EQUINE INTERNAL PARASITES

Effective control programs for equine internal parasites. Don Hudson, Extension Veterinarian Dale Grotelueschen, Extension Veterinarian Duane Rice, Extension Veterinarian Major Parasites There are five major kinds of equine internal parasites: large and small strongyles, ascarids, bots, and pinworms. Large and Small Strongyles The most common and most destructive of all internal parasites in the equine are the large strongyles (blood worms). Strongyles can be seen in horses of all ages, except in very young foals. Strongyles range in length from 1/2" to 2". The sexually mature strongyles are found, for the most part, in the large intestine. The larval stages travel via the blood vessels to the heart, liver, and lungs, leaving damaging tracks or scar tissue behind by destroying healthy tissue. The mature female lays her eggs which are passed in the manure. The eggs hatch into infective larvae that contaminate grass and hay, and when ingested, the cycle starts again. When horses are kept on the same pasture year after year, the number of infective larvae accumulate and multiply. The large strongyle group contains three main species: Strongylus vulgaris, Strongylus equinus, and Strongylus edentatus. Strongylus vulgaris, the most destructive, migrates via the arteries of the intestine, creating a thickening in the wall of the anterior mesenteric artery where it attaches to the aorta. The resultant thrombi (blood clot in bloodstream) or aneurysm (ballooning of vessel wall) create a significant reduction in blood flow to a large portion of the bowel. Periodic bouts of colic shortly after feeding or exercise are common due to showering or movement of thrombi into small vessels of the intestines. Severity of the colic episodes depends on the amount of circulatory damage. Total blockage or rupture of an aneurysm can result in death of the horse. There are about 40 species of small strongyle (cyathostome) and they are increasing in numbers due to drug resistance. In many areas, the small strongyle may be more of a problem than the large strongyle. Migration is limited to the intestinal lining. Numerous encysted small strongyles emerging from the intestinal wall can induce colic. The life cycle of strongyles is continuous; therefore, horses may need to be dewormed every 8 to 10 weeks year round to control these blood sucking parasites. Ascarids Parascaris equorum (large roundworms) are the largest internal parasite affecting horses, ranging in length from 5" to 15". Ascarids reach up to 1/2" in diameter when mature and look much like a white earthworm. These parasites are common in young horses and are usually not found in horses more than five years old. Immunity normally develops following exposure to these large roundworms during adolescence. The female roundworm deposits eggs in the intestine and the eggs pass out in the manure. The larvae develop to infective stage within the eggs, which are swallowed by the horse with contaminated feed or water. The eggs hatch in the intestine, releasing larvae that penetrate the intestinal gut wall. They migrate through the liver, then through the lungs, and then to the alveoli where they are coughed up to the windpipe to the pharynx where they are reswallowed. The roundworms then develop to maturity in the small intestine and the cycle repeats itself. The life cycle is completed in 10 to 13 weeks. Respiratory problems in young horses can be started and intensified due to larval migration of roundworms. Worm impactions of this worm species can be seen in heavily infested young horses not on a routine worming program. Bots Bots come in three types: Gastrophilus intestinalis, the most common; Gastrophilus haemorrhoidalis, the nose bot; and Gastrophilus nasalis, the throat bot. The buzzing of the hairy, brown bot fly is very annoying to the horse and owner. It is about the size of a honey bee, does not bite but lays yellow eggs on the hair of the forelegs, shoulders, and flanks of the horse. These eggs are stimulated, hatched, and ingested by the horse when they try to lick off the eggs. Larvae of all three types of bots enter the mouth and embed themselves in the mucous lining of the gums. After about a month, they migrate to the stomach and become attached, leaving the stomach lining inflamed and ulcerated. After 8 to 10 months of development, the larvae pass out in the manure. Once outside, the bot hatches into an adult fly, and the cycle begins again. The bot fly population is most active in the late summer and fall. Bot flies do not feed. Control is directed at egg removal from the hair and a dewormer to kill the bots in the stomach. One month after a killing frost which will kill the remaining eggs on the hair, a boticide dewormer is administered. Pinworms Oxyuris equi (pinworms) are found in the cecum, colon, large intestine, and rectum. Female worms are normally full of eggs which pass out in the feces. Additional female pinworms crawl out the anal opening and deposit their eggs on the surrounding skin, causing irritation and itching to the host. For relief, the horse usually rubs against a fence post or other solid object, resulting in hair loss near and on the tail and occasionally producing a secondary infection. The mature female has a slate-grey or brownish color and a narrow tail which may be more than three times as long as the rest of the body. Females are 3" to 6" in length. The life cycle is completed in five months. Pinworms are actually less damaging to the equine system than any other internal parasite group. Yet the constant annoyance and irritation can spoil the looks and action of an otherwise attractive horse. Pinworms can sometimes be seen in the manure of heavily infected animals. Control and Treatment Horse owners need to understand that an internal parasite control program is a continual battle. Management practices include: Feeding hay in bunks or mangers; avoiding feeding on the ground. Regular cleaning of stables and paddocks. Avoiding overcrowding of pastures. Avoiding wet pastures--rain, dew, flooding--especially with young animals. Not spreading manure where horses can come in contact with it. Working dirt lots with a harrow, springtooth harrow, or disk to bury manure and destroy weed growth. Periodical grazing of cattle in horse pastures decreases exposure as equine parasites do not mature in cattle and breaks the life cycle. Treatment programs consist of: Proper drugs at the proper dosage and proper time (Figure 1). Deworming all animals in the group or lot. Deworming pregnant mares within 30 days of foaling to minimize passage to foal. Keeping lactating mares and their foals on a rigid treatment schedule (every 6 to 8 weeks). Rotating anthelmintic classes of drugs to prevent development of parasite resistance. Resistance generally develops with repeated usage over time (Figure 1). Number of horses, space allotted per horse, age of horses, contact between horses, type of feed (i.e. pasture or dry lot) all have a bearing on frequency of deworming. Your veterinarian should evaluate each individual circumstance and determine the proper drug and frequency needed. Veterinarians can also provide fecal examinations 7 to 10 days post treatment to evaluate efficacy of a control program. Figure 1. Three Classes of the Most Commonly Used Wormers I. BENZIMIDAZOLES Brand Name Active Ingredient Distributor Worms Affected Cutter Paste Wormer febantel Cutter Animal Health ascarids strongyles pinworms Panacur fenbendazole Hoechst ascarids strongyles pinworms Safe-Guard fenbendazole Hoechst ascarids strongyles pinworms Telmin mebendazole Pitman-Moore ascarids strongyles pinworms Benzelmin oxfendazole Syntex ascarids strongyles pinworms Anthelcide EQ oxibendazole SmithKline Beecham ascarids strongyles pinworms Equipar oxibendazole Cooper ascarids strongyles pinworms Equizole thiabendazole Merck ascarids strongyles pinworms II. TETRAHYDROPYRIMIDINES Strongid T pyrantel Pfizer ascarids strongyles pinworms Strongid P pyrantel Pfizer ascarids strongyles pinworms Strongid C (for continuous feeding) pyrantel Pfizer ascarids strongyles pinworms III. AVERMECTINS Eqvalan ivermectin Merck bots ascarids strongyles pinworms Zimecterin ivermectin Farnam bots ascarids strongyles

BLOOD PARASITES OF HORSE

Blood parasites are organisms that live in the blood of their animal hosts. These parasites can range from single-celled protozoa to more complex bacteria and rickettsiae. The method of transmission varies, depending on the parasite, but often they are transmitted through the bites of ticks or flies. Babesiosis Babesiosis is a disease transmitted by ticks. It affects a wide range of domestic and wild animals and occasionally humans. In horses, babesiosis is caused by protozoan parasites of the genuses Babesia andTheileria, which infect red blood cells. Equine babesiosis occurs in Africa, Europe, Asia, South and Central America, and the southern US. Infection of unborn foals, particularly with Theileria protozoa, is relatively common. The incubation period is approximately 8 to 10 days. Signs of infection in adult horses may include reluctance to move, lack of appetite, and fever. Swelling of the fetlocks may occur, and episodes of colic are common. In young horses, signs may be more severe and can include jaundice, weakness, and pale mucous membranes. The disease lasts for about 10 days, but death may occur in the first 24 to 48 hours. Some horses develop chronic, or longterm, infections and can become carriers for several years after the initial infection. Babesiosis can be confused with other conditions that cause fever, anemia, destruction of red blood cells, or jaundice. Therefore, laboratory tests should be performed to confirm the diagnosis. Treatment generally involves using one or a combination of effective antiprotozoal drugs. There is no vaccine for use in horses. Controlling ticks by periodic spraying and inspection of the horse can help reduce the chance of transmission. African Trypanosomiasis (Tsetse Fly Disease) Tsetse flies are small, winged biting flies that feed on the blood of humans and other animals. They only occur in sub-Saharan Africa, where they are responsible for transmitting a group of diseases caused by protozoa of the genus Trypanosoma, which affect all domestic animals. Tsetse flies are restricted to Africa; however, horseflies and other biting flies can transmit the disease in other locations such as Central and South America. In horses, Trypanosoma congolense, T. vivax, and T. brucei brucei are the trypanosomes most likely to cause disease. Domestic animals may be a source of human infections. The severity of disease varies with the species and age of the animal infected and the species of trypanosome involved. The incubation period is usually 1 to 4 weeks. The primary signs are fever that may come and go, anemia, and weight loss. Internally, the lymph nodes and spleen are usually swollen. The diagnosis is confirmed by finding trypanosomes in laboratory tests. Several drugs can be used for treatment; however, most drugs only work if the correct dose is given. It is very important to follow the prescribed dosage exactly. Some trypanosomes have become resistant to certain drugs, which may be the cause in cases that do not respond to medical treatment. The risk of infection can be reduced in areas where the disease is common by getting rid of tsetse flies and using preventive drugs, which are given to stop an infection from getting started. Flies can be partially controlled by using sprays approved for use on horses, spraying insecticides on fly-breeding areas, using screens coated with insecticide, and clearing brush to reduce the habitat for the flies. Animals can be given preventive drugs in areas with a high population of trypanosome-infected tsetse flies (portions of Africa and Central and South America). There is no vaccine. Surra (Trypanosoma evansi Infection) Surra is separated from the tsetse-transmitted diseases because it is usually transmitted by other biting flies that are found within and outside tsetse fly areas. It occurs in North Africa, the Middle East, Asia, the Far East, and Central and South America. It can be a deadly disease in horses. Trypanosoma evansi in other animals appears not to cause disease, and these animals serve as a source of the infection. The development and effects of the disease, signs, physical changes, diagnosis, and treatment are similar to those of the tsetse-transmitted trypanosomes (see above). Dourine Dourine is a venereal disease of horses that is transmitted during sexual intercourse. It is caused by a species of trypanosome named Trypanosoma equiperdum. The disease occurs on the Mediterranean coast of Africa and in the Middle East, southern Africa, and South America; however, the distribution is probably wider. Signs may develop over weeks or months, and infection may become chronic. Early signs include mucous and pus-filled discharge from the urethra in stallions and from the vagina in mares, followed by swelling of the genitals. Later, characteristic scaly patches ¾ to 4 inches (2 to 10 centimeters) in diameter appear on the skin, and the horse becomes dangerously thin. If untreated, 50 to 70% of infected horses will die. Getting definitive proof of this disease can be difficult. However, your veterinarian can perform certain tests to find and identify the trypanosomes in the discharges, the skin patches, or the blood. In areas prone to this disease, horses may be treated with several different medications. When completely eliminating the disease from a stable or group of horses is desired, strict control of breeding, euthanasia of positively identified infected horses, and elimination of stray horses has been successful. References http://www.merckvetmanual.com/pethealth/horse_disorders_and_diseases/blood_disorders_of_horses/blood_parasites_of_horses.html

DJD

Degenerative joint disease (DJD) is a type of osteoarthritis that causes lameness in affected horses and is one of the most common causes of lameness in sport horses. DJD develops when the cartilage protecting the bones of the joint is destroyed.

Degenerative joint disease, is a progressive deterioration of the joint cartilage and represents the end stage of several other diseases including traumatic arthritis involving the synovial membrane and joint capsule, joint fractures, traumatic damage to cartilage, osteochondritis dissecans, cysts beneath cartilage, and infective arthritis.

Cartilage, which is made up of collagen fibers, glycosaminoglycans, and proteoglycans, is associated in direct proportion with the severity of the disease. When the articular cartilage loses its elasticity and ability to bear and transmit forces efficiently, it creates a cascading cycle of more cartilage damage, and the complex process results in the net loss of cartilage.

The joints that are usually affected are the lower joints of the legs because they are the major shock absorbers.

In addition to loss of cartilage, degenerative joint disease often leads to the growth of bone in the affected limbs. In the forelimb, it is usually the carpus (knee). In the hind limb, it is commonly the hock, also know as bone spavin. In the coffin joint, it is called low ring bone and, in the pastern, it is known as high ring bone.

Because of the bone growth, horses will show signs of lameness and pain with flexion of the involved joints. Swelling occurs in the affected joint; and, if the process has been ongoing, decreased range of flexion occurs.

The joints most commonly affected are the upper knee joint, front fetlocks, hocks, coffin joints in the forefeet, and the spine, including the neck and back.

The form of degenerative joint disease known as osteochondritis dissecans occurs when the immature joint cartilage separates from the underlying bone. Fluid enters the space, and cysts may form under the cartilage. The cartilage may break away completely or, if the joint is rested or protected, reattach itself to bone.

Osteochondritis dissecans usually is seen in young animals (less than 1 year old), most commonly at the femoropatellar (knee) joint, tarsal joint, fetlock joints, and the shoulder. The exact cause is unknown, but contributing factors likely include a genetic predisposition in the animal, rapid growth, high caloric intake, disproportionate levels of copper and zinc in the diet, and hormonal factors

Symptoms

• Reduced activity level
• Slow or stiff movements after rest or in cold weather
• Stiffness or lameness that disappears with exercise
• Difficulty getting up from a lying down position
• Abnormal gait or lameness during exercise
• Swollen joints that are warm to the touch
• Change from normal behavior or temperament
• Decreased appetite
• Loss of muscle mass

Causes

Two major factors control the development and progression of DJD: biomechanical forces and biochemical substances. The biomechanical forces are the excessive forces that the horse puts on its joints through repetitive stress and strain during exercise.

The biochemical damage occurs when enzymes are released into the joint, resulting in the breakdown of the joint cartilage. This leads to more enzymes being released, causing further cartilage damage resulting in a self-perpetuating destructive cycle. Cartilage in the joints is made up of cells known as chondroctyes and a matrix of proteins. These cells have a very limited ability to regenerate, resulting in irreversible cartilage destruction.

Usual causes of DJD include:

• Injury
• Abnormal growth pattern
• Inherited factors
• Traumatic injury to hock, stifle, pastern and fetlock joints
• Old age
• Genetics - heavy breeds can be prone to DJD because their weight puts extra demand on their joints. The same goes for horses that are overweight
• Overworking of the joints
• Poor fitting/unbalanced shoes

Prevention

The best way to control DJD is to prevent it. Unfortunately, because this disease is often secondary to a traumatic incident, prevention is difficult. However, several areas of care can help reduce the possibility of developing DJD from an injury.

A diet with balanced vitamins and minerals plus the correct ratio of roughage to grain should be formulated to help with the proper development of cartilage.

As a foal, the conformation of the limbs will greatly influence the way the joint will wear as the horse matures. When proper alignment is missing, abnormal wear may lead to premature DJD of the joint.

Hoof care is an area that is often overlooked but has a lot to do with the proper alignment of the lower pastern region. Adequate trimming and shoeing can help maintain alignment.

Finally the training regime must be reasonable for the animal. It is important that the training ground is level and that the surface is not too hard or too soft. Each animal should have a work schedule tailored to its unique fitness level and injury status.

Adequate muscling will help reduce the likelihood for injury and reduce the chances for DJD

Treatment

Treatment of degenerative joint disease is generally limited to reducing joint pain and stiffness. Nonsteroidal anti-inflammatory drugs (for example, firocoxib, ketoprofen, and phenylbutazone) or corticosteroids may provide relief.

Chronic use of many of these agents can decrease or suppress chondrocyte metabolism and cause further degradation of the cartilage matrix by the inhibition of normal collagen and proteoglycans synthesis.

Physical therapy may prove helpful. In advanced cases, surgical fusion may be performed on selected joints. Some horses return to athletic soundness following surgical fusion of the pastern or tarsal joints. For very valuable animals, the fetlocks may be surgically fused, making the horse comfortable and capable of breeding

Some NSAlDs can cause gastrointestinal ulceration and hemorrhage. The problems and limitations of NSAlDs and steroidal anti-inflammatory agents have recently led to a search for agents that relieve pain and inflammation and limit or reverse cartilage degeneration side effects.

In all cases involving degenerative joint disease, the services of a knowledgeable veterinarian are invaluable. With proper treatment accompanied by an appropriate work load and exercise based on the particular horse's capacity, the effects of degenerative joint disease can be minimized.

Reference

Equimed.com

STOMACH ULCERS

A common case of heartburn can bring intense discomfort, even pain, to a person. Imagine your horse trying to perform with a stomach ulcer. Did you know that the clinical signs of ulcers in horses are subtle and nonspecific and might be reflected in a slight attitude change, a decrease in performance, or a reluctance to train?

Gastric ulcers are common in horses. Their prevalence has been estimated to be from 50% to 90%, depending on populations surveyed and type of athletic activity horses are engaged in.

Gastric ulcers can affect any horse at any age. Foals are particularly susceptible because they secrete gastric acid as early as 2 days of age and the acidity of the gastric fluid is high. Foals that have infrequent or interrupted feeding, or are recumbent for long periods have been found to have lower gastric fluid pH (aqueous solutions with a pH less than 7 are acidic), suggesting that milk has a protective effect against ulcers and that recumbency increases exposure of the stomach to acid.

In adult horses, gastric ulcers occur more frequently in horses that perform athletic activities, with the highest frequency found in Thoroughbred racehorses (80-90%), followed by endurance horses (70%), and show horses (60%). Researchers have found that exercise increases gastric acid production and decreases blood flow to the gastrointestinal (GI) tract.

In addition, when horses exercise, the acidic fluid in the stomach splashes and exposes the upper, more vulnerable portion of the stomach (squamous mucosa) to an acidic pH.

Why are gastric ulcers so common in horses? First, the stomach of the horse is smaller compared with the stomach of other species. Because of this, horses cannot handle large amounts of food; rather, they are built to graze and eat frequent, small portions of feed for extended periods of time.

In a natural grazing situation, the horse requires a steady flow of acid for digestion, so a horse's stomach produces acid 24 hours a day, 7 days a week--up to 9 gallons of acidic fluid per day, even when not eating. In a natural, high-roughage diet, the acid is buffered by both feed and saliva.

Second, understanding the horse's anatomy, it is possible to see how ulcers could be considered a "manmade" disease. When horses are fed two times per day, the stomach is subjected to a prolonged period without feed to neutralize the acid. Furthermore, high-grain diets produce volatile fatty acids that can also contribute to the development of ulcers.

Other risk factors for developing gastric ulcers include physical and environmental stress such as transport stress and stall confinement (intermittent feeding and lack of exposure to other horses). Recent studies have demonstrated that a few hours of transport can induce gastric ulceration in horses that had none prior to departure, as determined by gastroscopy.

Finally, chronic administration of some non-steroidal anti-inflammatory drugs (NSAIDs)--such as phenylbutazone, flunixin meglumine or ketoprofen--can decrease the production of the stomach's protective mucus layer, making it more susceptible to ulcers.

Anatomy of the Horse Stomach

The horse's stomach is divided into two distinct regions: the squamous region at the top (considered a continuation of the esophagus lining) and the glandular mucosa at the bottom (similar to the human stomach). The bottom part is glandular and secretes gastric acid. However, this region also produces mucus and bicarbonate, which protect the mucosa from acid exposure. So even though this region is also exposed to acid for several hours a day, it is not a common place for ulcer formation. When ulcers do form in this region of the stomach, they are usually secondary to chronic NSAID administration.

The top portion of the stomach is designed for mixing of the contents of the stomach and does not have as much protection from the acid. This is the most common place to find gastric ulcers. The lining of this section of the stomach is very thin and does not have many mechanisms for acid protection. Because the horse's stomach produces gastric acid at all times, even when not eating, the squamous mucosa is exposed to acid several hours a day, which can easily erode the lining of this region.

Clinical Signs

The majority of horses with gastric ulcers do not show outward clinical signs. They have more subtle signs, such as:

• Poor appetite;
• Dullness;
• Attitude changes;
• Decreased performance;
• Reluctance to train;
• Poor body condition;
• Poor hair coat;
• Weight loss;
• Excessive time spent lying down;
• Low-grade colic; and
• Loose feces.

More serious cases will show abdominal pain (colic) and/or grinding of the teeth. Some horses are found on their backs, commonly seen in foals, since this position seems to provide some relief from severe gastric ulceration. Others will walk away from food for a period of time as if they experience discomfort when the food first hits the stomach.

Clinical signs of ulcers in foals include intermittent colic (after suckling or eating), frequently lying down, intermittent nursing (interrupted nursing due to discomfort), diarrhea, poor appetite, grinding of teeth, and excess salivation. When a foal exhibits clinical signs, the ulcers are likely to be severe and should be diagnosed and treated immediately.

Note that horses that look completely healthy can also have gastric ulcers. Approximately half of the horses presented for colic at UC Davis have gastric ulcers and often it is hard to know whether the colic is the result of the ulcers or the other way around.

Diagnosing Ulcers

The only way to definitively diagnose ulcers is through gastric endoscopy, or gastroscopy, which involves placing an endoscope into the stomach and looking at its surface. This procedure is easy to perform, is minimally invasive, and allows us to evaluate the esophagus, squamous and glandular regions of the stomach, and proximal segment of the small intestine in horses. (See a video of gastroscopy from UC Davis here.)

Since feed material can prevent a complete evaluation of the stomach, horses are fasted for a minimum of 12 hours and water is withheld for four hours before examination.

To minimize stress, we sedate the horse slightly with a short-acting tranquilizer. We then insert the endoscope through the nostril and down the esophagus into the stomach. The light and camera on the end of the endoscope allow the veterinarian to observe the stomach lining. The procedure is very safe, and a complete evaluation takes from 10 to 20 minutes.

Some practitioners will treat a horse for gastric ulcers and look for a change in clinical behavior. This can be helpful but does not answer the question of when to discontinue treatment. Horses that improve with treatment should be scoped prior to discontinuing therapy.

Prevention and Treatment

As always, prevention is preferable to treatment. We have described some common risk factors that can contribute to the formation of gastric ulcers in horses. The following management techniques may assist in preventing ulcers:

• Feed horses frequently or on a free-choice basis (pasture). This helps to buffer the acid in the stomach and stimulate saliva production, nature's best antacid.
• Reduce the amount of grain and concentrates and/or add alfalfa hay to the diet. Discuss any feed changes with your veterinarian so that medical conditions can be considered.
• Avoid or decrease the use of anti-inflammatory drugs. If anti-inflammatory drugs must be given, consider newer ones such as firocoxib, if appropriate.
• Limit stressful situations such as intense training and frequent transporting.
• If horses must be stalled, allow them to see and socialize with other horses as well as have access to forage.

A common question asked by horse owners is, "If the prevalence of gastric ulcers is so high, do I need to treat my horse for the rest of its life?" Considering that treatment is expensive and that acid in the stomach is there for a reason, we do not recommend that horses be treated continuously.

Antacids are commonly used in humans to buffer or neutralize gastric acid and protect the mucosa. However, in horses, the dose of antacids required to buffer the pH is high and would need to be used several times a day to be effective. If antacids are used for treating gastric ulcers in horses, they should be used in combination with agents that decrease acid production.

Acid pump inhibitors such as omeprazole and pantoprasole stop gastric acid secretion completely.

Other effective types of drugs for the treatment of ulcers are the histamine type 2 (H-2) receptor blockers such as cimetidine, ranitidine, and famotidine, which partially block acid production.

H-2 receptor blockers work in a similar way to antihistamines used for allergies, except that antihistamines act on type 1 histamine receptors, while the acid blockers act on type 2 histamine receptors. H-2 receptor blockers are less expensive than acid pump inhibitors, but they need to be administered three times a day and only partially block acid production.

Currently, there is only one treatment--omeprazole--approved by the U.S. Food and Drug Administration (FDA) for gastric ulcers in horses. In 2000, the Fédération Equestre Internationale allowed the use of the gastric ulcer medications omeprazole and ranitidine during competition.

Omeprazole is available as a paste formulation and it has been very effective in preventing and treating gastric ulceration in all types of horses. Although the commercial paste is expensive, it is very effective and requires administration once a day. Due to the cost of this product, some compounding pharmacies prepare and sell paste or liquid omeprazole at cheaper prices. However, several studies have shown that the amount of active omeprazole in those products is lower than the label. In addition, the ability of those products to inhibit gastric acid production and their ability to resolve gastric ulcers has been variable.

Horse owners should be wary of claims for products that are not controlled or regulated by the FDA (compounded products) or evaluated in scientific studies. While those products might be less expensive, they could cost you more in the long run.

We recommend treating (1) horses with severe gastric ulceration, (2) horses with clinical signs of gastric ulceration, and (3) horses that are under stressful conditions and at risk of gastric ulceration. Under these circumstances, treatment with a product that is labeled specifically to prevent and/or treat gastric ulcers and approved by the FDA should be used. Treatment should be given for a full month, followed by a recheck endoscopy to confirm complete healing.

A preventative dose of omeprazole is commercially available for use around transport or stressful events. Horses with a history of gastric ulceration may benefit from proactive treatment to decrease the chances of ulcer recurrence. At this dosage, the omeprazole is less costly and could serve as a good investment in your horse's well being.

by Jorge Nieto, DVM, PhD, Dipl. ACVS--Reprinted from The Horse Report with permission from the Center for Equine Health, School of Veterinary Medicine, University of California, Davis (UC Davis).

PULSED MAGNETIC THERAPY

Pulsed Magnetic Therapy

Veterinary professionals, animal physiotherapists and individual owners are enthusiastically using pulsed magnetic therapy (PMT) equipment for a wide range of musculoskeletal disease and degenerative conditions.

All animal organisms consist of a large number cells that function electrically. Cells have a basic electrical potential that is necessary for normal cellular metabolism. If there is no electrical potential then a cell is no longer viable. Damaged cells have an altered electrical potential. If the ions — electrically charged particles surrounding the cells — move into a pulsed magnetic field area, they are influenced by the rhythm of the pulsation, and ion exchange is enhanced resulting in greater oxygen utilisation, faster absorption of nutrients and elimination of waste products.

Treatment can be used on a variety of conditions including, but not limited, to:

• Orthopaedic trauma — fractures and bone damage
• Open wounds and circulatory problems
• Soft tissue problems — sore backs, muscle tightness, body soreness
• Acute inflammation
• Chronic pain

Hundreds of studies have been completed worldwide documenting the effectiveness of PMF. From these clinical experiments we know that pulsated magnetic fields can reduce pain sensations almost immediately. This is due in part to the increase in the oxygen partial pressure in the terminal tissue and the increase in the local perfusion and velocity of the capillary blood flow, alleviating the accumulation of metabolises due to small vascularisation and blood flow.

There are no contra-indications to magnetic therapy except in cases of haemorrhage. In contrast to chemical medica­ments, there is no chance of overdosing, at least within the field range that is presently used for treatments.

The PMF therapy is heatless; therefore all implants (metal or plastic) can be treated. Hospitals use PMF therapy to accelerate the healing of patients with pins and bone plates because no damaging heat is produced in the implants.  Fractures can be treated, even through a bandage, since magnetic fields permeate most materials.

The therapeutic effect of such treatments lasts for approx­imately six to eight hours. Most chronic cases require treat­ments twice a day. After five to ten days, the treatment regime can be reduced to one treatment daily or every other day. In chronic or extremely difficult cases, this may take longer.

There are several various Pulsed Magnetic units available, ranging from the Centurion Mini Pulse through to our 4PH + Hoof Pad option. Units are either self powered rechargeable battery or mains powered.

Centurion Systems also offers cold compression therapy, which is one of the most highly recommended treatments for recovery from soft tissue injuries and everyday training stress that may lead to more serious athletic injuries.

Centurion’s Boreas cold therapy machine helps to:

• Reduce Pain
• Reduce Swelling and inflammation
• Improve recovery from orthopaedic surgery
• Controls muscle damage
• Reduces heat

For full details on this treatment and how it works visit www.centurion-systems.co.uk 

HEAD SHAKING

Head shaking syndrome exhibit repetitive,involuntary headshaking that is more vertical.
Head shaking is a clinical signs of variety of disease.
Guttral pouch and paranasal sinus lesions.
This behavioral problem is most commonly seen in the warmer months of the year.

Causes
Insect bites
Ear mites
Dental problems
Allergies
Sunlight sensitivity

Signs
Damage of the sensory nerve of the skin.
Snorting
Head tossing
Violent shaking of head
Wiping of the nose

Affected horse will try to rub the nose on a foreleg or the ground at the canter.
In many cases horse is unrideable or dangerous to ride.

Treatment
In allergic rhinitis systemic antibiotics is required.
Ear mites should treated topically.

TENDINITIS IN HORSES

Inflammation of a tendon can be acute or chronic, with varying degrees of tendon fibril disruption. Tendinitis is most common in horses used at fast work, particularly racehorses. The problem is seen in the flexor tendons and is more common in the forelimb than in the hindlimb. 

Etiology

• Fast exercise  overextension
• Poor conditioning,
• Fatigue,
• Poor racetrack conditions,
• Persistent training when inflammatory problems in the tendon already exist.
• Improper shoeing may also predispose to tendinitis.
• Poor conformation
• Poor training

Clinical Findings and Diagnosis

acute stage, the horse is severely lame and the involved structures are hot, painful, and swollen.

chronic cases, there is fibrosis with thickening and adhesions in the peritendinous area. 
The horse with chronic tendinitis may go sound while walking or trotting, but lameness may recur under hard work.

Treatment

• Tendinitis is best treated in the early, acute stage.
• The horse should be stall-rested, and the swelling and inflammation treated aggressively with cold packs and systemic anti-inflammatory agents.
• Some degree of support or immobilization should be used, depending on the amount of damage to the tendon.
• Intratendinous corticosteroid injections are contraindicated. When a distinct hypoechoic or anechoic core lesion is present on ultrasound examination, tendon splitting has been recommended.
• More recently, cases have been treated with shock wave therapy, intralesional injection of fat-derived stromal cells or cultured bone marrow-derived mesenchymal stem cells, or autologous conditioned plasma.
• The horse should be rehabilitated using a regimen of increasing exercise. Superior check ligament desmotomy has been used as an adjunctive treatment to minimize recurrence of the problem when the horse is returned to training.
• Annular ligament desmotomy is also used when tendinitis involves the area of the digital tendon sheath.

 PREVENTIONS

• Checking the Legs: especially after hard work, it is important to feel each leg for swelling and heat, and to palpate it for pain.
• Correct Trimming and Shoeing: a good farrier will trim the horse's feet correctly, preserving the pastern-hoof angle, and will properly support the horse’s heels.
• Bandaging: using properly applied exercise bandages can help prevent the overextension of the fetlock.
• Correct Conditioning: with a base of long, slow distance work, and a fitness schedule that is not increased too rapidly.
• Suspending Training: if any sign of heat, swelling, or pain is detected

Reference

http://www.merckvetmanual.com/mvm/musculoskeletal_system/lameness_in_horses/tendinitis_in_horses.html

URTICARIA OR HIVES IN HORSES

Urticaria or Hives Urticaria (hives) is one of the most common skin problems faced by horses.

It is the result of a hypersensitivity (allergic) reaction and identified as multiple raised, oedematous(fluidy), flat topped swellings, which often will dent or ‘pit’ when pressure is applied to them.

Although occasionally itchy they usually cause no discomfort to the horse. Any age or type of horse can be affected, though thoroughbreds are probably over-represented.

CAUSES

• Food
• medication
• insect bites
• stings
• pollens
• mould 
• fungal spores
• extreme temperatures
• stress and many others

TREATMENT

• The majority of sudden onset cases of urticaria will spontaneously resolve in 24-48 hours, so if the horse is not otherwise affected it may be best to hold off any treatment, initially.
• However, if the horse shows any signs of discomfort or distress then treatment should be sought immediately.
• The most common and usually the most effective treatment is an intravenous injection of corticosteroid, which blocks the production of inflammatory substances which are what cause the wheals to form.
• Steroids need to be used with care, particularly in horses at risk of other conditions, such as laminitis and in competition horses, where it is a restricted substance.
• Vigorous exercise may help to reduce the reaction.
• Antigen desensitisation, or ‘self-vaccination’, is a costly process with very variable results. There is little scientific evidence for its use.
• Anti-histamines are expensive and generally produce only poor results. If all else fails a complete change of environment and placing the horse on an exclusion diet of hay and grass only,may be the solution.

Reference

http://www.minstervets.co.uk/uploads/Files/Urticaria%20or%20Hives.pdf

ANHIDROSIS IN HORSES

Anhidrosis is a condition in which the horse is unable to produce sweat.This is also called as Dry coat or Equine anhidrotic syndrome.

certain indiduals have a poor response to sweat stimulation by adrenalin.

Horses reared in temperate climates and transported to region of high huminity and temperature may fail to acclimatize.

Horses that sweat lightly or only in patches such as under the mane, in the saddle area, and on the chest are known as shy sweaters.

Signs

Acute sweating is much reduced or absent ,this is accompanied by respiratory distress,labored breathing,fever,collapse and occasionally death.

Chronic is characterized by dry coat, seborrhea and alopecia particularly face and neck.

Horse shows poor exercise tolerance.

Treatments

Application of cold water to reduce body temperature.

Air conditioned stable should be provided for affected horses.

Electrolyte supplementation seems to trigger a return to normal sweat

Management practices to help an anhidrotic horse include:

• Moving the horse to a cooler climate.
• Hosing with cold water as needed after exercise or periodically during hot weather.
• Limiting training and exercise to the coolest part of the day.
• At competitions, requesting that the horse be scheduled to perform early in the morning.
• Installing stall fans, misting machines, or air-conditioning in stables.
• Giving pasture-kept horses access to shady areas, ponds, or streams.

Reference

The Equine manual

by Andrew J.Higgins and Jack R.Snyder