Equine Articles

Owning a horse is hard work, but it’s one of the most rewarding experiences one can have. To help make caring for your horse a little easier, we’ve gathered a list of equine-related articles that contain a wealth of helpful information. Whether you’re looking for information on keeping your horse healthy, tips on bringing out the best in his or her performance or just learning how you can keep your horse happy, you’ll find everything you need here.

Angular Limb Deformities

Angular limb deformities are either congenital (present at birth) or acquired (caused by disease that affects bone growth). The condition describes a deviation in the shape of the limb bones from what is considered normal. When present, the bones bow toward or away from the center of the foal’s midline as observed from the front of the animal. It is most common that this deformation occurs at the ...

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Angular limb deformities are either congenital (present at birth) or acquired (caused by disease that affects bone growth). The condition describes a deviation in the shape of the limb bones from what is considered normal. When present, the bones bow toward or away from the center of the foal’s midline as observed from the front of the animal. It is most common that this deformation occurs at the knees. “Bow-legged-ness” is called carpus varus, whereas “knock-kneed-ness” is called carpus valgus. The most common angular limb deformity seen in foals is carpus valgus.

Bones of the limbs are capped with a growth plate that accommodates the bones’ lengthening while the foal matures. Excessive intake of energy-dense feed during rapid growth phases in addition to imbalance of mineral intake are thought to cause the growth plates to develop more prominently on one side of the joint than the other. This problem affects the left and right limbs symmetrically. Crib feeding may cause competition between foals which often ends in one foal hoarding more grain. This “gluttony” leads to nutritional overloads in the dominant foal which may result in acquired angular limb deformity.

Congenital defects may cause the cuboidal bones in the knees to remain soft and susceptible to deformation during exercise after the foal is born. Once the bones finally do harden by a process called ossification, the limbs will permanently deviate from a normal angle unless corrected.

Thoroughbreds may be slightly more at risk for developing angular limb deformities, but any breed or sex horse may be affected. Visual inspection usually leads to a presumptive diagnosis. The foal is observed from the front and the rear and while walking on level ground to confirm lateral deviation in the limb at the carpus (knee), fetlock (ankle) and/or tarsus (hock). Many times the affected joints will be swollen by synovial effusion (inflammatory joint fluid). Lameness is likely in the cases of cuboidal bone damage, but is not necessarily present in acquired limb deformity caused by diet until later in life. Abnormal hoof wear will be present in either case and is proportional to the degree of limb angle deviation.

If limb deformities are seen at birth or shortly after birth, the foal should be treated by a veterinarian as soon as possible before complete bone ossification. Splinting or casting the limbs for several weeks after birth may help “set” the bones at a more normal angle. Sometimes x-rays are taken in older foals to help confirm the condition and calculate the limb angle. Corrective farriery is usually very helpful in treating these horses. Surgery will be indicated when the angle of deviation is greater than 10 to 12 percent from normal (>12° anglation).

There are numerous techniques employed in the surgical correction of angular limb deformities. The orthopedic surgeon will determine the best option depending on the particular case. It is very important that the foal is examined early if surgery is to be considered. The success rate is inversely proportional to age of the animal.

In order according to the severity of the condition, treatment starts with a conservative approach. This may include stall rest for up to 8 weeks, repeated x-rays to assess bone ossification progress, splinting or casting, corrective hoof trimming and shoeing, periosteal stripping (minor surgery), and orthopedic surgery.

The prognosis for angular limb deformities depends upon severity of the condition, how early recognition and intervention occurs, and the expected use of the horse. About 2/3 of horses diagnosed with incomplete cubodial bones ossification of the tarsus (hock) will not be able to be used productively.

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Blister Beetle Toxicity

Blister Beetles are extremely toxic to horses when the insects are accidentally ingested. They may contaminate alfalfa hay which is a very popular feed for its excellent nutritional profile. Only six grams, or two tenths of one ounce, of blister beetle parts are potentially lethal to a fully grown horse. The insects’ toxic potency does not decrease upon death of the beetle; the whole insect is...

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Blister Beetles are extremely toxic to horses when the insects are accidentally ingested. They may contaminate alfalfa hay which is a very popular feed for its excellent nutritional profile. Only six grams, or two tenths of one ounce, of blister beetle parts are potentially lethal to a fully grown horse. The insects’ toxic potency does not decrease upon death of the beetle; the whole insect is not required to induce toxicity.
Blister Beetles produce a chemical called cantharidin that causes “blisters” (thus the name) in the mucous membranes of the gastrointestinal tract. High blood levels of the toxin can also result in lesions of the heart, kidneys, and urinary bladder. None of these symptoms are obvious to the horse owner, whose only clues to the problem maybe colic, inappetence, drooling, “thumps” or “hiccups”, diarrhea, or bloody stool or urine. Unfortunately, outward signs may be subtle despite a lethal toxicity, and death may occur without much warning.

On blood-work, the veterinarian will see evidence of renal damage and reduced levels of blood calcium and magnesium. The doctor may also detect abnormal heart rhythms associated with toxic shock.

There is no antidote for the Blister Beetle toxin. Horses are treated supportively and sources of the beetles are removed to avoid further toxicity. Intravenous fluids, electrolyte supplementation, and parenteral nutrition may all be given to avoid dehydration and subsequent kidney damage. If the horse has recently ingested the blister beetle contaminated alfalfa, the veterinarian may administer activated charcoal to absorb the toxin. Sucralfate is a drug that forms a protective layer over gastric ulcers and may provide some relief of pain and avoid further tissue damage. Other medications given may include H2 blocker antacids and proton pump inhibitors to reduce acid production and absorption of the toxin, mineral oil to accelerate passage of the ingesta, and prophylactic antibiotics to prevent sepsis (systemic bacterial infection).

The only way to prevent this deadly toxicity is to secure a reputable source of alfalfa (which could still become contaminated) or eliminate alfalfa from the horse’s diet. The veterinarian can help guide the horse owner in this manner.

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Anthrax

Anthrax is a very serious, often lethal, reportable disease that is caused by toxins produced by bacteria called Bacillus anthracis.  In most livestock, mass die-off may be the first indicator that anthrax has infected the herd; horses have a slight resistance to the effects of the toxins, so a sick horse may be seen before the disease causes death.  Anthrax is deployable as a military weapon...

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Anthrax is a very serious, often lethal, reportable disease that is caused by toxins produced by bacteria called Bacillus anthracis.  In most livestock, mass die-off may be the first indicator that anthrax has infected the herd; horses have a slight resistance to the effects of the toxins, so a sick horse may be seen before the disease causes death.  Anthrax is deployable as a military weapon against people and livestock, so the disease must be reported to a veterinarian if it is suspected.  Bacillus anthracis can form spores that lie dormant in soil for years, so sporadic natural infections are known to occur in several parts of the country.

Anthrax naturally spreads by accidental inhalation or ingestion of the dormant spores from soil contaminated by the carcass of an animal that succumbed to the disease.  Bison bones have been shown to harbor viable spores for at least 100 years.  Anthrax spores may be distributed over a wide area after flooding.  Once the spores enter the horse, they are reactivated and become the vegetative form of the bacteria.  They multiply rapidly within the bloodstream and produce toxins that are responsible for disease.  Biting flies are another possible vector of anthrax, carrying spores or vegetative bacteria from one animal to another during interrupted feeding.

Anthrax develops rapidly, causing fever as high as 1070F, followed by death.  Horses may have swelling in the underside of the barrel, decline food, and seem very depressed and lethargic.  Horses found already deceased will lack rigor mortis and have black blood seeping from the mouth, nose, and anus.  A horse carcass will be a reservoir of bacteria that can infect other animals and humans, so careful precautions must be taken if a horse is discovered with these signs.  The veterinarian should be immediately notified so that anthrax can be verified in the lab.

Surviving horses in the herd and on adjacent farms (as well as other livestock) should be vaccinated at once if a positive animal is detected.  All horses that have normal temperatures may receive the vaccine with the exception of pregnant mares, and any horse showing a fever will be treated with antibiotics.  The earlier an animal is treated, the more likely it is to survive.

Because anthrax persists in the environment, the veterinarian and health department will be consulted for safe disposal of the carcass and site disinfection.  Disturbing or transporting the carcass before a diagnosis is known may make complete disinfection impossible.

If anthrax is ever suspected, these steps should be taken to minimize exposure to people and other animals:

  • Contact the veterinarian immediately.

  • Do not handle or disturb a carcass with signs of anthrax.

  • Disinfect / decontaminate before handling other animals.  (skin, clothes, boots, equipment)

  • Take temperatures of other herd members daily for 10 days.  Vaccinate / treat according to veterinary recommendations.

  • Notify the family doctor if human exposure has occurred.

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Botulism (Clostridium botulinum toxin)

What is Botulism?

Botulism is widely known as a severe form of food poisoning in people, but horses, especially foals, are also susceptible. The disease is caused by the effects of toxins produced by several strains of bacteria in the genus Clostridium. Specifically, C. botulinum is responsible for the neurotoxins that result in generalized weakness, flaccid paralysis of the tongue, difficulty...

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What is Botulism?

Botulism is widely known as a severe form of food poisoning in people, but horses, especially foals, are also susceptible. The disease is caused by the effects of toxins produced by several strains of bacteria in the genus Clostridium. Specifically, C. botulinum is responsible for the neurotoxins that result in generalized weakness, flaccid paralysis of the tongue, difficulty swallowing, and eventually respiratory failure. Another species of Clostridium, C. tetani, causes Tetanus in horses and other mammals; however the classical symptoms and the routes of entry of the two diseases are easy to differentiate. Botulism most often occurs after the ingestion of contaminated feed, whereas Tetanus is a secondary complication of infected wounds. In foals, Botulism is the cause of “Shaker Foal Syndrome”, which likely proves fatal if not treated aggressively.

How does a horse get exposed to Botulism?

A horse’s feed and water may become contaminated by Botulinum toxin in several ways. Rodents, snakes, or other small animals carrying the bacteria may become trapped during harvesting and baling methods, or may drown in a horse’s water supply. As oxygen is depleted in the decaying animal’s body, C. botulinum will begin rapidly forming toxin-releasing spores. The spores form only under anaerobic conditions such as this, where there is little to no oxygen in the bacteria’s environment. As the small animal decomposes, the powerful botulinum toxins are released and contaminate the surrounding feed and water. Any horse that ingests enough of the toxin will succumb to its devastating effects.

Fermented forage feeds (haylage) may also become contaminated with C. botulinum by the same process. The conditions inside a sealed bag of haylage, with high moisture content and low oxygen levels, are ideal for Clostridium to sporulate unless the fermentation process maintains a very acid pH (< 4.5)="" throughout="" the="" bale.="" it="" may="" not="" be="" possible="" to="" detect="" a="" “spoiled”="" bag="" of="" haylage="" by="" sight="" and="" smell="" alone.="" one="" may="" find="" as="" many="" endorsements="" as="" there="" are="" precautions="" about="" feeding="" haylage="" to="" horses.="" for="" horses="" that="" may="" benefit="" from="" haylage="" supplementation,="" such="" as="" those="" requiring="" ultra="" low-dust="" feeds,="" contract="" a="" reputable="" source="" for="" the="" bales="" and="" consult="" your="" veterinarian="" as="" to="" whether="" the="" benefit="" outweighs="" the="" risk="" of="" botulism="">

Foals may be exposed to botulinum toxin through contaminated feeds or from the environment. Because very young foals have underdeveloped immune systems, it may be possible (although rare) for a foal to develop Botulism by ingesting the bacteria alone – from soil or contaminated manure, etc. On the other hand, it would be very unlikely for an adult horse to be made ill by these otherwise harmful bacteria which may normally reside in very small populations within the GI tract. The normal bacterial flora in the healthy adult horse naturally inhibits C. botulinum sporulation.

Occasionally, Botulism may occur from infection of a wound with C. botulinum. This is more commonly the route by which Tetanus affects the horse, however.

What are the symptoms of Botulism?

In foals and adult horses, as well as humans, botulinum toxin causes profound neurological deficits. It interferes with the transmission of normal electro-chemical signals between targeted motoneurons and muscle tissue, resulting in the inability of certain muscles to contract. Generalized weakness and depression is soon followed by flaccid paralysis of the upper and lower GI tract and eventually the muscles that control respiration. (In contrast, Tetanus causes rigid paralysis, where the muscles fail to relax.) The tongue may hang from the side of the mouth, the nursing foal will drool milk, the eyelids will sag, and there will be difficulty swallowing food and water. The tail will also begin to fall, and the superficial muscles of the horse will fasciculate, or tremble. This appearance is what lends the name “Shaker Foal Syndrome”.

As the disease progresses, the horse will become unable to rise or remain standing. Internally, the digestive tract loses its normal contractions, called peristalsis, and constipation occurs – although rarely noted as an observed symptom. At complete ileus (intestinal paralysis), watery diarrhea may occur.

Ultimately, the neurotoxin inhibits the muscles that control breathing. Death occurs as a consequence of suffocation, dehydration, or secondary complications from the horse being down.

The cascade of symptoms can begin within a matter of hours after ingestion of a significant amount of botulinum toxin or may take days to become evident, depending upon the exposure. When adult horses, or especially multiple horses in a group, become symptomatic, contaminated feed or water should be suspected as the primary source of toxin.

What is the treatment for Botulism and how can we prevent the disease?

 

In order for treatment to be effective, the exposure to botulinum toxin must be recognized early. Plasma transfusions containing antitoxin are administered intravenously in addition to penicillin. The plasma antitoxin will block any free botulinum toxin in the bloodstream from binding with healthy motoneurons, while the penicillin will help to kill any toxin-producing bacteria in the GI tract or other tissues. There is no treatment available to reverse the damage that has already occurred to affected nerve cells; instead, the horse’s body will require several days to weeks to rebuild new neuromuscular junctions and regain normal use of the dysfunctional muscles.

Supportive treatment, once the horse is unable to eat, drink, and rise on its own - and especially if respiratory paralysis has occurred – is extremely difficult and costly. Pressure sores, colic, and secondary infections can be as challenging to address as the primary illness itself.

Obviously, it is better to prevent exposure to Botulism in the first place. Harvesting and baling methods must assure that moisture is kept to a minimum. Never feed hay that contains decayed, discolored, moldy, or off-smelling content. Round bales can be especially difficult to assess for quality until the bales are opened. Consult a veterinarian for recommendations before feeding haylage, since it is especially susceptible to contamination.

Fortunately, approved vaccines are available to prevent Botulism in foals, broodmares, and other adult horses. Mares should be vaccinated before foaling, and vaccination is suitable for foals as early as two weeks of age in high risk situations. Other adults are typically boostered yearly. Your veterinarian will advise you on an appropriate vaccination schedule for your horses’ particular exposure risk.

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Castration: why, when, and how?

Castration means the complete surgical removal of the testicles.  There are three common reasons that this procedure is performed:  to prevent breeding, to reduce aggressiveness / unruliness, and in the case of undescended testicles (cryptorchidism). Castration surgery is very common and is not considered technically challenging to the veterinarian; nonetheless, it should be left to the trained...

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Castration means the complete surgical removal of the testicles.  There are three common reasons that this procedure is performed:  to prevent breeding, to reduce aggressiveness / unruliness, and in the case of undescended testicles (cryptorchidism). Castration surgery is very common and is not considered technically challenging to the veterinarian; nonetheless, it should be left to the trained and licensed professional, because serious and sometimes life-threatening complications are possible if the procedure is not done correctly.  Diligent aftercare by the horse owner is also very important to minimize problems associated with post-op negligence or inappropriate treatment.

The testicles are dual-purpose organs.  Part of the male reproductive system, they produce and incubate spermatozoa; and as an endocrine gland, they secrete numerous hormones including testosterone.  Testicles are located in the scrotum, which is a retractable sac that helps control the temperature of the testicles by moving them closer to, or further away from, the body.  (Sperm develops at a slightly lower temperature than normal body-core temp.)  A cord suspends each testicle within the scrotum, and contains several components:  a blood supply, a duct to carry sperm to the urethra and outside of the body, a gubernaculum muscle, and nerve branches.  During castration, the cords are severed and each testicle is removed.  The scrotum is usually opened yet not removed and will retract on its own over time.  The procedure cannot be reversed (it is not similar to a vasectomy performed on men that is sometimes reversible).

Castrations can be done on any age of horse, precluding any animal with health problems that would prevent the surgery.  Ideally, it should be done at a young age, less than one year preferably, to prevent aggressive behaviors from developing and accidental breeding.  Once a stallion becomes aggressive, castration may not fully resolve his unruliness.  Some owners prefer to wait as long as three years in order to allow the male horse to develop a more muscular and masculine appearance.

Cryptorchidism is a condition in which one or both of the testicles fail to descend from the abdomen, where they develop in the fetus, into the scrotum just before birth.  After birth, the inguinal rings through which the testicles should have moved will close.  The testicles will usually not descend afterward, except in rare cases of “temporary inguinal retention”.  The retained testicle(s) will not be able to produce viable sperm (because of increased temperature within the body), but will continue to produce testosterone.  One retained testicle is referred to as unilateral cryptorchidism (the descended testicle is fully functional).  With both testicles undescended, the condition is called bilateral cryptorchidism (the horse will be sterile).  Retained testicles are usually abnormal in structure as well, and may become problematic later in life, possibly forming a tumor.  Cryptorchid horses are just as likely to become aggressive as would an intact stallion.  The condition is thought to be heritable, or genetically passed from the parent to the colt, although this is open to debate.  Nonetheless, it is not a desirable trait, and unilaterally cryptorchid males should not be allowed to breed, despite being able to do so.  The surgical procedure for cryptorchid animals is more invasive and is not described here.

Normal castrations are performed in several ways according to the preference of the veterinarian.  A standing castration involves sedation and local anesthesia of each testicle.  The surgical site is disinfected, and an incision is made through the scrotum over each testicle.  The testicle is exteriorized, the cords crushed with an emasculator or ligated with sutures, then cut free from the body.  The veterinarian will examine the remaining portion of the cords for bleeding and intervene with additional ligatures if there is persistent hemorrhaging.  The incisions in the scrotum are left “open” to heal by second intention (without suturing).  Problems that can occur during the standing castration include injury to the animal, the veterinarian, and assistants should the horse object, kick, and struggle.  Many veterinarians choose not perform standing castrations for these reasons.  If an emergency such as excess bleeding occurs, the horse will have to be immediately anesthetized and the problem corrected.

Recumbent castrations require the horse to receive a general anesthetic, and may be performed in the field or at the veterinary hospital.  The latter is preferred because of the cleaner controlled environment and improved sterility.  Still, most are done in the field.  After the horse is fully anesthetized and laid on its side, the same surgical procedure described above will be performed.  In the hospital however, there is the option to close the incisions, in hopes of preventing some of the potential complications that may arise after surgery.

Many owners worry about their horse surviving a general anesthetic.  Actually, anesthetic accidents are very rare.  Albeit more expensive, recumbent castrations are overall safer for the animal (not to mention the doctor) in minimizing risk and avoiding complications.

After surgery, the owner should follow the veterinarian’s aftercare instructions.  These will include keeping the incision clean and watching for excessive swelling or any protrusions from the openings.  The first 12-24 hours after castration, the horse should be confined to his stall to fully recover from the anesthetic drugs.  Afterward however, the horse will require forced exercise if the incisions are left open.  This will encourage the drainage of accumulating serum from the incisions.  If the horse is kept overly confined, the retained serum may form a seroma (fluid filled mass) and may lead to pain, infection, self-trauma, and delayed healing.  On either surgical technique, there is a slight risk of inguinal eventration (hernia).  Eventration is a life threatening emergency where a loop of intestine becomes strangulated through the inguinal ring and incision.

Some swelling is expected after surgery, but if it becomes severe, or the incisions appear angry and inflamed, there is pus (milky discharge) or protrusions of tissue from the wounds, or the horse seems especially uncomfortable, the veterinarian should be consulted immediately.

One important consideration before castration that has not been mentioned thus far is the possibility of tetanus infections post-surgically.  Tetanus is a severely debilitating to life-threatening disease caused by Clostridium tetani bacterial infections.  All horses being scheduled for castration should be current within the last six months on tetanus vaccination.

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Causes of Weight Loss in Horses

Horses may lose weight for a number of reasons, but three primary causes are most common: intestinal parasites, malocclusion of the teeth, and malnutrition (improper diet or feeding regimen).  The Henneke scale is commonly used to assess the “body condition” of horses, rating them on a scale of one to nine.  Body condition scoring (BCS) can indicate whether a horse is underweight to begin with,...

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Horses may lose weight for a number of reasons, but three primary causes are most common: intestinal parasites, malocclusion of the teeth, and malnutrition (improper diet or feeding regimen).  The Henneke scale is commonly used to assess the “body condition” of horses, rating them on a scale of one to nine.  Body condition scoring (BCS) can indicate whether a horse is underweight to begin with, but an unexplained shift from one body condition type to another that is lower on the scale would indicate weight loss.  The lowest score (1) indicates the horse is completely emaciated, and the highest score (9) indicates that the horse is morbidly obese.  A BCS of five is ideal for most horses, but some breeds may average slightly higher or lower.  For all practical purposes however, a horse that shifts downward on the scale for no known reason my may be suffering from disease leading to weight loss.

Intestinal Parasites:

Intestinal parasites do not rob the horse of nutrition, but they cause inflammation and blood loss in the gastrointestinal tract that may lead to malabsorption of nutrients.  Parasites can devastate a foal and can cause general loss of body condition over time in adults.  Severe parasite burdens are life-threatening to any age animal.  Horses must be protected from parasite infestation by regular testing, appropriate deworming schedules, and proper management of the horses’ environment.

Malocclusion of the Teeth:

Dental problems are a very common cause of weight loss in horses.  Proper mastication is necessary to derive all of the essential nutrients from plants.  Mastication is the veterinary term for chewing, the first stage of digestion.  Food that is not chewed sufficiently passes through the digestive tract unutilized.  It may also lead to colic and serious complications like choke.

A horse’s teeth continue to erupt or grow out of necessity, in order to compensate for the huge amount of wear that takes place in consuming abrasive plant material.  Abnormal wear of the teeth leads to malocclusion; the teeth do not align properly to achieve complete mastication.  Malocclusion also leads to pain when surfaces of the abnormally worn teeth irritate the soft tissues of the oral cavity.

Problems affecting the teeth are many times a result of modern horse husbandry practices, despite the best intentions by owners.  Wild equines had to pick through many tougher stalks in unmanaged savannahs to get to tender, more desirable shoots.  These plants contain a higher silica content which is abrasive to tooth enamel.  The rate of tooth wear was much higher than for today’s horses kept in lush pastures of fine, soft grasses.  Wild equines had (and still have) shorter life spans as a result of rapid tooth “wear-out”, but today’s domesticated horses are more prone to tooth overgrowth and subsequent dental disease which can cause weight loss and compromise their extended life expectancy despite better overall provisions and care.

Very old horses may “outlive” their teeth.  The rate of tooth wear may exceed the rate of tooth eruption in geriatric animals.  Fractured and missing teeth are common and may lead to digestive interruption.

Malnutrition:

Except in the case of abuse, malnutrition is usually not caused by starvation, but it may be a possibility for overly confined horses denied adequate grazing time.  More often, malnutrition occurs as a result of improper feeding regimens or an unbalanced diet.  Poor quality feed may lead to nutritional deficiencies as well as dental problems that exacerbate GI irritation and malabsorption.

Other causes of weight loss include tumors of the GI system, endocrine glands, and oronasal cavity.  Stomach ulcers may lead to malnutrition and diet intolerance.  Severe generalized infections and diseases of the kidneys, liver, lungs, and urogenital system are also causative factors.

Any weight loss should be investigated by a veterinarian.  Early intervention is much easier to address than advanced disease.

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Causes and Prevention of Choke

In horses, “Choke” describes the affected animal’s visible symptoms and the possible outcome of an episode, but it is only secondarily a disease of the airway and respiratory system, even if this is the more serious manifestation of the underlying problem.  It is first caused by an obstruction of the esophagus, or the passage between the mouth and the stomach.  Choke occurs when food becomes...

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In horses, “Choke” describes the affected animal’s visible symptoms and the possible outcome of an episode, but it is only secondarily a disease of the airway and respiratory system, even if this is the more serious manifestation of the underlying problem.  It is first caused by an obstruction of the esophagus, or the passage between the mouth and the stomach.  Choke occurs when food becomes lodged in the esophagus, often the result of having not being chewed properly.  In most cases the horse can still breathe, but in an effort to dislodge the obstruction, it may cough, gag, expel food and mucous from the nares, and potentially aspirate the material into the trachea and lungs.  If the obstruction is not cleared, the horse will be unable to eat and drink, and it may eventually dehydrate.  If the horse aspirates, it can develop pneumonia or die from asphyxiation.  It wouldn’t seem that horses would often choke on their food; but, this is a very common emergency seen by veterinarians, and its underlying etiology (reason for occurring) must be corrected to prevent its likelihood and recurrence.

Accidentally choking on food and foreign bodies can happen to any animal, but there are certain pathological processes and husbandry / behavioral issues that might leave a horse predisposed to this disorder.

Choke is most often a consequence of improper mastication (the first stage in the digestion process).  The food a horse consumes must first be broken down physically by chewing.  This not only reduces the size of the food particles, it is vital for digestion by increasing the surface area of the nutrients that will be chemically reduced by enzymes in the rest of the digestive tract.  If for any reason, the animal cannot – or opts not – to properly chew its food, it will be at an increased risk to develop esophageal obstructions, a.k.a. Choke.

Horses’ teeth are worn down and replenished by new growth continually over a lifetime of chewing on rough sources of nutrition like grasses and grains.  If wear does not occur evenly, the horse will develop a malocclusion; the teeth will not meet properly and effective grinding / crushing of the food will be reduced.  Severe malocclusion can cause sharp edges to form on the teeth which may irritate or injure the soft tissues of the mouth.  The animal may begin to avoid chewing in painful areas of the mouth, which further exacerbates the problem.

Malocclusion, and dental problems in general, are very common in domestic horses, because the modern sources of fodder provided to them are less likely to result in a sufficient rate of wear to keep up with normal tooth eruption.  In older horses, missing teeth may be a reason for improper mastication.  Congenital malocclusion (over bite / under bite) may also predispose a horse to problems with chewing.  Any of these problems that interrupt the process of chewing may lead to swallowing an abnormally large bolus of unprocessed food that is likely to become trapped on its way down the esophagus.

Diseases of the esophagus itself can also lead to Choke.  Tumors and scarring from previous obstructive episodes can reduce the diameter, elasticity, and muscle tone of the esophagus.

Despite good dental health and normal esophageal function, a horse that “bolts” its food may still be susceptible to Choke.  This behavior is most often associated with malnutrition or inappropriate offerings (treats, table scraps).  Also, if water is not accessible, dried feeds may be more likely to become obstructions.

Horses with esophageal obstructions will swallow compulsively and repeatedly.  They may drool and expel food particles from the mouth and nose.  Often, the horse will extend its neck and cough.  Excessive coughing may lead to respiratory distress, in which case the horse may aspirate saliva, water, or food into the trachea during a fit.  Any horse suspected of choke should be immediately denied access to food and water, calmed as much as possible, and be examined / treated by the veterinarian as soon as possible.

The veterinarian will pass a nasogastric tube (nose to stomach) in order to clear the obstructed bolus of food and assess any degree of physiological restriction in the esophagus.  Also, sedatives and spasmolytic drugs may be administered to relax the muscles of the esophagus and calm the distressed animal.  Failure to reach the stomach will indicate a complete blockage, in which case general anesthesia may be required to further evaluate and treat the horse.  An endotracheal tube will be placed which ensures an open airway and avoids aspiration while clearing the obstruction in the esophagus.  Severely distressed horses may be immediately anesthetized at the discretion of the veterinarian.  Extreme care to avoid aspiration and suffocation is the goal in treatment.

Once a horse has experienced an episode of Choke, it should be evaluated and treated for an underlying cause.  The owner should take certain measures to help reduce the chance of recurrences.  These same measures may help prevent Choke in the first place.

Most importantly, all horses should have regular dental examinations.  Senior horses should be examined twice a year.

Also, allow as much natural grazing time as possible.  This will help prevent rapid feeding on processed feeds and aid in more normal tooth wear.

Provide plenty of water at all times.  Dampen dry and pelleted food before feeding.

Slow horses from bolting their food by placing large rock(s), too large to consume of course, in the middle of the feeder.

Consult a veterinarian on feeding recommendations for senior horses, those with dental problems, and horses with a prior history of Choke.

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Colic and its Causes

Colic simply means abdominal pain, but the term doesn’t suggest what caused it or the degree of its severity.  Horses are especially susceptible to colic, so it is important to understand the factors that can result in this condition.  The problem can be mild, or it can become life-threatening.  Colic can occur as a result of primary gastrointestinal (GI) tract disease.  It can be secondary to...

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Colic simply means abdominal pain, but the term doesn’t suggest what caused it or the degree of its severity.  Horses are especially susceptible to colic, so it is important to understand the factors that can result in this condition.  The problem can be mild, or it can become life-threatening.  Colic can occur as a result of primary gastrointestinal (GI) tract disease.  It can be secondary to illness in other parts of the body.  It may even be attributable to husbandry and feeding practices.  Colic is the number one health problem seen by veterinarians and the number one reason for death in horses.

One cause of colic may be intestinal parasites.  Large strongyles migrate through and cause damage to the blood vessels that supply the intestines.  Roundworm burdens can be so great as to block the intestinal tract.  Tapeworms may cause ulceration and occasionally intusseption of the small intestine into the cecum, and botfly larvae may cause severe inflammation in the stomach lining and may even block the opening into the intestines.  These parasites are certainly responsible for causing colic pain and must be ruled out first on any symptomatic horse.  Regular deworming protocols and botfly control measures should be established.

Diet and feeding practices are perhaps a very common cause of colic.  Sudden diet change, spoiled feed sources, withholding water, or over-supplementing with processed diets may lead to bacterial overgrowth in the gut or obstruction from bolting.  Horses confined to overgrazed paddocks can develop “sand colic” from ingesting too much soil, which irritates the mucousal layer and may become impacted.  Salmonella is a common cause of colic that may stem from unsanitary conditions around the horse farm.

Colic may also be secondary to other disease processes in the animal.  Respiratory and urinary tract infections are common contributors.  Teeth malocclusion problems that may develop as a result of improper feeding practices and a lack of regular dental exams can cause colic when food is swallowed before it is fully chewed.

Over-confinement may lead to cribbing or wood chewing from boredom, which may also contribute to colicky symptoms.  Even lameness and laminitis can play a role.

While it may have so many contributing factors, colic is pretty easy to recognize.  A colicky horse will become restless and may paw at the ground.  It may roll on its back frequently, and repeatedly look back at the abdomen.  Rolling can become violent, or the horse may lie motionless on its back.  It may have a distended (swollen) abdomen, and may be unable to pass stool.

If colic is suspected, the veterinarian should be summoned to perform an exam sooner rather than later.  Because so many disease processes can lead to abdominal pain, it is important to reveal the underlying cause.  If the horse is approachable, it should be walked at a slow pace until the doctor arrives.  This may help release trapped gas within the GI tract.  Use caution while leading the horse if the it insists on rolling.

The veterinarian will take a history of symptoms and assess contributing factors, perform a complete physical exam, and collect a fecal sample for parasite screening and a blood sample for basic lab work.  A stethoscope will be used to listen for normal abdominal sounds.  An absence of sounds could indicate colic.  The pulse and respiration rates are counted to detect early signs of shock and pain, and a stomach tube may be passed to relieve built up ingesta in the stomach.  Advanced diagnostics may require an ultrasound of the abdomen, or an abdminocentesis (passing a needle into the abdomen to collect any free fluid or gas present).

The treatment will completely depend upon the source of the colic.  This can include anything from a simple change in feeding habits, to floating the teeth to correct malocclusions, to abdominal surgery.  Often, pain medications are administered, and mineral oil as a laxative is delivered to the GI tract via the stomach tube.

Even mild colic needs to be monitored after treatment.  The horse can relapse quickly, developing a life-threatening obstruction in the intestines.  Contact the veterinarian immediately if the horse’s condition worsens.  If colic pain is not controlled by medications and other supportive care, colic surgery may be indicated.

 

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Cushing’s Disease – Causes and Consequences

Cushing’s Disease (Pituitary Pars Intermediate Dysfunction; PPID) is an endocrine hormonal imbalance caused dysfunction of the pituitary gland. The dysfunction overproduces several hormones that are responsible for critical functions throughout the body. One of which is ACTH. ACTH in turn stimulates the adrenal glands to produce cortisol, a hormone that is released when the body is stressed....

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Cushing’s Disease (Pituitary Pars Intermediate Dysfunction; PPID) is an endocrine hormonal imbalance caused dysfunction of the pituitary gland. The dysfunction overproduces several hormones that are responsible for critical functions throughout the body. One of which is ACTH. ACTH in turn stimulates the adrenal glands to produce cortisol, a hormone that is released when the body is stressed. Cortisol conserves energy by inhibiting glucose uptake and temporarily suppressing the immune system. It is important in survival, but at constantly high levels Cortisol has devastating consequences on the health of the horse.

Cushing’s affects primarily older horses. There is no apparent breed or sex predilection for the disease. There are numerous symptoms associated with Cushing’s, the most obvious of which is hirsutism, or abnormal hair growth. Affected horses will become shaggy as a result of hormonal imbalance. Other notable symptoms include:

  • Increased thirst and urination

  • Increased appetite

  • Chronic laminitis

  • Sweating

  • Lethargy

  • Redistribution of weight (muscle wasting, abdominal fat deposit)

  • Other fat pad formations on the crest of the neck and tail head

  • Immune suppression causing increased susceptibility to infection, disease, and parasitism

  • Decreased regulation of body temperature due to variation in ambient environment (standing out in the sun on hot days, in the shade are very cold days)

Cushing’s develops over a period of time, so these symptoms may be overlooked as they gradually increase in intensity. Before and after “snapshots” of the animal show obvious changes, but it may be difficult for an owner to become aware of the disease until symptoms are pronounced and the horse is obviously ailing.

Horses showing signs of Cushing’s Disease should be examined by a veterinarian who will perform a complete physical examination, take a detailed history of symptoms, and collect samples for laboratory analysis. There is unfortunately no one definitive test for the disease. Biopsy of the pituitary is impractical and dangerous because of its location at the base of the brain. A combination of blood and urine tests are run instead, sometimes repeatedly to help confirm the disease. Not all are necessarily performed, but the tests may include:

  • ACTH level

  • Low-dose dexamethasone suppression test

  • thyrotropin releasing hormone

  • Insulin

  • Blood glucose

  • ACTH stimulation test

  • Urine cortisol:creatinine ratio

  • Domperidone response test

It is not recommended to treat horses based upon a presumptive diagnosis alone. There is no approved (labeled) treatment for Cushing’s Disease, but an off-label use of pergolide mesylate can help reduce circulating ACTH levels and control some symptoms. ACTH levels may be checked until a proper dosage is found. Over-dosage causes anorexia and depression, and this drug must be administered with great care. Because of the instability of Pergolide, environmental storage should be of a concern and discussed with the veterinarian.

Adjunct management of horses with Cushing’s includes grooming (body-clipping) the coat, frequent hoof assessment and proper farriery, maintaining vaccine status, frequent deworming, and feeding a low-grain diet. The horse is more susceptible to external parasites and subsequent bacterial infection of the skin, so proper prevention steps should be established.

Even though there is no cure for Cushing’s Disease in horses, they can still live a comfortable life if managed properly. The disease itself causes no pain or discomfort. If laminitis cannot be controlled and lameness becomes chronic, humane euthanasia should be considered.

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Dental Care Basics

“Don’t look a gift horse in the mouth.” We are all familiar with this old adage instructing us to be gracious for what we receive, no matter its monetary value. However, most of us have not stopped to think about exactly why the condition of the horse’s mouth has a direct relationship to its “value”. A valuable horse is a healthy horse; its dental health has a profound impact upon the animal’s...

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“Don’t look a gift horse in the mouth.” We are all familiar with this old adage instructing us to be gracious for what we receive, no matter its monetary value. However, most of us have not stopped to think about exactly why the condition of the horse’s mouth has a direct relationship to its “value”. A valuable horse is a healthy horse; its dental health has a profound impact upon the animal’s overall condition and vitality. Nutrition provides the building blocks for life, growth, and protection from illness. Despite an abundant supply of quality feed and pasture, dental disease may interfere with the delivery of nutrition into the body, leaving the horse susceptible to many other health problems.

Primary teeth (aka baby teeth, milk teeth, or deciduous teeth) are usually shed by the age of five, and replaced by 36 to 44 permanent teeth depending upon the sex and breed of the horse. The forward most teeth are called the incisors. They are used for cutting grass during grazing, opposing each other in the upper and lower jaws like the blades of scissors. Directly behind the incisors are the canine teeth. These are sharply pointed “fangs” used only during male sparring, and are rarely present or significantly underdeveloped in females. Wolf teeth may come next, after a natural gap in the tooth distribution along the jawbone. Wolf teeth are vestigial structures that are no longer used by modern horses. They are present in less than a third of all horses, male and female. The rearmost teeth in the horse’s dental anatomy are the premolars and molars, also called cheek teeth. These are used for thoroughly grinding and pulverizing (masticating) food before swallowing. Proper mastication is necessary to derive all of the essential nutrients from plants. Food that is not chewed sufficiently passes through the digestive tract unutilized. A horse’s teeth continue to erupt or grow out of necessity, in order to compensate for the huge amount of wear that takes place in consuming abrasive plant material.

Problems affecting the teeth are many times a result of modern horse husbandry practices, despite the best intentions by owners. Wild equines had to pick through many tougher stalks in unmanaged savannahs to get to tender, more desirable shoots. These plants contain a higher silica content which is abrasive to tooth enamel. The rate of tooth wear was much higher than for today’s horses kept in lush pastures of fine, soft grasses. Wild equines had (and still have) shorter life spans as a result of rapid tooth “wear-out”, but today’s domesticated horses are more prone to tooth overgrowth and subsequent dental disease which can compromise their extended life expectancy despite better overall provisions and care.

Horses fed processed diets may have more abnormalities with their cheek teeth. These abnormalities can be sharp points that arise due to abnormal wear because of less chewing action during mastication. These edges may cause ulceration of the cheek and tongue, which causes pain and may lead to infection.

Horse anatomy also plays a role in premolar and molar wear patterns. The lower jaw is narrower than the upper, which correlates with a 15 degree angle (approximately) of the cheek teeth.

Canine teeth in stallions can grow tall and sharp, posing an increased risk of severe injury and fight-wound abscesses in other animals during sparring. They are not used for mastication whatsoever and do not wear down much naturally. Overgrown canines may cause difficulty when placing and removing the bit during bridling. Wolf teeth may interfere with proper bit placement as well and are often removed if present.

Symptoms associated with dental problems are vast and not always easily recognized as originating in the mouth. Furthermore, horses try to conceal pain in an effort to avoid the attention of predators. Therefore, oral health is always examined regularly and if the animal shows any signs of illness.

Mouth discomfort can lead to improper mastication and swallowing of large food particles that may not be processed fully in the GI tract. This can lead to colic, weight-loss, and malnutrition derived diseases. Occasionally, severe dental problems can lead to a condition called choke, where a large bolus of un-chewed food becomes lodged in the esophagus. Symptoms more obviously related to dental pain include head tossing, fighting the bit, unruly riding behavior, unilateral nasal discharge and odor or blood from the mouth. A simple change in behavior however, may be the only evidence of oral health problems.

A thorough dental exam should be performed by the veterinarian at least once a year, and more often for problematic horses. The doctor will float the teeth – a process involving sedation and filing of any overgrown or irregularly worn teeth – and inspect the oral cavity for signs of infection or disease. The idea of floating is to create a symmetrical profile of the upper and lower teeth to cause them to wear more evenly. In addition, retained primary teeth, that are a source of infection and odor, will be removed when needed.

It is clear that the horse’s mouth is directly linked to its overall health, performance, and potentially its lifespan. Regular preventive measures and minor wear corrections are far easier to deal with than established and secondary complications of poor dental health.

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Dermatophilosis: Rain Scald / Mud Fever / Rain Rot

In warm, wet conditions, an opportunistic organism called Dermatophilus congolensis may infect a horse’s skin causing sticky, crusty scabs that entangle and mat the hair coat. It also invades the skin of ill-kempt goats, sheep, and cattle – and not as commonly – pigs, dogs, cats, and people. Common terms for this disease are Rain Scald, Mud Fever, and Rain Rot.

D. congolenis is an actinobacterium ...

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In warm, wet conditions, an opportunistic organism called Dermatophilus congolensis may infect a horse’s skin causing sticky, crusty scabs that entangle and mat the hair coat. It also invades the skin of ill-kempt goats, sheep, and cattle – and not as commonly – pigs, dogs, cats, and people. Common terms for this disease are Rain Scald, Mud Fever, and Rain Rot.

D. congolenis is an actinobacterium that has fungal qualities in that it produces filamentous hyphae, or threadlike projections that extend from its outer capsule like tentacles or feeler roots. These “tentacles” probe and infiltrate the skin tissues causing a significant inflammatory response from the horse’s immune system resulting in oozing, scabby lesions. The bacteria can live benignly on a healthy animal’s skin, multiplying rapidly and causing disease when conditions become ideal.

Suspected to originate in soil, however yet to be isolated and confirmed, D. congolensis thrives especially on horses exposed to wet, muddy environments for prolonged periods of time. Biting insects, which are more prevalent in warm, humid weather may also play a role in defeating the skin’s natural defenses to bacterial infections such as rain scald.

D. congolensis is considered to be an opportunistic pathogen; rather than being directly contagious to a healthy horse, it takes advantage of an animal whose skin health is compromised by environmental conditions. Animals are the only proven reservoirs of the organism however, so it is wise to separate infected horses from others that are susceptible. In addition, equipment and tack used on an infected horse should be thoroughly disinfected to eliminate a possible source of infection to another member of the herd.

Before rain scald produces visually obvious lesions, the horse owner may feel small bumps along the back and over the rump. While grooming or rubbing down the animal, the bumps may break loose to reveal scabs or irritated patches of hair loss on the skin. Although the inflammation caused by D. congolensis leads to significant skin disease, the horse is not typically itchy or bothered by these infections.

In some cases, rain scald lesions resolve spontaneously in 2 to 4 weeks without treatment. In chronic cases however, smoldering or dormant lesions may seed new sites of infection as environmental conditions become ideal for the bacteria to colonize. A culture and sensitivity test performed in the laboratory is the only method to confirm the causative organism in any bacterial or fungal skin infection. Still, a visual and physical examination along with the horse’s environmental history may lead to a presumptive diagnosis and warrant treatment.

Horses diagnosed with rain scald are treated with antibiotics. A typical protocol includes a single intra-muscular injection of penicillin and streptomycin. Topical antibiotic sprays, washes, and rinses are also often employed to reduce the spread of infection to other parts of the horse’s body and other animals. Scabs should be soaked in betadine or chlorhexidine solution, then gently brushed or rinsed away. The horse should then be towel dried and moved to a clean, well ventilated, dry location. Populations of biting insects must be kept in check to prevent coincidental recurrences of rain scald.

Your veterinarian should always be consulted if you suspect rain scald even though it is typically straightforward to diagnose and treat. Secondary infections are common and can quickly complicate the diagnosis and treatment of skin diseases.

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Equine Protozoal Myeloencephalitis (EPM)

Opossums of North and South America carry and shed a parasite called Sarcocystis neurona that is capable of infecting equines and causing a devastating neurological disease named Equine Protozoal Myeloencephalitis, or EPM for short. The parasite spreads by fecal to oral transmission when the horse inadvertently consumes feed or water contaminated by opossum excrement. Many horses (greater than...

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Opossums of North and South America carry and shed a parasite called Sarcocystis neurona that is capable of infecting equines and causing a devastating neurological disease named Equine Protozoal Myeloencephalitis, or EPM for short. The parasite spreads by fecal to oral transmission when the horse inadvertently consumes feed or water contaminated by opossum excrement. Many horses (greater than half) in opossum-infested areas will at some point be exposed to sarcocystis, but only about two percent of those animals will develop advanced neurological symptoms as they are for some reason unable to fight the infection. About four out of ten symptomatic horses will die from the disease eventually despite treatment. If detected and treated very early however, before the disease has progressed, around eighty percent of infected horses may survive.

After ingestion by the horse, the parasite crosses the blood-brain barrier and takes up residence within the cells of the central nervous system (CNS) where it is able to reproduce. The offspring abandon the now damaged cells and seek healthy ones to infect, leaving lesions of scar tissue and inflammation (swelling) behind in their wake. Most horses are able to control the sarcocystis populations with an antibody response from the immune system. Once harbored within the CNS cells however, the horse’s immune system is unable to detect and kill the parasite. It is speculated that stress to the animal may at some point allow the parasites to reproduce at uncontrolled rates, causing neurological disease as a result of numerous and advanced lesions within the CNS. Immune stress can stem from exercise, transport, diet change, subsequent illness, anesthesia and surgery, certain medications, or even inclement weather.

It is not known why ninety-eight percent of exposed horses are able to eradicate the parasite without treatment or evidence of disease, leaving the other two percent defenseless. There is no remarkable breed, age, or sex predilection to explain the susceptibility to sarcocystis.

Neurological symptoms of EPM are often vague at first and almost always asymmetric – meaning that one side of the animal may be affected while the other is normal. They are a direct result of nerve inflammation due to cellular damage. Un-attributed lameness and mild ataxia (incoordination) are the most common first observed symptoms, followed by a head-tilt and muscle atrophy (wasting) especially in the hind-quarters due to inactivity or reluctance to exercise. More subtle neurological symptoms include one-sided facial paralysis (drooping of the lips and eyes), nystagmus (rapid eye movement), regurgitation (expelling of food and water from the mouth), and behavioral changes. Advanced disease may result in seizures, inability to stand, and death.

Equine Protozoal Myeloencephalitis is difficult to diagnose. Its symptoms may be confused with numerous other disease processes and may affect any part of the animal. Ruling out all other causative factors is the first step in diagnosing EPM (i.e.: most horses with EPM will not have an elevated temperature). Age, history of symptoms, stressful events, geographic location, and the season of the year will all be considered in a diagnostic workup.

The veterinarian will perform a neuro-exam on suspected animals, whereby the horse will be observed for any neurological deficits. The Mayhew Scale is a standardized method to record and grade any abnormalities arising from neuromuscular disruptions. The horse is lead through a series of maneuvers designed for this purpose.

Blood tests and cerebrospinal fluid (CSF) taps measure the horse’s immune (antibody) response to the parasite. A positive result can only prove that the horse has been exposed to sarcocystis but doesn’t confirm an active infection. Remember that as many as half of all horses have been exposed to S. neurona. These tests are still useful as a rule-out test nonetheless (there are very few false negative results), and are performed during the diagnostic workup on the symptomatic horse. The only definitive laboratory test available at this time is the positive identification of the parasite microscopically in the CNS tissue after the horse is deceased – not very useful during the attempt to save the animal, however.

A presumptive diagnosis of EPM can be made when a response is seen to antibiotic therapy. Sixty percent of horses will respond positively to treatment within a month. The percentage is higher, the sooner the antibiotics are begun. If no response is seen within 14 days however, other disease processes should be considered. If the horse is improving, therapy will be continued for at least 12 weeks, or until a negative CSF test is seen. Other drugs used in conjunction with antibiotics are helpful to reduce swelling in the CNS tissues, enhance immune response, and to reduce the severity of symptoms. These include non-steroidal anti-inflammatory drugs (NSAIDS), folic acid, thiamine, and vitamin E. Steroids, which effectively reduce swelling but also suppress the immune system, are generally avoided. After remission, about a third of horses will experience a relapse. This is usually because the treatment was stopped too early (expense becomes a factor). Horses that have survived EPM should be considered susceptible for re-infection at any point.

EPM occurs so sporadically that it is difficult to prevent. There is no approved vaccine, so the best measures are to control opossum populations in close proximity to the barns and stables. Keep in mind that horses can become infected in the pasture as well, but obviously avoiding contact by opossums with prepared feeds, water troughs, and stable bedding would be beneficial. General sanitary procedures where horses are kept are essential to prevent all sorts of disease.

In order to improve the prognosis for a horse with EPM, it is vital to consult a veterinarian at the earliest signs of any neurological symptoms.

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EIA – Equine Infectious Anemia (swamp fever)

Sometimes still called “swamp fever”, Equine Infectious Anemia is caused by a retrovirus that is transmitted primarily by blood-sucking insects. Once thought to occur only in humid regions such as the Southeast United States, its actual distribution is nearly worldwide, regardless of climate. The EIA virus is a member of the genus Lentivirus, one species of which is human immunodeficiency virus...

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Sometimes still called “swamp fever”, Equine Infectious Anemia is caused by a retrovirus that is transmitted primarily by blood-sucking insects. Once thought to occur only in humid regions such as the Southeast United States, its actual distribution is nearly worldwide, regardless of climate. The EIA virus is a member of the genus Lentivirus, one species of which is human immunodeficiency virus (HIV). Similar to HIV, this equine-specific virus invades and multiplies within macrophages – white blood cells that when functioning properly, destroy bacteria and other disease causing agents. Since it suppresses the immune system, the symptoms of EIA can be vague, vast, silent, or severe. Thanks to stringent pre-transport testing regulations, the disease prevalence within the US has been reduced to a fraction of what it was as little as three decades ago. However, EIA has not been completely eradicated and remains a threat to horses everywhere. There is no cure once the animal becomes infected; all horse owners should be aware of this disease and take measures to prevent its resurgence.

Once a horse is infected by EIA, and the virus begins to replicate, it will be present in many bodily fluids. Biting flying insects transmit the virus when their feeding attempt is interrupted, causing them to rotate between horses until satiated. The EIA virus, which is carried on the mouthparts of the vector, does not utilize the insect as an intermediate host and will not survive beyond a couple of hours unless introduced into another horse. Horse flies and deer flies make suitable vectors as their feeding attempts are often interrupted; horses are particularly annoyed by and aware of these large, noisy fliers and the painful bites they inflict.

More obscure, yet still possible ways that Equine Infectious Anemia can be spread include iatrogenic infection (contaminated syringes and needles, for example), or by bodily fluid to blood contact (open wounds). Dental and surgical equipment can be another pathway for infection if not sterilized between uses. EIA may also spread from the mare to the unborn foal.

Some horses infected by the virus, as is the case with HIV in humans, may go undetected for quite some time after exposure. Acutely affected cases may experience fever, loss of appetite, nosebleed, anemia (reduced red blood-cell count), jaundice (yellowing of the mucous membranes and skin), depression, and / or death. Often, if and after the acute stage subsides, the infected horse will become an asymptomatic carrier of EIA. Stress, coincidental illness, and excessive exercise / work can trigger a relapse of symptoms or sudden death in these animals. Other horses will develop chronic and recurring symptoms, with fatality impossible to predict. Unexplained weight loss is a common reason to suspect EIA in a horse that fails to thrive.

Equine Infectious Anemia exists almost worldwide. Transmission is more likely in areas with heavy insect burdens. All equids can become infected, although donkeys and mules are more likely to become asymptomatic carriers of the disease and possibly less likely to be suspected as reservoirs of the EIA virus. The virus is especially capable of modifying its antigenic structure, making it difficult to develop vaccines that are effective at protecting against constantly changing viral strains.

In 1970, Leroy Coggins, DVM developed the agar gel immunodiffusion (AGID) test for EIA. The “Coggins” test has been widely employed to stop the spread of EIA from endemic populations. An enzyme-linked immunosorbent assay (ELISA) test, developed later, is slightly more sensitive, but also delivers a few false-positive results. Positive ELISA’s are usually confirmed with the Coggins test. Both methods measure the animal’s antibody response to the virus. DNA testing (PCR) is capable of detecting the EIA virus itself, regardless of antibody response in exposed equids. PCR is effective at detecting EIA in mules and donkeys that may have sequestered infections.

All 50 United States and many other countries have regulations in place that require a negative EIA test before the importation or sale of an animal. The only effective vaccine that has been used in a large number of horses was developed and distributed in China. While providing protection from the disease, it also causes horses to test positive for EIA, preventing the animals from ever being allowed to enter other horse populations. There is no approved vaccine in the US.

If an animal tests positive for Equine Infectious Anemia, it is required to be indefinitely isolated from healthy horses. It may not be transported, moved across state lines, shown, sold, or bred. There is no way that is currently known to remove the virus from the animal, and treatment is merely supportive. That said, a horse may survive for years with the disease. Laws do not require euthanasia of positive horses; however, it must be carefully considered whether resources are available to continually treat the infected animal. Inhumane suffering is no alternative to euthanasia, and the potential exposure risks to adjacent populations must be realized and avoided.

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Equine Respiratory Herpesvirus Infections (Viral Rhinopneumonitis, “Rhino”)

What is Viral Rhinopneumonitis, or “Rhino”?

Equine herpesvirus type 1 (EHV-1) and type 4 (EHV-4) are highly contagious pathogens responsible for a variety of symptoms in horses including mild to moderate respiratory disease, fever, poor appetite, and depression. More serious manifestations of disease include neurological symptoms and spontaneous abortion by pregnant mares (EHV-1). The...

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What is Viral Rhinopneumonitis, or “Rhino”?

Equine herpesvirus type 1 (EHV-1) and type 4 (EHV-4) are highly contagious pathogens responsible for a variety of symptoms in horses including mild to moderate respiratory disease, fever, poor appetite, and depression. More serious manifestations of disease include neurological symptoms and spontaneous abortion by pregnant mares (EHV-1). The disease process caused by these infectious agents is more commonly called Viral Rhinopneumonitis, or “Rhino”; true equine rhinovirus, closely related to the human rhinovirus that causes the common cold, inflicts similar yet less progressive upper respiratory disease than EHV.

What are the symptoms of Rhino?

Horses contracting Rhino will usually develop a serous (transparent) or mucopurulent (milky) nasal discharge as the disease becomes established 2 to 10 days post exposure. They will typically have an increased temperature ( > 102 F) and will sometimes develop a cough. Lymph nodes beneath and at the back of the jaw will become enlarged, and interest in food will wane. Infections with EHV may then become complicated with neurological manifestations or spontaneous abortion. Foals are more likely than adults to develop serious pneumonia.

Pregnant mares infected with Rhino may abort late in pregnancy and show little or no obvious clinical symptoms prior. Aborted foals rarely survive. EHV-1 has been shown to be responsible for sweeping outbreaks of abortions in groups of mares on common grounds or stabled together.

Neurological symptoms (equine herpesvirus myeloencephalopathy), caused by EHV-1, may include mild to significant hind-limb ataxia, or incoordination, and may present alongside urinary incontinence, and/or fecal retention. Horses affected by this manifestation of the disease may begin to sit on their haunches (dog sitting position) and may eventually become completely unable to stand.

Secondary respiratory bacterial infections are common with Rhino and may further complicate the disease, increasing recovery time or decreasing the overall prognosis.

How is Rhino spread?

Rhino is easily spread by direct contact with infected horses, inhaling aerosolized respiratory secretions, and by the use of contaminated equipment, feed, or water. Immunity after exposure lasts only a few months at best; therefore, disinfection and quarantine procedures are critical to stop the disease from spreading throughout a group. Under ideal conditions, the virus may survive in the environment without a host for up to 14 days. The Equine Herpes Virus may lie dormant in an infected horse and cause illness only after a period of stress or coincidental disease. This is called a latent infection.

How is Rhino treated?

There are currently no antiviral drugs known to specifically treat equine herpes type 1 and type 4 infections. The treatment for Rhino is mainly supportive and is targeted at alleviating symptoms and reducing stress which may further compromise the animal’s immune system. Broad-spectrum antibiotics with good respiratory system perfusion are often prescribed prophylactically and in the case of secondary infections. Non-steroidal anti-inflammatory drugs (NSAIDs) are sometimes used to help reduce fever and respiratory tract swelling, and bronchodilators may help to relieve respiratory inflammation and breathing distress.

When horses refuse to eat and drink, they become susceptible to the systemic effects of dehydration. An electrolyte-fluid replacement solution may be given orally; or for more advanced cases, it may be administered intravenously to reduce stress and improve the outcome.

The horse affected by EHV requires rest and recovery time, and should never be worked or ridden until a full recovery is seen.

Mares who abort usually require no specific treatment unless symptomatic or if injury has occurred during parturition. Still-born foals should be packaged in heavy plastic, refrigerated (not frozen) if possible, and delivered to the veterinarian or diagnostic laboratory as soon as possible for examination and a confirmation of EHV. Improper care and disposal of the fetus may result in the spread of the disease to other horses. Consult a veterinarian about when the mare can again be bred safely.

If the horse is persistently recumbent and will not / is unable to rise, you should keep its bedding clean at all times of waste, and contact a veterinarian for guidance.

How can I prevent my horse from getting Rhino?

Vaccination for type 1 and type 4 EHV is available. Unfortunately, it offers only short immunity (2 to 3 months) from the abortive form, 6 months for the respiratory form, and no protection from the neurological form of the disease. Nevertheless, it is recommended for healthy horses in groups where an individual has acquired the disease or has been exposed to Rhino (especially horses <5 years="" old).="" consult="" your="" veterinarian="" about="" vaccinating="" pregnant="">

Thorough sanitation procedures of stalls and equipment, and quarantine of EHV infected (or suspected) horses is the best method to prevent the spread of Viral Rhinopneumonitis. Any food, water, bedding, etc exposed to an infected horse should be disposed of, and all contaminated surfaces should be cleaned with disinfectant and rinsed with clean water. If you have any questions about Rhino, vaccination protocols, or suspect your horse may be at risk, you should contact your veterinarian as soon as possible.

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Equine Viral Arteritis (EVA)

“EVA” is a highly contagious disease caused by equine arteritis virus. It is most notable as a reason for spontaneous abortions in pregnant mares. More subtle symptoms include fever, respiratory problems, reduced appetite, eye swelling and discharge, and edema of the limbs, mammary glands, and male genitals. The virus may be spread by contact with nasal and respiratory secretions as well as...

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“EVA” is a highly contagious disease caused by equine arteritis virus. It is most notable as a reason for spontaneous abortions in pregnant mares. More subtle symptoms include fever, respiratory problems, reduced appetite, eye swelling and discharge, and edema of the limbs, mammary glands, and male genitals. The virus may be spread by contact with nasal and respiratory secretions as well as transmitted sexually. While most adult horses develop high immunity to re-infection after the illness runs its natural course, stallions often become silent carriers of EVA for years after exposure, thus becoming reservoirs of disease. Infected broodmares rarely bear live offspring; infected foals delivered alive rarely survive beyond a few days.

Numerous outbreaks of equine viral arteritis have occurred in breeding facilities over the past years. It is in these concentrated populations of animals that the disease sustains the highest morbidity. Abortion rates vary considerably but may occur in as many as 70 percent of infected broodmares. Stallions who become carriers may spread the virus during natural breeding or through artificial insemination (AI) techniques with EVA positive semen. Respiratory transmission of EVA occurs rapidly at horseshows, racetracks, and other locations where horses may come together in large numbers.

EVA does not usually lead to fatality in an adult horse. In fact, many infected horses are clinically asymptomatic. Horses that do exhibit signs of illness will typically run a high fever for 2 to 10 days, combined with any of the following symptoms: clear nasal discharge which may become colored after secondary bacterial infection; swelling of the conjunctiva (tissue surrounding the eyes); skin rashes and hives; depression and lameness; respiratory distress; and edema with tenderness in the limbs and reproductive organs. Horses with respiratory symptoms will typically lose interest in food as well.

The mechanism by which arteritis virus causes disease is associated with its tendency to localize in the arterioles, the branches of arteries that narrow into capillary vessels. Vasculitis, or inflammation of the vessel walls, causes fluid (serum) leakage into surrounding tissues. The most severely affected tissues correspond with the symptoms mentioned above. The virus is shed along with the fluid leakage into almost all secretions and wastes from the body, including semen, tears, respiratory mucous, urine, and feces, for up to 3 weeks following infection.

While most adult horses make a full recovery, untreated stallions can remain infertile for several months following severe edematous damage in the reproductive tract. Once a stallion becomes a carrier of EVA, the only known method to clear the virus is castration. Occasionally, but not predictably, a carrier stallion may eliminate the virus spontaneously. These stallions are no longer considered a reservoir of infection, and none have been shown to begin shedding equine arteritis virus at a later date.

Foals born live should be considered a potent source of infection to naïve (previously unexposed), unvaccinated foals and horses in the herd. Even with aggressive supportive treatment, infected foals rarely survive more than 2 to 3 days, during which they may spread the virus to healthy animals despite efforts to quarantine and disinfect. There is no specific treatment for EVA in foals, and humane euthanasia is preferred to the suffering the animal will endure.

Unprotected mares will contract EVA from infected stallions by sexual contact or through EVA positive semen during artificial insemination (AI) more than 75% of the time. Because of the low survival rate of infected foals, all broodmares should be vaccinated prior to breeding. Pregnant mares should not receive the vaccine, especially during the last two months of gestation, unless the risk of exposure to EVA outweighs the risk of possible adverse reactions (fetal infection, abortion) associated with the vaccine, albeit rare.

The vaccine is also contraindicated in foals less than 6 weeks of age, therefore maternal antibody protection of the foal through colostrum is the only way to protect them from contracting arteritis virus.

Stallions should be confirmed negative with a blood test for EVA prior to the initiation of the EVA vaccine.

The symptoms of equine viral arteritis closely mimic those seen in equine herpesvirus infections; therefore, confirmation of the disease by diagnostic testing is necessary to institute appropriate containment and prevention measures. The testing method that achieves the quickest results (PCR assay) should be utilized where available.

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First Aid

It is very important to be prepared for an emergency should a horse become injured. Taking proper steps before the veterinarian arrives can mean the difference between life and death in some cases. First Aid means to provide the first care necessary to preserve health and safety in an emergency situation. First Aid does not imply how to do it yourself in order to avoid a vet bill; it can however, ...

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It is very important to be prepared for an emergency should a horse become injured. Taking proper steps before the veterinarian arrives can mean the difference between life and death in some cases. First Aid means to provide the first care necessary to preserve health and safety in an emergency situation. First Aid does not imply how to do it yourself in order to avoid a vet bill; it can however, save expense in treatment if the owner takes appropriate action to reduce the severity of the problem and avoid complications. Some minor “emergencies” are completely treatable by the owner and will not require a visit from the veterinarian. These are some ways to be prepared for various emergency situations.

Prepare

Before an emergency occurs, the horse owner should establish a first aid kit. The kit will include essentials needed for almost every kind of situation, and it should be located on the farm as to provide quick access. Below are some items that should be contained in the first aid kit.

1 in. and 3 in. medical tape – breathable and waterproof kinds
6 in. vetrap or its equivalent (only sticks to itself)
4 in. x 4 in. gauze sponges
wide cotton roll padding
bandage scissors – paramedic style (serrated, blunt nose)
betadine solution (povidone-iodine)
betadine soap (povidone-iodine)
handtowels
exam gloves
emergency flashlight
stethoscope
watch or kitchen timer (to count pulse / respiration)
triple antibiotic ointment
ophthalmic antibiotic ointment
fly repellant paste
wire cutters (linesman’s pliers)
thermometer (large animal rectal type)
bucket with lid and handle (carrying case and water bucket)
pistol with soft nosed cartridges
When an emergency occurs

It cannot be stressed enough how important it is for the owner to remain calm during an emergency. If the owner is panicked and not thinking clearly he or she may do more harm to the animal or even become injured themselves. A stressed horse can be very dangerous; give the animal time to settle down, and take a moment to think through the next steps that will be taken. A deep breath and a count to ten will not compromise the situation at all. Instead, it will likely yield a better outcome.

If the horse becomes injured, the owner must determine where and to what degree. There may be multiple locations of injury, and each will have a different priority. If the animal is able to rise and move, secure the lead to the nearest immovable object. Do not tie the horse to something that could be pulled loose. A thrashing horse swinging a broken post or tree limb is not an ideal situation to say the least!

The order in which to approach multiple injuries depends upon how likely each one is to compromise the horse’s health and safety. Active bleeding, especially arterial bleeding (spraying blood) is of the first concern. Apply pressure to the wound with gauze sponges or towels, or affix an absorbent bandage and allow time for the bleeding to cease. Depending upon the size of the severed vessel, this can take 20 to 30 minutes. The amount of pressure to apply should be enough to stop blood from spraying or flowing, but not enough to completely occlude circulation. Clots form only as platelets leave the vessel, so circulation to the wound is necessary.

A tourniquet should be fashioned only if there is arterial spray from a limb. It is always applied above the wound (closer to the body). Tourniquets are very dangerous if they are too tight for too long. Keep in mind that the rest of the limb is not receiving a blood supply while the tourniquet is in place. If used, it should be just tight enough to slow bleeding to a trickle, and a pressure bandage at the site of the wound should do the rest. The tourniquet must be loosened every five minutes to allow circulation to the rest of the limb. Use with great caution and only if absolutely necessary!

Never try to remove a foreign object from a wound. This can increase bleeding substantially. The object will be removed by the veterinarian in a controlled environment (operating room).

After bleeding stops, it is time to assess the extent of the wound. Deep punctures and large lacerations always require veterinary attention. If the horse is current on its tetanus vaccination, small lacerations (not punctures) can be treated on the farm with antibiotic salve. It will be important to keep the wound clean and dry and prevent insect infestation.

Being careful not to cause bleeding to start again, the wound should be washed with saline (or fresh water if saline is not available) and dilute betadine soap (it is okay to get soap in the wound, as long as it is rinsed well). The area should then be rinsed with betadine solution (for acute wound management) and thoroughly dried before applying loose bandage where possible. Fly repellant should be applied around, not in, the site to keep insects away. Be aware that betadine and even water may sting when introduced to the wound, so begin very carefully to see what the horse will tolerate. Diluting the betadine with water first will help.

The horse’s vital signs should also be assessed at this time. Check the animal’s gum color for a healthy pink color. Depressing the tissue for a moment and releasing should cause the color to go pale and return to pink within a second or two. Longer times and overall abnormal color of the gums indicates shock or some other circulatory and systemic problem.

Take the horse’s temperature with a thermometer and count the pulses and respirations with a stethoscope and watch for 15 seconds. Multiply your findings by four to arrive at a beats per minute and respirations per minute figure. These numbers will be very important to the vet in assessing the animal’s condition. This procedure should be practiced before an emergency event as there is a bit of a learning curve in proper technique.

Normal vitals:

Temperature: (if mercury thermometer, be sure to shake down the thermometer first!) 100.50F +/- 10

Pulse:

adult: 26 to 44 beats per minute
foal: 60 to 90 beats per minute
Respirations:

8 to 16 resp per minute (slightly higher in foals)
Report the findings to the veterinarian before he or she arrives. They may have instructions to carry out based on the horse’s vital signs.

Heatstroke

Overheating is common especially when the humidity is as high as the temperature outside. If a worked horse suddenly seems lethargic or reluctant, takes a stumble, or is panting, it may be overheated. Heatstroke occurs when the horse’s core temperature exceeds 1050F. Check for an increased pulse rate at rest, and cool the horse immediately if the temperature is elevated.

To cool an overheated horse, get the animal to shade and circulating air. Do not ride the horse. Remove the saddle and blanket. Use room temperature (not cold) water if available to drench the horse’s head, thorax, and abdomen. If the horse’s temperature exceeds 1050F, contact the veterinarian immediately.

Broken limbs

If there is bone protruding through the skin, if the animal cannot rise at all after a period of calming, or if there is obvious displacement of the limb (pointing in the wrong direction), a veterinarian will need to be immediately consulted about surgical options and stabilization procedures prior to arrival. More and more horses are able to recover after surgical intervention for a fractured limb, but there is still a very guarded prognosis overall.

If a veterinarian cannot be summoned quickly, or if there is no way to transport the animal, a decision may need to be made about whether the animal will suffer needlessly. It may be more humane to euthanize the horse in certain circumstances. The decision is certainly not taken lightly.

This is the point of the pistol in the first aid kit. If used properly, this tool of violence can become a tool of compassion for a horse in severe pain. Please see Humane Equine Euthanasia for information about the proper procedure.

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External Parasites of Horses

There are so many “bugs” that parasitize the skin of horses, it’s difficult to name them all in one attempt; however, they can be categorized into several different groups including: biting flies, non-biting flies, mosquitoes, mites, lice, and ticks. All are very common, and all cause disease to a varying degree. Populations of flies and mosquitoes fluctuate according to season; but mites, lice,...

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There are so many “bugs” that parasitize the skin of horses, it’s difficult to name them all in one attempt; however, they can be categorized into several different groups including: biting flies, non-biting flies, mosquitoes, mites, lice, and ticks. All are very common, and all cause disease to a varying degree. Populations of flies and mosquitoes fluctuate according to season; but mites, lice, and ticks stay with their hosts once they have established a “home”. Parasite species also vary according to geographic location. It is important to become familiar with the characteristics of each so that a prevention strategy can be established.

Common Biting Flies:

Horse fly, deer fly, stable fly, black fly, horn fly, sand fly, biting midge

All are blood-suckers that in large numbers can lead to significant anemia (blood-loss). All biting flies leave the skin susceptible to secondary bacterial infections.

Horse flies, deer flies, and stable flies inflict very painful bites, and may cause panic in horses. They are often interrupted in their feeding attempts, causing them to move from horse to horse, and making them suitable vectors for diseases like equine infectious anemia and anthrax. All three flies reproduce in high moisture areas, around tanks and in moist rotting vegetation. Larvae burrow beneath the soil and pupate (form hard, chemical resistant shells) before emerging as adults, making them difficult to kill with insecticide. Topical repellants are utilized to give temporary relief from bites and prevent disease transmission to horses. Providing drainage to low lying areas and clearing plant debris may help to reduce populations.

Black flies are known to cause death by overwhelming their victims in such large numbers as to cause weakness, toxemia, and anaphylactic shock. They prefer the mucous membranes of the animal for feeding and are seen around the eyes, ears, nares, mouth, anus, and genitals. They are most common around moving waters.

Horn flies reproduce only in cattle manure, but will migrate to nearby horse populations. They are capable of causing anemia in very large numbers, but are associated more with skin lesions and secondary infections as a consequence. Topical insecticides and repellants are used to control Horn flies.

Sand flies and biting midges are common in wet, swampy areas. They are so small that they may go unnoticed (also called no-see-ums in some parts of the country). Horses kept near these breeding grounds are susceptible to skin lesions called Sweet Itch. Some horses rub and bite incessantly as a result of the allergic reaction caused by the bites of these flies, while others do not react significantly. Repellants are the only control measure in lieu of moving the horses away from infested areas.

Non-Biting Flies:

Botfly, house fly, blow fly

Though not blood-suckers, the flies of this group cause disease in horses in a different, but still significant manner.

Botflies are probably the most significant threat in this group, but they parasitize horses internally by laying the eggs on the horse’s coat. The eggs enter the animal’s mouth and hatch into infective larvae when the horse grooms itself. See Intestinal Parasites of Horses for more information and control measures for this species.

House flies breed prolifically in manure, farm and household waste, and rotting plant material. They feed on organic debris and mucous around every opening on the horse. While they don’t bite the horse, the huge numbers of flies can be so annoying to the animal to cause it to stop eating and lose weight. House flies carry hundreds of bacteria and viruses and are significant vectors of infections. Control is an ongoing battle in sanitation, insecticide / larvicide application, topical repellants, and fly baits.

Blow flies that parasitize horses are also called screwworm flies. Flies lay their eggs which hatch into larvae (maggots called screwworms) in necrotic flesh and decaying organic material. Screwworms feed on the necrotic material within a wound on the animal, but unlike other maggots, do not stop there. They move onto healthy tissue, burrowing deeper anytime the wound is disturbed. The “blow fly eradication program” officially ended the threat of screwworms in the United States, but with reproducing flies just over the border in Mexico and parts of Central America, it is possible that they make a reappearance. The parasite is a reportable species in the United States, meaning they must be brought to the attention of the State Veterinarian if sighted.

Mosquitoes:

Mosquitoes require relatively stagnant or slow moving water on which to deposit their eggs. Larvae develop under the water’s surface, pupate, and emerge as flying insects. Only the females are blood suckers, which must do so in order to reproduce. Female mosquitoes can transmit encephalomyelitis (West Nile Virus, EEE, WEE, and VEE) and possibly other diseases known to be transmitted by biting flies. Usually, their numbers aren’t so great as to cause significant blood loss, but it is certainly possible. Breeding areas, which can be as seemingly insignificant as an abandoned soda can, can produce thousands of mosquitoes in a matter of days after a rain shower. Drainage of stagnant reservoirs is the best method to prevent an infestation. Mosquito “dunks” can be tossed into tanks and troughs and are safe for fish, invertebrates, and all animals that drink from the body of water. They contain a dormant stage of a bacterium called Bacillus thuringiensis that parasitizes and kills mosquito larvae. Topical repellants can be applied to horses to provide temporary protection.

Mites:

Sarcoptic Mange mite, Psoroptic Mange mite, Demodectic Mange mite, Chorioptic Mange mite, chiggers, Straw Itch mite

All mites are microscopic. Sarcoptic, Psoroptic, and Demodectic Mange (mites specific to horses) are all rare to very rare in the United States. In addition, Sarcoptic and Psoroptic mites are reportable to the State Veterinarian if found on a horse.

Chorioptic Mange mites feed on the surface tissues of the skin causing considerable irritation. They are common on the legs of heavy draft breeds of horses and are spread by direct contact. The mites cause intensely itchy papules to form, followed by hair loss. The skin will become thickened, crusty, and oozing. Infected horses may bite and chew at the limbs to the point of mutilation. Secondary bacterial infection is very common. The mites have an unusual life-cycle in that they become most infective during the cooler months of the year. Lesions may improve during the summer, and return in the winter. There is no approved (labeled) product for the treatment of Chorioptic Mange in horses, but many veterinarians treat the legs topically with ivermectin mixed into antibiotic / anti-inflammatory paste, or with fipronil (Frontline spray),a product labeled for fleas and ticks on dogs. Horses with long hair should be clipped before topical treatment is applied. Both treatments are found to be effective.

Chiggers are not specific parasites of horses, but they may opportunistically infest a horse if their numbers become great within a pasture. They feed on the surface of the skin in the same manner as Chorioptic Mange mites, and cause itchy papules to form. Unlike Chorioptic Mange mites, chiggers do not remain on the animal, so treatment to kill the mites on the horse is not necessary. Horses are usually administered glucocorticoids (cortisone) to reduce itching and skin inflammation. Topical repellants can be used to temporarily protect the horse from infestation.

Straw Itch mites live within straw and grain and occasionally infect a horse if their numbers become great (unchanged bedding straw). Lesions may or may not be itchy and appear on the legs, muzzle, face, and neck. No treatment specifically to kill the mites on the horse is necessary. The source of the mites should be removed, and the itch can be controlled with steroids.

Lice:

Biting louse, sucking louse

Lice are small but visible to the naked eye. They are species-specific, meaning the horse louse only infects horses. Lice are contagious by direct contact between animals and by contact with contaminated fomites (brushes, tack, etc.). They do not survive off of the host for more than a few days. Both kinds of lice are more prevalent in winter months when hair coats are longer and horses are more stressed. Biting lice may cause more symptoms of itchiness, while sucking lice in great numbers may cause anemia. Severe lice infestations on foals can cause stunted growth. There are numerous products available to kill lice, and they are easily controlled. All exposed equipment, tack, and grooming supplies should be disinfected before reuse.

Ticks:

Numerous species according to geographical location

Ticks are visible to the naked eye, ranging in size from that of a pin head to the end of one’s pinky finger. They are blood-suckers that can transmit diseases and cause anemia in large numbers. Male ticks are tear drop shaped, grey, red, brown, and / or patterned with symmetrical markings. Female ticks are usually seen fully engorged with blood and eggs, and appear like fat grey beans, their legs barely visible. Ticks have 6 to 8 legs depending upon their stage of development, and pincer-like mouth parts that tightly grasp the host while they feed and reproduce. Often, the smaller male tick will be found attached to the horse’s skin directly beneath the engorged female. Females drop off of the host to lay their eggs which hatch into larvae (seed ticks) that climb up the nearest vertical surface. They hang hook-like legs out into the wind to catch a ride on the next passer-by.

Ticks cause swelling at the attachment site, blood-loss in large numbers, and are capable transmitting several diseases including Piroplasmosis (Horse Tick Fever), Anaplasmosis (was Ehrlichiosis), Lyme Disease, and Tularemia. Spinose ear ticks can cause severe damage to the inner and middle ear canal.

Killing ticks on the animal can be achieved by the use of numerous sprays or dips labeled for use on horses. Environmental control is also very important as well, since ticks can survive off of the host for a long period of time without a blood meal. Vertical surfaces of fences, trees, shrubs, buildings, etc. must be thoroughly treated.

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Foaling a Mare

Foaling is the process of giving birth to a baby horse. The broodmare carries the foal for about 11 months from conception (fertilization) to delivery. This time period is referred to as the gestation period and can range from 320 to 365 days depending upon breed, variation within a breed and season of the year. While wild equines have successfully handled the entire process of breeding on their...

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Foaling is the process of giving birth to a baby horse. The broodmare carries the foal for about 11 months from conception (fertilization) to delivery. This time period is referred to as the gestation period and can range from 320 to 365 days depending upon breed, variation within a breed and season of the year. While wild equines have successfully handled the entire process of breeding on their own un-aided for eons, domestic horse owners can take steps to ensure that a healthy foal is delivered and there is no danger to the mare should something go wrong.

Pre-foaling concerns:

Mares should be dewormed and vaccinated prior to and during the gestation period. The veterinarian should be consulted as to which diseases are threats in their geographic location. Deworming ensures that no parasites are passed from the mare to the foal shortly after birth, and vaccinating causes the mare to pass antibodies that fight diseases to her foal in the colostrum, or “first milk”. The vaccines and dewormer need to be safe for the mare if given during pregnancy.

Sometimes mares leak the colostrum before giving birth. This is a concern, because the foal may not receive the benefit of antibody protection. Some slight leakage is considered normal a few days before foaling, but if colostrum is flowing, it should be collected in a sterile container and frozen, to be given by bottle to the foal four to six hours after birth. If this is not possible, the foal may receive killed vaccines sooner that normally scheduled (they are pointless or possibly harmful given early to a foal that has received colostrum from a vaccinated mare). In addition, foals can be given plasma IV by a veterinarian to increase its immune function.

Preparing the foaling stall:

A mare can foal at pasture, but observing her for problems is a challenge.

A clean quiet stall should be prepared for the foaling mare as far from other animals as possible to avoid stress and a source of infection. All bedding should be removed, the floors and walls de-soiled, and every surface disinfected. After the stall is completely dry, fresh bedding straw is brought in – enough to provide warmth, but not so much as to impede the little horse from learning to stand. The stall should be warm and well ventilated. Bedding should be changed daily until the foal arrives.

Predicting the date:

About one month to two weeks prior to giving birth, the mare will show signs that the birthday is near. These will include the vulva dropping, the udder filling, and milk veins becoming prominent. Clear to milky fluid (waxing) may leak from the teats for several days before parturition (delivery).

Birthday:

Foaling occurs in three stages. The first stage lasts from 1 to 2 hours typically (up to 24 hours), and begins as uterine contractions start to push the fetus toward and into the birth canal. The mare may be anxious. She may lie down and rise often, pace, sweat, and urinate repeatedly. During this stage the foal is turning into position for delivery, and this movement may be noticed in the mare’s abdomen.

The second stage is marked by the water breaking. The sac that surrounds the fetus ruptures, and amniotic fluid pours from the vulva. This stage includes the delivery of the foal and may take a few minutes to half an hour. The mare may repeatedly reposition herself in the stall. It is very important to not disturb the mare during this process. If she is stressed or distracted, it may delay or stop the contractions. If full delivery does not occur within 30 minutes, the foal may be malpositioned. Foals are born front feet first, soles pointed downward; head next, nose forward; then the shoulders, and so on. If the foal is turned otherwise, the veterinarian will need to assist. Malposition may appear as only one forelimb showing, more than two limbs visible, the nose is not between the fore limbs (head turned backward), nose appears before the forelimbs, or the soles are upside down. In addition to malpositioned foal, if a red bag is seen and you cannot see the foals legs, blunt transection (opening) of the bag may need to be made. A veterinarian should be called immediately in any of these situations.

Very occasionally, the foal will pass without the amniotic sac breaking. If this is the case, the mare may groom the foal to open the sac, or she may need assistance. It should be opened immediately. Do not use a sharp implement; it will tear fairly easily by hand. The foal will need the mouth and nose cleaned with a towel and fluid removed from its lungs by rubbing the thorax vigorously to stimulate breathing. The less responsive the foal is, the more stimulation it needs. Leave the sac attached to the umbilical cord until there are no pulses seen in the cord (20 minutes). Then, cut the cord about 3 to 4 inches from the foal’s body and wipe the stump with dilute betadine solution.

The third stage is the passing of the afterbirth, or the placenta, and this can take a few minutes to several hours. It may be necessary to tie the placenta in knots to shorten its length so the mare does not step on it. If she pulls it out prematurely, there can be damage to the uterus. If the afterbirth is not completely delivered in 3 hours, contact the veterinarian. A retained placenta can lead to life-threatening infections.

After delivery, the mare may seem colicky. This is normal as the uterus is contracting back to its normal size.

Right after birth, the mare should begin cleaning the foal aggressively. Despite her concerns, the foal will be anxiously trying to stand. A foal that cannot stand after 4 or 5 hours may need veterinary attention. The foal should also begin to nurse within the first 6 hours of life in order to receive the benefit of colostrum.

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Gastric Ulcers

Gastric ulcers are erosions in the protective lining of the stomach. The lining is a mucosal barrier that keeps the stomach’s acids and enzymes from digesting its own tissue. Several factors contribute to the development of ulcers in horses. They include any stressful event(s): extended confinement, sporadic feeding cycles, long travel, and extreme exercise. Also, certain concentrated diets may...

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Gastric ulcers are erosions in the protective lining of the stomach. The lining is a mucosal barrier that keeps the stomach’s acids and enzymes from digesting its own tissue. Several factors contribute to the development of ulcers in horses. They include any stressful event(s): extended confinement, sporadic feeding cycles, long travel, and extreme exercise. Also, certain concentrated diets may accelerate ulcer formation. The prevalence of gastric ulcers in horses is surprising high with as many as half of all foals, and a third of all adults, possessing mild erosions. In dressage and race horses, the majority of animals are affected and the lesions tend to be more severe. Ulcerative disease is sometimes referred to as Equine Gastric Ulcer Syndrome (EGUS).

When allowed to do so, horses graze continually throughout the day. Unlike ruminant animals, their stomachs are relatively small and are not used to store large amounts of food. By design, the horse’s stomach continually produces acid to digest the constant supply of food. Confinement practices may lead to a build up of acid that begins to erode the protective mucosal layer.

The type of food a horse eats also plays a role in EGUS. Concentrated feed contains less roughage which requires chewing. Chewing stimulates saliva production which neutralizes stomach acids to some degree. Also, concentrated feed may not contain as much calcium as is found in alfalfa hay. Calcium may neutralize acid and helps protect the stomach wall.

Highly exercised horses suffer from gastric ulceration due to all of these factors combined. In addition, stress from training and competition causes increased levels of certain hormones that weaken the stomach’s ability to inhibit erosion. Stress slows gastric emptying, giving the stomach acids more contact time with the mucosal layer.

Non-steroidal anti-inflammatory drugs (NSAIDs) and Glucocorticoids (i.e.: prednisone) can also accelerate ulcer formation when used at high doses or for extended periods of time. These drugs are especially likely to lead to ulcer formation if used in combination.

Foals that have advanced gastric ulceration will show signs of colic especially after nursing and eating. They may nurse reluctantly and stop eating. A symptom called bruxism, or clenching and grinding of the teeth, along with drooling is also sometimes noted in foals. They may develop diarrhea, fail to thrive, and lose weight.

Adult horses will show a poor body condition and poor coat quality. They will have a reduced appetite and a depressed attitude. Symptoms of mild colic include lying down frequently and rolling. Dressage and race horses will decline to perform. Weight loss is eventually seen as the ulceration becomes more prolific. In the worst cases, gastric ulcers may become life-threatening.

Changing horse management practices is absolutely necessary to treat and prevent the recurrence of gastric ulceration. In addition, the veterinarian may prescribe several medications that help reduce acid production, bind with or block the action of stomach acid, and protect the eroded areas in the stomach lining while they heal. These drugs include:

Antacids (pH buffers) – require very large doses and have limited duration of effect. Still, may be used to provide immediate relief from pain.

H2 histamine blockers and proton pump inhibitors – block the mechanisms of acid production.

Protectants – form a protective coating over the eroded portion of the stomach lining protecting the ulcer from contact with stomach acid.

Probiotics – supplements of beneficial bacteria that help reestablish the normal gut flora and have been shown to produce anti-inflammatory effects on the GI tract.

Prevention requires the animal to live a more natural lifestyle. Reducing confinement time, allowing more grazing, decreasing concentrated feeds, and feeding high quality hay will all help to prevent ulcer formation. For very mild signs of EGUS, these changes in routine may be all that is necessary.

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Geriatric Care and Considerations

Thanks to advances in equine veterinary knowledge, technological improvements from the industry, and diligence on the part of horse owners when it comes to good management practices, domestic horses are living beyond their twenties and into their thirties now days. Very occasionally, a horse may even reach forty years of age. Compared to the average 15 to 18 year lifespan of wild equines, it is...

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Thanks to advances in equine veterinary knowledge, technological improvements from the industry, and diligence on the part of horse owners when it comes to good management practices, domestic horses are living beyond their twenties and into their thirties now days. Very occasionally, a horse may even reach forty years of age. Compared to the average 15 to 18 year lifespan of wild equines, it is clear that man’s intervention has increased the lifespan of the domesticated horse. What is not guaranteed however is whether the quality of life for the geriatric horse will remain good into those extended years. Geriatric horses have special needs that must be met in order to ensure that their golden years are happy, healthful, productive, and pain free.

Today’s horse’s lifespan is a little more than one third of the average human’s, meaning a one year old horse is the equivalent of a three year old child; a thirty year old horse has similar age-related issues as a ninety year old person.

Like the geriatric person, the older horse has experienced deteriorative changes in all parts of the body. Arthritic damage in the joints, reduced immune response to disease, dental problems, decreased tolerance to stress, and other age-related changes all leave the older horse more susceptible to illness.

Deteriorative changes are seen as result of a myriad of contributing factors. Wear and tear on joints leads to reduced range of motion, joint pain, and reduced activity. Obesity tolerated as a youth, heavy labor, and exorbitant exercise demands in race and show animals accelerates this degradation. Dietary intolerance, dental disease, and hormonal imbalance may reduce nutritional supplies to the body tissues. Stress from weather changes, harassment by younger horses, and increased frequency of bacterial and parasite infections may all together result in weight loss and an inability to build muscle mass. Poor body condition is a common complaint from owners of geriatric horses.

Despite the “natural” wear and tear, there are elements in all of these processes over which the owner has some considerable control. Two major factors are diet and dental health. Anyone who has cared for a horse into its older years realizes the link that connects the two. Horses are not ruminant animals which are able to process plant material to a great extent within the stomach; therefore, the first stage of digestion is mandatory for all other digestive functions to proceed correctly in the horse. Mastication is the process of chewing and pulverizing food so that its nutritional constituents can be absorbed by the digestive tract. Horses’ teeth continually erupt throughout their lives and are worn down by the mastication process. When tooth wear is irregular, a condition called malocclusion develops which causes discomfort and an interruption in mastication. Food is either rejected or swallowed in large un-chewed boluses causing indigestion and possibly colic. Over-confinement and feeding processed diets, thus denying natural grazing in the pasture to a great extent can accelerate malocclusion formation.

Geriatric horses may have also “outlived their teeth”. At some point, wear exceeds eruption of new tooth enamel, and horses are left chewing with the softer dentin that comprises the inside of the tooth. Geriatric teeth are more prone to irregular wear and fracture. The older horse’s “slower” immune system may also leave it more susceptible to periodontal abscesses.

In lieu of a dental examination by the veterinarian, observation of the horse’s manure may give evidence of a dental problem. Intact grains and large portions of un-chewed hay point to incomplete mastication. A history of mild recurrent colic supports this finding as well. In severe cases, malocclusion and periodontal disease may lead to a condition called Choke. Choke occurs when un-chewed food becomes lodged in the esophagus.

A dental exam should be performed on all horses regularly, but even more often on geriatric animals. The effects of a dental related malnutrition can be devastating in a short period of time. As said before, other age-related issues may cause the geriatric horse to be unable to recover from significant weight-loss.

In order to prevent dental problems, the horse should be allowed to graze as much as possible and have frequent dental exams. Confinement from natural grazing has no benefit whatsoever, and is linked to numerous other husbandry-related health issues.

Gastric ulcers may be more prevalent in older horses, especially those that are suspect for developing Cushing’s disease, a hormonal imbalance caused by a dysfunction of the pituitary gland. Increased levels of cortisol associated with Cushing’s may predispose the stomach lining to erosion by stomach acid and decrease the horse’s immune defense against bacterial overgrowth within the GI tract. Here too, the ulcers are exacerbated by excessive confinement, sporadic feeding, and poor diet.

Geriatric horses should also avoid high-carbohydrate (starch, aka sugar) supplemental feeds, especially if they are diagnosed as having metabolic syndrome (sensitivity to sugars). It is important that older horses are instead fed increased levels of fiber (bran, psyllium) to reduce the chance of ulcers, colic, and other diseases like laminitis (founder). Probiotics may also be of benefit to maintain normal bacterial gut-flora and digestion since older horses are susceptible to bacterial overgrowth in the GI tract.

Older horses can lead happy, productive, and pain free lives if they are given a little special attention when it comes to their care. For the geriatric horse, an ounce of prevention is worth another year of faithful companionship.

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Santo, TX 76472

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