Signs of Knee Injuries

The horse will “walk wide,” swinging the leg to the outside to move it forward without bending the sore knee. The involved joint might be puffy (called “hygroma”) and warm, depending on the severity and freshness of the injury and depending on whether it involves bone or soft tissue or both. In most cases, the problem is obvious when the foot is picked up and the joint is forced to flex—the horse will flinch or otherwise display a painful response. In the normal horse, you should be able to bend the leg to easily touch the heel to the elbow. The horse with a sore knee will tense the leg and prevent the flexion if it hurts, and the lameness will be exaggerated temporarily when you put the foot back down. Other signs: the horse might resent having the joint manipulated, and the joint might be tender to the touch.

Causes of Knee Injuries

There are three main types of sudden, severe knee lameness common in performance horses:

1. bone fractures
2. ligament strains
3. inflammation of the joint capsule

Fatigue plays a major role in knee injuries, and some activities predispose to each type of injury.

The most dramatic knee joint injury involves chip and/or crushing fractures of one or more bones inside the carpal joint. With fatigue, the muscle allow the carpal bones to move out of proper alignment when the joint is stressed, and since they’re supposed to intelock perfectly during maximum load, fractures are highly likely when they’re out of position and 1,100 pounds of mass are barreling down the leg at high speed. The most common victims are youngsters in training, especially heavy-bodied, fast-sprinting Quarter Horses that can pour on the speed early in their careers, without prior conditioning. Youngstres in jump training are at risk particularly when asked to jump before they’ve developed adequate strength in their legs. Carpal chip fractures are frequent findings in horses that run downhill, an activity that is common during endurance races, delivering a concussive beating to the knees. Weekend warriors’ horses are at risk because of lack of conditioning and marshmallow-soft muscles that are unable to absorb much of the stress of load-bearing.

One of the most common soft tissue injuries in the knee is inflammation of the ligaments that hold the rows of carpal bones in position. This is most often seen in youngsters in early training and is a result of stress on the knee joints from a training program that is too strenous too soon. Rather than concussive insults, it’s quick changes in direction, jack-rabbit starts, sliding stops, and extended trots that are most often implicated&mdahs;any moves that tend to twist, or bend the little cube-shaped bones out of their neat, orderly rows, or that ask the hinge-like joint to overextend (common in youthful, poorly executed trots) or bend sideways (common in young cutting horses.)

The other common non-bony carpal joint injury is inflammation of the joint capsule, also known as synovitis/capsulitis. It is the result of excessive stress on the joint under load, particularly when the ligaments are loose.

Emergency Care

1. CONFINE Strict stall confinement for 48 hours is a must to further limit damaging forces to the injured leg. As soon as it’s safe to do so (the leg is well protected and the quickest route has been mapped out), the horse should be transported to a competent equine orthopedist for a specific diagnosis.
2. ICE Ice the knee, using crushed ice packs, bags of frozen peas, chemical cold packs, or cold water rinses. Ice on: 5 minutes. Ice off: 15 minutes. repeat cycle for 48 hours.
3. IMMOBILIZE Apply a Class III or Class IV knee bandage to limit movement and minimize swelling. Until the exact nature of the injury is known, it’s critical that further damage to the inside of the joint be prevented by immobilizing the leg. Shredded ligaments, torn cartilages, and shrp bone fragments can combine to make the problem much worse if the horse is permitted to move the leg freely.
4. GIVE AN ANTIINFLAMMATORY An intramuscular injection of an antiinfalmmatory medication can keep inflammation and its byproducts from worsening the damage, and its pain-killing action will help to make the horse more comfortable. Do not give the medication if for some reason you can’t properly bandage the leg—if you relieve the pain without restricting leg movement, you set the stage for massive additional damage.

Locate the problem

Your first task is to identify what area of the leg has been injured; whether it’s hoof, lower leg, or upper leg.

Stop All Activity

Don’t let the horse continue to hobble around in the hope that he’ll “walk out of it.”

Restraint

Ideally, while you’re working on your horse, he’ll be restrained by a trusted assistant at his head. If you’re working on a hind limb, the assitant should stand on the same side, ready to pull the horse’s head toward himself and lever the hindquarters away from you if problems arise. If you’re working on a forelimb, the assistant should stand on the opposite side, ready to pull the forequarters toward himself, away from you. Physical restrain devices, such as a twitch, lip chain or rope, chain chain or rope, war bridle, etc., can be both potentially helpful and dangerous depending on the horse and on your own experience; use these tools only if you’re well versed in their proper use.

If it’s necessary to tie the horse, don’t cross-tie him; he can rear and lunge forward when in cross-ties. And avoid close quarters so you can get out of harm’s way should the horse lash out in pain or fall or otherwise make a sudden change of position. Never attempt to examine an injured horse in a standing tie-stall or in a horse trailer.

No Drugs

The use of chemical restraint; tranquillizers, sedatives and pain killers; is unwise in the field lameness situation. Such drugs can mask the signs, making your horse detective work more difficult, and they can also affect the horse’s balance, making it less likely that he’ll be able to stand during your examination without risk of stumbling or falling; in addition to being hazardous to your health. Furthermore, when under the influence of a mood-altering sedative ot tranquillizer, some horses seem oblivious to pain, but can suddenly overreact in an excessive and illogical manner.

Puncture Wounds of the Foot

If you see that a foreign body (“poker”) is still in place in the horse’s hoof, you can only guess where the tip of the poker reached inside the hoof. At this moment, your horse’s freshly wounded hoof is not infected; it’s just contaminated. Quick action might be able to prevent infection.

After meticulously cleaning the foot and carefully excavating and irrigating the puncture wound, a plastic hoof boot is invaluable for preserving the clean environment. Bandages and duct tape are fine if the horse is to be confined to a stall with soft bedding, but if he must walk any distance to get to veterinary assistance, tha bandage is likely to wear through and expose the foot to dirt, mud, grit, and a whole host of contaminants. The boot should be water tight (the plastic models seem to hold better than the rubber ones), tall enough to encompass the pastern, large enough to put on over the foot bandage, and somewhat contoured to the shape of the foot. It should be removed and cleaned daily along with the bandage.

It’s a good idea, within 24 hours of the initial injury, unless you’re positive that the poker penetrated less than one-half inch. In that case, cleaning the foot thoroughly, carefully excavating and irrigating the puncture wound, plugging the hole, applying water-proof and air-proof bandages and boots and giving anti-inflammatory drugs would probably be enough. Nevertheless, it shouldn’t be difficult for you to get to a competent equine veterinarian in 24 hours. In doing so, you’ll benefit from getting a second, experienced opinion, backed by x-rays and ultrasound. And if the horse becomes more, rather than less, sore over next few days, take that as a sign that there’s trouble brewing, and get to a vetrinarian right away.

Choke occurs when a bail of food sticks in the esophagus, the tube leading to the stomach. Try as it might, the horse cannot get the feed all the way down. Saliva continues to be produced, and the horse drools excessively. You may see green feed coming out of the nostrils.

The horse may panic, throwing itself about and trying to rid itself of the annoyance. Or it may eventually stretch out its neck, drooling all the while. remember, though, the horse can still breathe. The food is lodged in the esophagus, not in the windpipe.

When your horse chokes, your first reaction should be a calm one. Your horse can still breathe since there is no blockage of the airway. Keep your horse calm and prevent him from injuring himself by slowly walking or by standing with him and talking calmly. Sometimes you can see a lump on the side of the horse’s neck where the ball of food is stuck in the esophagus. You may try to massage the throat area to help move the bolus of food down.

Choke usually occurs because the horse doesn’t chew and lubricate his food properly before swallowing, so the food cannot pass normally. A greedy eater is the usual victim of choke. Also, horses that are fed in groups may eat faster than usual due to competition for feed, and so suffer from choke. Horses trying to eat in a swaying trailer can choke when they accidentally swallow a bolus of food before they are ready. Finally, the horse that is overdue to have its teeth floated is a prime candidate for a choke episode; the feed just can’t be chewed normally.

Most cases of choke can be prevented. If you feed horses in a group, provide several feeding areas to reduce competition for feed. Avoid feeding grain in a trailer, since grain is more likely to cause choke than is hay (do not provide any feed in the trailer to a horse that gobbles its feed or has a history of choking).

The greedy eater is the horse that is most difficult to protect from choke. Several methods have been tried, and one may work for a particular horse but be useless for another. Feed hay before grain, so the horse is slightly full and less likely to bolt the concentrated feed. Place large rocks in the grain bucket, forcing the horse to pick its way around the rocks to eat the grain. Finally, spread out the feed over a large area to prevent the horse from gulping it down. Yearly dental exams ensure that the horse’s teeth are in good shape and can perform their needed function. Horses with teeth in very poor condition can be given specially prepared feed.

After substantial exercise-induced muscle glycogen depletion, ingestion of starch-rich meals only minimally affects net muscle glycogen concentrations after exercise, despite marked differences in soluble carbohydrate ingestion and availability of glucose to skeletal muscle. “Dietary supplements may actually inhibit repletion”, says Hyyppä, licentiate in Veterinary Medicine from MTT Agrifood Research Finland. Maintaining horses in a good state of hydration seems to have a moderate positive effect on repletion of muscle glycogen stores. Providing horses with an isotonic glucose-electrolyte rehydration solution soon after exercise helps to overcome dehydration significantly better than providing them with plain water.

High starch intakes increase the risk for metabolic disorders and therefore alternative feedstuffs are of interest. High-fat oat varieties have a lower starch and higher energy content than regular oats. High-fat oats can replace regular oats in the diet of athletic horses without any adverse effects on metabolism and exercise response. Due to the high energy content and a high digestibility of dietary components in high-fat oats the daily allowance of oats can be reduced and thus the intake of starch.

Muscle glycogen synthesis depends on glucose availability. Dietary carbohydrate composition may influence the rate of repletion of glycogen and support the hypothesis that molassed sugar beet pulp can replace oats in a hay based diet without impairing nutrient utilisation and metabolic response in exercising horses.

Muscle disorders are a common cause of disability in horses. For many years, clinical manifestations such as muscle pain, exercise intolerance, weakness, and stiffness were believed to be caused by a single syndrome. However, in the past years a broad spectrum of muscle disorders have been recognized including glycogen and polysaccharide storage myopathies, malignant hyperthermia, mitochondrial myopathy, hyperkalemic periodic paralysis and others.

Canadian researchers have found that muscle glycogen storage in horses during a 6 h period after exercise was enhanced by IV glucose administration (3 g/kg) but not by an equivalent glucose dose administered by mouth. While oral administration of glucose achieved a level of hyperglycaemia and hyperinsulinaemia that markedly accelerates glycogen storage in other species, the rate of glycogen storage following oral supplementation was not different to control conditions. Glucose supplementation via the IV route should be considered when rapid replenishment of muscle glycogen stores is desired.

Horses that are inadequately trained or have other systemic or musculoskeletal problems or those that are competing in hot conditions may develop a variety of metabolic problems. It is hoped that knowledge of the fluid and electrolyte losses may help in treating horses with metabolic problems and, more importantly, in improving management of horses in training and competition to prevent any loss of performance.

It happens often at endurance races and is, therefore, commonly viewed as a problem of the endurance horse. But heat exhaustion happens in polo ponies, steeplechasers, eventers, trail riders – any horse exerting himself for more than just a quick sprint, and particularly when it’s hot and humid outside. At endurance races, the scenario is common to the point of being a stereotype: one of the horses has been pulled from the race for failing to recover adequately during a vet check, and now his condition is worsening despite several minutes of rest, and suddenly the reality hits his worried owner like a freight train: his horse might not make it. The event’s on-site veterinarian is summoned, and the drama unfolds.

But what if your horse is stricken and you’re at an unsanctioned event, where there’s no veterinarian available? Or you’re on a training run, rather than at an official event? Or it wasn’t intentional exercise at all – your show horse somehow got out of his stall and has been running, terrified, with snarling dogs at his heels, for the past hour as the outside thermometer creeps up to 95°F and the relative humidity is close behind? What do you do?

What You See

The hallmark of advanced heat exhaustion is lack of interest in eating or drinking after a workout, despite the absolute certainty, after the rigors of his exercise, the horse desperately needs the liquids and electrolytes that water and food would provide. The full list of signs includes:

• shortened stride, lack of impulsion
• elevated rectal temperature (as high as 104-107° F
• depression, acts profoundly tired
• inattention:shows no interest in surroundings
• unstable or persistently elevated heart rate
• persistently elevated respiratory rate, or panting
• the “thumps” (what appears to be a rhythmic jerking of the abdominal muscles with each breath, almost like violent hiccups)
• no appetite, no desire for water
• glazed look in the eyes
• “quiet gut” – the normal motility of the intestines has slowed
• sweat-soaked or less than expected sweating
• scant and very concentrated urine

The goal in dealing with this dangerous condition is catching it in its earliest stages, before the diagnosis is obvious and before the horse’s cardiovascular system breaks down.

Why Is Heat Exhaustion Dangerous?

This is much more than just a bad case of fatigue. It’s a dangerous buildup of heat in the horse’s body which, if unresolved, can lead to cardiovascular instability, collapse and death.

It is caused by electrolyte deficits in the exhausted horse that can be astounding, and since the sensation of thirst is linked to the detection of excess salt in the system, the salt deficient horse feels no desire to drink. This means that, if left to his own devices, he would be unlikely to recover because despite his dehydration he has no natural urge to replace the liquids he so desperately needs.

To naturally replace electrolytes, the horse must eat. However, of his mineral deficiency is severe enough to cause his gut motility to slow down, he’s got a belly ache – it might be very mild and subtle, or it might appear as full-blown colic – but even the mildest colic pain can squelch his desire to eat. He must eat, but he won’t.

Meanwhile, he continues to pant in an attempt to blow off the heat that is killing him from the inside. But with each breath he can become more dehydrated, and the muscular activity involved in panting can actually stoke the fire, creating more heat.

As his cardiovascular system collapse, blood vessels to the muscles and skin begin to constrict. This keeps his too-hot blood close to his core, away from the body’s surface where it had the best chance of dissipating the extra heat. It also sets the horse up for myositis, because those muscles, which are sorely in need of nourishment after their workout, are suddenly being cut off.

Early in the course of heat exhasution, the horse might appear bright and normal, but he needs to be pushed to keep up the pace, and if you checked his rectal temperature it might be as high as 104° F. Horses that are stricken with heat exhaustion while performing some short-term, high-intensity exercise such as 3-day eventing or polo are likely to have less critical need for fluids and are simply in need of help of lowering their core temperature. For these horses, repeated cool (not cold) water baths and slow, relaxed walking in a light breeze is likely to do the trick. Getting the horse to eat and drink is rarely a challenge, so he’ll probably replenish his fluids and electrolytes on his own.

The endurance horse is a different case – his fluid and electrolyte debts are likely to be heavy and possibly life-threatening, and without the option of administering intravenous fluids and electrolytes, you’re severely limited. However, even though you’re in serious trouble in this situation and should move heaven and earth to get a competent equine veterinarian to come to your aid, you should still be able to help the horse if you’re prepared.

Prevention. Heat stroke can be prevented by limiting the horse’s exposure to predisposing situations and by insuring that hard-working and endurance horses drink frequently during prolonged exercise.

Heat Exhaustion Treatment

1. CHECK VITALS Check the rectal temperature, the number of heart beats per minute, the number of breaths per minute, and listen to the abdomen for gut sounds and write all your findings. Re-check every half hour and record your progress. The normal temperature is 99-100.5°ree; F. The normal number of heart beats is 32-44 beats/min (adult). The normal respiratory rate is 8-15 breaths/min.
2. ELECTROLYTES AND FLUIDS Gently but persistently get electrolytes and fluids into the horse orally. If he won’t eat or drink voluntarily, you’ll have to use some initiative to coax him.

• Offer a bucket containing a half gallon of plain, cool (not cold) water and, right next to it, a second bucket containing a half gallon of electrolyte-treated water using a commercially prepared electrolyte powder designed specifically for endurance horses. Do not , under any circumstances, give this horse an electrolyte product made for calves or foals with scours (diarrhea) or for sprinting-activity performance horses&mdahs;the sodium bicarbonate in these products can make his heart unstable, and it can guarantee that he will be stricken with myositis on top of all his other problems.
• If he shows no interest, rinse his mouth gently with a 20 cc syringe full of electrolyte-treated water, then offer the buckets again.
• If he still shows no interest, you’ll have to force him. Remember, he’s still losing more water and electrolytes, probably a gallon or more per hour, even though he’s just standing there—they’re literally pouring out of him in his sweat and in his breath.
• Start with the elctrolytes first. Read the instructions on the label of your elctrolyte product and calculate how much of the product would be required to prepare one quart of treated water. Mix the calculated amount with something yummy, then give him your concoction with the syringe. Still no luck? Then you need to be more aggressive. Give him one cup of water, by syringe, every five minutes, and give him another dose of elctrolyte mix, by syringe, every half hour. Do this for 2 hours, or until he begins drinking on his own.
• If you don’t have an elctrolyte powder, you can make your own concoction with ingredients you can buy at any grocery store:

1 tablespoon regular table salt (sodium chloride) 1 tablespoon Morton’s salt substitue (potassium chrolide)
2 crushed tablets of extra-strength TUMS_TM (calcium carbonate)
500 mg (2 crushed 250-mg tablets) of magnesium pills (magnesium oxide)
2 tablespoons Karo syrup or honey or molasses or pancake syrup
1 jar of baby food

1. COOL HIM Meanwhile, be working on bringing his body temperature down by swabbing him every ten minutes with cool (not cold), dripping-wet cloths over his body, being sure to get him behind and between his ears, on his forehead, and on the underside of his neck, and in his armpits and groin. Do not run cold hose water over his back and rump—you could cause the blood vessels in those muscles to clamp closed even more than they already are, which will slow down his heat dissipation and threaten myositis.
2. GIVE ASPIRIN As soon as you see signs of improvement: a bright look in the eye, heart rate beginning to drop to within normal range, respiratory panting beginning to resolve, body temperature coming back down to earth, and a return to voluntary eating and drinking, give a tiny dose of aspirin paste or gel orally to relieve residual muscle pain, encourage the still-spasming muscles to relax, and guard against the damaging effects of inflammation and toxicosis.
3. MUSCLE TREATMENT If your horse is showing any signs of impending myositis (stiffening gait, tight or hard-feeling muscles over his back, croup, and loins, and/or coffee-colored urine), or if he has a history of tying-up in the past, he might benefit from a judicial dose of a medication that will help to dilate the constricted blood vessels in his major muscles. Again, if he is in a very tough shape, he might not be able to tolerate any medication smoothly. Rule of thumb: if he’s eating and drinking well on his own, and he seems to be showing general signs of recovery, he should be able to tolerate the medication.

Clostridium tetani spores are also commonly found in the feces of domestic animals, especially those of horses, and in soil contaminated by the feces. Clostridium tetani spores may stay in soil for many years and are resistant to many standard disinfection processes, including steam heat (100º C for 15 minutes).

Although all species of domestic animals are susceptible to tetanus, horses are most sensitive to tetanus toxin. If the germ enters a deep wound and the wound closes too soon, the horse may easily contract the infection through his blood stream. A horse that receives a bad wound, particularly if there is known to be tetanus in the area, should at once receive the anti-tetanus vaccine which will prevent the disease.

Signs of Tetanus

The earliest symptom of tetanus is extreme sensitivity. Within 10 to 14 days following injury, horses become increasingly nervous. They jump violently on being touched. Some seem unwilling to be handled and may respond with aggression. Protrusion of the third eyelid, and stiff gait are the most common clinical signs. Spasms of the masseter muscles–muscles that bring the upper jaw and lower jaw together–occur early in the disease which results in “lockjaw”. Loud noises, colic, and sweating usually appear at a later stage of the disease.

Treatment of Tetanus

Treatment usually consists of administration of antibiotics, tranquilizers, tetanus toxoid, and antitoxin. Persistent treatment and much nursing care are needed. Affected horses need to be protected from light and sound that can stimulate nervousness. Horses are placed in darkened stalls and their ears are plugged with cotton. Antitoxins, antibiotics and sedatives are usually administered for several weeks.

Prognosis for Tetanus

If the animal has been vaccinated prior to the injury, responds to the tranquilizers, the prognosis is usually good.

Prevention of Tetanus

Prevention is twofold. Unvaccinated horses usually receive tetanus antitoxin with 24 hours following injury or surgery. This provide temporary protection for 10 to 14 days. If healing is not complete by that time, vaccination is repeated. No horse should live its life without being immunized with tetanus toxoid which provides a very stable immunity. Annual boosters and vaccinations following injury or surgery provide good protection against tetanus.

Signs of Summer Pneumonia

Foals rarely show definitive signs until abscesses and bronchopneumonia are well established. Signs include rapid and labored breathing, cough, nasal discharge, a persistent, slightly elevated temperature, poor appetite and weight loss as the disease progresses. The prognosis may be grave in cases with multiple lung abscesses and particularly if the abdomen is involved.

Treatment of Summer Pneumonia

Rhodococcus equi is an intracellular organism which provokes an inflammatory reaction. Although the organism is sensitive to several antibiotics and a combination of them have proved successful in some cases, treatment is difficult. Affected foals need prolonged treatment because of the persistence of the bacteria within abscesses in the lung and because immunity to lung infection is poor, the disease tends to recur. The combination of erythromycin and rifampicin have improved the survival of foals infected with R. equi; however, erythromycin can cause adverse reactions in foals and mares, which has prompted the search for alternative therapies.

Prevention of Summer Pneumonia

Rhodococcus equi is a robust soil organism widespread in the environment. The organism will potentially multiply wherever there is horse manure. Because the organism reaches the lung by inhalation, dusty manure-contaminated environments (such as are commonly found in loafing paddocks on horse breeding farms in the summer) are potentially lethal sources of infection. It is also important to ensure that loafing paddocks are well grassed, and not totally grazed, reducing them to dusty sandpits.

Rhodococcus equi, a recognized bacteria in horses, is emerging as a human pathogen, especially in immunocompromized hosts with an overall mortality of 75%. Wound infections and skin abscess, have been reported in humans.

The life cycle of this parasite has some unique, important features. The eggs are laid by adult worms in the intestine. They pass out in the feces and hatch into larvae in 1 to 2 days. Larvae feed on manure and continue to develop. After about a week, larvae become infective, move up on the blades of grass, and the horse eats them. Once inside the horse, they migrate to various organs and tissues where they do extensive damage. After the young adult worms return to the small intestine, they attach themselves to the gut wall, feed themselves on the gut lining, reach maturity and lay eggs. The life cycle of the small strongyle is different from that of the large strongyle in that the larvae penetrate the large intestine and become encysted. after 1 to 2 months, the larvae emerge and return to the intestine where they mature [1].

A horse gets infected by ingesting larvae present in grass and forage.

Large Strongyles, Bloodworms

One of the three species, Strongyle vulgaris, is the most harmful because its larvae enter the arteries, creates blood clots which block small vessels. This destroys part of the blood supply to bowels and other digestive organs.

The larvae live in the arteries for about 5 months, then return to the intestine and develop into adult worms, where they attach to the wall of the bowel. A heavy infection can cause severe anemia

Small Strongyles

Small strongyles are the most common internal parasites in adult horses and occur frequently in foals. Larvae produce colic, bleeding and anemia, protein loss, and intestinal malabsorption.

Prevention of Strongyles

Control of strongyles is most important in all deworming programs. Since the arterial worms are not killed by most dewormers(except for ivermectin), it is extremely important to eliminate the larvae at early stages. An occasional treatment does not offer protection and will not prevent the potentially devastating consequences of these parasites. Most veterinary experts recommend the inclusion of ivermectin in all deworming programs.

Signs of Stringhalt

The horse exaggeratedly flexes one or both hind limbs when in motion. The abnormality is sometimes evident at all paces, but it is usually most apparent at walk, especially if the horse is turned or backed, and may disappear at trot. The condition may be intermittent and remain static or deteriorate.

Treatment of Stringhalt

Most often, the cause of the condition is unknown. Some horses are successfully treated by the removal of a piece of the lateral digital extensor tendon at the level of the hock.

Prognosis for Stringhalt

Unless the gait abnormality is extremely severe, affected horses are usually able to perform adequately, including jumping, but are unsuitable for dressage. A guarded to fair prognosis is warranted after surgery. Some horses improve initially but subsequently relapse.

Sometimes stringhalt may develop a complication following trauma to the dorsal metatarsal region. Potential causes include tendon injury that result in abnormal flexion of the tarsocrural joint. Horses may develop stringhalt within 3 months after injury. They can be treated with exercise, including daily hand-walking with pasture turnout, followed by lunging; or surgically, using lateral digital extensor myotenectomy. Of the horses treated with exercise, some may have resolution of stringhalt. Horses treated surgically have varying degrees of improvement, or no change.

remains one of the most commonly diagnosed and important infectious diseases of horses world-wide. Strangles infection is extremely contagious. Contaminated tack, feeding utensils, water tubs and bedding are all potent sources of infection. The organism gains entry to the body at the back of the throat and rapidly settles in the tonsils and lymph nodes. From there it spreads to the lymph glands of the head and neck, and causes the swelling and abcess formation so typical of the disease. Most horses recover with no complications, and some 70% develop life-long immunity. It is thought that other 30% become carriers of the disease.

Signs of Strangles

Affected animals have a fever, a nasal discharge at first watery then mucous, and poor appetite. Head carriage may be stiffer than normal, swallowing may be difficult and a soft cough heard. Lymph nodes beneath the lower jaw enlarge. These swelling can impair breathing, (hence “strangles”) by compressing the airways.

Usually horses recover rapidly once the swelling ruptures. Occasionally lymph nodes fail to filter the infection, which spreads to other systems (bastard strangles) producing abcesses, aspiration pneumonia and pleuritis  and even brain damage by inducing metastatic brain abscesses.

Diagnosis of Strangles

Diagnosis is made based on clinical signs and confirmed on bacteriological culture, since the presence of swollen lymph nodes under the jaw can indicate many other respiratory diseases (Equine Herpesvirus etc.) Recent findings suggest that S. equi meningoencephalomyelitis should be considered for foals with neurologic signs that have a history of strangles or exposure to affected horses.

Treatment of Strangles

The nostrils should be cleaned, hot pads applied to the swelling, and soft, easily swallowed feed provided. Strict hygienic measures should be observed as the organism can be transmitted on hands and clothes. Treatment of choice is administration of potassium penicillin and fluids. Antibiotics are used in severe cases, particularly when the infection spreads to lungs and abdomen.

Prevention of Strangles

Prevention is possible. In a closed herd situation, new arrivals should be isolated for 2 weeks. Since the organism can be shed from draining abscesses for up to 4 weeks and can remain viable for another month or longer, affected horses should be isolated. In-contact animals should be quarantined and observed for signs. However, current antibiotic therapy is often ineffective and thus recent attention has focused on vaccine development.