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By Amanda Hedges, DVM, cVA, CVSMT, published in the San Mateo County Horsemen’s Association (SMCHA) Newsletter, Q1 2021 An Immune System Gone Awry Molecules that irritate our horse’s bodies are all around. One of the jobs of the immune system is to protect us from the harmful effects of these irritants, maintaining the balance between stimulus and an appropriate response that keeps a horse healthy. Equine allergies can occur when an irritant or combination of irritants disrupts or overwhelms the immune system’s balance. An allergic reaction may be severe and life-threatening (anaphylaxis), sudden (acute), or more slow/insidious in onset (chronic). Signs of an Allergic Reaction Signs of allergies often appear as an immune system overreaction, resulting in local or systemic inflammation. We see hives, itching, oozing, scabs, hair loss, tearing, coughing, breathing changes, nasal discharge, hair loss, poor performance, and even gastrointestinal upset. Anaphylaxis is a severe acute allergic reaction characterized by increased respiratory effort, rate, or noise, recumbency, and/or shock. Anaphylaxis is a medical emergency necessitating immediate veterinary intervention. Sometimes an allergic episode (e.g., hives) is a one-off and other times a horse has developed allergies to something in his/her environment. Restoring Balance To restore balance to the immune system in non-life threatening cases, we need a two-fold approach: 1) decrease the irritants 2) calm down the immune system. Let’s look at some common equine allergens and what we can do about them. Common Allergens Changes in the environment and the horse’s immune system can make it difficult to identify the cause of a horse’s allergic response. Some common equine allergens include: Insects: The most common culprit of chronic skin allergies is the saliva of the Culicoides fly (a.k.a. gnats, no-see-’ums). Other fly species, other insects, and even arachnids (spiders) can cause an allergic response. Environmental: Components of dust, different molds and mildews, different plants and pollens, and even some topical products can all cause allergies. Note that food allergies are not common or well-understood; it is more common for a horse to be allergic to the components of dust on hay than the hay itself. Treatment Strategies for Equine Allergies Treatment strategies focus on minimizing the presence of the allergen and influencing the immune system to restore balance. Common treatments include: Environmental management: if you know what your horse is allergic to from an allergy testing profile (see “Desensitization Injections” below), then you can minimize his/her exposure to specific irritants. General recommendations to decrease irritants revolve around fly control and dust control, both of which will add fuel to the fire of an overactive immune system. Fly control: Remove manure from the living area at least once daily. Make sure that your horse is stabled far from the manure collection area. Consider feed-through fly products, fly traps, automatic fly spray systems that use permethrin, overhead fans, fly sheets including belly coverage, fly masks including ears, fly boots, natural predators (bats, birds, wasps), and other fly control strategies. Dust: Consider wetting down your horse’s hay at each feeding. Stable your horse away from dusty arenas, and avoid riding during times of peak arena use. Good ventilation is also good. Diet change: While food allergies are not common, it is even more challenging to diagnose allergies due to dusts, molds, and contaminants in hay. A trial diet can help assess the contribution of diet to an allergy response. A novel food source, for example timothy pellets, is fed for 3 months, and the horse’s allergy signs are monitored. If allergy signs improve, then a food allergy is suspected. Other feeds can then be added to further identify the allergen. Often wetting down the feed is helpful to minimize the amount of inhaled aerosolized allergens. Medications: Steroids: Short- or long-acting steroids may be used to help suppress the immune system. Steroids can have some unwanted side effects, so use the lowest dose needed for the shortest amount of time. Combine with environmental management, antihistamine, and omega3 fatty acid supplementation for better effects. Antihistamines: A key molecule in the allergic response is histamine. Oral antihistamines, such as hydroxyzine, cetirizine, or diphenhydramine, can suppress the histamine response. Unlike steroids, these drugs are safer for long-term use though they can make some horses a bit sleepy. Your vet can advise on which drug may be the best for your horse, and the ideal duration of treatment. In horses these medications are better at preventing an allergic reaction than at treating a current one. Supplements: Some supplement ingredients can help support the body’s immune system. In addition to good quality hay or pellets and a vitamin/mineral supplement, horses with allergies may benefit from: Omega3 fatty acids: Research supports that horses fed a high dose of omega-3 fatty acids may have a decrease in allergy signs, possibly by decreasing the inflammatory response. This should be used long term as effects are not immediate. Equine-specific research is poor or lacking for other compounds reported to help with allergic reactions such as ashwagandha (found in some plants in the nightshade family), American ginseng (plant in the ivy family), astragalas (herb in the legume family), MSM (an organosulfur compound), quercetin (a plant flavanol), spirulina (a biomass of cyanobacteria), and turmeric (in the ginger family). Combinations of these ingredients can be found in brand-name supplements and in traditional Chinese herbal medicine formulations. Immunotherapy (aka allergy shots): For a personalized treatment, consider requesting an allergy test. Two test protocols are available to identify the specific allergens to which your horse is reacting. The most precise test for skin allergies is called intra-dermal skin testing. To perform this test, a veterinary dermatologist injects a small amount of different environmental irritants under the skin and then monitors the strength of the horse’s immune response at 30 min, 4 hours, and 24 hours. The second option is blood sample, while this is a more convenient way to test for allergens, it is thought to be less specific than intra-dermal testing. Following testing, a personalized allergy shot protocol is developed for your horse, with a dosing regimen to slowly introduce the allergens to your horse’s immune system without overwhelming it, resulting in a more appropriate response. Environmental management is again key to maximizing the success of this treatment plan. While the frequency of injection decreases over time, most horses require life-long treatment to keep allergy signs at bay. Allergy desensitization is a great way to manage skin allergies long-term; it greatly reduces the allergic response in most horses (though give it up to a year to work fully). There’s not much proof that allergy desensitization shots work very well for respiratory allergies. Allergies and Aging With time, both the environment and your horse’s immune system will change. New irritants can come in the form of new landscaping, new products, changes in air quality, etc. As horses age, there is some evidence that they can experience immunosenescence, or the gradual weakening of the immune system over time. Both of these factors may mean that your horse’s allergy status and immune system needs may change with time. If you notice any allergy signs, contact your veterinarian to discuss further options! Setting Expectations It may take weeks, months, or even years to find the perfect combination of immune-support and environmental control to rebalance your horse’s body. This plan may need to be regularly adjusted depending on the season. After establishing a treatment plan with your veterinarian, it may take weeks to see results. Complete resolution of all clinical signs may not be possible. With patience and persistence, almost every horse can find some degree of relief from allergies.

Watch this video of a presentation on equine allergies by Dr. Amanda Hedges. (Be sure to turn up your sound!) Related resources you may also be interested in: “Equine Allergies” (Article) by Amanda Hedges, DVM, cVA, CVSMT “Maximizing the Golden Years: Care for the Aging Horse” by Amanda Hedges, DVM, cVA, CVSMT and Nora Grenager, VMD, DACVIM

Equine dentistry is more than just floating teeth. It's much broader and examines the horse’s health more systemically, which is why it’s important to have your veterinarian perform annual dental exams. The general goals of equine dentistry include: Improving the chewing of food Relieving pain and treating or curing infection and disease Promoting general health, productivity, and longevity Preventing more painful and costly problems later According to the American Association of Equine Practitioners (AAEP), these 10 signs suggest that your horse needs a dental exam:

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 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.