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- Glycerine 4L A clear, colorless, syrupy liquid, used as a humectant and as a solvent for drugs
- Copper Sulfate 400G used as a vermicide against small nematode worms, germicide, fungicide, viricide, astringent, antiseptic agent and ophthalmic solution. It is also indicated for urethral infection, ring worm, alopecia and wound treatment (caustics).
- Sulfur Powder 2KG Used as an orchard spray and topically as an ectoparasiticide and antifungal in the treatment of skin diseases. Can cause skin irritation in some animals. Called also calcium sulfide, calcium polysulfide, sulfurated lime.
- Borax Powder 400G used as a herbicide, an insecticide, and a soil sterilant. It is toxic to animals if consumed in moderate to large doses (>0.5 g/kg).
- Citric Acid 400G is a versatile material and can aid in solving solubility problems for a variety of water administered products in poultry, swine, and other livestock.
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Dominion Veterinary Laboratories guarantees you top quality made-in-Canada products. For instance, horse supplies, horse drugs, horse medications, horse liniment, horse products, horse supply, horse supplements, cattle supplies, livestock supplies, cattle medicine, cattle prod, cattle feed, cow supplies, livestock antibiotics, and horse medicine. Horse and Cattle Supplies: Tying-up is a less severe form of azoturia.
CAUSES Horses worked at irregular intervals and fed high-grain diets are most susceptible to azoturia. Ingested grain is converted to glycogen, which is stored in muscles and elsewhere. If the horses is rested for periods of one or two days whilst on a high-grain diet, large quantities of glycogen are stored in the muscles. Glycogen is used my the muscles as a source of energy when work is being done; the waste product from the chemical change that takes place is lactic acid. If a large volume of glycogen is stored, a large volume of lactic acid is produced when the horse exercises. If the lactic acid cannot be expelled from the muscle tissue, it damages the muscle fibers, causing the condition known as tying-up. If large areas of muscle fibers are damaged or even destroyed, asoturia results.
some horses that are not on grain diet tie up because they are hypersensitive to lactic acid or because their particular metabolism does not cope with it efficiently.
SIGNS These can vary widely. In mild cases, during or after exercise, the horse steps short in the hindlimbs, giving the appearance of stiffness. In severe cases, the horse will show stiffness, pain, sweating and muscle tremor. The stiffness, involving both the hindlimbs and the frontlimbs, may progress to the point at which the horse cannot move and may lie down. The affected muscles are very hard to the touch, indicating cramp, and the urine may vary in color from dark brown to reddish black, according to the severity of the condition.
TREATMENT Call your veterinarian, who can confirm the condition not only by its history and clinical signs but also by taking a blood count and by doing certain serum enzyme tests.
Stop exercising the horse when you notice that it is tying-up. In all cases except severe ones, walk the horse for thirty minutes. If it appears no better, call your veterinarian. Walking aids in the circulation of blood to the muscles with consequent removal of lactic acid, thus helping to prevent severe cramping.
Keep the horse warm by seeing that it is well rugged. Tempt it with fluids containing electrolytes, which, if drunk in any quantity, will help to flush out the kidneys.
With the aid of information gained form a blood count, the veterinarian can administer a muscle relaxant, diuretics, tranquillizers and anti-inflammatory agents if required, as well as specially prepared fluids and electrolytes by stomach tube or intravenous methods.
All grain should be eliminated from the diet and the horse should be offered a bran mash as a mild laxative. Horses susceptible to frequent tying-up should have a low-level grain diet. Normally the grain level in the diet should be in proportion to the amount of work done. For example, if any one week a horse works for six days, followed by a day off, reduce the quantity of grain in the feed for that day. Recovery can take place within hours, though in severe cases it may take weeks.
Exercise the horse every day, even if it is just walking exercise and consult your veterinarian about the regular use of a particular vitamin supplement as a preventive measure.
Degenerative Joint Disease, commonly known as bone spavin, is a bony swelling onnthe lower, inner side of the hock, caused by arthritis of the bones in the area. Some horses with an obvious bone spavin show little or no signs of lameness; others may be very lame but with no signs of swelling. Horses with bone spavin may still be useful, but fluctuating lameness may recur at varying intervals.
When a horse is viewed from behind, a line should bisect the gaskin, hock, cannon, fetlock, pastern and foot. If the horse's hocks turn inward, the horse is considered cow-hocked. When the legs are viewed from the side, a straight line drawn downward from the back of the buttock should touch the back of the hock, cannon and fetlock. If the horse has too much angle in the hocks, then it is considered to be sickle-hocked. If the leg is forward of this line and too straight, the horse is considered post-legged.
CAUSES In many cases, bone spavin is due to poor conformation, such as sickle and cow hocks. Despite what many people think, the condition is not hereditary. What is inherited is the poor conformation. Bone spavins, bogs, thoroughpins and weakness are common among sickle-hocked horses. The condition can also be caused by stress and strain being placed on the hock because of participation in such activities as polo, calf roping and racing, especially by young horses.
SIGNS These include a hard, bony enlargement that can be felt and seen in the lower and inner side of the hock. Lameness is evident when the horse is cold but often disappears as it warms up with exercise, although in some cases the lameness may worsen. The lameness is characterized by reduced flexion of the hock and a shortening of the stride in the affected leg.
TREATMENT Accurate diagnosis is important to determine the severity of the condition, and this in turn will determine the type of treatment. The diagnosis can only be made by your veterinary surgeon with the aid of X-rays.
Your veterinarian may advise any one of a number of treatments or a combination of them, if necessary. These treatments include rest in a spelling paddock for a minimum of six weeks and corrective trimming and shoeing. In the latter treatment, the toe of the foot should be rasped square and a shoe with a raised heel and a rolled square toe should be fitted. This causes the leg to move in a straight line rather than deviating outwards, thus alleviating strain on the inside of the hock.
Other treatments are radiation, anti-inflammatory drugs, pin firing and surgery to sever a section of the tendon that runs over the spavin.
The little yellowish dots on your horse's lips and front legs appear harmless at first, but several months from now those bot fly eggs will have developed into larvae in your horse's stomach. Your horse is sure to be infested with bots unless your area is entirely free of flies.
Bots are the larvae of the Gasterophilus fly. Since these flies can't live through the cold months of winter, they have developed a unique method of ensuring the survival of future generations. The small, yellowish flies (which look a little like bees) live only for a week or so as adults, spending most of their lives as immature bots in the horse's stomach.
Bot flies start laying their eggs in the spring and summer, with a peak egg-laying period in the fall. The season can extend almost year-round in warmer climates. The eggs hatch when the horse rubs or licks his legs with his lips or tongue. Tiny immature larvae latch onto the horse's mouth and burrow into the tissues. A large infestation may cause tenderness and ulcers throughout your horse's mouth.
The larvae spend a month or two maturing in the tongue before they emerge and are swallowed. Over the next several weeks, they grow and develop into stomach bots. Bots create deep pits in the stomach wall producing ulcers. severe cases may cause perforation of the stomach or blockage of its outflow into the small intestine. Bots can live attached to the stomach wall for up to a year before finally release their hold and are expelled in the manure. They spend another month or two on the ground and then hatch into adult bot flies.
There is no simple way to diagnose bot infestation. You can assume that horses with eggs on their legs and face are infested with bots. A bot treatment has traditionally been recommended after the first killing frost each year, when all adult flies have died. While this advice is well taken, you are leaving your horse open to infestation the rest of the year if you don't treat more often.
Bot flies begin to deposit their eggs in early spring. Studies show that the highest average number of bot larvae per infected stomach occurred in the winter and spring with about 44-94 percent infection rate. If you don't use a boticide (bot treatment) until November, you're leaving bots in your horse's stomach all summer long. Treatments in spring, summer , and fall are a good idea. The organophosphates and invermectin kill both bots at the tongue-migrating stage and bots in the stomach.
Fly control is as important as regular bot treatments. Since fecal piles of the horse are used as the mating site for the newly hatched flies, regular manure cleanup will keep any hatching bot flies away from your horse. Remember to shave the eggs of your horse's hair after your last bot treatment in the fall.
Several products provide feed-through fly control. These products contain low levels of organophosphates, which remove the bots from the horse's stomach. The drug persists in the manure, killing the larvae of flies that lay eggs in compost.
The low levels of drug in feed-through products may not be enough to remove all the bots from your horse. If you're using a feed-through products regularly, be aware that you may overdose your horse by deworming him with organophosphates paste or tube product. Also be sure you're environmentally responsible in the disposal of manure that contains chemicals.
You should not take bot infestation lightly. There has been reported a case of septic peritonitis due to bot infestation. The larva was embedded deep in the horse's colon which eventually caused perforation of the colon and leakage of intestinal content into the gut. The horse developed acute colic and fever and was euthanatized.
Botulism is caused by the toxin Clostridium botulinum. Horses are among the most susceptible species. The toxin may be produced in food, such as silage or vaccum-packed moist hay, which has been contaminated by decaying matter containing the organism. Also known as "Shaker foal" disease, the toxicoinfectious form of botulism affects foals, with the highest incidence in the United States seen in Kentucky and the mid-Atlantic region.
Clostridium botulinum is a spore-forming anaerobic bacterium which reproduces in decaying animal or plant matter. Under favorable conditions of warmth and humidity spores multiply and produce a highly lethal toxin. There are at least 7 different toxin types. Botulinum neurotoxins (BoNTs), produced by spore-forming anaerobic Clostridium botulinum, are the most toxic substances known. Ingestion of preformed toxin is the major route of infection in adults.
SIGNS
The rapidity of onset, i addition to severity of clinical signs, is toxin dose related. Affected foals are usually less than 8 months and often less than 2 months old. Signs include impaired sucking, inability to swallow, decreased eyelid and tail tone and dilated pupils. There is progressive muscular weakness and tremors, leading to collapse and inability to rise. Muscle tremors over the shoulders and flanks are evident. Saliva drools from the mouth. The gait is weak, shuffling and unsteady. Death results from respiratory paralysis within 24 to 72 hours of the onset of clinical signs.
TREATMENT
Equine antitoxin (pentavalent vaccine against A-E toxin types) can only target the toxins at extracellular level, and can not reverse the paralysis caused by botulism. Intensive care is often difficult to provide and always expensive in the face of a guarded to poor prognosis. Treatment often is unrewarding unless a case is identified early and the proper antitoxin is readily available.
PREVENTION
Prevention involves common sense approaches to feeding and care of the horse and, where possible, judicious use of vaccination in endemic areas.
Chronic Obstructive Pulmonary Disease (COPD), also known as heaves, broken wind, alveolar emphysema and equine asthma, is a chronic respiratory condition caused by development of a narrow airway in the horse's lungs. It is caused by an allergic reaction to fungal infections.
The condition is mostly seen in stabled horses and is associated with a dusty atmosphere and mold in hay and straw. Micropolyspora faeni (which causes farmer's lung in man and cattle) and Aspergillus fumigatus fungus appear to be the cause of COPD in most cases.
Symptoms--The disease affects horses of two years old and above, becoming more common as horses get older. Early signs may include mild cough, slight increase in respiratory rate and effort, thick yellow mucous. heaves-affected horses have normal temperature and appetite. An affected horse may show signs as rapidly as one hour after exposure, with the horse becoming increasingly breathless. Removal of the offending material allows most cases to improve gradually over a few days.
The allergic reaction brings about serious changes in the lungs. These include inflammation of the very small airways, production of excessive, thick mucous and spasm of the airways which may result in their complete collapse. This makes exhalation difficult and an increased volume of air is retained in the lungs which have an overinflated appearance.
The changes in the lungs are reversible with a proper care, but once a horse becomes affected with heaves, it remains hypersensitive for many years if not for life.
Treatment and Prevention--The most important thing in treating heaves-affected horse is to provide minimum-dust environment together with medical therapy, if necessary. Use substitues for hay and straw. Bedding should be changed on a daily basis. The stable should be at least at least 70 yards to the windward side of the hay store, according to the direction of the prevailing wind. Dust should be removed from the stables on a regular basis.
The alternative method of environmental control is to keep COPD-affected horses at grass. No supplementary hay should be fed and grazing areas should not be near to hay or straw stores. Any supplementary feeding should be in the form of a cubed diet, as even good-quality hay and straw
DELAYED RELEASE OF THE PATELLA
The clinical signs of this condition depend of its severity. It occurs most often in young horses and ponies, especially those which are unfit and poorly muscled. In the most severe cases the leg becomes stuck in extension and the patella is "locked." The horse may hop on 3 legs, dragging the affected leg behind it. The horse may release itself spontaneously. Some horses remain unable to flex the leg and it may be necessary to force the horse either to back or to jump forward in order to release the patella, which has become stuck on the upper part of the femur. This may happen intermittently several times a day, especially if the horse is kept in. One or both hind legs may be affected.
In less severe cases the patella moves jerkily and its release from the position when the leg is extended is slightly delayed. This may be most obvious when the horse walks up or down a slope or when pushed sideways. If moved over in the box, the horse may move the leg very stiffly. It may find it difficult to make smooth downward transitions from trot to walk and the back legs may appear slightly uncoordinated and jerky.
Treatment
In many horses and ponies the condition appears to be related to poor muscular tone of the quadriceps muscles. If the horse is kept in work and got fitter, the condition frequently improves and with enough time disappears completely. Hill walk is particularly beneficial, as are long, slow canters. Work in straight lines is often preferable to work in circles. Some people feel that elevation of the heels of the hind feet with special wedge-heeled shoes is helpful.
In horses and ponies which fail to respond to conservative treatment, a simple surgical procedure, cutting the medial patellar ligament, usually effects a cure. There are potential complications of this procedure and it should be reserved for those horses for whom regular work has failed to produce adequate improvement.
OSTEOCHONDROSIS
The lateral trochlear ridge of the femur is one of the most common sites for osteochondrosis. This condition is usually seen in young horses (6 months to 3 years old) but is occasionally identified in older horses. There is marked distension of the femoropatellar stifle joint capsule and slight to moderate lameness characterized by a stiff limb flight, lowered arc of flight of the foot with or without an intermittent roe-drag. Lameness may be aggravated by flexion of the limb. The condition may affect one or both limbs. Young horses with both stifles affected may become slightly roach-backed and have difficulties in getting up after laying down.
Diagnosis
Diagnosis is confirmed by radiographic examination.
Treatment
Without treatment lameness usually persists. Provided that the lesions are not too severe, surgery is generally successful.
SUBCHONDRAL BONE CYST
The stifle joint is a common location for subchondral bone cysts, which almost always occur at the point of maximum weight bearing in the lower end of the inside of the femur, the medial femoral condyle. They occur most often in young horses when first starting serious work, but are also found in older horses.
Signs
The horse shows a sudden onset of a variable degree of lameness. The lameness may be extremely subtle or very severe. The horse usually improves with box rest but the lameness recurs when work is resumed. There is only slight distension of the stifle capsule, if any.
Treatment
Prolonged rest (6 to 9 months) results in soundness in approximately 60% of horses. In horses which fail to respond to rest surgery can be performed with a fair prognosis. Evidence of partial subchondral bone cyst filling and cartilage repair has been reported in many cases along with increased comfort and accelerated return to performance after using Vet-Stem Cell™Therapy
SPRAIN OF THE STIFLE JOINT
There is a sudden onset of lameness associated with some swelling of the stifle joint capsule.
Diagnosis & Treatment
Diagnosis is based on the clinical signs. Rest usually resolves the lameness. The duration of rest depends on the severity of the initial injury. If lameness persists, the stifle should be radiographed.
BRUISING OF THE STIFLE REGION
Bruising of the stifle region is a common injury either as a result of a kick or hitting a fixed fence when jumping. The latter is a common injury of event horses. There is a variable degree of swelling and lameness.
Treatment
Anti-inflammatory analgesic drugs are extremely helpful in reducing swelling and removing pain. Plenty of slow exercise prevents the horse from becoming excessively stiff, so if it can be turned out in a small paddock or walked in hand regularly, this is helpful. Provided that there is no underlying bony damage the prognosis is good. If the horse does not improve rapidly the stifle should be examined radiographically. A fracture of the patella or other bony damage might otherwise be missed.
Contagious Equine Metritis (CEM, CEMO) is a highly infectious disease of mares caused by Taylorella equigenitalis (previously called Hemophilus equigenitalis). The disease was first diagnosed in 1977 and subsequently spread to many nations. The disease was confirmed in the United States in 1978. Specific regulatory procedures for this disease have been established in the United States and 37 other countries.
The organism is carried on the external genitalia of stallions and transmitted at mating to mares, most of which are highly susceptible. The disease is self-limiting and usually clears with sexual rest after about 3 months. Some individuals may take longer to recover and require treatment, and others remain as carriers (harboring the organism but showing no symptoms) for years. Colt foals born to infected mares may be carriers and thus are capable of starting an epidemic by infecting mares during mating. The disease can be the cause of short-term infertility and, very rarely, abortion in mares.
SIGNS
There is genital inflammation, vaginal discharge and lowered fertility. Affected mares may return to heat unexpectedly, often with shortened interheat periods, but usually breed successfully once the infection has been eliminated. Stallions do not show clinical signs.
TREATMENT
Most cases resolve without treatment. However, infection appears to persist longer in older mares and recently foaled mares. Treatment is with antibiotics over a 7 to 10 period. Aggressive systemic antibiotic therapy accompanied by routine topical therapy might be required to treat some CEM-positive stallions.
PREVENTION
Prevention and control of CEM is achievable through a comprehensive programme of breeding farm management that includes early detection and treatment of carrier mares and stallions.
Corneal Ulcers follow injuries to the cornea that progress instead of healing; decreased tear production, or entropion. Ulcers which do not heal promptly often become infected. Large ulcers may be visible to the naked eye. They appear as dull spots or depressions on the surface of the corneas. Most ulcers, however, are best seen after the eye has been stained with fluorescein.
SYMPTOMS
Horses with corneal ulcers often have blepharospasm (tight shutting of the eye in response to the presence of an eye irritant or foreign body on the surface of the cornea), epiphora, and often are extremely sensitive to light (photophobic). These horses may also appear head shy and reluctant to allow physical examination of the head region.
TREATMENT
Corneal ulcers are dangerous and most receive prompt veterinary attention. Early treatment is vital to avoid serious complications or even loss of the eye. Corneal scrapings examined under the microscope will show if the ulcer is infected.
Uncomplicated small surface ulcers respond to topical ophthalmic antibiotic ointment applied 4 times a day. Atropine ointment is used to dilate the pupil.
Deep or infected ulcers require intensive antibiotic therapy by subconjunctival injection, or by the intravenous route. Cultures are taken by corneal scraping and antibiotics selected according to the sensitivities. The eylid may have to be sutured together to protect the eye and keep it from drying out.
Soft contact lenses also have been used for this purpose. Eye surgery to create a flap of conjunctiva to cover the cornea may be required in difficult cases. White spots of the cornea may persist after healing. If these scars are large enough to interfere with vision, they can be removed by eye surgery.
PREVENTION
All painful eye disorders should receive immediate veterinary attention. In particular, foreign bodies should be removed as soon as possible to prevent corneal damage.
Corticosteroids, which are incorporated into many eye preparations used for treating conjunctivitis and inflamed eyelids, should not be put into eye suspected of having corneal injury. This may lead to rupture of the cornea.
Horses wearing fly masks must be checked on a regular basis as they may develop ulcers despite the protection. Unless masks are removed daily, ulcers may go unobserved and progress to a severe stage, before the damage is discovered. As a rule, take masks off at night, to avoid this potential complication.
Urinary calculi or stones may form in any part of the equine urinary tract, but the most common site is the bladder (cystic). Calculi are formed by material dissolved in the urine (solutes) being precipitated upon a collection of bladder or other cells, such as red or white blood cells. The factors favoring this precipitation are not well understood but include urine pH—alkalinity increases the formation of carbonate calculi—and the concentration of urine solutes. This can be affected by diet, water intake and loss. The concentration increases when the horse is deprived of water or loses water excessively, as in sweating or diarrhea. If the diet or water fed to a horse has a high mineral content, this also increases solute concentration, while a high-concentrate, low-roughage ratio may allow the deposited solute to cement together more easily. Usually only one calculus occurs at a time, often composed of calcium carbonate.
SIGNS
All breeds and both sexes are equally likely to develop calculi, athough in mares they become very large before symptoms appear. These are similar to those seen in cases of cystitis, which often is present at the same time. Affected individuals urinate more frequently, with straining and dribbling of urine. Less commonly there may be mild recurrent colic, loss of condition and stilted gait. Occasionally a calculus passes into the male urethra, causing acute obstruction of urine flow.
DIAGNOSIS
Veterinary help should be always sought in cases in which there is obvious difficulty in passing of urine. Diagnosis of cystic calculi involves urine analysis (the changes are similar to those of cystitis), passage of urinary catheter, and occasionally in the mare, passage of an endoscope into the bladder.
TREATMENT
Surgical removal of the calculus is the only effective method of treatment. The approach and type of surgery is determined by the size of the stone and the sex of the patient. Some cases may also require treatment for concurrent cystitis.
PROGNOSIS
Prognosis for cases treated successfully by surgery is guarded because the affected horse may remain predisposed to chronic cystitis and calculus formation. Preventive measure are limited to correct dietary management, particularly in regard to moneral and concentrate proportions, adequate sources of drinking water and prompt veterinary attention to any case of suspected cystitis.
In case of osteophyte, there is an abnormal development of bone from surface of joint. Osteophyte is the earliest sign of arthritic change at the margins of the small tarsal joints. The location of the osteophyte formation may vary with the type and/or use of the horse and the stage of the disease.
Degenerative joint disease may occur as a result of joint infection (septic arthritis). Most septic arthritis occur fllowing surgery or a puncture wound. Septic arthritis may occur in any joint. Horses with septic arthritis present with severe lameness, joint swelling, fever, loss of appetite, stiffness and pain. Bone changes are more severe and progress rapidly and are usually visible during radiographical examination. Septic arthritis treatment include antibiotics and surgery (in severe cases).
Degenerative joint disease may occur as a result of untreated Osteochondritis dissecans (OCD), a disease associated with defective development of bone from cartilage leading to inflammation in affected joints. Often loose fragments of cartilage and/or bone present in joint, usually stifle, hock, fetlock and shoulder. The disease may occur in any joint, but is most commonly seen in the tarsus (hock). Breeds with a high-incidence of tarsal osteochondrosis include Standardbreds, Quarter Horses, Warmbloods and Arabians.
Medical reports show that about 76 percent of treated horses raced successfully or performed their intended use following surgery. In many cases, however, additional techniques to improve the healing response in bone and cartilage are needed so as to preserve articular function.
The principles of treatment of Degenerative Joint Disease include prevention or treatment of septic arthritis and osteochondritis dissecans; treatment of active soft tissue disease contributing to articular cartilage degeneration, including rest, physical therapy, synovectomy and administration of anti-inflammatory drugs, sodium hyaluronate and polysulfated glycosaminoglycans; treatment of articular cartilage loss or degeneration, including articular cartilage curettage (removal), subchondral bone drilling, and osteophyte removal.
The equine practitioner is faced with many choices for controlling inflammation in osteoarthritis (OA.) The proper combination of systemic nonsteroidal anti-inflammatory drugs (NSAIDs), intraarticular steroids, viscosupplementation (injection a preparation of hyaluronic acid into the joint that acts as a lubricant to enable bones to move smoothly over each other and as a shock absorber for joint loads), and chondroprotectants (supplements which work to maintain cartilage health) can be used to treat the disease and stop further progression of degenerative changes to the cartilage surface.
Although the whole nutraceutical industry is essentially unregulated, with manufacturers making outrageous claims on products that have never been tested at all, are often of poor quality, and occasionally lacking in any active ingredient, ongoing research shows that oral administration of nutraceutical products, such as Glucosamine and chondroitin to the horse is common and easy and is perceived to be a benign treatment for OA in horses. The main goal for use of nutraceuticals is to use them in OA cases to attempt to lower the dose of other drugs that are more problematic while potentially preventing further progress of DJD.
Clinical findings have revealed that glucosamine sulfate and chondroitin sulfate are effective and safer alternatives to alleviate symptoms of OA (Glucosamine and chondroitin sulfates in the treatment of osteoarthritis: a survey by de los Reyes GC, Koda RT, Lien EJ). Glucosamine is an amine-sugar that has been marketed as a natural product for the treatment of osteoarthritis. It has been popularized in the complementary section of pharmacies as a safe over-the-counter treatment for osteoarthritic pain.
Recent research suggests that it may not only provide symptomatic pain relief, but may have a role in chondroprotection. This is due to the fact that articular cartilage is critically dependent upon the regular provision of nutrients (glucose and amino acids), vitamins (particularly vitamin C), and essential trace elements (zinc, magnesium, and copper). Therefore, dietary supplementation programs and nutraceuticals based on antioxidant vitamin C, polyphenols, essential fatty acids, used in conjunction with non-steroidal, anti-inflammatory drugs (NSAIDs) may offer significant benefits to patients with joint disorders, such as OA and OCD.
There is also evidence that the combination of oral nutraceutical joint supplements containing high quality glucosamine (GU) and chondroitin sulphate (CS) may be more effective in preventing or treating osteoarthritis in horses than either product alone.
Dermatophilosis, also known as mycotic dermatitis, rain scald, mud fever, and greesy heel, is a skin disease caused by fungal organism Dermatophilus congolensis which gains entry to the horse skin when it is saturated by prolonged rain. It is mainly seen in mild wet winters.
Symptoms--Lesions are seen on the back, belly and lower limbs. Horses in poor condition and badly cared for at pastures are at risk. Horses with shaggy coats or with feather are particularly at risk.
Diagnosis is based on the appearance of the sores and microscopic examination of the organisms.
Treatment Dry conditions and improved hygiene should be the first step in therapy. Affected animals must be housed. Long hair shielding the sores must be removed by clipping (sterilizing the blades after use). Astringent lotions are beneficial and antibiotics may be given when the sores are severe. Cracking of the skin may require prolonged careful treatment.
Remove long hair and wash with mild soap and tepid water. Areas must be kept dry after initial washing. Dressing with antibiotic ointments is helpful. Rest in a dry area for several weeks will be helpful.
Prevention is better than cure. Practise good husbandry, prevent prolonged wetting by providing some shelter, examine regularly for parasites, and never expose a horse or groups of horses to confinement in small muddy paddocks without shelter.
Colic refers to abdominal pain, the external signs of which is uneasiness, sweating, biting at the flanks and other signs of pain. The horse gets up and lies down again. Very acute colic may be caused by a twisted gut and generally requires surgery.
Studies show that colic may result from congenital (present at birth) malformation of the large colon, enteroliths (pathological formations of mineral concentrations) which cause colonic obstruction, and equine gastric ulcers.
There are three main types of colic:tympanitic, spasmodic and obstructive.
Tympanitic colic (bloat, gastric tympany, wind colic)
Symptoms usually include continuous pain, caused by an overproduction of gas which distends the gut, sweating, a high pulse and a tense abdomen. The horse might take violent attempts to lie down. Frequent attempt to urinate and flatulence is common. This type of colic occurs when a horse is fed large quantitis of grain or coarse mix. Rich green grass grazed in the spring has the same effect. Treatment include analgesics to control pain; anti-spasmodic drugs; vegetable oils to reduce the fermentation process. The treatment of uncomplicated cases is usually successful.
Spasmodic colic
The most common type of colic, mild in character and short in duration (only a few hours). Seen more often in young horses. Bouts of acute pain, sweating, restlessness, frequent rolling and a tense abdomen are common symptoms. The horse looks repeatedly at its flank. May be caused as a result of blocking the normal passage of gas and intestinal contenets through the gut by migrating strongyle worm larvae; often seen in exhausted, dehydrated horses because of lack of sodium and chlorine ions. Treatment includes anti-spasmodic drugs and sedatives.
Obstructive colic
This type of colic is further subdivided into obstructive, and less severe impacted types.
Obstruction of the stomach and small or large intestine all cause acute pain. The horse rapidly becomes shocked due to the release of toxins into the system. The obstruction can occur on the stomach when it is due to overeating, especially dry material such as nuts, or unsoaked sugar beet. It can also occur in the small intestine as a mechanical obstruction caused by developing tumors, or by a twist, and as a result of hernia. Mechanical obstructions are rare, while food materials are common causes. A sudden change in diet, such as from grass to dry hay or straw, or sand impactions can cause obstruction.
Obstructive colic should always be treated as an emergency and is one of the conditions where professional help should be obtained immediately. The decision to operate has to be made quickly, as irreversible changes soon occur in the obstructed tissues.
Impacted colic is less obvious in nature. As the impaction builds up, the horse stops eating and passes increasingly dry and scanty feces. The horse spends a lot of time lying down and frequently looks at its flank. Impacted colic responds well to treatment that consists of softening the impacted mass and massage. This may take a few days, but in complicated cases surgery may be necessary.
Equine herpesvirus 1 (EHV1) and equine herpesvirus 4 (EHV4) are important equine viruses, causing much damage to the horse industry. EHV1 strains are associated with respiratory disease, abortion, and paralysis, whereas EHV4 strains are primarily associated with respiratory disease.
Young horse are at greatest risk to be infected by herpesvirus. The herpesvirus rarely occurs in foals younger than three months of age because they still have their vaccinated mothers' immunity. The great majority of infected foals is seen in sucklings and weanlings between 4 and 12 months of age which develop what veterinarians call "foal snots". The risk of developing the URTD increases with overcrowding, heavy parasite infestation, poor nutritional state, climatic extremes, existing disease, and the intermingling of animals from different social groups.
The infection is transmitted by contact with another infected horse and its respiratory discharge. Diagnosis of herpesvirus respiratory disease in horses is performed through laboratory tests. Vaccination of young horses does not prevent the infection, but diminishes the intensity of the disease.
The outbreaks of infection are common in large broodmare farm operations, annual yearling sales events and race or show barns in which horses from different places are kept together in enclosed, confined spaces. Two- and three-year-olds usually develop an acute form of herpesvirus URTD with neurological complications and increased risk of abortion. The virus remains in an individual horse over the lifetime and periodically reactivates and transmits from horse to horse and mother to foal. The factors contributing to herpesvirus reactivation include surgery, boarding, prolonged transport, weaning, lactation, extreme weather, and stress.
Symptoms of the herpesvirus URTD vary from horse to horse and may range from mild illness to a life-threatening lung inflammation. Most common signs include watery nasal discharge that occurs during the first day of the disease. By the second or third day the nasal discharge often dries to form crust in and around the nostrils and becomes thicker and yellowish. In some horses signs may include loss of appetite (anorexia), fever, lethargy, cough, labored breathing and discharge from the eyes (conjunctivitis). In uncomplicated form of infection, the prognosis for full recovery is usually good and signs usually disappear by the end of second week. With the secondary bacterial infection, primarily by primarily by Streptococcus equi zooepidemicus, the disease is much more severe.
Even though the infection by herpesvarus affects mainly the upper respiratory tract, it may lead to other serious complications including abortion, neonatal foal death, brain, lung and eye infections.
Treatment includes medications for fever reduction and anti-inflammatory agents for reduction of respiratory tract inflammation and antimicrobials. Horses unwilling to eat or drink may require fluid-electrolyte replacement therapy.
Prevention of herpesvirus URTD is the most effective way to control the disease outbreaks. Foals become maximally susceptible to infection by 5 - 6 months of age. Vaccination against EHV-1 and EHV-4 respiratory disease is recommended as part of the preventive, herd-health program for all horses at risk for acquiring infection. Vaccination of young horses does not prevent respiratory infection, but diminishes the intensity of clinical signs and both the magnitude and duration and amount of shedding of infectious virus. Because immunity to EHV-1 and EHV-4 generated by vaccination is of short duration, frequent booster doses are necessary for maximal effectiveness.
Equine Infectious Anemia Virus (EIAV) is a lentivirus, of the Retrovirus family with an almost worldwide distribution, infecting equids - horses, mules and donkeys. The EIAV belongs to the family of RNA viruses which generally cause slowly progressive, often fatal diseases. The virus is closely related to the human immunodeficiency virus (HIV), which causes acquired immunodeficiency syndrome (AIDS) in humans.
Animals may be acutely or chronically infected. The incubation period is variable, from a matter of days to a few months but generally 1 to 3 weeks. Antibodies usually develop 7 to 14 days after infection and last for life. Infected animals remain carriers of the virus for life.
The clinical signs of the acute form of equine infectious anemia are nonspecific; in mild cases, the initial fever may be short lived (often less than 24 hours). As a result, horse owners and veterinarians may not observe this initial sign when a horse is infected with EIAV. These infected horses often recover and continue to move freely in the population. The first indication that a horse was exposed to, and infected with, EIAV may well be a positive result on a routine annual test.
The majority of horses are inapparent carriers: they show no visible abnormalities as a result of infection. The inapparent form may become chronic or acute due to severe stress, hard work, or the presence of other diseases.
Equine infectious anemia acute form symptoms--These depend upon the stage of the disease. Bleeding, edemas ( excessive accumulation of fluids in body tissues or cavities), rapid breathing, and jaundice occur in the acute disease. During the attack, which usually lasts three to five days, the animal will try to shift its weight from one leg to another because of weakness. It will have shaggy coat and be sluggish.
Equine infectious anemia chronic form symptoms--If the horse survives this first acute bout, it may develop enlargement of the liver, spleen and lymph nodes, anemia ( the blood experiences a marked drop in its red corpuscle count and appear thin and watery), fever, different sizes of hemorrhage into the skin (petechia), an irregular heartbeat, and a jugular (located in the region of neck or throat) pulse may become evident.
Equine infectious anemia is considered a classic bloodborne infection. People have played an important role in EIAV transmission over the years by using blood–contaminated materials on different horses. The EIAV most frequently is transmitted between horses in close proximity by large biting insects, such as horseflies and deerflies.
Control of equine infectious anemia is currently based on detection of anti-EIA virus (EIAV) antibodies through AGID test. However, the current diagnostic methods may fail to diagnose the disease at its early stage. infection.
There is no vaccine or treatment for the disease. It is often difficult to differentiate from other fever-producing diseases, including anthrax, influenza, and equine encephalitis.
Equine protozoal myeloencephalitis (EPM) is one of the most common neurologic diseases of horses in the United States. It is caused by the protozoa Sarcocystis neurona. The parasite is ingested by the horse through infected food or water, or through direct contact with sporocytes in infected animal feces. Opossums, striped skunks, raccoons, armadillos and cats are intermediate hosts that spread the spores, but horses do not transmit the infection to other animals. The parasite damages the brain, brainstem and spinal cord of the horse. EPM can affect a horse of any age, breed, or sex.
Diagnosis--Blood tests detect antibodies to the Sarcocystis neurona but do not indicate if the horse will develop the disease. If antibodies are found in the cerebral spinal fluid along with neurolical signs are positive indicators of the disease.
Symptoms--Only a small percentage of horses become sick after ingesting the parasite. Signs include dragging a toe, incoordination, dropped eyelid, malposition of a limb, muscle atrophy, wobbling, head tilt, and occasional lameness. All neurologic disease in horses is not EPM and a complete work-up by your veterinarian is needed in many cases to arrive at a specific diagnosis of the problem.
Treatment--Horses are treated for EPM until they have negative test results for antibodies to S. neurona. Many horse develop complications and adverse reactions to medications: fever, loss of appetite, depression, incoordination, mild anemia and abortions.
Prognosis--The disease is progressively debilitating to the horse and requires extensive treatment. A vaccine for EPM is available but has unknown efficacy. Response to treatment is an important indicator of survival. Treatment with ponazuril minimizes, but does not eliminate, infection and clinical signs of EPM in horses [1-2].
Prevention--Use good hygiene when it comes to storing a horse's food containers, water buckets and tubs.
Equine recurrent uveitis (ERU), also known as periodic ophthalmia or moon blindness, is one of the most common causes of blindness in horses. Classic treatment of ERU includes mydriatics, corticosteroids and nonsteroidal anti-inflammatory drugs. Despite vigorous topical and systemic treatment, however, in many cases, the prognosis for preserving vision remains poor.
Symptoms--The signs of this disease are acute pain with the eye closed, discharge, and unwillingness to expose the eye to light. The cornea is cloudy. The eyelids remain tightly shut and tears often run down the cheeks. The conjunctiva and iris are red and inflamed. Recurent attacks diminish the sight until complete blindness results.
Causes-- Despite extensive clinical research, the causes of equine recurrent uveitis (ERU) are still unknown. In general, the diseases is thought to be an exaggerated response of the immune system to a wide range of organisms, including leptospires bacteria and and Onchocerca cervicalis parasites.
Diagnosis is made based on detailed examination of the eye.
Treatment--Long and vigorous treatment is necessary to control the inflammation. Antibiotic treatment is used if a bacterial cause is suspected. Corticosteroids and atropine applied to the eye are also essential.
New surgical techniques for ERU have been recently developed giving horses with equine recurrent uveitis a chance of a cure, and the possibility of maintaining their eyesight. The surgery involves making an incision through the sclera and removing the infected base where the organisms are. Then, antibiotics are flushed into that tissue to kill any residual organisms. Any clouded up and inflammatory debris is also removed.
Researchers at the ophthalmology department at North Carolina State UniversityWe have developed a drug delivery device (a micro-implant) for treating uveitis. The implant, which delivers a constant amount of cyclosporine (an immunosuppressive agent) within the eye, is made at NCSU and currently is being distributed free of charge to ophthalmologists who request one.
PrognosisProper treatment improves the course of the disease, especially if started early. However, the disease is often complicated by secondary catarcts and detachment of retina usually result in irreversible loss of vision. Conventional treatment does not prevent recurrence and horses that have had one attack will almost invariably have another at unpredictable intervals.
Prevention—Some eye problems are more preventable than others. Professor Brian Gilger, DVM, MS, Dipl. ACVO, Chief of the Ophthalmology Service, the ophthalmology department at North Carolina State University recommends that horse owners minimize the risk of eye trauma and infection by using a fly mask, and feeding hay on the ground, not from nets, bags, or elevated mangers. "They're horrible about causing eye trauma," he warns.
What type of horses are affected most? —Racehorses are the population of horses most often affected by gastric ulcers with an ulcer prevalence between 63 and 90%. In contrast, a much lower prevalence (37%) of stomach ulcers is seen in pleasure horses and the degree of ulceration is less severe. Several endoscopic surveys have indicated that the frequency of gastric ulceration in Thoroughbreds in training is fairly high. Ulcers appear to be chronically progressive during training, but to regress during retirement.
Symptoms—Clinical signs that typically are associated with gastric ulceration include recurrent colic for seven or more days, acute colic, poor bodily condition, and/or chronic diarrhea, poor appetite, and weight loss. Often symptoms are less obvious (such as poor performance), or not even noticeable. Foals with ulcers suck only half-hearted, grind their teeth and frequently chew on straw.
Causes Large amounts of concentrated high-energy feeds, small rations of forage and a low feeding frequency per day as well as the use of spoiled food can contribute to the development of colics and ulcers. An extended period of diarrhea or treatment with NSAIDs also predisposes to gastrointestinal ulceration.
Acids also are the important causes - severe ulceration of the stomach, caused by excess acidity, can develop rapidly in horses deprived of feed or not consuming feed. Compared with being turned out to pasture, stall confinement alone appears to be an important factor in the development of gastric ulcers in horses. Current therapy targets the suppression of gastric hydrochloric acid (HCl) and creation of a suitable environment for ulcer healing. Diagnosis is based on history, clinical signs, gastroscopy, and response to treatment.
Treatment—Of the products available, only GastroGard (FDA approved) and ranitidine have been shown to be efficacious in the treatment of EGUS. Ranitidine is often associated with treatment failure as a result of incorrect dosing and lack of owner compliance, because of the three times daily dosing required. Also, EGUS occurs in critically ill neonatal foals, but the underlying cause may be different than in adult horses and acid-suppressive therapy may not be as effective.
Other studies demonstrated that omeprazole paste is highly effective in healing gastric ulcers in Thoroughbred racehorses and that the omeprazole paste effectively prevents the recurrence of EGUS. The study also indicates that gastric ulcers in untreated horses did not demonstrate a significant rate of spontaneous healing (contrary to an existing theory of self-healing equine ulcers).
Severe ulceration of the gastric squamous epithelial mucosa, caused by excess acidity, can develop rapidly in horses deprived of feed or not consuming feed. Suppression of gastric acidity with the histamine type-2 receptor antagonist ranitidine effectively minimized the area of ulceration caused by feed deprivation. Compared with being turned out to pasture, stall confinement alone appears to be an important factor in the development of gastric ulcers in horses, probably as a result of altered eating behavior.
Foal heat, or "ninth day diarrhea" (which actually occurs form days 6 to 14), affects nearly all newborn foals. The stools is soft, pasty-yellow, and not profuse. The foal appears unaffected, remains bright and alert, and nurses at regular intervals. The diarrhea usually lasts fewer than 7 days.
Since the diarrhea happens to occur when the mare enters her first heat after foaling, it was believed that hormones in the mare's milk caused the diarrhea. In fact, the same diarrhea also occurs in orphan foals. Newborn foals normally eat manure and feedstuffs such as grain and hay. It appears that the ingestion of these substances may upset the flora of the foal's immature intestinal tract and cause temporary diarrhea. Recent studies show that foal heat diarrhoea is most likely caused by hypersecretion in the small intestinal mucosa (the membrane of the four coats of the intestinal wall), which may overwhelm an immature colon that is unable to compensate by increased fluid and electrolyte (substance that while in solution or its pure state will conduct an electric current by means of the movement of ions; examples of electrolytes: sodium, potassium, chloride, and calcium) absorption.
Treatment—Diarrhea of short duration associated with the foal heat requires little treatment. Keep the foal dry and clean around its tail. Zinc oxide ointment is applied to prevent scalding of the buttocks. Luxatives, purgatives and variety of untested equine probiotic products that are commercially available are not recommended as they will make the diarrhea worse.
Bacterial Pneumonia--One of the major causes of pneumonia in foals aged between 1 and 6 months with most cases occurring before 4 months is Rhodococcus equi bacteria. Inhalation of the soil-borne organism, Rhodococcus equi, can lead to a chronic and severe pneumonia in young horses and people with weak immune system. In addition, ulcerative colitis is a common result to infection in foals, and dissemination from the lung to other body sites is common in either the horse or man.
Rhodococcus equi is largely a soil organism but is widespread in the feces of herbivores (animals that eat only plants). Its growth in soil is considerably improved by simple nutrients it obtains from herbivore manure. About one-third of human patients who have developed R. equi infections had contact in some way with equines or their manure. Others may have acquired infection from contact with soil or wild bird manure.
Studies show that foal management practices, environmental management, and preventative health practices are risk factors for development of Rhodococcus equi pneumonia in foals. Housing foals in stalls with dirt floors may increase the risk for development of R equi pneumonia. Also breeding farms with large acreage, a large number of mares and foals, high foal density, and a population of transient mares and foals are at high risk for foals developing pneumonia caused by R equi.
Symptoms--The intestinal form of the disease may manifest itself by fever, depression, loss of appetite, weight loss, colic or diarrhea, lameness, nostril flaring and reluctance to move. Heat, pain and severe lameness are characteristics of R. equi septic arthritis.
Viral Pneumonia--Equine herpes virus 2 (EHV-2). The EHP-2 is ubiquitous in the general equine population. Foals are born free of EHV-2 infection but virtually all acquire the infection during the first months of life. The common signs of EHV-2 infection include uveitis, nasal discharge, pneumonia and colic.
Parasitic Pneumonia--Parasitic pneumonias are not common in horses, especially with today's deworming programs. The typical case involves horses pastured with donkeys infested with the lungworm, Dictyocaulus arnfieldi. In foals, Parascaris equorum is a more common parasite and because its life cycle involves migration through the lung, which can potentially cause signs of respiratory disease. A diagnosis of parasitic pneumonia is often difficult to obtain because it may be difficult to identify larvae in tracheal washes. Parasitic pneumonia could be suspected in foals with a poor deworming history, coughing, nasal discharge and poor response to antimicrobials.
Common Symptoms of Foal Pneumonia--The earlier signs of lower airway infection in foals are probably abnormal lung sounds on auscultation, nasal discharge and/or coughing, coughing when they get up or run, respiratory rate above 30 - 40 breaths per minute, or an increased respiratory effort. Crusting may be found at the nostrils or on the bones where the foal may wipe its nose. Nasal discharge, however, may be absent or undetectable if the lower airway discharge is swallowed.
Foals with lower respiratory tract infection will often cough while forced to take deep breaths, appear restless or distressed because of the rebreathing bag or show a prolonged recovery after the bag is removed. In severe cases, abdominal breathing, nostril flaring, cyanosis and pronounced exercise intolerance will be present. While most foals with early disease continue to be bright and alert, individuals with severe lesions may be depressed or lethargic and anorexic. Some foals with pneumonia will be reluctant to lie down because of increased breathing difficulties and may become very weak.
Treatment--Foals of 1 to 6 months of age will commonly experience respiratory tract infections, which may not necessarily require therapy. However,when labored breathing, fever, depression or appetite, leukocytosis (an abnormal large increase in the number of white blood cells in the blood during an acute infection) occur, antimicrobial therapy should be initiated without delay.
Prognosis--A favorable outcome is expected in most cases of foal pneumonia when an appropriate antimicrobial therapy is initiated early in the course of the disease.
WHITE LINE DISEASE (Seedy Toe)
In this disease the white line disintegrates as the result of infection caused by bacteria, yeast, or fungus. The infection starts at ground level and works its way up the white line to the coronary band. The region commonly affected is the toe back to the quarter. The loss of horn creates a hollow space between the hoof wall and the sole that becomes mealy or "seedy."
Eventually, a deep recess, filled with cheesy material and debris, develops between the sole and hoof wall. White line disease seldom occurs in barefoot horses on pasture. Like many other hoof conditions, it is a disease of domestic horse management. The typical horse with white line disease is given limited exercise, bedded in damp wood shavings, kept in a wet stall, and exposed to frequent wet-to-dry episodes such as daily wash-downs or walks in wet grass.
TREATMENT. With advanced disease, special shoeing techniques are required. All predisposing conditions should be corrected.
CANKER
Canker is a chronic infection of the horn tissue of the foot. It begins at the frog and progresses slowly to involve the sole and sometimes the wall. The disease is rare and is found almost exclusively in tropical climates.
Canker develops in horses who stand in mud, or in bedding soaked with urine and feces, and who do not receive regular foot care. The cankerous horn tissue of the frog loosens readily, and when removed discloses a foul-smelling, bleeding corium covered with a curdled-white discharge.
TREATMENT. consists of moving the horse to a clean, dry stable, or preferable a dry rocky pasture. Remove the shoe and thoroughly clean the frog. Apply a drying agent and bandage the foot to prevent contamination. Consult your veterinarian for best treatment regimen. Because canker often involves the corium, treatment is generally prolonged.
THRUSH
Thrush is a painful infection involving the frog. It is characterized by a black discharge along with poor growth and degeneration of the horn. The disease can be caused by a number of bacteria, but Fusobacterium necrophorum seems to be the most common.
Treat the foot as described for canker. The prognosis is good when the sensitive structures are not involved.
Acute gastric dilation is a sudden painful distention of the stomach due to a buildup of fluid or gas. The most commmon cause is grain engorgement. The grain forms a packed mass in the stomach that ferments and draws fluid into itself. Allowing a horse to drink cold water after a heavy workout is another cause of gastric dilation.
A secondary type of gastric distention occurs when there is an obstruction in the small intestine or colon. The fecal contents of the bowel back up into the stomach. The stomach progressively enlarges because the horse cannot vomit to relieve the pressure.
The pain of acute gastric dilation is severe and violent. It is accompanied by rolling, sweating, kicking at the abdomen, and turning the head as if to bite at the abdomen. Heart and respiratory rates are increased. The horse may exhibit shock with cold extremities.
Chronic gastric dilation is a milder condition found in horses who crib and swallow large amounts of air. It also occurs in horses who suffer from gastritis, and those who eat and drink immediately after strenuous exercise.
TREATMENT
If the horse shows signs of abdominal distress, notify your veterinarian at once. Gastric rupture is a fatal complication of acute gastric dilation and is likely to occur if the distended stomach is not decompressed.
Irrigating and flushing the stomach will relieve the problem caused by overeating or over-drinking. Dioctryl sodium sulfosuccinate (DSS) helps to soften a grain impaction. Most horses with gastric dilation are dehydrated and have electrolyte and acid-base imbalances. These are usually corrected by appropriate intavenous therapy.
Acute laminitis (founder) may accompany or follow an episode of acute gastric dilation.
The equine eye gets its nutrition from fluids that run through special pathways in and out. Obstruction of this outflow of fluid can be the result of an abnormally developed drain (i.e., primary glaucoma) or through damage to the drain from scarring, or accumulation of debris (i.e., secondary glaucoma). The result of this obstruction is retention of fluids and increase in the pressure within the eye.
Symptoms include inflammation of the iris, tumors, cataracts, cornea swollen with an excessive accumulation of fluid. At the advanced stages of the disease, the size of the eyeball may increase and eye lenses may dislocate.
Equine practitioners usually consider glaucoma as the cause of any unexplained corneal edema or ocular cloudiness and in cases of severe unrelenting ocular inflammation. Accurate measurement with a portable tonometer is essential to make the definitive diagnosis and to monitor the response to therapy.
Causes: The most common cause of glaucoma in horses is chronic or recurrent uveitis. Primary glaucoma usually affects both eyes, therefore the unaffected eye usually requires preventive therapy. Secondary glaucoma may not affect both eyes unless the horse has recurrent uveitis in both eyes.
Treatment consists in reducing the inflammation using anti-inflammatory medications, decreasing the production of fluids or laser therapy.
An outbreak of hives on a shiny coat of a performance horse might seem like an emergency because of the effect it has on plans to show or compete, but in reality it's a potential emergency for another good reason: it signals an ongoing hypersensitivity reaction, one that could escalate to full-blown allergic or anaphylactic shock.
Does this mean you you should push the panic button every time your horse gets a case of so-called alfalfa bumps? Yes and no. Most cases of equine hives resolve as quickly as they appear, usually within 24 to 48 hours, and the cause is never figured out. But to shrug them off without a second thought is to invite disaster, because the horse is a practiced and infamous over-reactor to a variety of stimuli, and in most cases of fatal hypersensitivity, the groundwork for the reaction was laid months, maybe even years earlier. Which means that every outbreak of "the bumps" could be a dress rehearsal for the big one.
The first bumps usually show up on the side of the neck, followed by the face, the chest, and the upper front legs. They may or may not be itchy. The bumps are initially distinct and steep-walled, and they retain a depression for several seconds when you press on them with your finger (this is called pitting edema). As they grow in size and number, they may coalesce into large plaques of swollen skin. If the outbreak also involves the tissues that line the respiratoty and digestive tracts, there may also be respiratory distress (like a severe asthma attack, with wheezing and an increasingly anxious struggle to get air) and colic pain that leads to diarrhea.
The skin condition itself is not dangerous. But it's only a sign of an allergic reaction going on inside the body, and if that allergic reaction is widespread enough to involve the major organ systems such as respiratory and digestive tracts, and it's escalating, the horse could be on a fast track to collapse and death.
The biggest mistake is complacency. Because the horse's body tends to be so overreactive, outbreaks of hives are seen pretty often, and as people become acclimated to the condition, they begin to see it as just a nuisance rather than a potential harbinger to a disaster, and it gets "diagnosed" as "alfalfa bumps," spider bites, beestings, creosote allergy, and a number of other unsubstantiated "conditions" that satisfy people's need to pin a reason on things. As a result, the gravity of the situation is completely missed, and the chance to get help early in the process is completely passed by.
TREATMENT Medical treatment is aimed at interrupting the allergic response, employing such agents as antihistamines and corticosteroids, but it should be remembered that this is only treating signs. Another thing to bear in mind is that corticosteroids can cause founder.
To truly resolve the problem, the underlying allergen must be identified and eliminated. To that effect, some diagnostic tests must be run, including blood tests and skin biopsy.
If you notice that your horse is woking harder than usual to get his air, making any wheezing sounds when he breathes, then he is developing a respiratory distress. Loose manure, belly pain or exceptionally gurgly gut sounds are all evidence that your horse might be in serious trouble. Get help. Meanwhile, give him a cool bath and hold ice packs on his swollen eyelids and sooth and help calm his irritated tissues. Do not give him and medications before diagnostic tests.
PINWORMS Pinworms (Oxyuris equi) are one cause of the "itchy-tail syndrome." The adult pinworm lives in the large intestine, but doesn't cause much disturbance there. Pinworms deposit their eggs around the anus, causing irritation, tail-rubbing, and hair loss. Eggs can fall to the ground wherever the horse rubs its rear end. Horses are infected with pinworms when they ingest larvae that hatch from eggs several days later. Your veterinarian will do a "scotch-tape prep" to diagnose pinworms, since there are other causes of tail-rubbing. A piece of scotch tape is pressed around the horse's anus, then pressed onto a microscope slide so the tiny pinworms eggs can be examined. Pinworms are easily treated with many dewormers, including the benzimidazole, ivermectin, and the organophosphates.
TAPEWORMS Anaplocephala perfoliata and Anaplocephala magna, the equine tapeworms, are less commonly diagnosed than the other parasites. Tapeworms have an interesting life cycle, which involves a stage inside a mite. The mite eats the worm egg in the manure, the horse eats the mite, and the immature tapeworm then emerges and develops into an adult. Adult tapeworms live in and near the horse's cecum, a large dead-end extension between the small and large intestine. Large numbers of tapeworm may cause blockage of the opening into the cecum, ulcers, or even rupture of the intestine. Tapeworms can be difficult to diagnose. A standard fecal egg count may or may not reveal the eggs, and the worms are seldom seen in the manure. Many of the dewormers in use today, including ivermectin, are not effective against tapeworms. Your veterinarian will help you choose the medication to eradicate this parasite.
There are many other worms that infest horse, but they probably won't be a problem for you.
HABRONEMA larvae live in the stomach wall, where they form tumor like growths. These worms are also the cause of summer sores on the horse's outer body. While the stomach parasite is difficult to diagnose, it is killed by ivermectin; so you are probably eliminating any problem by using this drug in your program.
DICTYOCAULUS is a lung worm of horses and donkeys. Infection with lung worms will cause a chronic cough. Immature lung worm larvae are coughed up and swallowed, so they may be seen by microscopic examination of your horse's manure. Ivermectin kills these parasites.
FASCIOLA HEPATICA, the liver fluke, is a parasite of cattle and sheep that occasionally infests the horse. Signs include weight loss, colic, and diarrhea. Fluke eggs may be found only with a specific type of fecal examination. Your vet will prescribe specific treatment for flukes since they are not killed with traditional deworming medications.
THELAZIA or eye worms are a problem in a few areas. They cause conjunctivitis and irritation of the cornea, which can lead to blindness if untreated. Your veterinarian removes the worms from the conjunctival sac with forceps.
Infections of the middle and inner ear can be recognized by signs of labyrinthitis. The labyrinth is a complex organ composed of three semicircular canals: the utricle, saccule, and cochlea. The labyrinth is like a gyroscope. Its purpose is to synchronize eye movements and maintain posture, balance, and coordination.
A horse with labyrinthitis will often assume an abnormal posture with a head tilt toward the affected side. Dizziness, incoordination, and loss of balance are evident in the staggering gait, turning and circling toward the affected side, and tendency to lean against walls and fences for support. The horse may exhibit rapid jerking movements of the eyballs, a condition called nystagmus.
The usual cause of inflammation of the labyrinth is a bacterial infection of the middle and inner ear. Encephalitis, meningitis, and ryegrass staggers can produce signs of labyrinthitis. These signs can also occur with brain tumors, antibiotic-induced damage to the auditory nerves, antifreeze poisoning, and a condition called idiopathic vestibular syndrome. This syndrome is thought to be caused by a virus.
TREATMENT
The treatment is directed at the primary disease. Bacterial infection require high-dose antibiotic therapy. The horse should be confined to a quiet, well-bedded stall. Horses that recover from labyrinthitis may exhibit head-bobbing or a coarse tremor of the head, evident during eating or drinking. They are prone to episodes of imbalance and may pose a hazard when used for sport or pleasure.
Widespread swelling of a limb below the knee or hock occurs for many reasons, including lymphangitis. A careful clinical examination of both the ffot and the swollen region of the leg is necessary to establish the cause of the swelling.
Signs
One or more legs are swollen. Hind legs are more commonly affected tha forelegs, and usually the entire leg is swollen up to the level of the stifle, resulting in moderate to severe lameness. Surface lymph vessels are prominent and local lymph nodes are enlarged. Serum may exude through the skin. The rectal temperature may be raised. Heavy-hunter types seem especially prone.
Diagnosis
The clinical signs are fairly typical. The inflammation is often secondary to a chronic low-grade infection of the leg and careful inspection usually reveals an old wound or wounds.
Treatment
Treatment aims to eliminate the primary infection and reduce the soft-tissue swelling. Relattively long-term treatment with appropriate antibiotics is combined with cold hosing of the leg, bandaging and exercise.
Prognosis
Vigorous treatment can produce rewarding results, although the leg may remain prominently thickened. The problem may be recurrent, especially in hind limbs, and careful vigilance is necessary to detect and treat small wounds as early as possible.
If your horse has lymphangitis, or is prone to it, never use sports massage.
SPORADIC LYMPHANGITIS
This non-contagious form of
Prognosis
normally occurs in horses that have been overfed and kept in with restricted exercise for a few days. Typically the disease would arise in working horses stabled over the weekend. The lymphatic vessels on the inside of the leg are very visible and the leg will be hot and swollen. The horse will stop feeding and exhibit thirst along with patchy sweatting. Constipation is also a coomon feature. Consider using Aconite in the very early stages and Apis or Bovista where the signs fit in later stages when the acute signs have subsided. According to Tim Couzens, author of "Homeopathy for Horses (Threshold Picture Guide)", the most valuable interim remedy to use is Bryonia.
ULCERATIVE LYMPHANGITIS
This is a mildly contagious form of lymphangitis caused by a variety of bacteria including Corynebacterium pseudotuberculosis, streptococci, and staphylococci. It occurs most frequently in horses kept in poor, unhygienic conditions or where overcrowding occurs and follows wounding or cracked heels. One of the first signs is swelling and pain around the pastern or fetlock joints. Nodules then develop in the tissues, following the course of the lymphatic vessels, especially around the fetlock region. These can grow quite large and burst releasing green pus. Affected areas then ulcerate. Local lymphatic vessels enlarge and become thickened. Affected areas will slowly heal, but more nodules and ulcers can occur over a period of several months. Tim Couzens, author of "Homeopathy for Horses (Threshold Picture Guide)", recommends Merc Sol as the main remedy to use where the nodules have bust and are discharging pus where there are ulcers that bleed easily when touched. Dose: 30c 3 times daily.. Anthracinum is useful where there is no response to Merc Sol, or where crops of discharging nodules keep appearing. Other useful remedies include Muriaticum acid 30c to help heal limb ulcers, Kali iod 30c to prevent more nodules appearing and Silica 30c to help remove scar tissue if the condition has become chronic.
Navicular disease is an inflammation of bursa, deep flexor tendon and navicular bone. Bone and tendon develop adhesions which cause pain and lameness. The genetic predisposition to navicular disease is proven nowadays, but otherwise, what causes it is still unclear. Horses with navicular disease have an increased load on the navicular bone in early stance. This has been suggested to be a response to pain in the heel region. The horse responds to heel pain (including pain in the navicular region) by contracting the deep digital flexor muscle to unload the heels. This increases the compressive load on the navicular bone, which may cause damage to the overlying flexor cartilage, which is then painful and identified as navicular disease.
Symptoms - Occasional lameness which decreases on rest and after work (horse warms up); standing with affected toe pointed; shuffling gait, especially if both forefeet affected.
Diagnosis
On X-ray navicular bone has ragged edge and areas of rarefied bone and nerve block.
Treatment - Navicular syndrome can be treated in a variety of ways. This is related to the fact that it has a variety of causes. Treatment may include stallrest, non-steroidal anti-inflammatory drugs, and orthopaedic shoeing plus intrabursal injections of short-acting corticosteroids and hyaluronic acid. Many veterinarians recommend shoeing as the primary therapy. Shoeing is performed to correct preexisting problems, enhance physiologic function of the foot, and ease breakover of the foot. Shoeing is reported to be most effective when performed within 8 months of the first signs of lameness. Nonsteroidal anti-inflammatory drugs are not used unless radical changes have been made in the shoeing. Approximately 75% of the horses improve in their performance. If therapy does not improve the horse within 6 to 12 weeks, surgery may give permanent relief.
Prognosis - The disease is progressive, and affected horses eventually will need to be retired because of lameness. Often horses with navicular disease remain undiagnosed until the disease has advanced to the stage where problems exist in the foot or to where the conformation-balance of the hoof is irrecoverable. The key to controlling the disease is prevention by maintaining good overall hoof husbandry.
Onchocerciasis (Ventral Midline dermatitis) is a skin isease caused by a hair-like worm called Onchocerca cervicalis. The adult worm lives in connective tissue of the horse's neck. The majority of horses in the United States are infected, but a few develop a dermatitis. It is believed that the skin response is due to an allergic reactionn to the dying microfilaria (prelarvae stage of worms released by female worm into the bloodstream).
The filaria migrate under the skin and settle primarily on the midline of the abdomen from the chest to the groin, especially around the umbilicus. Other sites are the withers, face, eyelids, and legs. At these sites the parasites produce an itchy skin disorder with redness, moist shallow sores, crusting and scaling, and patchy hair loss. Spots up to 10 inches in diameter can develop. Scarring and loss of skin pigmentation may also develop.
These open sores attract Culicoides gnats and other flying insects. Gnats feeding on the open sores pick up filaria and introduce them to a new host. Biting flies and other insects aggravate the skin disorder and create pyoderma.
TREATMENT
Ivermectin paste is completely effective in ridding the horse of filaria within 2 to 3 weeks. Minor reactions can occur with the use. Veterinary supervision is advised.
Adult worms are not affected by deworming agents and therefore serve as a reservoir for recurring infection. To keep the skin free of disease, ivermectin must be repeated at 4-month intervals. A deworming program incorporating ivermectin will effectively control the onchocerciasis.
NOTE:The filaria are capable of penetrating the eye and producing uveitis, a leading cause of blindness in horses.
Osteochondrosis occurs particularly in young, rapidly growing individuals. There is probably a genetic predisposition in foals. Encouraging a horse to grow quickly using high planes of nutrition may increase the risk of the disease. The stifle and hock are most commonly affected in the hind leg and the shoulder joint in the front leg. The clinical signes are usually evident in the first two years of life.
During development of bone, cartilage is converted to bone. Impaired blood supply to the cartilage will delay conversion of the cartilage to bone and result in abnormally thick cartilage on the joint surfaces, the lower layers of which may die. THerefore the cartilage on the joint surface is only loosely attached to the underlying bone and may become detached. This causes inflammation within the joint and production of excess synovial fluid, with the result that the joint capsule becomes distended. Although some joints may have mild osteochondrosis without clinical signs, the majority of lesions cause lameness and deteriorate if not treated.
Diagnosis is based on clinical signs and is confirmed by a combination of physical examination, scintigraphy, and radiography. Arthroscopy (examination with a camera inserted into the joint through a small incision of about 1/2 inch) can be used to confirm the diagnosis and treat cartilage and subchondral bone lesions. The disease often affects both stifles, so it is important to take radiographs of both joints even if only one is obviously affected.
Symptoms include joint swelling and lameness.
Treatment is by surgery. Abnormal cartilage is stripped off the underlying bone and the bone is scraped until healthy bleeding bone is exposed.
Prognosis--Young and middle-aged horses with mild osteochondral lesions of the shoulder joints have a good prognosis for return to performance following arthroscopic treatment.
Intestinal parasites are an important cause of death in horses of all types. The prevalence of many intestinal helminths is high and, within any population of horses, certain individuals can harbor large numbers of parasites, which may lead to disease.
Pinworms (Oxyuris Equi)are nematodes that occur in the large intestine of horse throughout the world. The males are small, but the females may reach 4 inches long and are white-gray in color, with a long tail tapering to a point, hence the name pinworm.
SIGNS
The presence of the female worms laying their eggs and particularly the presence of the eggs themselves stuck in a gelatinous mass around the anus are irritating, so affected horses will rub their tails.
TREATMENT
There are several types of deworming compounds: Ivermectin, Moxidectin, Fenbendazole, Pyrantels (Pyrantel Pamoate), and Quasiquantels. Each compound works differently in the horse to destroy internal parasites. Ivermectin paste administered to horses orally continues to be highly effective for treatment and control of a broad range of small and large strongyle species as well as other species of gastrointestinal parasites.
PREVENTION
Measures are not usually applied specifically for the control of pinworms. Any program of treatment to control the strongyles will control the infection with pinworms. In fact, the presence of pinworms may suggest that the srongyle control program is not being applied properly and the complete worming program should be reviewed. All incoming or returning horses should be quarantine drenched with an effective product. This product should also be able to remove inhibited (and potentially resistant) larvae. Moxidectin appears to have an advantage here. Ddon't breed from wormy horses. In time this should lead to reduced pasture pollution. Use pasture management. Pick up feces.
Pyoderma is a bacterial skin infection that drains pus. Many cases are the result of self-mutilation. When a horse rubs or bites at a persistent irritant to its skin, the skin becomes infected. Always look for another skin disease before concluding that pyoderma is the only problem the horse has.
CELLULITIS is an infection of the deep layer of the skin. Most cases are caused by puncture wounds, scratches, and cuts. Horses are aprticularly prone to such injuries. Many wound infections can be prevented by proper early treatment of wounds.
Signs of cellulitis are pain (tenderness to pressure), warmth (the skin feels hotter than normal), firmness (not as soft as normal), and change in color (it appears redder than normal).
As infection spreads out from the wound, you may feel tender cords which are swollen lymphatic channels. Regional lymph nodes may enlarge. This is a stage beyond cellulitis and is characterized by two disease (ulcerative lymphangitis and malignant edema).
A skin ABSCESS is a localized pocket of pus. Pimples, furuncles, and boils are examples of small skin abscesses. An abscess is fluctuant and feels like fluid under pressure.
The following skin infections are of particular importance:
FOLLICULITIS ("Summer Rash"). This is a hair-pore infection nearly always caused by a Staphylococcus bacteria. It tends to occur in hot weather as a consequence of excessive sweating and friction to the skin from ill-fitting tack. Small pimples appear, usually at points of contact in the saddle or harness areas. These pimples enlarge and form pustules. The pustules rupture and exude pus. Crusts form and the hair becomes matted.
Folliculitis can be prevented by good hygiene, such as brushing and cleaning the skin and coat after workouts, and using clean dry blankets beneath saddles.
FURUNCULOSIS. This is a deep-seated hair-pore infection with draining tracts and patchy hair loss. It is a progressive form of folliculitis and more difficult to treat.
Tail Pyoderma. This condition begins as an itchy skin disorder caused by mange mite or pinworms. As the horse scratches, rubs, and abrades the skin of its tail, secondary staph infection occurs and pustules develop. The ailment is complicated by furunculosis, and by abscesses that rupture and drain in an unending cycle. Hair is lost on the top of the tail. Treatment is most difficult.
TREATMENT OF PYODERMA
Any underlying itschy skind disorder should be treated to eliminate rubbing, biting, and self-mutilation.
Localize the skin infection by clipping away the hair and applying warm soaks for 15 minutes 3 times a day. Saline soaks, made by adding a cup of Epsom salts to a gallon of warm water, make a good poultice. Daily Betadine scrubs help to loosen scabs and promote cleanliness. Topical antibiotics such as nitrofurazone or Triple Antibiotic Ointment are of value and should be applied 2 to 3 times a day.
Oral or injectable antibiotics are used to treating wound infections, cellulitis, abscesses, furuncles, and tail pyoderma. Most skin bacteria respond well to penicillin, oxytetracycline, or trimethoprim-sulfadiazine.
Rhinopneumonitis virus (rhino) can cause respiratory disease, abortion, or neurological signs. Rhinopneumonitis is caused by an equine herpes virus, EHV-1. The equine herpes virus labeled EHV-2 does not cause disease, and EHV-3 causes a venereal disease).
One thing that all herpes viruses have in common is their ability to live within their host indefinitely. Once a horse is infected with rhinopneumonitis, it seems that infection can be reactivated later when the horse is stressed.
Young horses are most often affected when they are brought together in groups. Rhinopneumonitis is spread between coughing horses or on the hands of unknowing people. An upper respiratory infection is a common result of virus invasion. Uncomplicated cases will resolve on their own in a week or two. Occasionally the illness will leave the horse susceptible to bacterial pneumonia or a guttural-pouch infection.
Another common result of rhino infection is abortion in pregnant mares. Some mares will carry their fetus to term, only to deliver a weak sickly foal with slim chances of survival.
The neurological form of rhinopneumonitis is less common. A high fever precedes the development of signs ranging from incoordination and weakness to paralysis. These horses may recover with nursing care, but it can take anywhere from a few days to several months.
Two different subtypes of the EHV-1 virus exist in nature. Subtype one usually causes abortion or nervous system disease (myeloencephalopathy), while subtype two (sometimes called EHV-4) is most often the cause of respiratory infections.
There are two kinds of vaccine available now to help protect your horse from rhinopneumonitis. One is a modified live-virus vaccine, while the other contains a killed product. Whether killed or live, many rhino vaccines contain only subtype one, the major cause of abortions. Recent studies show that a protection induced by the modified-live virus vaccine is superior to that induced by the inactivated combination vaccine (1).
Many vaccines that are currently available contain only EHV-1 subtype one. It's hoped that the two strains of virus have enough in common that vaccination offers some protection against subtype two, the cause of respiratory disease. Vaccines have recently been produced that contain subtype 2, of EHV-4.
While respiratory infection is not prevented, its severity is reduced and the length of illness shortened when any vaccine is used. For the competitive show or race horse, any advantage is better than none. Rhino vaccinations are not necessary for the adult pleasure | |
