the more common viruses and bacteria that cause upper respiratory tract infections. Endoscopy of the upper airway is when a small camera is passed into the upper airway to evaluate the nasal passages, pharynx, guttural pouches, and entrances to the sinuses. This is useful to visualize where the discharge is coming from, to see masses in the nasal passages, to look in the guttural pouches, to evaluate the larynx, and even to look down into the trachea. Radiographs of the skull would be used to evaluate for disorders of the sinuses or nasal passages not identified with endoscopy. Radiographs can often be done in the field, and endoscopy can be done in the field or at a veterinary hospital, depending on your veterinarian’s setup. Oral examination may be performed if a tooth root infection is suspected. Thoracic ultrasound can be performed in the field or at a veterinary hospital (a more complete exam can be done in the hospital with a larger ultrasound) and is useful for evaluating the lungs when lower respiratory tract disease (such as pneumonia) is suspected. Airway sampling can be Thoracic Ultrasound performed in a variety of ways – through the endoscope, through a small hole in the trachea, or directly through the chest wall in cases of pneumonia; this is done to evaluate the type of cells present, and sometimes to culture if there is an infection. Serous (clear or watery) to mucoserous (mixed mucoid and serous) nasal discharge can be benign due to wind or dust irritation, can be due to allergies, can be indicative of an upper respiratory tract viral infection, or can be the early stages of a more serious infection. Wind or dust can cause mild upper airway irritation and serous nasal discharge that is usually mild, bilateral, intermittent, and not associated with any clinical signs of systemic disease. Allergic upper airway disease can have serous nasal and ocular (from the eyes) discharge that is mild, bilateral, intermittent, and not associated with any clinical signs of systemic disease, and is more common in young performance horses. Both could have an intermittent dry cough. Horses that have “heaves,” or recurrent airway obstruction, which is similar to asthma in people, can have mucoid nasal discharge, cough, increased respiratory rate, or other signs of lower airway disease. This is typically a more chronic condition, and is more common in older horses. Horses with viral infections of the upper respiratory tract typically have a high fever, are depressed, inappetent, and may have other systemic signs of disease. The most common upper respiratory tract viruses are equine influenza virus, equine herpes virus, and equine arteritis virus. Purulent or mucopurulent (mixed mucoid and purulent) nasal discharge occurs when there is a bacterial infection in the respiratory tract. Unilateral purulent nasal discharge is most common with a sinus infection, guttural pouch empyema (bacterial infection), or infected nasal passage mass. Bilateral purulent nasal discharge can also be due to guttural pouch empyema, strangles (an upper respiratory tract infection caused by Streptococcus equi subspecies equi), or lower respiratory tract disease such as pneumonia. Sinus infections are most often secondary to a tooth root infection because the cheek teeth in horses protrude into the paranasal sinuses; this is particularly common in older horses. Sinus infections can also be primary (no underlying cause), or secondary to a sinus cyst (benign mass), progressive ethmoid hematoma in the sinus (benign mass), or neoplasia. Guttural pouch empyema most often occurs weeks to months after a strangles infection, but can occur without any previously noted clinical signs of upper respiratory tract infection. Masses in the nasal passage can be benign (cysts or progressive ethmoid hematomas or foreign bodies) or malignant (neoplasia such as adenocarcinoma). Sinus cysts are benign fluid-filled masses that can get very large and even cause deformation of the facial bones (so the face looks swollen on one side). Progressive ethmoid hematomas are benign blood-filled masses that most often cause an intermittent bloody unilateral nasal discharge, but can get secondarily infected and cause mixed bloody-mucopurulent unilateral intermittent nasal discharge. Foreign bodies, other types of masses (such as fungi), or neoplasia in the nasal passages or sinuses are not very common, but could also cause unilateral mucopurulent nasal discharge if secondarily infected. Strangles is an upper respiratory tract infection that causes fever, bilateral mucopurulent nasal discharge, enlarged lymph nodes, and is most common in younger horses. Pneumonia, or infection of the lungs, typically causes fever, increased respiratory rate, cough, lethargy, inappetence, and can have bilateral mucopurulent nasal discharge. Horses with pneumonia are quite ill and generally require extensive treatment. Unilateral bloody nasal discharge can occur with progressive ethmoid hematoma, nasal foreign body, or occasionally with fungal infection of the guttural pouch or exercise induced pulmonary hemorrhage (EIPH) (the latter two can cause bilateral discharge also). Bilateral bloody nasal discharge can occur with fungal infection of the guttural pouch, EIPH, blood clotting abnormalities, or occasionally with severe pneumonia. Fungi can grow on the arteries that course through the guttural pouch and these fungi can eat through the arteries and cause potentially fatal bleeding. Typically there is initially a small amount of bloody nasal discharge, followed by possibly fatal severe bleeding episode. EIPH is a condition that most often happens in performance horses that work at high speeds; a small amount of blood can be seen coming from the nostrils after intense exercise. In EIPH the small blood vessels in the lungs, called capillaries, burst under the pressure of high-intensity exercise and cause mild bleeding. Horses with bilateral bloody nasal discharge can have abnormalities of blood clotting secondary to eating a toxin, to systemic disease, to infection, or can rarely be born with a bleeding abnormality. Horses with severe pneumonia can occasionally have blood-tinged mucopurulent nasal discharge if the infection damages blood vessels in the lungs. Feed or saliva coming from the nose is indicative of acute esophageal obstruction (known as “choke”), swallowing disorders, or uncommonly with congenital abnormalities of the upper airway. Acute obstruction of the esophagus can happen in horses that eat too fast, have poor teeth, or for a variety of other conditions that prevent the esophagus from functioning normally. Horses with acute esophageal obstruction are stressed, can be seen to gag or cough, and often have feed or saliva coming from the nose and mouth. This is an emergency situation that requires immediate removal of food from the horse’s surroundings and a phone call to your veterinarian. Laryngeal or upper airway or esophageal dysfunction can also cause feed and saliva to come from the nose. Swallowing is a complex reflex that involves many nerves and muscles to work in coordination. Discussion of the numerous disorders that can cause dysfunction of swallowing and abnormal nasal discharge secondary to that is beyond the scope of this article. This is again an emergency situation because horses can get severe pneumonia if any feed goes down the trachea instead of the esophagus. Depending on the history and physical examination findings, your veterinarian will decide on what, if any, further diagnostic procedures need to be performed. Treatment will vary depending on the suspected cause. Hopefully this brief discussion on nasal discharge will help you be better prepared to talk about your horse’s nasal discharge with your veterinarian.

By Nora Grenager, VMD Published in Bay Area Equestrian Network April 2007 Biosecurity is the undertaking of management practices that can reduce the risk of outbreaks and minimize the spread of infectious disease. Until fairly recently this word was not often associated with the horse industry even though many horse operations maintain some general biosecurity practices. However, recent infectious disease outbreaks (such as neurologic herpes virus and diarrhea caused by Salmonella) have brought to light the necessity for applying biosecurity practices, to some extent, at all horse facilities. There are many aspects of the horse industry that make implementation of biosecurity practices potentially challenging. The horse population is increasingly mobile – horses travel to shows, clinics, go on trail rides, and even travel abroad. Many facilities have a transient resident population. There is also a lot of human traffic associated with horse facilities and events, and this is obviously an integral part of the industry. With an awareness of the importance of biosecurity, and a degree of conscientious planning, practical measures can be put in place that will benefit everyone in the long run. There are numerous benefits of having a good biosecurity protocol at both an individual horse and facility-wide level. The most obvious benefit is the decrease in the risk of illness or death of a horse from infectious disease. This extends to include prevention of a stable-wide outbreak of infectious disease. Infectious disease has not only the potential to cause suffering, but it can be devastating emotionally and very expensive in terms of veterinary costs, loss of time in training, and even loss of event entrance fees. Decreasing the risk of an infectious disease is, therefore, valuable on many levels. The most frequently implicated modes of infectious disease transmission are horse-to-horse contact, human and equipment contact, and wildlife and pests. Infectious diseases of concern affect a variety of different body systems and therefore have a wide range of clinical signs (symptoms). Special consideration should be given to the different categories of horses: pregnant mares, weanlings, yearlings, horses in training, geriatric horses, breeding stallions. Some diseases should be reported to the state veterinarian for tracking purposes, and some must be reported by law. There are a few infectious diseases that can be zoonotic, or transmitted from animals to humans. Part of the Routine It should become a habit to follow basic biosecurity measures as a part of your daily horse routine. Hand-washing is under-utilized as an indispensable way to control the spread of infectious disease. Wash your hands before and after working with each horse. Do not share equipment if possible – if necessary, clean and disinfect thoroughly between uses. Monitor and know your horse’s appetite, attitude, and manure production. Consult with your veterinarian if you have any concerns, as catching an illness early is pivotal in minimizing duration of illness and limiting the exposure of other horses. Maintain clean feed and water sources. Store feed in closed bins to prevent fecal contamination from other animals. Clean stalls as frequently as possible and dispose of manure promptly and properly. This not only limits the fecal-oral route of transmission but also decreases insect populations. Incorporate insect prevention into the daily routine; for example – frequent manure removal, feed-through insecticides, fly larvae predators, topical insecticides, good deworming programs, removal of any standing water. Traveling Try to prevent nose-to-nose contact with unknown horses at events. Do not share equipment such as water or feed buckets, brushes, tack. Clean and disinfect your equipment and trailer prior to returning home. Ideally every horse should be isolated for 2 weeks after traveling to an event to prevent the spread of any infectious diseases to which the horse was possibly exposed at the event. If even one horse on the property travels, all the horses in contact with that horse should be up-to-date on vaccines. Consult with your veterinarian as to which vaccines your horse needs, as it can vary with geographic location, activity level, and age of horse. New Horses Every new horse on the property should be isolated for 30 days. During this time, any evidence of illness (such as nasal discharge, cough, enlarged lymph nodes, inappetance, diarrhea) warrants consultation with your veterinarian. Ideally the rectal temperature should be obtained once daily because often an increased rectal temperature (greater than 101.5 o Fahrenheit) is the first detectable sign of illness. New horses should meet the vaccination and deworming recommendations or requirements of the facility. This may include having a negative Coggins test, or a recent health certificate. Sick Horses It is important to have a plan on how to isolate sick horses that can be easily put into effect. The stress of having a sick horse does not need to be added to by inadequate planning. Length of isolation time will vary with type of illness. Isolation As previously discussed, new horses, sick horses, and horses returning from traveling should all be isolated. “Restricted Access” signs should be posted at the clearly demarcated perimeter of the isolation area. Ideally, isolation stalls should be completely separate from the remainder of the horses, as some infectious diseases can be aerosolized and travel up to 50 meters. Quarantined horses should be worked with after all the other horses on the property. Alternatively, or additionally, separate clothing and shoes should be worn when working with quarantined horses, or coveralls/disposable gowns and disposable booties should be worn. Hands should be washed before and after, and disposable gloves must be worn. All of these items can be kept in a plastic tub with a lid near the stall. A separate trash bag should be placed stall-side. Equipment should not be shared; the specified isolation equipment can be marked with colored tape to prevent confusion. If equipment must be shared it should be used last in the day and thoroughly cleaned and disinfected afterwards. A foot dip tub containing disinfectant at the entrance to the isolation facility is an excellent way to minimize foot traffic contamination. This tub can contain any one of a number of disinfectant types. Disinfection Recommendations Hands should be washed for a minimum of 15 seconds with a pump-dispensed liquid soap. Alternatively, hands that are not visibly dirty can be cleaned with an alcohol-based (at least 62% ethyl alcohol) gel or foam disinfectant and allowed to dry. Equipment and non-porous surfaces (metal, varnished wood, concrete, stall mats, etc.) should be thoroughly cleaned with a detergent (such as Tide  ) and water (allow detergent to sit for 5-10 minutes), rinsed, then disinfected, followed by a final rinse. Equipment that cannot be effectively disinfected should not be shared between horses. Cloth items can be laundered and dried completely. Disinfectant can be purchased at a veterinary or farm supply store. There are many types of disinfectants on the market. Choose one with which you are comfortable working, and that has documented efficacy in the presence of 10% organic matter. Diluted bleach (typically 2oz:1gallon of bleach:water but check the bottle as there are different concentrations available) is often used. It is very important to thoroughly clean with a detergent to remove organic debris (visible dirt and grime) otherwise disinfects are rendered ineffective. Be familiar with the proper safety precautions for the disinfectant you use and wear proper safety gear. Manure and bedding from isolated horses should not be spread onto pastures or put into open air piles/pits. All infectious agents, not just organisms shed in the manure, can be spread via used bedding. Conclusion Formulating an effective and straightforward biosecurity protocol for your horse and facility is essential in this day and age of mobile horse and human populations. Routine daily biosecurity measures as well as isolation protocols for horses that are new, sick, or returning from travel is imperative. Infectious disease can cause loss of productive time, financial losses, and even loss of life. While the task of implementing a biosecurity protocol may seem daunting, the risks of not having one in place are even more so. Think about your situation and consult with your barn manager and veterinarian as to what will best suit your situation. Time spent now will minimize problems in the future.