EQUINE ARTICLES

Heaves: Recurrent Airway Obstruction in Horses

“Heaves” is the common name historically given for chronic obstructive pulmonary disease in horses. It is characterized by lethargy and exercise intolerance, coughing and gagging, blood-tinged mucoid discharge from the nostrils, and abnormal respiratory sounds (wheezing or heaving). The disease is probably better described as RAO, or recurrent airway obstruction, because the symptoms usually come ...

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“Heaves” is the common name historically given for chronic obstructive pulmonary disease in horses. It is characterized by lethargy and exercise intolerance, coughing and gagging, blood-tinged mucoid discharge from the nostrils, and abnormal respiratory sounds (wheezing or heaving). The disease is probably better described as RAO, or recurrent airway obstruction, because the symptoms usually come and go over time. It is similar to asthma in people, in that inhaled irritants and coincidental respiratory infections are significantly responsible for the onset and flare-ups of this disease.

The symptoms associated with RAO are caused by inflammation and narrowing of the bronchioles, or the air passages within the lungs. Excessive mucous production further obstructs the airways. Bronchospasm, constriction of the muscles that support the lung structures, reduces the horse’s ability to expel air effectively, causing the animal to use its abdominal muscles to force air out of the lungs during exhalation. This repetition over time causes the overdevelopment of specific abdominal muscles, resulting in a classical “heave line” that projects from the bottom sides of the ribcage into the flanks, despite overall muscle atrophy (wasting) from exercise intolerance.

RAO generally affects horses 6 years of age and older that have developed an immuno-hypersensitivity from repeated exposure to allergens and inhaled particulate irritants. Hay and bedding are common sources of dust and mold. Mold spores, toxins produced by mold, and other organic allergens are believed to be responsible for the development and recurrent episodes of this disease. Stable-kept horses and horses eating from a round bale of hay are most prone to RAO, but some genetic predisposition appears to be involved in an animal’s susceptibility. A diagnosis almost always corresponds to a large amount of the horse’s life being stabled and fed poor quality hay.

Horses fed hay in the pasture or stable may develop symptoms of airway obstruction and respiratory distress within 90 minutes to several hours after exposure to dusts and molds. The lung tissues become thickened, airways constrict, inflammatory mucous forms, and smooth muscle contractility in the lungs decreases. This leads to reduced blood-oxygen saturation, lethargy, and weakness. The affected animal will begin to cough and wheeze in an effort to ventilate the lungs and expel the accumulating mucous. Copious amounts of nasal discharge are seen especially when the horse’s head is lowered after being tethered for several hours. Blood may be seen in the exudates if coughing is especially forceful.

In RAO, the ability to exhale air from the lungs is compromised, while the ability to inflate the lungs remains fairly normal. This causes emphysema, or pressure damage to the alveoli (tiny air sacs in the lungs) that is reversible in quickly treated horses, but may lead to permanent lung damage in chronic or poorly managed cases. Persistent failure to respond to treatment is a sign that permanent damage has developed, and lung biopsies can confirm this, but it is difficult to determine when it may occur.

In addition to fatigue and exercise intolerance, chronic obstructive pulmonary disease will lead to appetite loss due to respiratory distress (i.e.: a feeling of suffocation while eating) and a decrease in the sense of smell and taste from mucous accumulation in the sinuses. The horse will lose muscle mass rapidly after the body’s fat stores are depleted.

A diagnosis is often made presumptively, based upon clinical signs and the horse’s history (age, stabling history, exposure to respiratory irritants such as hay dust). A bronchoalveolar lavage (BAL) performed by the veterinarian, where a sterile fluid is introduced by endoscopy into the lungs and collected for laboratory analysis, is useful to determine the level of inflammatory response. This test may be used to help rule out other disease processes causing similar symptoms. Chest x-rays, blood cell counts, and blood chemistry profiles may also be assessed as part of a diagnostic work-up.

Treatment for acute episodes of RAO includes first removing the source of the respiratory irritants. This will also be vital in the long-term management of the disease, since once-affected horses will be very prone to recurrences. If possible, the horse is moved to pasture to reduce exposure to dust, while stables are cleaned thoroughly and ventilation is improved to remove airborne contaminates. Horses in respiratory distress are treated with anti-inflammatory drugs and bronchodilators to reduce swelling in the lung tissues and aid respiratory function. Corticosteroids like dexamethasone and aerosolized fluticasone are preferred to non-steroidal anti-inflammatory drugs because of their broader spectrum of benefit despite potential side-effects associated with long-term administration. Corticosteroids reduce tissue edema, open airways to some degree, and also increase appetite. The dosage is then tapered to establish the minimum effective dose while the horse recovers.

Bronchodilators are used in conjunction with steroids to give more immediate relief from respiratory distress. Albuterol and clenbuterol are commonly used just before and in conjunction with aerosolized steroids to enhance their delivery and effectiveness. Bronchodilators are also used as rescue drugs in severely compromised horses.

Management of RAO requires diligence. Every effort to reduce the horse’s exposure to dust and molds should be taken, since there is no way to predict how much the animal can tolerate without relapse. The first recommendation, when feasible, is to allow the horse to graze naturally and avoid feeding hay. Even hay bales from a reputable source – especially round bales – may prove to cause a relapse in an especially sensitive horse. Rolled grains also have a high dust content. Poorly cured hay may contain molds and bacteria that trigger diseases like RAO when inhaled, or botulism when ingested.

Feeding silage, a high-moisture fermented hay product, will reduce the dust exposure, but carries the risk of Clostridium botulinum contamination if not properly processed and stored. Follow the recommendation of your veterinarian and consider vaccinating for botulism when weighing this option.

In cooler climates, many horse owners avoid keeping horses at pasture despite the fact that they do very well if provided protection from wind and precipitation. Their well-being also depends upon available nutrition and unfrozen water supplies, of course. Pelleted food is a good alternative to hay when pastures grasses are low or unavailable.

In the stable, there are options for bedding materials that may help control dust levels. Shredded cardboard or paper bedding are proving useful in this effort. Regular cleaning of manure and wastes, and frequent bedding changes will help to reduce molds from growing. Better ventilation methods may also reduce dust when the stable is dry, as well as deter mold from growing in moist conditions between cleanings.

The most effective way to help prevent RAO from developing in a healthy animal is to allow the horse to graze at pasture as much as possible. The pasture is a horse’s natural and best food source, and avoids many of the hazards that processed feeds and man-made shelters, despite the best intentions, may introduce accidentally.

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Injuries of the Eyes

Horses have prominent eyes that are susceptible to injury. Tree branches, hay stalks, and other foreign bodies may scratch or lacerate the cornea leading to infection and ulceration. If the condition is not recognized and treated early, the horse may risk going blind in the eye and suffering a lot of pain along the way.

The cornea is the clear membrane that encapsulates the front of the eyeball....

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Horses have prominent eyes that are susceptible to injury. Tree branches, hay stalks, and other foreign bodies may scratch or lacerate the cornea leading to infection and ulceration. If the condition is not recognized and treated early, the horse may risk going blind in the eye and suffering a lot of pain along the way.

The cornea is the clear membrane that encapsulates the front of the eyeball. It is comprised of numerous layers of tissue not unlike the layers of an onion. When an outer layer is compromised by a foreign body, bacterial contamination may be introduced between the subsequent layers of the membrane. Infection will lead to tissue necrosis and sloughing. Eventually, the full thickness of the cornea may be jeopardized, allowing the inner membrane of the eye to protrude. This condition is called a desmetocele, and it is very fragile. The horse risks losing its eye in this situation.

A severe eye injury would probably be noticed immediately, but a tiny corneal scratch may go undetected, at least at first. It doesn’t take long for a small injury to turn into a complete disaster, however. In a few days, the problem may threaten the horse’s eyesight. Swelling of the eyelids, conjunctivitis (red inflamed tissue around the eye), photophobia (avoidance of bright light and guarding of the eye), increased tearing of the eye, and cloudy areas on the cornea are all reasons to suspect an injury may have occurred. If any of these symptoms exist, contact the veterinarian immediately.

Do not apply medications to the eyes before the doctor has a chance to examine the horse. Ophthalmic ointments can contain corticosteroids that may accelerate corneal ulceration. Also, medications used previously for other eye problems may introduce infection into the eye.

The veterinarian will apply a fluorescein stain to the cornea which will only adhere to damaged tissue if present. The healthy cornea is normally so slick and non-porous that the stain is easily rinsed away with saline. A lesion will appear as a bright green area of stain uptake when the doctor shines a black light called a wood’s lamp onto the cornea.

Eye ulcers are extremely painful. If not treated, they may lead to permanent scarring or rupture of the cornea. If a foreign body remains trapped in the eye, the horse may require sedation to facilitate removal of the contaminant. Medications that may be prescribed will include a topical pain reliever, a drop or ointment that dilates the pupil, and an antibiotic preparation for the eye. Dilating the pupil will help prevent adhesions from occurring between the inflamed cornea and the iris. If drugs are used to dilate the pupil, precautions should be used to make sure the eye is protected from sunlight and watch for colic as a side effect of the drug. If there is no corneal damage, a steroid drop may be used to treat redness and swelling.

The prognosis for even minor injuries to the eye depends on swift recognition, assessment, and diligent treatment. All eye injuries should be considered emergencies and be immediately examined by a veterinarian.

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Humane Equine Euthanasia

Humane euthanasia is a preferred alternative to unnecessary suffering when a horse has a fatal injury or an unmanageable disease. It is the greatest and most difficult responsibility of being a horse owner to be sure that the animal does not suffer an agonizing end of life. It is also difficult to know when euthanasia is justified. While there are numerous factors to be considered when assessing treatment options for various ailments (side-effects, expense, rate of success, etc.), the only real measure to indicate that it is time to euthanize is...

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Humane euthanasia is a preferred alternative to unnecessary suffering when a horse has a fatal injury or an unmanageable disease. It is the greatest and most difficult responsibility of being a horse owner to be sure that the animal does not suffer an agonizing end of life. It is also difficult to know when euthanasia is justified. While there are numerous factors to be considered when assessing treatment options for various ailments (side-effects, expense, rate of success, etc.), the only real measure to indicate that it is time to euthanize is prognosis. Prognosis is a prediction of the most likely outcome of an illness. It may be influenced by what treatment options are available to the horse owner, but in the end prognosis will be what determines the most humane course of action. Once a decision has been made to euthanize, the next question will be how to end life humanely. The process itself must not cause unnecessary suffering.

The veterinarian will be most helpful and experienced in determining the prognosis for the horse fallen ill. For acute injuries and sudden onset diseases, the doctor will assess the animal for level of pain, underlying factors that predisposed the horse to the problem, the risk to other exposed horses in the herd, and likely secondary complications. In chronic conditions, factors that play a role in determining prognosis are whether the horse is responsive to therapy, the ability to control pain on a long-term basis, side-effects that have occurred or are likely to occur, and the horse’s ability to eat, drink, and rise unassisted.

Expense is a factor in either situation and cannot be overlooked as a justification for humane euthanasia. Some owners may be in denial about whether they can truly afford a long-term and complicated treatment regimen. This may result in the horse receiving less than adequate relief from suffering, which will be regretted after the owner realizes that the end was inevitable. Expense should be considered as well for its negative impact on the care that is provided for the other animals on the farm, not to mention the horse owner and his or her family. The owner should not be ashamed to recognize this fact.

Some of the common terms used by the veterinarian to describe the horse’s prognosis are good, fair, guarded, poor, and grave. A guarded prognosis may warrant an attempt at treatment, which may turn out to be successful; however, the owner is forewarned to be on the lookout for a possible decline in the animal’s response to therapy. At that point, alternate treatments if available should be explored, or euthanasia should be considered. A poor prognosis may indicate that palliative care (relief from pain) may be administered while the owner makes arrangements for burial or cremation, but the actual disease or injury will not be addressed per se. A grave prognosis would mean that immediate humane euthanasia is the only option.

Humane euthanasia is performed by one of three acceptable methods: lethal injection, gunshot, or penetrating captive bolt gun. Each requires a careful technique to ensure that the horse does not suffer needlessly. There are pros and cons to all three methods, which are described below:

Lethal injections require the animal to be completely unconscious, usually requiring anesthesia. Some drugs formulated for the sole purpose of euthanasia combine a barbiturate that induces coma, along with a drug that causes heart and lung paralysis which leads to brain death. If administered properly, the animal feels absolutely nothing and dies in its “sleep”. Most owners prefer this method because it is peaceful and bloodless when everything works as intended. Sometimes, illness in the horse such as reduced circulation can cause an increased time for the drugs to take effect. The animal may twitch or convulse before expiring, which is obviously upsetting for the owner to see. Some animal care professionals that are unlicensed to carry controlled substances have access to only the drugs that only stop the heart and lungs. These should not be used on a conscious horse, as death may be cruel and cause suffering.

Horses that are euthanized by the lethal injection method must be disposed of in such a manner as to not allow accidental exposure of domestic animals and wildlife to the carcass. Immediate disposal by deep burial or cremation is mandatory. Check with local ordinances about burial regulations.

Euthanasia by gunshot seems atrocious to some owners, as guns are perceived as tools of violence. However, if performed properly this method is just as humane as a lethal injection. It is also sometimes the only method available (i.e.: in emergencies, no vet available, no anesthesia available, burial or cremation will be delayed). The drawback to this method is primarily the emotional distress for the horse owner and family witnessing the event, as it is very loud and sudden. The horse may be fully conscious at the time which is also upsetting to observers. If performed correctly however, euthanasia by gunshot is extremely quick (avoiding stress and suffering in the horse), very reliable (little movement afterward, no chance of drug failure), mostly bloodless, and very humane. The horse feels nothing as brain function ceases immediately. Guns can be very dangerous to the operator, bystanders, and other animals if handled improperly.

A description is given below on the proper method to administer euthanasia by gunshot. This is intended ONLY to prepare a horse owner for an emergency situation, where the expertise of a veterinarian is not available or if time does not permit.

Gun type:

A handgun or long rifle may be used, but a handgun is preferred if no one is available to assist. A rifle is also more likely to create a significant exit wound which will not be bloodless. With a handgun, the owner can hold the lead in one hand and the gun in the other. With a rifle, an assistant can hold the lead at a safe distance behind the gun operator. In either case, the gun is held at point-blank range (but never up against the head), and never from a long distance.

Bullet type:

The type of bullet is critical. A soft-nosed, lead bullet or hollow point may be used, but full metal jacket bullets are to be avoided. The first two types will expand, rapidly slowing upon impact, and transfer all of their energy to the tissue, causing immediate death. Full metal jacket bullets will pass through the animal without expansion, and may put other people and animals even at great distances at risk if the bullet were to ricochet. There is the possibility of the horse taking a long time to expire if the wrong type of bullet is used.

Bullet caliber:

Nothing smaller than a .22 caliber long-rifle bullet (.22LR) should be used to euthanize the horse. Some people say the .22LR may not have enough energy when fired from a handgun barrel, but from a rifle it would develop the speed and energy necessary. The .32 cal, 9 mm, or .38 spl are also acceptable calibers.

Bullet placement:

The bullet should enter the animal at exactly the correct location to ensure humane treatment. Never shoot the animal between the eyes or in any other location besides the following. If an imaginary “X” is drawn from the base of each ear to the top of the opposite eye, the bullet will enter where the lines intersect. The gun barrel must be held perpendicular to the skull at the point of entry, which will cause the bullet path to point straight down the center of the neck.

Technique:

Hold the horse’s lead in order to keep its head from moving, but keep your lead hand behind the gun barrel at all times. The end of the barrel should be held 1 to 2 inches from the horse, never pressed up against the skull. If possible, the horse should be on soft ground to prevent a ricochet should the bullet pass through the animal. In any case, every one involved – people, other horses, dogs, etc. – everyone should be behind the gun except for the horse to be relieved of its misery.

The horse will usually buckle straight downward, but be prepared that it could fall forward, injuring the owner. Also, if it is possible to blindfold the horse, it may help to reduce anxiety of having a shiny object waved in front of its face. A blanket can be used for this purpose, but be sure that shot placement is exact.

Keep in mind that the horse will have to be removed from the location where it was euthanized, so consider the use of equipment if the horse is able to move before performing the procedure.

No one should attempt to use a gun in this situation that is not completely comfortable with their use beforehand.

A penetrating captive bolt gun accomplishes the same immediate brain death induced by gunshot. This method also requires careful technique to ensure a humane treatment of the horse. Most bolt guns are designed to be placed firmly against the skull, but otherwise placement and precautions are nearly identical to euthanasia by gunshot. Bolt guns are designed specifically for euthanasia and have the benefit of being supplied with an instruction manual. Follow the manufacturer’s directions carefully to avoid improper application of the device and needless suffering in the animal.

Unacceptable methods of euthanasia which would be inhumane (and may be considered animal torture or abuse) include:

Blunt trauma to the head or any part of the horse’s body

Injection of any chemical or drug not labeled specifically for euthanasia

Electrocution

Poisoning – by ingestion or otherwise

Gunshot other than as described above

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Intestinal Parasites of Horses – Deworming

Various parasites infect the gastrointestinal tracts of horses. Despite the widespread availability and use of anthelmintic drugs, “worms” continue to compromise the health of many horses in all parts of the country. It appears that drug-resistant parasites have emerged over time, most likely as a consequence of the misuse of deworming agents. Intestinal parasites may be responsible for sub-acute ...

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Various parasites infect the gastrointestinal tracts of horses. Despite the widespread availability and use of anthelmintic drugs, “worms” continue to compromise the health of many horses in all parts of the country. It appears that drug-resistant parasites have emerged over time, most likely as a consequence of the misuse of deworming agents. Intestinal parasites may be responsible for sub-acute to life threatening disease in horses and should not be underestimated as a significant threat to your horse’s health.

Of common farm livestock, horses may possess the largest average worm burdens, or the number of parasites that infect the host at one time. Compared to sheep and cattle, horses can sustain two to three times as many live worms in their intestinal tract – two thousand times as many as would parasitize a dog or a cat. This equates to approximately 100,000 live worms per infected horse.

Intestinal parasites spend their “adult” lives inside of the host animal, feeding and reproducing at incredible rates. It is during this stage that they cause disease. However, they begin life outside of the animal as eggs and larvae shed in feces. In fact, worms that infect horses cannot complete their life-cycle entirely within the intestinal tract. Microscopic eggs and larvae that lay waiting outside of the host are ingested by horses during grazing. It is by this design that these parasites are easily able to infect other animals that graze in common pastures. It is also the reason that despite treatment, horses are continually re-infected. With some female worms able to lay up to 200,000 eggs per day, it may be impossible to eradicate all sources of infection.

It is very important to follow a veterinarian’s recommendations for deworming regimens. Under-dosing, sporadic dosing, inadequate period of treatment, and use of no longer effective medications contributes to increasing drug-resistance in parasites. Every horse on the farm should have a strictly followed deworming schedule as established by the veterinarian.

While many parasites are capable of infecting horses, the most common types of intestinal parasites responsible for causing disease are bots, large strongyles, small strongyles, ascarids, pinworms, tapeworms, and threadworms. Below is a description of these parasites’ life-cycles, routes of infection, and mechanisms of disease. Deworming drugs and protocols are ever-changing in a response to resistance, so they are not described here. Consult the veterinarian for up-to-date strategies that are most effective in your geographical region and for your herd’s exposure risk.

Bots:

Bots are the larvae of botflies. While in the adult, flying stage of their life cycle, these arthropods do not bite horses or feed at all. Bots only develop into botflies for the purpose of finding a mate and reproducing. They lay their eggs in the hairs of the horse’s forelimbs, face, and neck, appearing as tiny pale yellow flecks. One female fly can lay as many as a thousand eggs during its short adulthood, which are accidentally ingested when the horse grooms itself. The larvae hatch immediately and burrow into the mucosal layers of the mouth tissues, where they remain for 3 to 4 weeks. After this period of time, they migrate down through the esophagus, finally attaching and feeding upon the stomach wall with tiny but very sharp mouth parts. Their attack on the delicate tissues causes significant inflammation, ulceration, and bleeding, and their numbers can be so great as to interfere with normal digestion or even obstruct the opening into the small intestine. The larvae will continue to mature for 8 to 10 months, then detach from the stomach wall in order to pass through the intestines in fecal material unharmed. Once outside of their host, larvae burrow into the ground for a period of time before emerging as adult botflies seeking a host to rear their offspring for them.

Large Stongyles:

Large strongyles are parasitic nematodes. Commonly called bloodworms, red worms, and palisade worms, the three species that most often infect equines are Stronglyus vulgaris, S. equines, and S. edentatus. They are spread effectively by fecal to oral transmission. When eggs of the parasites are shed in an infected horse’s stool, they hatch into infective larvae which are ingested during grazing. The infective stage larvae are protected from stomach acid and digestion by resistant outer capsules. Once in the small intestine, the larvae molt into burrowing juvenile worms that migrate through various tissues of the horse’s body before settling in the large intestine at full maturity. The development into adulthood takes at least 6 months before the worms are able to reproduce and deliver eggs that are detectable under the microscope during a fecal exam. The migrating larvae can cause arteritis (inflammatory disease of the arteries) and lesions throughout the liver, pancreas, and vasculature of the kidneys. As adults, the worms are voracious blood-suckers equipped with sharp, pincer-like mouthparts. In large numbers, adult large strongyles can cause anemia, weight-loss, weakness, and diarrhea that leads to dehydration, protein loss, and electrolyte deficits. The migrating larvae can significantly decrease blood supply to the horse’s intestines which may result in severe colic, perforation of the gut wall, and death to the animal.

Small Strongyles:

Small Strongyles are also parasitic nematodes; however, unlike their larger cousins, the larvae of the numerous species that infect horses do not migrate through tissues outside of the intestines. They also pass by fecal to oral transmission and are protected from digestion by a resistant capsule, but when they arrive in the large intestine, the parasites can form cysts that imbed deep within the intestinal wall. At this stage, the small strongyles are very resistant to deworming medications. After a sometimes long period of dormancy, the cysts finally emerge as young adult worms that feed on the mucosal layer and reproduce, delivering eggs that are detectable under the microscope during fecal examinations. Because of their unique life cycle and tendency to remain encysted for long periods of time however, the eggs are passed sporadically and in lower numbers than would be the case with large strongyles. A fecal exam is often negative despite the horse being infected by the worms. Small strongyles cause damage and bleeding in the intestinal wall while emerging from dormancy. Adult worms cause inflammation while feeding on the mucosal layer of tissue. In general, small strongyles cause milder gastrointestinal disease (and no symptoms due to larval migration) than large strongyles, but in very large numbers they may cause unexplained weight loss and severe diarrhea. Mild transient colic and poor coat condition may be the only symptoms seen in some cases.

Ascarids:

Ascarids are large roundworms that reach between 6 to 12 inches long during their reproductive adult phase. Although strongyles are technically in the roundworm family, ascarids are the parasites in equines that are commonly called by that name. They are passed by fecal to oral transmission. Like large strongyles, the immature larvae of ascarids migrate throughout various tissues in the body before reaching full maturity in the intestines. One strange aspect of their lifecycle is that the developing larvae must burrow outside of the intestines, through the liver and then the heart, finally into the lungs to be coughed up and swallowed by the horse, in order to reach adulthood in the intestines again. This migration pattern, when followed by a large number of larvae, can cause severe damage to the lungs and lead to pneumonia. In addition to coughing, ascarids cause colic and diarrhea, and may even block the intestinal tract when the adult worm burden is extremely heavy (also seen when all worms die at one time with deworming). Roundworm infection is especially common in foals. Female worms can deliver as many as 200,000 eggs per day.

Pinworms:

Pinworms are also spread by fecal to oral transmission. Even though they are an intestinal parasite, pinworms are more likely to cause external symptoms than gastrointestinal disease in horses. The adult female worms travel to the opening of the anus to deposit their eggs in a sticky substrate that adheres to the horse’s skin. As the material dries and flakes off, it causes irritation and itching. Infected horses may rub incessantly on any convenient object to find relief. This may lead to hair-loss on and around the tail, and occasionally broken skin.

Tapeworms:

Tapeworms are so named because of their flat, ribbon-like appearance as adults. They require an intermediate host to cause infection in horses. Mites in the pasture feed upon tapeworm egg-sacs and become infected. Horses inadvertently consume the mites while grazing. While the mite will be digested by the animal, the tapeworm larvae remains unharmed and matures to adulthood within the stomach and small intestines. Tapeworms cause disease when they attach firmly to the gut wall with sharp mouth parts, causing ulceration that is susceptible to infection, telescoping of the small intestine into the cecum (causing colic), and rarely perforation of the gut wall. They are not associated with emaciation in horses. The adult worms are segmented, and each segment at the tail end of the female worm contains egg “baskets”. The segments detach one by one and find their way to the horse’s anus. Once in the environment, the segments desiccate and are consumed again by mites.

Threadworms:

Threadworms (Strongyloides westeri) are a problem for foals, which ingest the parasite larvae present in a mare’s milk while nursing. Larvae in the foal’s bedding can also penetrate the skin and migrate to the intestinal tract. The threadworm usually causes little harm to an adult horse. Infected foals show signs of colic, diarrhea, and overall failure to thrive. Horses develop immunity to threadworms after several months of age, but very young foals can acquire significant parasite infestations that may lead to dehydration, electrolyte imbalance, protein loss, and other consequences of severe diarrhea.

In addition to following a recommended deworming protocol established by the veterinarian, it is important to institute environmental control measures in the areas a horse owner is able. Keeping stables and paddocks sanitary by removing manure regularly and providing good water drainage will help to reduce the incidental ingestion of parasites. Use elevated feeders for hay. Over population is also a factor that leads to parasite infestations (as well as other contagious disease) in the herd and should be avoided. Establish an effective fly control program to reduce botfly numbers. These efforts will all help to reduce the frequency and severity of intestinal parasite outbreaks.

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Keratoma of the Foot

Keratomas are locally invasive (non-spreading) tumors comprised of keratin, the primary substance making up the hard wall of the hoof. They are located between the coffin bone (3rd phalanx) and the hoof wall. Keratomas are fairly uncommon, but can be a significant source of lameness when the mass extends to the sole of the hoof. The tumors grow anywhere within the hoof capsule, exerting pressure...

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Keratomas are locally invasive (non-spreading) tumors comprised of keratin, the primary substance making up the hard wall of the hoof. They are located between the coffin bone (3rd phalanx) and the hoof wall. Keratomas are fairly uncommon, but can be a significant source of lameness when the mass extends to the sole of the hoof. The tumors grow anywhere within the hoof capsule, exerting pressure upon and displacing the coffin bone opposite of the tumor’s contact with the hoof wall. They are most common in the toe, but may exist in either quarter. Any foot may be affected.

The cause of Keratomas remains elusive, but some experts speculate that the tumors form in response to a previous insult to the coronary band. The coronary band is the junction between the hoof and the pastern and contains the epidermal cells responsible for making keratin.

In some cases, there is a visible bulge in the hoof wall at the site of the keratoma. The white line may deviate toward the frog, or may separate leaving the hoof susceptible to infection. In many cases however, there is no outward clue to the tumor’s existence other than unattributable lameness. A hoof tester may be helpful to reveal pain at the site of the mass. X-rays are used to confirm the diagnosis.

Keratomas, once diagnosed, require surgical removal under a general anesthetic. The hoof wall is removed to reveal the keratoma tumor, which is also excised as fully as possible to prevent re-growth. The defect created in the hoof is then packed with betadine soaked gauze, and the entire foot is wrapped to prevent contamination of the wound by soil and pathogens. A farrier can then build a special plate that covers the defect and is attached by removable screws. This facilitates changing of packing gauze every 3 days and keeps contamination out while the hoof heals.

Before surgery, if the horse was not current on tetanus vaccination, it will be administered to prevent the often fatal disease caused by bacterial infection of deep wounds. Afterward, the horse may receive antibiotics to prevent bacterial infection overall. It can take many months for the hoof to completely heal after Keratoma surgery, so diligence and patience are required to a great extent.

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Lameness – Navicular Syndrome

Navicular Syndrome (NS) is a cause of incurable lameness in mainly the front feet of horses that are predisposed and subjected to extreme exercise and burdensome work. Middle aged to older animals are diagnosed more frequently with NS than younger horses. Changes in gait due to heel pain are the initial symptoms, due to inflammation and degenerative changes in the navicular bursa, a fluid-filled...

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Navicular Syndrome (NS) is a cause of incurable lameness in mainly the front feet of horses that are predisposed and subjected to extreme exercise and burdensome work. Middle aged to older animals are diagnosed more frequently with NS than younger horses. Changes in gait due to heel pain are the initial symptoms, due to inflammation and degenerative changes in the navicular bursa, a fluid-filled cushion between navicular bone and deep digital flexor tendon of the horse’s foot. The bone and tendon will also become degenerative as the disease progresses. This problem usually affects both front feet, but the symptoms may alternate from side to side as the horse favors the most painful foot of the moment. Rest will help alleviate pain initially, but symptoms quickly return upon activity.

When observing the horse with NS, a few classical symptoms may be noted: The animal may constantly fidget, shifting weight from side to side in order to alleviate pressure on the heels. It may also point the front feet, and alternate which foot is pointed. Abnormal wear may be seen on the toe of the hoof or shoe due to heel avoidance during walking. And, one or both hoofs may contract in width at the heel due to poor circulation.

The mechanism that causes navicular degeneration is not completely understood, but there are several theories. They all result in the de-vitalization of the navicular bone, compromising its function and structural integrity, and causing persistent heel pain due to one or more of the following: decreased blood circulation and tissue necrosis, impact damage and excessive bone remodeling, and / or degenerative joint disease – a breakdown of synovial fluid and cartilage (lubricant and cushioning in the joints).

A diagnosis of NS is based upon a number of supporting indicators: typical clinical signs, a history of intermittency and heavy work load, localization of pain within the heel, and navicular bone lesions if present on an x-ray or bone scan (scintigraphy). A hoof tester and “wedge tests” may be used to confirm and isolate pain at the frog (soft part of the heel) and in the navicular region. Local anesthetics can also be helpful in diagnosing NS by ruling out another source of the pain. When a palmar digital nerve block is placed, the horse will experience great improvement in the anesthetized heel. When both heels are blocked, the horse may appear practically normal.

There are numerous protocols that have been developed for treating Navicular Syndrome, all of which attempt to achieve the same goals: to alleviate pain and to slow the progression of the disease. Treatment may include hoof trimming, corrective shoeing, and rest in young animals with mild symptoms. As pain becomes more chronic, non-steroidal anti-inflammatory drugs (NSAIDs) may be administered. These steps will be a foundation upon which further treatment options may be added.

Bar shoes and rubber frog pads can be used to protect and cushion the heels from further impact damage. Intra-articular injections can also be considered for advancing cases. Cortisone, injectable NSAIDs, vasodilators, and restorative nutraceuticals like hyaluronic acid and polysulfated glycosaminoglycans may be injected alone or in combinations into the navicular region of the foot in an effort to control symptoms.

At some point, surgical options may be investigated. The risks / benefits of these procedures are weighed when a poor response to the aforementioned therapies is seen. There are two surgeries commonly performed to provide pain relief and improve mobility. A palmar digital neurectomy severs the nerve that is responsible for communicating sensations from the palmar surfaces of the foot, eliminating pain entirely if its source is indeed originating from navicular bone degeneration. Side effects are fairly rare, but this surgery performed on a horse without NS can increase the risk of injuries due to lack of sensation. The nerve may also re-grow, defeating the procedure, and occasionally a painful neuroma may form. A navicular suspensory desmotomy is preferred in moderately affected horses that may benefit from reduced compression on the navicular bone before completely denervating the palmar aspect of the foot. In either case, infection is a serious possible complication of surgery, and the horse must be strictly rested for at least 6 weeks post-operatively while it recovers.

The prevention of NS is difficult since there is no organism responsible for the disease that could be combated by vaccination strategies, testing, or quarantine efforts. It is impossible to predict how much exercise a susceptible horse may tolerate before developing degenerative problems of the navicular regions. Aside from exercise avoidance, which could lead to other serious problems, NS can only be prevented by early recognition of animals that may be predisposed. Horses with hoof confirmation problems, i.e. narrow hoofs, and those exposed to extreme abuses of the feet (racing, cutting, and roping horses), should be monitored for the development of NS. Early detection is key to slowing the progression of the degenerative effects that lead to permanent lameness. Proper and preventive shoeing is also vital to avoiding the development of NS.

Once horses are obviously affected by NS, the prognosis is guarded to poor, depending upon the diligence and aggressiveness of therapy. If the underlying causes are caught early, i.e. inappropriate shoeing or exorbitant stresses on the feet, the disease can be reversed or slowed for a period of time, significantly extending the quality of life for the animal.

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Lameness – Founder (Laminitis)

Founder is a severe form of lameness caused by laminitis of the horse’s foot. Laminae are the flexible interwoven layers of transitional keratinous material that form the shock-absorbent attachment between the coffin bone and the rigid hoof wall. They are responsible for transferring the animal’s weight evenly onto the hoof and dispersing the impact of locomotion on the skeleton. Laminitis means...

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Founder is a severe form of lameness caused by laminitis of the horse’s foot. Laminae are the flexible interwoven layers of transitional keratinous material that form the shock-absorbent attachment between the coffin bone and the rigid hoof wall. They are responsible for transferring the animal’s weight evenly onto the hoof and dispersing the impact of locomotion on the skeleton. Laminitis means inflammation of these supporting structures, the causes of which are variable and not fully understood.

Founder affects primarily, but is not limited to, the front feet. In severe cases, there may be complete detachment of the hoof from the coffin bone. The animal’s weight, unsupported by the laminae, is transferred onto the sole through the end of the bone, causing excruciating pain and sometimes protrusion of the bone outside the hoof. Founder describes the symptoms of a horse with severe laminitis.

If founder affects the front feet exclusively or to a greater extent than the rear, the horse may assume a “founder stance”. The rear limbs will be drawn as far under the body as possible to relieve weight from the forward limbs, and the front feet will be thrust forward with the weight on the heels, as if squatting or sitting on the haunches. Turning while walking will require raising the front limbs and spinning around on the rear. When all four feet are affected by laminitis, the horse will be reluctant to rise at all. The limbs will be tucked under the body to protect the toes from bearing any pressure, and standing will be slow and cumbersome as the horse avoids bearing weight on the points of the coffin bone.

Episodic laminitis will leave rings of abnormal layer formations on the outside of the hoof, but this is not always profound. Separation of the white line at the toe and in the forward quarters of the hoof is evidence of increased pressure on the sole by the coffin bone. Secondary infection (seedy toe) is common when this occurs.

Many factors contribute to founder. An overweight body condition plays a big role. Stress from foaling, repeated exuberant exercise, chronic systemic infection or disease, and standing or walking on hard grounds may all result in laminitis.

Any sign of lameness (with or without overt evidence of laminitis) should be evaluated by a veterinarian as soon as possible. X-rays of the feet will be taken after a complete physical examination and assessment of symptoms. Medications for inflammation and pain may be prescribed, and corrective farriery will be necessary. Modifications to exercise and diet will be instituted to facilitate healing and prevent flare-ups. Management will be a long term effort. In refractory / severe cases, euthanasia may be the most humane option.

Treating and preventing founder requires attention to diet, disease prevention, and avoidance of repeated injury to the feet. The horse should stay current on vaccinations, deworming schedules, and wellness examinations by the veterinarian. Despite so many possible causes, laminitis occurs most frequently as a result of improper husbandry and horse management.

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Lameness – Osteochondritis Dissecans (OCD)

OCD is short for Osteochondritis Dissecans, a developmental disorder of the bones and joints that is somewhat common and may affect any breed of horse. The condition may also be referred to as an OCD lesion or an OCD fragment after radiographic evaluation of the affected joint. It is thought to be an inherited problem, although other factors are shown to contribute to the risk of developing...

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OCD is short for Osteochondritis Dissecans, a developmental disorder of the bones and joints that is somewhat common and may affect any breed of horse. The condition may also be referred to as an OCD lesion or an OCD fragment after radiographic evaluation of the affected joint. It is thought to be an inherited problem, although other factors are shown to contribute to the risk of developing symptoms of advanced joint disease. These include abnormally rapid growth spurts while bone and articular cartilage is not yet fully developed, diets that may contribute to rapid growth, mineral deficiency, and certain hormone imbalances. OCD is likely to be painful and left untreated may become eventually crippling.

After a foal is born, its bones and joints are still not completely developed. This is to allow for growth until the horse reaches its full stature at about three years of age. The ends of the bones adjacent to the animal’s various joints continue a process called endochondral ossification which produces the cartilage, or padding between the bones in the joint, and the hardened smooth surfaces that cap the ends of the bone. An interruption in this process leads to irregularly shaped, weakened cartilage and bone surfaces leading to instability, decreased range of motion, and a propensity to develop fractures within the joints.

OCD is one such “interruption” in joint development. The term literally means a separating (dissec-) section of bone (osteo-) and cartilage (chondro-) caused by inflammation (-itis). Inadequate blood supply to malformed articular tissues leads to necrosis, or tissue death, and eventual separation from their normal anatomical positions. Partially attached flaps and free floating fragments cause pain and further inflammation in the joint when the pieces impede normal joint movement and cause injury to healthy cartilage. Exercise or trauma to the affected joint will accelerate this process of fragmenting and articular damage. The abnormal joint will develop arthritic changes at an increased rate causing swelling and debilitation at a young age.

OCD lesions may cause symptoms of lameness at a few months of age or remain undetected until adulthood. The disease is usually confirmed by taking x-rays at about 12 months old. It is difficult to assess how many horses will become symptomatic from OCD lesions, but between 25 and 60 percent of horses show radiographic joint abnormalities on pre-purchase exams. Progressing disease will often result in joints swollen with effusions (inflammatory joint fluid). Swelling may suddenly occur after an exercise regimen is begun (i.e., formal training program).

Lesions may occur in any of the joints of the limbs, with the hocks, fetlocks, and stifles being most commonly affected. A diagnosis of OCD usually requires surgical intervention to remove the abnormal tissues and fragments. An arthroscopic procedure (performed by a surgical specialist) is preferred to an open surgery to avoid the risk of joint infections post-operatively. Healing times are quicker after this less invasive method as well, because the incisions through the skin and joint capsule are smaller. Surgery will require general anesthesia, so preliminary blood work will be assessed to minimize the risk to the patient. An arthroscope is a thin flexible tube with a lens or a tiny camera attached to the end that is inserted through one incision to visualize the internal joint anatomy and guide other instruments through another small incision in order to remove OCD fragments.

The horse will be rested for a period of time after surgery depending upon the complexity and location of the surgery. Low-impact physical therapy will follow according to the surgeon’s recommendations. Full recovery will usually take several months. Often, the surgical site will require bandaging for a week or two to minimize post-operative swelling and protect the incisions from contamination. Also, non-steroidal anti-inflammatory drugs (NSAIDs) for pain relief, and antibiotics to prevent bacterial infection, are typically prescribed to horses undergoing OCD surgery.

Most horses that are treated early in the onset of OCD of the distal (lower) limb joints have a good long-term outlook. OCD lesions in the shoulders carry a more guarded prognosis. This depends upon the owner’s diligent adherence to rehabilitation recommendations from the veterinarian.

Osteochondritis Dissecans is strongly suspected of being hereditary. Careful breeding may indeed reduce its prevalence in subsequent generations of horses. The trouble is that so many horses may show evidence of joint abnormalities on screening x-rays without ever exhibiting clinical symptoms attributed to OCD. Until a stronger association can be made, controlling the other factors that contribute to the development of OCD lameness is the most reasonable prophylactic effort at this point. Preventing excessively rapid growth during development is vital. A veterinarian can help the horse owner determine an appropriate diet and mineral supplement, if deemed necessary, most beneficial to growing foals.

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Laryngeal Hemiplegia (Roaring)

“Roaring” is a term used to describe the observed respiratory symptoms in a horse afflicted by the medical condition called laryngeal hemiplegia. Somewhat rare, it affects mainly thoroughbreds and other highly exercised horses. Laryngeal hemiplegia is caused by nerve damage (paralysis) that results in one of the arytenoid cartilages failing to open and thus obstructing the airway. Arytenoid...

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“Roaring” is a term used to describe the observed respiratory symptoms in a horse afflicted by the medical condition called laryngeal hemiplegia. Somewhat rare, it affects mainly thoroughbreds and other highly exercised horses. Laryngeal hemiplegia is caused by nerve damage (paralysis) that results in one of the arytenoid cartilages failing to open and thus obstructing the airway. Arytenoid cartilage controls the function of the vocal cords. The problem is more common in the left cartilage, although it is not understood exactly why. Owners complain of a roaring or whistling sound from the animal when ridden at high speeds. When severe, the horse will become gradually more intolerant of exercise.

Almost all cases of left laryngeal hemiplegia are idiopathic in nature, the specific cause of the nerve damage eluding veterinarians. Rarer still, right laryngeal hemiplegia is almost always attributable to a secondary complication of an inflammatory disease or infection. Treatment for the former (left LH) may require surgery, while treating the latter (right LH) involves addressing the underlying disease mechanism.

All other causative disease possibilities ruled out, laryngeal hemiplegia is diagnosed by observation of clinical signs, a history of exercise intolerance, and laryngeal endoscopy. An endoscope is a rigid or flexible tube with a lens at the tip and an eyepiece or camera at the handle. The horse will require restraint in order to place the endoscope into the pharynx (back of the throat) and observe the laryngeal cartilages functioning during respiration. In a healthy animal without laryngeal paralysis, both sides of the cartilaginous “voice box” will open and close fully and at the same time. In laryngeal hemiplegia, one side will hesitate to open and obstruct the trachea during inspiration. In some cases, the endoscope will be passed through the nostril, into the pharynx, and fastened to the bridle. A digital video camera will be attached to capture the function of the laryngeal cartilage while the horse is conscious and at heavy respiration during exercise. This can be accomplished on a treadmill in the hospital or in the field by a wireless connection to an observation monitor.

Horses diagnosed with mild laryngeal hemiplegia can simply be retired from heavy exercise, and should remain comfortable. These animals should be especially protected from subsequent respiratory disease by appropriate vaccinations, avoiding exposure to known infections, feeding low dust diets, and providing good ventilation in stables. For more severe respiratory obstruction, surgical intervention may be considered. There are three procedures that may provide relief from symptoms. The first is called a Hobday operation wherein the obstructive part of the laryngeal tissue is removed, causing scarring which holds the larynx open. More modernly, a “tie-back” procedure can be done (usually in addition to a Hobday operation), using sutures to tack the larynx open. The scarring from the Hobday operation will help to hold the airway open should the tie-back sutures fail. Finally, a tracheostomy tube can be surgically and permanently implanted to circumvent the larynx entirely. This is rarely performed, as the wound in the neck through which the tube is permanently sutured will be constantly susceptible to infection and suture failure. Humane euthanasia should be considered in the most severe cases to prevent unnecessary suffering.

Differential diagnoses for symptoms of roaring include infections such as equine protozoal myeloencephalitis (EPM), laryngeal cysts and tumors, lymphoid hyperplasia (inflammatory lymph tissue enlargement of the pharynx), and Epiglottic entrapment, whereby the epiglottis’ normal movement is restricted by excess tissue (usually the soft palate).

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Melanomas: Skin Cancer in Horses

Melanomas are malignant tumors comprised of abnormal melanocytes, cells that produce the pigment melanin that tints the skin. In horses, melanomas are slow growing and locally invasive. They usually do not cause disease when confined to the skin, but occasionally a tumor may metastasize, spreading to other tissues within the animal’s body. Gray horses possess more melanocytes in their skin than...

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Melanomas are malignant tumors comprised of abnormal melanocytes, cells that produce the pigment melanin that tints the skin. In horses, melanomas are slow growing and locally invasive. They usually do not cause disease when confined to the skin, but occasionally a tumor may metastasize, spreading to other tissues within the animal’s body. Gray horses possess more melanocytes in their skin than do other colors of horses, giving them a higher propensity to melanoma formation. More than three quarters of gray horses over the age of fifteen will develop a tumor of this type. Melanomas in the skin vary greatly in size and shape, sometimes mimicking other skin masses like warts, and they are usually darkly pigmented (dark brown or black) by melanin. They may be found as solitary masses or in undifferentiated clusters. Melanomas tend to be found around the anus, vulva, prepuce, and base of the tail, around the eyes, ears, and neck; usually non-painful, the masses may become inflamed and ulcerated, attracting flies and secondary bacterial infection, or may interfere with normal feeding or defecation. While in the skin, the tumors may remain inconsequential or may require surgical removal; however, if they originate in, or metastasize to internal organs, melanomas carry a grave prognosis.

In people, melanoma tumors are associated with excessive sunlight exposure and fair skin lacking melanin. Damaged melanocytes begin to divide at an uncontrolled rate, forming a mass. It is unclear if sunlight exposure is the direct cause of melanomas in horses, however. There may be genetic factors or other environmental stresses at play. All that is known is that grays tend to be at a higher risk, despite the fact that melanin protects the skin from ultraviolet radiation. Melanoma occurs less frequently in dark-skinned people; the rule holds untrue for dark-skinned horses. Other colors of horses account for about one third of all skin melanomas.

If and when a mass is discovered, a veterinarian should be consulted. It is important to confirm a diagnosis whether treatment will be immediately pursued or delayed. A biopsy and microscopic evaluation by a pathologist, along with a history of the growth of the tumor and the gross appearance, are necessary to determine a course of action. Small tumors may be observed for growth or removed at once in an effort to avoid complications. Some veterinarians believe that attempting to excise a melanoma may actually cause it to become more aggressive in nature. Most prefer to not take any chances with the tumor exploding in size or metastasizing. The location of the mass will have an impact on the veterinarian’s decision. Very small tumors can typically be removed after the placement of a local anesthetic; while larger, more invasive tumors will require a general or epidural anesthetic to be administered. Laser surgery has proven beneficial in removing precariously located tumors. Melanomas removed and shown by histopathology to have clean margins (healthy cells surrounding the mass) generally result in a cure. Surgery on very advanced tumors may require the expertise of a specialist in equine surgery.

Non-surgical options for treatment of melanoma that have shown mixed results include oral cimetidine (Tagamet), an H2 blocker – antacid drug; topical therapy with cisplatin or frankincense oil; and melanoma vaccine. These therapies may cause the tumor to shrink in size, delaying complications or facilitating removal, but will not ultimately stop the tumor from progressing over time.

The prognosis for a quickly detected, diagnosed, and removed melanoma is good. Tumors that are invasive, wide-spread, or internalized are much more likely to result in dire outcomes.

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Leg Bone Fractures

In the past, a horse with a broken leg was a dead horse. Even though fracture repair surgery has long been possible and is internally very similar to the techniques used in humans and domestic animals, the successful healing of fractures in horses is heavily dependant upon the stabilization done in the field and the ability to immobilize the limb after surgery. Great strides have made in the...

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In the past, a horse with a broken leg was a dead horse. Even though fracture repair surgery has long been possible and is internally very similar to the techniques used in humans and domestic animals, the successful healing of fractures in horses is heavily dependant upon the stabilization done in the field and the ability to immobilize the limb after surgery. Great strides have made in the post-surgical immobilization of fractures meaning more and more horses are able to survive leg fractures, but the owner must take certain crucial steps before surgery is attempted to ensure that repair is a possibility.

In the case of a leg fracture, call the veterinarian immediately. The owner will need assistance in immobilizing the limb, and the veterinarian is best equipped to help with this task.

The horse must be calmed before any assessment or treatment of the injury can or should be attempted. A thrashing animal is not only very dangerous to handlers; it may cause more damage to the fracture which may make healing more difficult. The veterinarian will administer tranquilizers and pain medications to facilitate examination and splinting.

Splinting requires immobilization of the limb to the greatest extent possible, without strangulation of soft tissue, above and below the fracture site. Inadequate splinting may cause a point of leverage to exist that exaggerates the movement and displacement of the broken bone pieces. Displacement causes damage to blood supply and inflammation around the injury which can impede the healing process.

A splint consists of soft padding, bandaging material, and a rigid device that extends beyond the nearest joints above and below the fracture. The rigid material may be any object that is stiff and relatively lightweight. The width of the splinting device should be equal to or narrower than the limb at all points of contact. This will help secure the limb firmly against the splint without excess movement or slack underneath the bandage. Splints may be fashioned from two by four lumber, wrapped t-posts, pipe, or any scrap around the barn suitable for the purpose.

To splint a fractured leg, first wrap the splinting device with soft padding that will prevent pressure sores and injury to the skin. Clean strips of blanket or cotton roll bandage may be used. Secure the padding to the splint with duct tape, medical tape, or anything available that does not stretch when applied. This will not contact the skin.

Next, tear two or more strips of porous 2” medical tape if available, duct tape in a pinch, the length of the bandage to be applied. Sections of soft rope can also be used. One end of these “anchors” will be secured to the limb with a band of tape at the lowest point of the bandage, preferably just above another joint before the diameter of the limb increases. If duct tape is used for anchors, it should be reversed to avoid contact of the adhesive with the skin; only the securing band needs “stick” to the skin. Do not cause restriction to blood circulation! The free ends of the anchors should hang below the cast.

Wrap the limb with soft bandaging beyond the nearest joints above and below the fracture, or wrap the entire limb. The more immobilized the limb is, the better. The bandaging is to protect the skin from contact with the splint device and provide compression space for the outer cast. The wrap should be made of breathable, absorbent material. Never use plastic, rubber, or any other waterproof material against the skin. Secure the bandage with pieces of tape, any kind, without going all the way around the leg to avoid a tourniquet effect.

Pull the anchors up and along side the bandage, and secure them with tape. This will keep the cast from sliding off the limb. Add the splinting device to the outside of the leg, wherever it lies most naturally without jabbing the body, and tape it all the way around the leg just tight enough to keep it in place. The final wrap will hold every thing together firmly.

The outer cast should also be made of breathable material. Vetrap works great, but keep in mind that it shrinks with time, so don’t stretch the bandage when applying. With the bandaging underneath, there is room for compression however, so when the cast is complete it should hold the limb securely with little movement and still allow circulation. If non-adhesive casting wrap is used, it may be secured with several bands of adhesive tape.

The horse will not appreciate the cast and will goose step once it is applied. Every effort should be made to keep the animal quiet and calm while moving into the trailer. The horse can throw a cast quite easily if not secured properly or allowed to panic. Move the trailer to the horse rather than the horse to the trailer. Use chest and butt bars to immobilize the horse once trailered. Distraction can be provided with treats or feed. Discuss transportation of the horse with the veterinarian.

Immediate (but safe) transport to a surgeon will help ensure that the fracture avoids further displacement and holds hope for repair and healing.

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Metabolic Syndrome

Obesity in horses used to be virtually non-existent. The majority of horses were kept as beasts of burden, only the rich possessing them as companion animals. Working horses couldn’t possibly consume more calories than they burned while pulling timber and cargo, transporting people, plowing fields, or driving livestock. Plump horses were suspected of lameness or inaptitude and were discredited at ...

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Obesity in horses used to be virtually non-existent. The majority of horses were kept as beasts of burden, only the rich possessing them as companion animals. Working horses couldn’t possibly consume more calories than they burned while pulling timber and cargo, transporting people, plowing fields, or driving livestock. Plump horses were suspected of lameness or inaptitude and were discredited at auctions. With the availability of calorie-dense processed feeds and people’s incomes justifying keeping horses for little more than the occasional weekend leisurely ride, more horses these days are carrying more fat than freight and more bulk than burden. As a result, more horses are seen with disorders and afflictions thought to be linked to obesity.

One such disease has had many aliases over the years. Once termed obesity-related laminitis, peripheral or pseudo- Cushing’s disease, hypothyroid laminitis, insulin resistance syndrome, and even syndrome-X, this devastating illness is now known as equine metabolic syndrome (EMS). Horses with EMS generally present with one or more of the following symptoms:

Excessive thirst and urination

Fat accumulation over the neck, shoulders, tail-head, and loins

A pot-bellied appearance

Un-attributable laminitis

Lethargy or exercise intolerance

An insatiable appetite

Irregular estrous cycles in broodmares

The primary disease mechanism responsible for symptoms in EMS is insulin resistance. When food is consumed, it is eventually broken down into glucose, a very basic sugar molecule that is the primary source of energy for every cell in the body. As glucose is absorbed through the gastrointestinal tract into the bloodstream, an organ called the pancreas is stimulated to produce the hormone insulin. Insulin is responsible for carrying glucose into the cells; without it, the cells will become starved for fuel and cease to function properly, regardless of the abundant supply of glucose circulating in the bloodstream. Insulin resistance describes an interruption in this energy transfer into cells. There may be enough insulin released by the pancreas, but for some reason the body’s tissues do not recognize its purpose.

Obesity may be a factor in the over-production of another hormone called cortisol. Cortisol is normally released by the adrenal gland in times of stress in order to suppress the activity of insulin. This causes an elevation of blood-glucose levels to be used as energy reserves in fight-or-flight situations. In Cushing’s disease, cortisol is overly secreted by the adrenal gland; in EMS however, the adrenal gland functions normally, and excess cortisol appears to instead originate in adipose tissues, or fat deposits.

Not every overweight horse will develop EMS, but obesity is certainly a risk factor. To diagnose metabolic syndrome, the veterinarian will rely on the animal’s history of symptoms, body condition, and the results of glucose tolerance testing. Most horses that have developed the syndrome are middle-aged, over seven and under 18 years of age. Certain breeds are predisposed to EMS, and this will be taken into account. Ponies, Morgans, European Warmbloods, Spanish Mustangs, Peruvian Pasos, and Paso Finos are over represented with EMS. Also, broodmares that have difficulty becoming pregnant may be suspected.

Though “gluttony” may have played a role at some point, veterinarians observe that some horses with signs of EMS are not apparently being overfed. Their owners describe them as “easy-keepers”, unable to lose weight despite being restricted from calorie-rich processed feeds. This causes further speculation about a genetic propensity to the illness.

Glucose tolerance testing involves taking several blood samples from the horse to measure serum-glucose and insulin levels before and after a bolus of glucose is administered. These results are compared to expected results from a healthy animal to determine whether the horse appears to have developed insulin resistance. Horses are usually fasted for a period of time before the test is performed.

There is no approved medical treatment for equine metabolic syndrome. Drugs administered to horses with Cushing’s disease are likely to exacerbate EMS. Instead, dietary management along with appropriate exercise is the best way to increase insulin activity and reduce the occurrence and severity of symptoms. (These are also the best methods by which to reduce the possibility of developing EMS.)

Horses should be fed just enough to maintain a good body condition. Some owners, in an effort to have an impressively large and imposing animal, confuse body weight with lean muscle mass. A horse’s ribs should always be easily palpable, but not protruding visibly. Horses that are not used for laborious chores will require little feed supplementation beyond access to a good pasture. Processed grains are especially high in carbohydrates (sugars) and should be a minimal portion of the diet. EMS horses should be restricted from grain and grain mixtures altogether. A proper weight-loss regimen should be developed through the advice of a veterinarian in order to see progressive benefits without causing starvation.

Exercise is the only way to burn calories ingested and stored as fat. Regular exercise not only helps to shed excess pounds, but also encourages better insulin activity. A veterinarian can help determine a safe and appropriate level of activity for an already obese animal. Obviously, any existing lameness and / or laminitis will need to be addressed with the help of the vet and farrier before the horse will be ready to run.

At best, equine metabolic syndrome can be reversed entirely if bad habits are stopped before serious symptoms develop. The further obese and symptomatic the horse becomes however, the more difficult it will be to slow the progression of the disease.

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Potomac Horse Fever

Potomac Horse Fever (PHF) is a sporadic cause of acute diarrhea in many parts of the country. The disease is caused by bacteria called Neoriketssia ristici, which is carried by aquatic insects that consume tiny parasites (cercariae; a fluke) of fresh water snails. A horse may be exposed by ingesting the insects while grazing; however, because of the unique life cycle of cercariae, the horse is...

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Potomac Horse Fever (PHF) is a sporadic cause of acute diarrhea in many parts of the country. The disease is caused by bacteria called Neoriketssia ristici, which is carried by aquatic insects that consume tiny parasites (cercariae; a fluke) of fresh water snails. A horse may be exposed by ingesting the insects while grazing; however, because of the unique life cycle of cercariae, the horse is not infected directly by the snails or the water that contains the parasites of the snails.

PHF is more prevalent in warmer months when large numbers of the parasites are released into bodies of water and aquatic insects are most active. Horses kept near ponds and creeks are more likely to be exposed to Neoriketssia ristici, but this is not prerequisite. Anywhere the carrier insects gather, a horse may be exposed.

Although the bacteria are shed in the infected horse’s stools, PHF is not considered directly contagious. Group outbreaks are usually associated with close confinement, where the horses were all exposed to insect contaminated feeds.

PHF occurs when cells that line the intestine become infected with N. ristici. The incubation period after ingesting the carrier insects is about 10 days to 2 weeks. The horse will become depressed and go off feed in most cases, accompanied by fever as high as 107 degrees. Moderate to severe diarrhea from cow-patty to watery consistency occurs in more than 60% of cases, and is often the indicative symptom. Horses are at risk of dehydration during this stage of the disease. Approximately 40% of cases will be complicated by laminitis. It can be severe and will most often affect all four feet. A few horses will develop edema in the skin over the limbs and the underside of the girth and flanks, and occasionally bruises (petechiae) will be noticed on the mucous membranes. Pregnant mares are at risk of spontaneous abortion even months after infection.

A presumptive diagnosis is based upon clinical symptoms and location within endemic areas. A positive blood and fecal DNA test, where available, for N. ristici is definitive, but antibody titers are unreliable. In any case, horses suspected of PHF should be treated aggressively to prevent dehydration and laminitis. Pretreatment x-rays of the feet should be taken as a reference should laminitis occur.

Treatment will consist of IV fluid and electrolyte replacement, antibiotics, frog pads, and anti-inflammatory drugs. Although vaccination is of little value to an infected horse, it may help reduce symptoms in other horses in case of an outbreak. The vaccine has limited duration of protection and will not prevent the infection, only reduce the severity of disease.

Consult your veterinarian about whether vaccinating for PHF is appropriate in your area.

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Ringworm (dermatophytosis)

Ringworm is very common in horses and may be confused with many other skin diseases due to its variable appearance. Veterinarians refer to ringworm as dermatophytosis, meaning an overgrowth of specific microbes that live on the skin. Not caused by a worm at all, ringworm is a fungal infection of the skin and hair follicles caused by the Trychophyton and Microsporum genera of fungi, closely...

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Ringworm is very common in horses and may be confused with many other skin diseases due to its variable appearance. Veterinarians refer to ringworm as dermatophytosis, meaning an overgrowth of specific microbes that live on the skin. Not caused by a worm at all, ringworm is a fungal infection of the skin and hair follicles caused by the Trychophyton and Microsporum genera of fungi, closely related to dermatophytes known for causing raised ring-shaped skin lesions on people and other animals. In horses, the disease generally appears as localized patches of hair-loss that grow larger as the infection spreads.

In many cases, horses seem undeterred by ringworm infections. The lesions may become irritated and inflamed however, and may start to itch and flake causing the animal to rub and scratch. The two species of fungus most commonly associated with ringworm in horses are T. equinum and M. equinum, but other genus / species of ringworm may spread to horses from other animals, including dogs, cats, pigs, and humans, especially if the horse is immuno-compromised. Equine ringworm is a zoonotic disease, meaning it has the potential to spread to and infect people.

Ringworm fungus grows on keratin-rich hair shafts near or just beneath the surface of the skin. The fungus causes the hair to become devitalized and break off, leaving a fine stubble in a dime to quarter-sized circular pattern. It may also invade the outer layer of the skin, causing flakes and scales to form. Hairs at the lesion’s borders pluck easily because of damage to the follicles.

The incubation period for ringworm – the time between exposure and the onset of symptoms – is between a few days and one month.

The fungus is spread most effectively by direct contact with other horses. Contaminated equipment, tack, blankets, and even handlers may spread the disease as well. Adult horses may become carriers of the fungus, never exhibiting obvious symptoms but spreading disease none-the-less. Younger animals are more susceptible to ringworm infection than their adult stable-mates.

Because shared blankets and tack can be a source of contamination, patches of hair-loss may first appear in the shoulders, flanks, and girth. Horses sweat under tack, lending warm, moist environments ideal for fungal growth. A species of Trychophyton carried by rats and mice can occasionally contaminate feeds and feeding supplies, causing lesions that originate on the face. Ringworm may then spread to other parts of the body as isolated circular lesions or generalized regions of hair-loss.

Because the disease is so highly contagious, horses suspected of having ringworm should be immediately segregated from the herd. All equipment, tack, and grooming supplies must be thoroughly disinfected with dilute bleach or an appropriately labeled anti-fungal cleaning product. Bedding should be properly disposed of to avoid contamination, and blankets should be scrubbed with bleach solution and completely dried before storage or reuse. The veterinarian may prescribe a shampoo containing miconazole, which is used daily for one week, then weekly until the lesions heal. Alternatively, chlorhexidine or betadine sprays may be employed to control the infection.

Ringworm infection should be confirmed by a veterinarian prior to treatment by a fungal culture on DTM, or dermatophyte test medium. Hair samples from the newest lesions are plucked, and while treatment is ensued, the fungus is grown for a week or more on DTM agar plates until it can be isolated and identified by species. Ringworm testing may help to preclude spreading of the disease to the rest of the herd (and handlers), as the horse may be contagious for several weeks while being isolated and treated.

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Pre-purchase Examination

One must not forget that owning a horse is an emotional investment in addition to a monetary expense. Once the horse becomes a resident on the family farm, who could deny it love and care if it becomes obvious that the animal has serious health concerns? Most purchases are “as-is”, so it is crucial to know ahead of time whether the horse will be able to meet its intended purpose, or if it will be ...

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One must not forget that owning a horse is an emotional investment in addition to a monetary expense. Once the horse becomes a resident on the family farm, who could deny it love and care if it becomes obvious that the animal has serious health concerns? Most purchases are “as-is”, so it is crucial to know ahead of time whether the horse will be able to meet its intended purpose, or if it will be a charity case that may test the owner’s limits financially as well as emotionally. It is obviously wise practice to be sure that a horse purchase is a good “business decision”, but it is still more important to understand who will be emotionally responsible for the humane care of the animal should there be a serious problem discovered after the purchase. Just like a used car should be inspected by a qualified mechanic to assess its condition, every horse no matter how perfect in outward appearance, should be thoroughly evaluated by the veterinarian to verify its current health and vitality. This evaluation is called a pre-purchase examination, or purchase exam for short.

Pre-purchase examinations vary greatly in the depth of investigation and screening that is undertaken by the veterinarian. The difference is dependant upon the intended use of the animal and directly affects the cost of the exam. Competition animals could undergo a battery of tests and be examined by multiple experts. Companion animals should be examined too, but possibly to a slightly lesser extent that still gives reasonable assurance that the horse is healthy. Keep in mind that the pre-purchase exam cannot absolutely rule out future health problems that may arise.

The buyer should feel comfortable with what will be assessed during the pre-purchase examination. If communication is unclear about what will be included in the exam, what can be ruled in or out, and what will remain uncertain about the horse during the exam, the owner may want to explore other avenues. The veterinarian should be very familiar with the breed and must be aware of the history and future intended use of the animal. Be sure to inform the doctor if you plan to breed or show the horse. The buyer and seller may both be present during the examination, but the veterinarian should represent the buyer. He or she should be willing to discuss the findings in private with the prospective new owner.

The owner should not expect a “buy” or “don’t buy” answer from the veterinarian concluding a pre-purchase exam on an apparently healthy horse. The doctor will instead help the buyer to make an informed decision by discussing the findings objectively. While it is difficult to predict the future, the veterinarian will try to explain any abnormal findings and their significance. If a connection to an active disease process can be found, the treatment options, other diagnostic tools that can be explored, and prognosis will be discussed so that the new owner is fully aware of what to expect.

Pre-purchase exams are designed to protect a buyer from investing in the proverbial money pit. They will also help preclude serious heartache after the emotional investment is made in an equine companion.

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Salmonella Infections (enteric salmonellosis)

Enteric Salmonellosis is a bacterial overgrowth and infection of the gastrointestinal tract by one or more of the hundreds of species of Salmonella. The bacteria are capable of infecting most mammals including humans and horses, as well as birds and reptiles. Most of the time, horses are exposed by a fecal to oral transmission route. Salmonella-positive feces may contaminate grazing pastures and...

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Enteric Salmonellosis is a bacterial overgrowth and infection of the gastrointestinal tract by one or more of the hundreds of species of Salmonella. The bacteria are capable of infecting most mammals including humans and horses, as well as birds and reptiles. Most of the time, horses are exposed by a fecal to oral transmission route. Salmonella-positive feces may contaminate grazing pastures and prepared feeds. The disease may also be contracted from water, especially when an infected bird, rodent, or reptile has drown and decomposed in a horse’s water supply.

Salmonellosis is probably the number one cause of infectious diarrhea in horses. Exposure to the bacteria does not always cause disease, however; the factors that influence the development and severity of symptoms include the bacterial strain of Salmonella, the quantity of the organisms ingested, the immune status of the animal, stress (extreme exercise, overcrowding, diet change, surgery), and antibiotic use (modification of the normal bacterial flora in the gut).

Salmonella causes intestinal disease resulting in diarrhea by invading the lining of the GI tract, releasing enterotoxins which cause the leakage of fluids, protein, and electrolytes through the gut-wall into the stool, and immune-mediated inflammation. Diarrhea is often severe and is accompanied by abdominal discomfort. Overt infection by Salmonella will cause acute symptoms, but a bacterial overgrowth may be responsible for intermittent or chronic diarrhea as well. Systemic toxemia, as seen in advanced cases, can lead to bleeding disorders and cardiovascular shock, represented by petechiae (bruises) and hyperemic (dark red or purple) mucous membranes. Sub-acute cases of Salmonella may cause mild to moderate colic with or without diarrhea.

Horses with Salmonella infections will usually become dehydrated (even without outward signs of fluid loss), have a rapid heart rate, run a fever, and exhibit abdominal distension (bloating). The animal may also experience gastric reflux, the uncontrollable backflow of stomach contents into the esophagus. Serious secondary concerns attributable to Salmonellosis include laminitis, hypoproteinemia, liver and kidney dysfunction, disseminated intravascular coagulation (DIC), and pneumonia.

Salmonella should be confirmed in suspected horses by positive fecal cultures or DNA (PCR) testing for the bacteria. Pending test results, the horse will be treated supportively with IV fluid and electrolyte replacement, plasma or colloid therapy in the case of shock or hypoproteinemia, and possibly parenteral nutrition supplementation. The use of antibiotics in presumed cases of Salmonella (lacking positive test results and verification of antibiotic susceptibility) is not recommended except in the case of immuno-compromised horses. There are many strains of antibiotic-resistant Salmonella, and the indiscriminant use of antibiotics is thought to contribute to the development of these hard-to-kill bacteria. This is a definite concern in human cases of Salmonella infection.

Aggressively treated horses should show good response to supportive therapies within a week. Horses that continue to have severe diarrhea beyond 10 days may not survive the disease.

Preventing Salmonella in unexposed herds is straightforward. General cleanliness is essential. Keeping stalls free of feces, changing bedding materials frequently, and regular disinfection of feed buckets, water troughs, and other equipment will prevent exposure to potential sources of Salmonella. Overcrowding causes stress, unsanitary conditions, and ideal scenarios for the spread of disease, and should always be avoided. Handlers may transport Salmonella from a contaminated area to a susceptible animal on hands, boots, and clothing; they can even become infected themselves. Good hygiene practices and regular hand washing in disinfectant soap is indispensable.

Horses with diarrhea should be segregated from the herd as soon as possible and while testing for Salmonella is pending. All exposed tack, stalls, buckets, water supplies, and equipment must be thoroughly de-soiled, washed, disinfected, and dried before reuse. Exposed feeds, which may have been the original source of the infection, should be disposed of properly or incinerated – never shared with healthy horses.

An infected horse should continue to be isolated from healthy animals for at least 2 weeks following remission. Some veterinarians delay turnout until the horse is no longer Salmonella-positive. A negative PCR test is reliable, but cultures should be repeated and confirmed to be negative five consecutive times.

Salmonella is zoonotic (can be transmitted to humans and cause illness). Sanitary precautions should be taken to prevent fecal oral exposure to humans also.

Equine diarrhea PCR panels are available to ensure that new horses are free from several causes of diarrhea before the introduction into the healthy herd.

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Sarcoids

A sarcoid is a slow growing tumor that occurs in the skin of a horse most often on the legs, in the flanks, on the abdomen, or anywhere on the head and neck. They are of an uncertain origin but are thought to be linked to a virus similar to the bovine papilloma virus. Sarcoids may also form in the location of a previous wound, but the relevance is not understood. Breed predilection might exist in ...

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A sarcoid is a slow growing tumor that occurs in the skin of a horse most often on the legs, in the flanks, on the abdomen, or anywhere on the head and neck. They are of an uncertain origin but are thought to be linked to a virus similar to the bovine papilloma virus. Sarcoids may also form in the location of a previous wound, but the relevance is not understood. Breed predilection might exist in Appaloosas, Quarter Horses, and Arabians, but this too is unconfirmed.

Sarcoids take on several outward appearances which may lead to a presumptive diagnosis. They can be wart-like (verrucose) – poorly defined margins with raised bumpy surfaces that may or may not be ulcerative; fibroblastic – cauliflower shaped, pedunculated (attached by a stem), and ulcerative; flat (occult) – hairless, smooth, or slightly scaly; or combination (transitional) types.

The physical appearance of the sarcoid may help to determine the level of urgency in taking action. In general, fibroplastic and transitional tumors pose more of a risk to the horse in terms of secondary infection (i.e. tetanus) and local invasion into surrounding tissues. They also attract the attention of flying insects which can cause greater damage and transmit pathogens (possibly even Sarcoids to other horses). An ulcerative tumor will be addressed with greater haste than a smooth, unremarkable mass.

Histopathological examination of the tumor cells and structure is the only definitive way to confirm a sarcoid. The tissue is fixed in formalin and delivered to the laboratory for microscopic evaluation by a pathologist, a veterinary specialist trained in the cellular appearance of disease. Many veterinarians believe from past experiences that a partial biopsy of the mass may cause it to become active; therefore, a complete excision (removal) is planned or performed before initial confirmation in the lab. Differential diagnoses for Sarcoids include granulation tissue over a wound or skin cancer (melanoma or squamous cell carcinoma).

Excision can be performed under general or local anesthesia, depending on the size and location of the tumor. Because complete removal with clean tissue margins is recommended and often curative, general anesthesia is preferred. (The term “clean margins” refers to the ideal finding that no tumor cells are seen within a comfortable distance of the edges of the mass under the microscope.)

Other treatments that may be needed if the tumor is poorly differentiated include radiotherapy (focused x-ray exposure), chemotherapy (drugs that target abnormal mutations of cells), immunotherapy (drugs and supplements that boost or suppress certain functions of the immune response), and follow up surgery.

Sarcoids are mostly locally invasive. They can become very large and difficult to remove, or ulcerated and infected, which obviously increases the risk to the horse and the expense of treatment. There is also new data that shows that sarcoids may metastasize (spread) to other areas of the skin.

Every mass discovered on a horse should be evaluated by a veterinarian.

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Strangles: Treatment and Prevention

“Strangles” in horses is a highly contagious disease caused by the bacteria Streptococcus equi. It is spread by inhalation or oral intake of the organism during direct contact with the respiratory secretions of an infected horse or by fomites – contaminated equipment, tack, stalls, feeding buckets, and water troughs. Insects, and even handlers can serve as vectors, though the causative bacteria...

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“Strangles” in horses is a highly contagious disease caused by the bacteria Streptococcus equi. It is spread by inhalation or oral intake of the organism during direct contact with the respiratory secretions of an infected horse or by fomites – contaminated equipment, tack, stalls, feeding buckets, and water troughs. Insects, and even handlers can serve as vectors, though the causative bacteria are only known to infect equids (horses, donkeys, mules).

Strangles gets it name from the clinical appearance and symptoms of infected horses. Lymph nodes of the face and neck often become quite enlarged, causing the horse to experience trouble breathing and painful swallowing. Most horses recover from Strangles within a few weeks; however some cases progress to life-threatening infections or persistent complications. The disease is often fatal in foals that did not develop adequate protection through colostral antibodies. Prevention measures are vital to keeping this disease from spreading throughout the herd.

The horse’s symptoms and the identification of S. equi through nasopharyngeal and lymph node cultures are used to diagnose Strangles. Symptoms develop in 3 days to 3 weeks after exposure and begin with a moderate fever, reduced appetite, and mucopurulent or snotty nasal discharge. The horse will begin to experience throat pain and stand with the neck extended as regional lymph nodes become infected and engorged with pus. Respiratory distress occurs when swelling becomes severe. At that point, the lymph nodes may abscess, or rupture and drain through the skin beneath the mandible, or lower jaw.

Streptococcus equi can occasionally invade the thorax and abdominal cavities through lymph circulation. This condition is referred to as “Bastard Strangles” and is certainly life-threatening. It can occur weeks or months after the outward symptoms of infection have abated.

Another possible complication of S. equi infections is an immune reaction called Purpura haemorrhagica. This is an inflammatory disease of the peripheral blood vessels resulting in severe edema (tissue swelling) in the limbs and head. Tiny bruises may be visible in the mucous membranes as this “allergic reaction” to the bacteria develops.

All suspected cases of Strangles should be immediately segregated from other horses and examined by a veterinarian. Infected horses can be contagious for as long as 2 months after symptoms develop, so quarantine measures are vital to prevent the spread of the bacteria. Thorough disinfection of all equipment, stalls, troughs, grooming supplies, etc., is crucial. Handlers should change clothing and wash with antibacterial soap to reduce the chance of infecting healthy animals.

Veterinarians sometimes avoid the use of antibiotics in the treatment of Strangles, especially after symptoms have developed, reserving the drugs for complicated cases. Some evidence indicates that symptomatic horses may be more likely to develop internal lymph node abscesses if they are started on antibiotics, but this is still open to debate. Prophylactic antibiotic dosing in exposed but asymptomatic horses may reduce the chance of contracting the disease, but this practice carries a risk of inducing resistant bacterial strains and inhibiting natural immunity in the animal. Nonetheless, Streptococcus equi is usually susceptible to Penicillin, so the doctor may choose to treat very early cases in order to head off advanced symptoms and avoid an outbreak in the herd.

Warm compresses can be applied to swollen areas to reduce pain. If swelling impinges upon breathing and eating, the veterinarian may lance the lymph nodes to provide relief.

Whether the veterinarian prescribes antibiotics or not, a culture and susceptibility swab will usually be collected to confirm the presence of S. equi in the laboratory. This can help to predict the risk to other horses that may benefit from vaccination or prophylactic treatment.

Strangles vaccination may be recommended to reduce the severity of the disease in exposed horses. Currently available vaccine is not able to entirely prevent the disease, but it may reduce the symptoms and make lymph node abscess less likely. The vaccines also have a risk. If the horse has a high M-protein titer (blood test), the horse has a higher risk of getting Purpura haemorrhagica from the vaccine. In addition, the modified live intranasal vaccine should be handled with caution (abscess formation in muscle if administered intramuscularly).

About 10% of horses will become chronic carriers of Streptococcus equi and continue to act as reservoirs of the disease. A DNA test can help to identify these horses.

New horses should be quarantined before introduction to the herd. If no symptoms develop within three weeks, it is usually safe to allow them into the group. A veterinarian should always examine new horses to reduce the risk of infecting other animals with contagious diseases like Strangles.

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Snakebites in Horses

Horses share common stomping grounds with many other creatures that would prefer that they didn’t. Snakes and horses are two animals that will be at odds from time to time.

Despite the horse’s enormous strength and size by comparison, the snake in a confrontation has the advantage of camouflage and covert weaponry. Tiny, needle-sharp fangs not only deliver a sharp sting to the curious muzzle, but ...

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Horses share common stomping grounds with many other creatures that would prefer that they didn’t. Snakes and horses are two animals that will be at odds from time to time.

Despite the horse’s enormous strength and size by comparison, the snake in a confrontation has the advantage of camouflage and covert weaponry. Tiny, needle-sharp fangs not only deliver a sharp sting to the curious muzzle, but may also carry with them biological and chemical agents of warfare.

While the superficial punctures inflicted by a snake’s teeth are quickly shrugged off by a horse, bacteria transferred from the snake’s mouth may continue the attack for days and weeks to come. Furthermore, venomous snakes may inject locally and systemically toxic compounds that can subdue a horse many times the snake’s size.

In North America, most venomous snakebites to horses come from members of the pit viper family of snakes – rattlesnakes, copperheads, or water moccasins. Their venom is capable of causing severe localized tissue damage but is rarely potent enough to cause direct systemic toxicity in an animal the size of a horse. Coral snakes are one exception whose venom is neurotoxic to even horses. They are unrelated to pit vipers and are found in the southern states.

You may not be immediately aware that your horse has been bitten by a snake. Bites are usually found on the nose, muzzle, or lower limbs. Horses will usually have stumbled upon a snake while grazing or being ridden, rather than the weary snake seeking out the horse for a confrontation. Bites can occur any time of year, although snakes are more active during warmer months.

Snakebites in early presentation will usually appear as two small punctures, about an inch apart, in the center of a swollen and bruised area. Reaction to venom can cause a great deal of tissue edema – intracellular fluid, and tissue sloughing – tissue death. The wound site may open and drain, and the original bite wounds may not be obvious after some time.

If a bite occurs around the face, swelling may affect the mucous membranes of the sinuses, mouth, and upper respiratory passages. Respiratory distress, or even suffocation, can ensue if left unchecked. Consult with your veterinarian about placement of rigid tubing (e.g. 60cc syringe casing) in the nostrils to keep an airway open until arrival by doctor.

In some cases, bacterial toxemia, which can occur as a result of either a venomous or a “harmless” snake’s bite, is a secondary complication that may be a bigger concern than venom toxicity. Systemic inflammation may result from endotoxins released from bacterial colonies that have been introduced via the bite wounds.

If you suspect or witness a snakebite to your animal, the first thing to do is to stay calm. Move the horse away from the snake to prevent subsequent attacks to the horse and yourself. Some have claimed that it is critical to observe the type of snake responsible for the bite in order to ensure appropriate treatment; furthermore, it has also been said that you should attempt to collect the snake for confirmation of species. This is not only unnecessary, but also unwise. Do not put your horse, yourself, or other people at risk of being bitten. You may only make the situation worse.

The treatment for snakebites is usually supportive and in response to symptoms that arise. Antivenin, an antidote for snakebite venom, would seem like an urgent solution that warrants a gallop to the vet; however, it is derived from equine antibodies, thus its use holds risks all its own for the horse and is controversial if not contraindicated.

Do not attempt to remove snake venom from the site of the wound by any method. Folkloric remedies such as cutting open the wound and sucking out the poison puts your horse and yourself at risk of more serious consequences. Never use a tourniquet on any part of the animal. Ice packs, heat packs, and other remedies are unnecessary and may also cause further problems. Instead, keep the horse calm and call the veterinarian as soon as possible. Halter and stable the horse if possible, and stay with him until the vet arrives.

If the bite wound is old, it may have abscessed. In which case, it will be irrigated with antiseptic solution and treated with antibiotic preparations. If it is fresh, the veterinarian will prescribe antihistamines or NSAIDs to reduce inflammation of local and respiratory tissues and antibiotics to prevent bacterial infection and toxemia. Usually corticosteroids are avoided in snakebite cases, but may be warranted in the case of extreme respiratory inflammation or as a life saving measure.

Oral or intravenous fluid and electrolyte replacement may be needed if the horse succumbs to the toxic effects of snake venom or if bacterial toxemia results from established infection.

In most cases, snakebites to horses have a fair prognosis; recovery however relies on quick but calm action by the horse owner.

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Tetanus

Any wound or incision on a horse, if not kept clean and dry, can become infected by opportunistic bacteria. Clostridium tetani is a spore-forming bacterium common in soil and manure that is responsible for the very painful and potentially fatal disease Tetanus. C. tetani is a real concern in deep puncture wounds due to being anaerobic bacteria which thrive in environments lacking oxygen; but, it...

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Any wound or incision on a horse, if not kept clean and dry, can become infected by opportunistic bacteria. Clostridium tetani is a spore-forming bacterium common in soil and manure that is responsible for the very painful and potentially fatal disease Tetanus. C. tetani is a real concern in deep puncture wounds due to being anaerobic bacteria which thrive in environments lacking oxygen; but, it may also infect castration procedures, retained placentas, unhealed umbilical stumps in foals, or any break in the skin. C. tetani produce a toxin called tetanospasmin that blocks specific nerve transmitters which normally allow muscles to relax after constriction. The result is rigid paralysis of affected muscle groups in the limbs, neck, face, and tail. Eventually, the toxin causes respiratory paralysis, and death results when starvation, dehydration, or suffocation occurs.

C. tetani and tetanospasmin are close cousins to C. botulinum and botulinum toxin; however, tetanospasmin causes rigid paralysis, whereas botulinum toxin causes flaccid paralysis.

Clostridium tetani cannot grow and reproduce in the presence of oxygen. When the bacterium is exposed to air, it forms protective spores in which to lie dormant. These spores are resistant to heat, desiccation, UV radiation, and common household detergents and disinfectants. They can remain viable in soil for years. C. tetani is then reactivated when conditions are again favorable for growth. Neurotoxins are created inside the active bacteria and released when the life cycle is complete.

Tetanospasmin is one of the most toxic substances known to man in terms of the minimum amount required to cause death. It ranks third in potency after botulinum and diphtheria toxin. Horses are one of the most sensitive domestic animals to the effects of tetanospasmin, with a minimum lethal dose of about 0.1 to 0.3 nanograms per kilogram of body weight. (One nanogram equals one billionth of one gram – one gram is about three hundredths of one ounce)

Tetanus, the disease, is not contagious to other horses, animals, or people. It requires an established C. tetani infection that facilitates tetanospasmin delivery into the surrounding tissues. Rarely, tetanus can be acquired after ingesting the toxin released from bacteria in contaminated feeds. The toxin is carried from tissue to the spinal cord by a process called axonal transport. There it binds permanently to receptors used for skeletal muscle control, specifically blocking muscle relaxation. There is no known reversal agent that can remove bound tetanospasmin from the receptors. It may take days to weeks for symptoms to develop while enough toxin makes its way to the receptors at the spinal cord; tetanospasmin has no local effect on tissues immediately surrounding the infection.

The symptoms of Tetanus can vary depending upon the size of the infection and the size of the horse. Foals are very susceptible due to their smaller size as well as the immaturity of their immune systems. Lameness or an altered gait may be the first thing an owner notices, followed by spasms – an overreaction to sounds, touch, and visual stimuli. A “saw-horse” stance is commonly described as the disease progresses; the limbs and neck will be fully and painfully extended. The colloquial name for Tetanus is “lock-jaw”, which describes the clenched jaw and pulled back facial muscles that is also common. The horse will have trouble eating and drinking, and may eventually be unable to stand at all.

Respiratory paralysis is usually the final stage of the disease, if the horse does not succumb to dehydration or starvation first.

A diagnosis is made based upon clinical symptoms, the presence of a wound, and unvaccinated status. There is no test for Tetanus other than a culture that will confirm the presence of C. tetani. Even an apparently healed wound can harbor the anaerobic bacteria, however.

Successful treatment for Tetanus relies on quick recognition of the disease and aggressive therapy. There are three objectives that must be met in the effort to save the horse: First, the source of the infection, and thus the toxin, must be determined and disinfected. Wound lavage (hydrotherapy) and debridement (removal of devitalized tissue) is necessary to physically reduce the numbers of bacteria. Former wounds may be reopened surgically and explored for signs of bacterial infection. The infected wounds will be left open to heal by second intention; suturing would only secure anaerobic reservoirs of infection. Injectable antibiotics like penicillin and tetracycline are then given to kill bacteria deep within tissues.

Second, any unbound toxin remaining in the animal must be captured and eliminated using Tetanus antitoxin injections. It has already been said that there is no way to reverse the already bound tetanospasmin, so it is vital to protect healthy neuro-receptors if the horse is to be rehabilitated. New motoneural connections can be made over time while the animal recovers. Unfortunately, the Tetanus antitoxin can cause liver disease over time, so risk should be discussed with your veterinarian.

Third, symptomatic treatment is used to control spasms and muscle paralysis. Also, dehydration and anorexia is combated with fluids and electrolyte solutions given intravenously. Feeding through a nasogastric tube may be necessary if the horse cannot eat for an extended duration. Tranquilizers, muscle relaxants, and anti-inflammatory drugs are given to improve symptoms of pain, spasm, and paralysis. In some cases, the horse may be catheterized and rectally palpated to remove urine and fecal material that has been retained. At the point when respiratory support is required, the prognosis is grave and humane euthanasia may be elected over prolonged suffering.

In any case, the prognosis for an animal with Tetanus is guarded at best. The fatality rate is 50 to 70% despite treatment. It is always better to institute prevention methods for this devastating disease. Tetanus toxoid vaccination is safe and effective and is considered a core vaccine for all horses regardless of location and purpose. Please see Vaccination Recommendations for Horses for recommended vaccination protocols.

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FIND US

Texas West Animal Health

16367 South FM 4,

Santo, TX 76472

Phone. 940-769-2222

Fax. 866-632-3365

Email. texaswestvet@gmail.com