Muscle and tendon defects

Joint defects

Defects of the skeleton

Relief of musculoskeletal pain

Several aspects about relieving pain in agricultural animals are important. Cost has always been a deterrent to the use of local anesthetics and analgesics but, with changing attitudes, the need to control pain is more apparent. Treatment of the causative lesion is a major priority but the lesion may be painful for varying lengths of time. Relief and the control of pain should be a major consideration. Details on the use of analgesics are presented in Chapter 2.

Analysis of gait and conformation

Inspection of the gait of the animal is necessary to localize the site of lameness. Evaluation of its conformation may provide clues about factors that may contribute to lameness. Details on the examination of farm animals for lameness are available in textbooks on lameness in horses and cattle.

Close physical examination

A close detailed physical examination of the affected area is necessary to localize the lesion. This includes passive movements of limbs to identify fractures, dislocations and pain on movement. Muscles can be palpated for evidence of enlargement, pain, or atrophy.

Radiography

Radiography is useful for the diagnosis of diseases of bones, joints and soft tissue swelling of limbs, which cannot be easily defned by physical examination. Detailed radiographic information about the joint capsule, joint cavity or articular cartilage can be obtained using negative (air), positive or double contrast arthrography. Ultrasonographic imaging can be used to differentiate the pathological changes in the soft tissue structures of digital flexor tendon sheaths of cattle.¹

Ultrasonography

Ultrasonography is used extensively in dogs and horses for the visualization of soft tissue structures of the joint. Most veterinary practices have an ultrasound machine that is used for small-animal imaging or transrectal pregnancy diagnosis in cattle and horses.² Ultrasonography is cheaper, faster and provides important information compared to radiography; it is also less invasive and cheaper than joint fluid aspiration and analysis.

The ultrasonographic anatomy of the elbow, carpal, fetlock, and stifle joints of clinically normal sheep using a 7.5 MHz linear transducer with a stand-off pad has been described.² The anatomical structures that could be consistently identifed in normal ovine joints included bone, articular cartilage, ligaments and tendons. In sheep with chronic arthritis/synovitis, the gross thickening of the joint capsule is visible as a hyperechoic band up to 20 mm thick.

The ultrasonographic examination of the stifle region in cattle has been described.³ The homogeneously echogenic patellar and collateral ligaments, the combined tendon of the long digital extensor and peroneus tertius muscles, the popliteal tendon, the anechoic articular cartilage of femoral trochlea, the echogenic menisci and the hyperechoic bone surfaces were imaged successfully. The boundaries of the joint pouches became partially identifable only when small amounts of anechoic fluid were present in the medial and lateral femorotibial joint pouches. The main indication for ultrasonography of the bovine stifle is evaluation of acute septic and traumatic disorders of the region, when specifc radiographic signs are often nonspecifc or absent. The cruciate ligaments could not be imaged in live cattle. The cruciate ligaments are identifable in the horse, in which flexion of the hindlimb is a routine procedure necessary for identifcation of these structures.

The ultrasonographic examination of the carpal region in cattle has been described.⁴ The main indication is the evaluation of septic and traumatic disorders of the carpal joints and tendon sheaths. Each tendon and tendon sheath in carpal region must be scanned separately. The use of a stand-off pad is recommended as it permits adaptation of the rigid transducer to the contours of the carpus. The carpal joint pouches and tendon sheath lumina are not clearly defned in healthy cattle. Thus the ability to image these structures indicates the presence of synovial effusion.

Ultrasonography is a valuable diagnostic aid for septic arthritis. Joint effusion, which is one of the earliest signs of septic arthritis, the accurate location of soft tissue swelling, the extent and character of joint effusion and involvement of concurrent periarticular synovial cavities or other soft tissue structures can be imaged by ultrasonography.⁵ The ultrasonogram can image the presence of small, hyperechogenic fragments within the joint, appearing very heterogeneous. Normal synovial fluid is anechoic and appears black on the sonogram. A cloudy appearance is usually associated with the presence of pus.⁶

Muscle biopsy

A muscle biopsy may be useful for microscopic and histochemical evaluations.

Arthrocentesis

Joint fluid is collected by needle puncture of the joint cavity (arthrocentesis) and examined for the presence of cells, biochemical changes in the joint fluid and the presence of infectious agents. The techniques and application of arthrocentesis for some of the joints commonly sampled in the horse have been reviewed.

Arthroscopy

Special endoscopes are available for inspection of the joint cavity and articular surfaces (arthroscopy). Diagnostic and surgical arthroscopy is now commonplace in specialized equine practice. Surgical arthroscopy is rapidly replacing conventional arthrotomy for the correction of several common surgical conditions of the musculoskeletal system of the horse. Accurate quantifcation of equine carpal lesions is possible when the procedure is performed by an experienced arthroscopist.⁷ Convalescent time following surgery is decreased and the cosmetic appearance improved compared to arthrotomy. The arthroscopic anatomy of the intercarpal and radiocarpal joints of the horse have been described. A synovial membrane biopsy can be examined histologically and for infectious agents and may yield useful diagnostic information.

Serum biochemistry and enzymology

When disease of bone or muscle is suspected, the serum levels of calcium, phosphorus, alkaline phosphatase and the muscle enzymes creatinine phosphokinase (CPK) and aspartate aminotransferase (AST), also known as serum glutamic oxaloacetic transaminase (SGOT), may be useful. The muscle enzymes are sensitive indicators of muscle cell damage; the serum levels of calcium, phosphorus and alkaline phosphatase are much less sensitive indicators of osteodystrophy.

Nutritional history

Because the most important osteodystrophies and myopathies are nutritional in origin a complete nutritional history must be obtained. This should include an analysis of the feed and determination of the total amount of intake of each nutrient, including the ratio of one nutrient to another in the diet.

Environment and housing

When outbreaks of lameness occur in housed cattle and pigs the quality of the floor must be examined to evaluate the possibility of floor injuries.

Enzootic nutritional muscular dystrophy

A nutritional deficiency of vitamin E and/or selenium is a common cause in young calves, lambs, foals, and piglets. Factors enhancing or precipitating onset include: rapid growth, highly unsaturated fatty acids in diet and unaccustomed exercise. The disease also occurs in adult horses.

Exertional or postexercise rhabdomyolysis

This is not known to be conditioned by vitamin E (selenium deficiency) and occurs as equine paralytic myoglobinuria (tying-up syndrome, azoturia) in horses after unaccustomed exercise or insufficient training.¹ It also occurs in sheep chased by dogs, in cattle after running wildly for several minutes and as capture myopathy during capture of wildlife. An acute myopathy of undetermined etiology occurred in horses at grass in Scotland.² The horses were not in training, creatine kinase levels were elevated and the urine was dark brown; most of them died and the muscles affected were those of posture and respiration rather than movement.²

Equine polysaccharide storage myopathy is a metabolic disease being recognized with increasing frequency in many breeds of horse.³ It occurs in Quarter-Horse-related breeds and more recently has been recognized in draught horse breeds. It is thought to be due to an inherited metabolic defect affecting carbohydrate metabolism (see Ch. 28).

Metabolic

Hyperkalemic periodic paralysis occurs in certain pedigree lines of North American show Quarter Horses.

Degenerative myopathy

This occurs in newborn calves, sheep and goats affected by Akabane virus infected in utero.

Inherited myopathies

The porcine stress syndrome, which is discussed under that heading, now includes herztod pale, soft, exudative pork encountered at slaughter and malignant hyperthermia following halothane anesthesia. Certain blood types in pigs have been used as predictors of stress susceptibility and malignant hyperthermia in Pietrain pigs is genetically predetermined. Most of these myopathies of pigs thus have an inherited basis and the stress of transportation, overcrowding and handling at slaughter precipitates the lesion and rapid death.

Congenital myopathy of Braunvieh– Brown Swiss calves is thought to be inherited.⁴ Affected calves become progressively weak and recumbent within 2 weeks of birth.⁴

Doubling-muscling in cattle and splaylegs of newborn pigs are also considered to be inherited. A dystrophy-like myopathy in a foal has been described and is similar to human muscular dystrophy.⁵ Dystrophy of the diaphragmatic muscles in adult Meuse– Rhine–Yessel cattle is thought to be inherited. Xanthosis occurs in the skeletal and cardiac muscles of cattle and is characterized grossly by a green iridescence.

Toxic agents

This is caused by poisonous plants, including Cassia occidentalis, Karwinskia humboldtiana, Ixioloena spp., Geigeria spp. and lupins. A special case is enzootic calcinosis of all tissues, especially muscle, and the principal signs are muscular. It is caused by poisoning by Solanum malacoxylon, Tricetum spp., and Cestrum spp.

Ischemia

Ischemic myonecrosis occurs in the thigh muscles of cattle recumbent for about 48 hours or more and is discussed in detail under the heading Downer cow syndrome. Iliac thrombosis in horses is an important cause of ischemic myopathy and has been reported in calves.

Neurogenic

Neurogenic muscular atrophy occurs sporadically due to traumatic injury and subsequent degeneration or complete severance of the nerve supply to skeletal muscle. The myopathy in arthrogryposis associated with the Akabane virus is thought to be due to lesions of the lower motor neurons supplying the affected muscles. It has been suggested that cattle with muscular hypertrophy may be more susceptible to the effects of exercise and the occurrence of acute muscular dystrophy. Suprascapular nerve paralysis in the horse (sweeney) is a traumatic neuropathy resulting from compression of the nerve against the cranial edge of the scapula.

Neoplasms

Neoplasms of striated muscle are uncommon in animals. Rhabdomyosarcomas are reported in the horse, affecting the diaphragm and causing loss of body weight, anorexia and respiratory distress.

Primary myopathy

The characteristic change in most cases of primary myopathy varies from hyaline degeneration to coagulative necrosis, affecting particularly the heavy thigh muscles and the muscles of the diaphragm. Myocardial lesions are also commonly associated with the degeneration of skeletal muscle and when severe will cause rapid death within a few hours or days. The visible effects of the lesions are varying degrees of muscle weakness, muscle pain, recumbency, stiff gait, inability to move the limbs and the development of respiratory and circulatory insufficiency.

In primary nutritional muscular dystrophy associated with a deficiency of vitamin E and/or selenium there is lipoperoxidation of the cellular membranes of muscle fibers resulting in degeneration and necrosis. The lesion is present only in muscle fibers and the histological and biochemical changes which occur in the muscle are remarkably similar irrespective of the cause. Variations in the histological lesion occur but indicate variation in the severity and rapidity of onset of the change rather than different causes.

Myoglobinuria

Because of the necrosis of muscle, myoglobin is excreted in the urine and myoglobinuric nephrosis is an important complication, particularly of acute primary myopathy. The degree of myoglobinuria depends on the severity of the lesion, acute cases resulting in marked myoglobinuria, and on the age and species of animal affected. Adult horses with myopathy may liberate large quantities of myoglobin, resulting in dark brown urine. Yearling cattle with myopathy release moderate amounts and the urine may or may not be colored; calves with severe enzootic nutritional muscular dystrophy may have grossly normal urine. In all species the renal threshold of myoglobin is so low that discoloration of the serum does not occur.

Muscle enzymes

An important biochemical manifestation of myopathy is the increased release of muscle cell enzymes that occurs during muscle cell destruction. CPK and serum glutamic oxaloacetate transaminase are both elevated in myopathy and CPK, particularly, is a more specific and reliable indication of acute muscle damage. Increased amounts of creatinine are also released into the urine following myopathy.

Exertional rhabdomyolysis

In exertional rhabdomyolysis in horses there is enhanced glycolysis with depletion of muscle glycogen, the accumulation of large amounts of lactate in muscle and blood and the development of hyaline degeneration of myofibers. Affected muscle fibers are richer in glycogen in the acute stage of ‘tying-up’ than in the late stages, suggesting an increased glycogen storage in the early phase of the disease compared with normal healthy horses. During enforced exercise there is local muscle hypoxia and anaerobic oxidation resulting in the accumulation of lactate and myofibrillar degeneration. The pathogenesis of postanesthetic myositis in horses is uncertain.⁶ A significant postischemic hyperemia occurs in horses that develop postanesthetic myopathy.⁶ Postanesthetic recumbency can occur in the horse with polysaccharide storage myopathy.⁷

Types of muscle fiber affected

In most animals skeletal muscle is composed of a mixture of fibers with different contractile and metabolic characteristics. Fibers with slow contraction times have been called slow twitch or type I fibers and those with fast contraction time are fast twitch or type II. Histochemically, types I and II fibers can be differentiated by staining for myofibrillar ATPase. Type II fibers can be subgrouped into type IIA and IIB on the basis of acid preincubations.⁸ Several different characteristics of these muscle fibers have been studied in the horse. There are variations in the percentage of each type of fiber present and in composition of muscle fibers dependent on genetic background, age, and stage of training.⁸ There are also variations in the muscle fibers within one muscle⁹ and between different muscles.¹⁰ The histochemical characteristics of equine muscle fibers have been examined:^11,12

The histochemical staining characteristics of normal equine skeletal muscle have been examined and serve as a standard for comparison with data obtained from skeletal muscles with lesions.¹²

Secondary myopathy due to ischemia

In secondary myopathy due to ischemia there may be multiple focal areas of necrosis, which causes muscle weakness and results in an increase of muscle enzymes in the serum. The degree of regeneration with myofibers depends on the severity of the lesion. Some regeneration occurs but there is considerable tissue replacement. In aortic and iliac thrombosis in calves under 6 months of age the thrombosis results in acute-to-chronic segmental necrosis of some skeletal muscles and coagulation necrosis in others.¹³

Neurogenic atrophy of muscle

In neurogenic atrophy there is flaccid paralysis, a marked decrease in total muscle mass and degeneration of myofibers, with failure to regenerate unless the nerve supply is at least partially restored.

Primary myopathy

In general terms, in acute primary myopathy there is a sudden onset of weakness and pseudoparalysis of the affected muscles, causing paresis and recumbency and, in many cases, accompanying respiratory and circulatory insufficiency. The affected animals will usually remain bright and alert but may appear to be in pain. The temperature is usually normal but may be slightly elevated in severe cases of primary myopathy. Cardiac irregularity and tachycardia may be evident, and myoglobinuria occurs in adult horses and yearling cattle. The affected skeletal muscles in acute cases may feel swollen, hard and rubbery but in most cases it is difficult to detect significant abnormality by palpation. Acute cases of primary myopathy may die within 24 hours after the onset of signs.

Acute nutritional myopathy

While acute nutritional myopathy in horses occurs most commonly in foals from birth to 7 months of age, acute dystrophic myodegeneration also occurs in adult horses. There is muscle stiffness and pain, myoglobinuria, edema of the head and neck, recumbency and death in a few days. A special occurrence of myopathy has been recorded in suckling Thoroughbred foals up to 5 months of age. The disease occurs in the spring and summer in foals running at pasture with their dams and is unassociated with excessive exercise. In peracute cases there is a sudden onset of dejection, stiffness, disinclination to move, prostration and death 3–7 days later. Lethargy and stiffness of gait are characteristic of less acute cases. There is also a pronounced swelling and firmness of the subcutaneous tissue at the base of the mane and over the gluteal muscles. There may be excessive salivation, desquamation of lingual epithelium and board-like firmness of the masseter muscles. The foals are unable to suck because of inability to bend their necks. Spontaneous recovery occurs in mild cases but most severely affected foals die.

Severe nutritional myopathy of the masseter muscles in a 6-year-old Quarter Horse stallion has been described.¹⁴ The masseter muscles were swollen and painful, and there was exophthalmos and severe chemosis with protrusion of the third eyelids. The mouth could be opened only slightly and masticatory efforts were weak. Serum enzymology supported a diagnosis of nutritional muscular dystrophy, and the concentrations of vitamin E and selenium in the blood and feed were lower than normal.

Tying-up

In tying-up in horses there is a very sudden onset of muscle soreness 10–20 minutes following exercise. There is profuse sweating and the degree of soreness varies from mild, in which the horse moves with a short, shuffling gait, to acute, in which there is a great disinclination to move at all. In severe cases, horses are unable to move their hindlegs, and swelling and rigidity of the croup muscles develops. Myoglobinuria is common.

Postanesthetic myositis

In postanesthetic myositis affected horses experience considerable difficulty during recovery from anesthesia. Recovery is prolonged and when initial attempts are made to stand there is lumbar rigidity, pain and reluctance to bear weight.⁷ Some affected horses will be able to stand in within several hours if supported in a sling.⁷ The limbs may be rigid and the muscles firm on palpation. In severe cases the temperature begins to rise – reminiscent of malignant hyperthermia. Other clinical findings include anxiety, tachycardia, profuse sweating, myoglobinuria and tachypnea. Death may occur in 6–12 hours. Euthanasia is the only course for some horses. In the milder form of the syndrome, affected horses are able to stand, but are stiff and in severe pain for a few days.

Exertional rhabdomyolysis

In horses, the clinical findings are variable and range from poor performance to recumbency and death. Signs may be mild and resolve spontaneously within 24 hours or severe and progressive.

The usual presentation is a young (2–5-year-old) female racehorse with recurrent episodes of stiff gait after exercise. The horse does not perform to expectation and displays a short-stepping gait that may be mistaken for lower leg lameness. The horse may be reluctant to move when placed in its stall, be apprehensive and anorexic, and frequently shift its weight. More severely affected horses may be unable to continue to exercise, have hard and painful muscles (usually gluteal muscles), sweat excessively, be apprehensive, refuse to walk and be tachycardic and tachypneic. Affected horses may be hyperthermic. Signs consistent with abdominal pain are present in many severely affected horses. Deep red urine (myoglobinuria) occurs but is not a consistent finding. Severely affected horses may be recumbent and unable to rise.

Many different manifestations of equine polysaccharide storage myopathy occur.³ All manifestations are related to dysfunction, which results in pain, weakness, segmental fiber necrosis, stiffness, spasm, atrophy or any combination of the above. The muscles most severely affected are the powerful rump, thigh and back muscles, including gluteals, semimembranosus, semitendinosus and longissimus.

In exertional rhabdomyolysis in sheep chased by dogs, affected animals are recumbent, cannot stand, appear exhausted and myoglobinuria is common. Death usually follows. A similar clinical picture occurs in cattle that have run wildly for several minutes.

Hyperkalemic periodic paralysis

Initially there is a brief period of myotonia with prolapse of the third eyelid. In severe cases, the horse becomes recumbent and the myotonia is replaced by flaccidity. Sweating occurs, and generalized muscle fasciculations are apparent, with large groups of muscle fibers contracting simultaneously at random. The animal remains bright and alert and responds to noise and painful stimuli. In milder cases, affected horses remain standing and generalized muscle fasciculations are prominent over the neck, shoulder and flank. There is a tendency to stand base-wide. When the horse is asked to move, the limbs may buckle and the animal appears weak. The horse is unable to lift its head, usually will not eat and may yawn repeatedly early in the course of an episode. The serum potassium levels are elevated above normal during the episodes.

Secondary myopathy due to ischemia

In secondary myopathy due to ischemia, e.g. the downer cow syndrome, the affected animal is unable to rise and the affected hindlegs are commonly directed behind the cow in the frogleg attitude. The appetite and mental attitude are usually normal. No abnormality of the muscles can be palpated. With supportive therapy, good bedding and the prevention of further ischemia by frequent rolling of the animal, most cows will recover in a few days.

In calves with aortic and iliac artery thrombosis there is an acute onset of paresis or flaccid paralysis of one or both pelvic limbs.¹³ Affected limbs are hypothermic and have diminished spinal reflexes and arterial pulse pressures. The diagnosis can be defined using angiography. Affected calves die or are euthanized because treatment is not undertaken.

Neurogenic atrophy

With neurogenic atrophy there is marked loss of total mass of muscle, flaccid paralysis, loss of tendon reflexes and failure of regeneration. When large muscle masses are affected, e.g. quadriceps femoris in femoral nerve paralysis in calves at birth, the animal is unable to bear normal weight on the affected leg.

Dystrophy of the diaphragmatic muscles

In dystrophy of the diaphragmatic muscles in adult Meuse–Rhine–Yessel cattle there is loss of appetite, decreased rumination, decreased eructation and recurrent bloat. The respiratory rate is increased with forced abdominal respirations, forced movement of the nostrils and death from asphyxia in a few weeks.

Severe diaphragmatic necrosis in a horse with degenerative myopathy due to polysaccharide storage myopathy has been described.¹⁵ Affected horses may have severe respiratory distress and respiratory acidosis, and do not respond to supportive therapy.

Muscle-derived serum enzymes

The serum levels of the muscle enzymes are characteristically elevated following myopathy due to release of the enzymes from altered muscle cell membranes. Creatine kinase (CK) is a highly specific indication of both myocardial and skeletal muscle degeneration. Plasma CK activity is related to three factors: the amount and rate of CK released from an injured muscle into plasma, its volume of distribution and its rate of elimination.¹⁶ CK has a half-life of about 4–6 hours and, following an initial episode of acute myopathy, serum levels of the enzyme may return to normal within 3–4 days if no further muscle degeneration has occurred. Levels of AST are also increased following myopathy but, because the enzyme is present in other tissues such as liver, it is not a reliable indicator of primary muscle tissue degeneration.

Because AST has a longer half-life than CK, the levels of AST may remain elevated for several days following acute myopathy. The daily monitoring of both CK and AST levels should provide an indication of whether active muscle degeneration is occurring. A marked drop in CK levels and a slow decline in AST levels suggests that no further degeneration is occurring whereas a constant elevation of CK suggests active degeneration.

In acute nutritional muscular dystrophy in calves, lambs, and foals the CK levels will increase from normal values of below 100 IU/L to levels ranging from 1000–5000 IU/L and even higher. The levels of CK in calves will increase from a normal of 50 IU/L to approximately 5000 IU/L within a few days after being placed outdoors followed by unconditioned exercise. There is some preliminary investigation into quantification of the amount of skeletal damage in cattle based on the amount of CK activity.¹⁶

The measurement of serum levels of glutathione peroxidase is a useful aid in the diagnosis of myopathy due to selenium deficiency.

In downer cows with ischemic necrosis of the thigh muscles, the CK and AST levels will be markedly elevated and will remain elevated if muscle necrosis is progressive in cows that are not well bedded and rolled from side to side several times daily to minimize the degree and extent of ischemic necrosis.

High levels of CK (1000 IU/L and greater) usually indicate acute primary myopathy. Levels from 500–1000 IU/L may be difficult to interpret in animals recumbent for reasons other than primary myopathy. This will necessitate a careful reassessment of the clinical findings, history and epidemiology.

In horses with acute exertional rhabdomyolysis (paralytic myoglobinuria) the CK levels will range from 5000–10000 IU/L. Following vigorous exercise in unconditioned horses, the CK and AST levels will rise as a result of increased cell membrane permeability associated with the hypoxia of muscles subjected to excessive exercise. Lactate dehydrogenase (LDH) has also been used as a biochemical measurement of the degree of physical work done by horses in training. With progressive training in previously unconditioned horses there is no significant change between rest and exercise in the levels of serum CK, AST, and LDH. In horses with postanesthetic myositis the CK levels may exceed 100000 IU/L, the serum calcium is decreased and the serum inorganic phosphorus is increased. In naturally occurring cases of exertional rhabdomyolysis in horses the most consistent acid–base abnormality may be a hypochloremia rather than metabolic acidosis as has been assumed.

Muscle biopsy

Investigation of the structural and biochemical alterations of muscle tissue in myopathy include biopsy techniques that have been described.^3,17 Needle biopsies require a specialized Bergstrom muscle biopsy needle, which most practitioners do have on hand. Open biopsy is recommended in order to obtain a strip of muscle. Biopsy of either the semimembranosus or semitendinosus muscles, at a site between the base of the tail and the tuber ischium, provides an adequate sample. Muscle biopsy samples can be processed for either frozen section or routine formalin-fixed, paraffin-embedded sections. The frozen section is considered the gold standard.

Inclusions of periodic-acid–Schiff (PAS)-positive, amylase-resistant complex polysaccharide are abnormal and characteristic findings in muscle of equine polysaccharide storage myopathy.³

Histochemical techniques can be used on muscle biopsies of horses with muscular disease and animals with congenital and inherited myopathies.⁴

Myoglobinuria

Myoglobinuria is a common finding in adult horses with acute paralytic myoglobinuria but is not a common finding in acute nutritional muscular dystrophy in young farm animals, except perhaps in yearling cattle with acute muscular dystrophy. The myoglobinuria may be clinically detectable as a red or chocolate brown discoloration of the urine. This discoloration can be differentiated from that caused by hemoglobin by spectrographic examination or with the use of orthotoluidine paper strips. Urine becomes dark when myoglobin levels exceed 40 mg/dL of urine. Discoloration of the plasma suggests hemoglobinuria. Both myoglobin and hemoglobin give positive results for the presence of protein in urine. Porphyria causes a similar discoloration although this may not be evident until the urine has been exposed to light for some minutes. The coloration is lighter, pink to red rather than brown, and the urine is negative to the guaiac test and fluoresces with ultraviolet light. Creatinuria accompanies acute myopathy but has not been used routinely as a diagnostic aid.

Electromyography is a special technique for the evaluation of the degree of neurogenic atrophy.

Acute myositis of limb muscles

This disease is accompanied by severe lameness, swelling, heat and pain on palpation. There may be accompanying toxemia and fever. In chronic myositis there is much wasting of the affected muscles and this is difficult to differentiate clinically from atrophy due to other causes. Biopsy of the muscles may be necessary to confirm the diagnosis.

Injury to the gracilis muscle can cause acute, severe lameness in performance Quarter Horses.² Horses competing in barrel racing may be susceptible to gracilis muscle injury because the muscle functions to adduct the hind limb. The prognosis is good for returning to athletic use after and an adequate period of muscle healing and mild exercise. However, fibrotic myopathy or muscle atrophy can be a complication of the injury resulting in persistent gait deficits.

In horses traumatic myositis of the posterior thigh muscles may be followed by the formation of fibrous adhesions between the muscles (fibrotic myopathy) and by subsequent calcification of the adhesions (ossifying myopathy). External trauma can result in fibrotic myopathy but it may also be associated with excessive exercise or secondary to intramuscular injections.

Occasionally similar lesions may be seen in the foreleg. The lesions cause a characteristic abnormality of the gait in that the stride is short in extension and the foot is suddenly withdrawn as it is about to reach the ground. The affected area is abnormal on palpation.

An inherited disease of pigs, generalized myositis ossificans, is also characterized by deposition of bone in soft tissues. In traumatic injuries caused by penetration of foreign bodies into muscle masses, ultrasonography may be used to detect fistulous tracts and the foreign bodies.

Extensive damage to or loss of muscle occurs in screwworm and sometimes blowfly infestation, although the latter is more of a cutaneous lesion, and by the injection of necrotizing agents. For example, massive cavities can be induced in the cervical muscles of horses by the intramuscular injection of escharotic iron preparations intended only for slow intravenous injection. Similarly, necrotic lesions can result from the intramuscular injection of infected or irritant substances. Horses are particularly sensitive to tissue injury, or are at least most commonly affected. Some common causes are chloral hydrate, antimicrobials suspended in propylene glycol, and even antimicrobials alone in some horses.

Injection site clostridial infections in horses

Clostridial myositis, myonecrosis, cellulitis, and malignant edema are terms used to describe a syndrome of severe necrotizing soft tissue infection associated with Clostridium spp. Affected horses typically develop peracute emphysematous soft tissue swelling in the region of an injection or wound within hours of the inciting cause. It can occur following the intramuscular or inadvertent perivascular administration of a wide variety of commonly administered drugs.³ In a series of 37 cases, the lesion occurred within 6–72 hours of a soft-tissue injection in most cases and most were in the neck musculature. Aggressive treatment can be associated with a survival rate of up to 81% for cases due to Clostridium perfringens alone; survival rates for other Clostridium spp. are lower. A combination of a high dose of intravenous antibiotic therapy and surgical fenestration and debridement is the recommended approach to treatment.

Injection site lesions in cattle

Muscle lesions associated with injection sites in the cattle industry are a source of major economic loss because of the amount of trim required at slaughter. The presence of injection-site lesions in whole muscle cuts, such as the top sirloin and outside round, limits their use and value. The occurrence of injection-site lesions in muscle is among the top five quality challenges for both beef and dairy market cows and bulls.⁴ Because injection-site lesions are concealed in muscles and/or are under subcutaneous fat, they are seldom found during fabrication at the packing plant and appear instead during wholesale/retail fabrication or at the consumer level. In 1998, the National Animal Health Monitoring System found that 47% of producers and 37% of veterinarians administered intramuscular injections in the upper or lower rear leg of cows; the need for further educational effort is apparent.

Monitoring the frequency of injection-site lesions allows educational efforts of state and national beef quality assurance programs to evaluate, more definitively, management practices of producers that can be changed to minimize occurrence of these defects. Audits done at abattoirs between 1998 and 2000 in the USA indicate that the frequency of injection-site lesions has decreased but the need remains for educational programs and continued improvements in beef quality assurance practices among beef and dairy cattle producers.⁴ Historically, most intramuscular injections were given in the gluteals and the biceps femoris muscles, which are prime cuts of beef. Surveys of injection sites in beef cattle in North America have found lesions in a significant percentage of prime cuts of beef.⁵ Lesions consisting of clear scars and woody calluses are mature and probably originated in calfhood; scars with nodules or cysts are less mature, occurring later in the feeding period. It is now recommended that intramuscular injections be given in the cervical muscles. Reducing the incidence of injection site lesions requires that manufacturers of biological and antibiotic preparations develop less irritating formulations. Products should be formulated for subcutaneous use whenever possible and administered in the neck muscles, which are not prime cuts of beef.

The outcome of an intramuscular injection depends on the nature of the lesion produced. Myodegeneration following intramuscular injections of antibiotics in sheep results in full muscle regeneration within less than 3 weeks.⁶ Necrosis following the injection results in scar formation with encapsulated debris, which persists for more than a month and leaves persistent scar tissue.

An outbreak of myositis, lameness and recumbency occurred following the injection of water-in-adjuvanted vaccines into the muscles of the left and right hips of near-term pregnant beef cattle.⁷ Within 24 hours, some cattle were recumbent, some had nonweightbearing lameness and, within 10 days, 50% of the herd developed firm swellings up to 24 cm in vaccination sites. Histologically, granulomatous myositis with intralesional oil was present. The swellings resolved over a period of 6 months. The acute transient lameness was attributed to the use of two irritating biological vaccines in the hip muscles of cows near parturition.

Nutritional causes

Inherited and congenital causes

There are many inherited and congenital defects of bones of newborn farm animals, which are described, and discussed in detail in Chapter 34. In summary, these include:

Angular deformities of joints of long bones due to asymmetric growth plate activity are common in foals and are commonly repaired surgically.² The distal radius and distal metacarpus are most often affected, the distal tibia and metatarsal less commonly. Physiologically immature foals subjected to exercise may develop compression-type fractures of the central or third tarsal bones. Some of these foals are born prematurely or are from a twin pregnancy. Retained cartilage in the distal radial physis of foals 3–70 days of age presents without apparent clinical signs.

Physitis is dysplasia of the growth plate, characterized by an irregular border between the cartilage and the metaphyseal zone of ossification, an increase in the lateromedial diameter of the physis, and distoproximally oriented fissures at the medial aspect of the metaphysis, which originate at the physis. In some cases, these may result in bilateral tibial metaphyseal stress fractures in foals.³

Abnormal modeling of trabecular bone has been recognized in prenatal and neonatal calves.⁴ Abnormalities included growth retardation lines and lattices, focal retention of primary spongiosa and the persistence of secondary spongiosa. Intrauterine infection with viruses such as bovine virus diarrhea (BVD) may be a causative factor.⁴

Physical and environmental causes

Moderate osteodystrophy and arthropathy may occur in rapidly growing pigs and cattle raised indoors and fed diets that contain adequate amounts of calcium, phosphorus and vitamin D. Those animals raised on slatted floors or concrete floors are most commonly affected and it is thought that traumatic injury of the epiphyses and condyles of long bones may be predisposing factors in osteochondrosis and arthrosis in the pig (leg weakness) and epiphysitis in cattle. Experimentally raising young calves on metal slatted floors may result in more severe and more numerous lesions of the epiphysis than occurs in calves raised on clay floors. Total confinement rearing of lambs can result in the development of epiphysiolysis and limb deformities. However, the importance of weightbearing injury as a cause of osteodystrophy in farm animals is still uncertain. In most reports of such osteodystrophy, all other known causes have not been eliminated.

Chronic osteodystrophy and arthropathy have been associated with undesirable conformation in the horse.

Vertebral exostoses are not uncommon in old bulls and usually affect the thoracic vertebrae (T2 and T12) and the lumbar vertebrae (L2–L3), which are subjected to increased pressure during the bending of the vertebral columns while copulating. The exostoses occur mainly on the ventral aspects of the vertebrae, fusing them to cause immobility of the region. Fracture of the ossification may occur, resulting in partial displacement of the vertebral column and spinal cord compression. The disease is commonly referred to as spondylitis or vertebral osteochondrosis and also occurs less commonly in adult cows and in pigs. It is suggested that the anulus fibrosus degenerates and that the resulting malfunctioning of the disk allows excessive mobility of the vertebral bodies, resulting in stimulation of new bone formation. A similar lesion occurs commonly in horses and may affect performance, particularly in hurdle races and cross-country events. The initial lesion may be a degeneration of the intervertebral disk.

Some types of growth plate defect occur in young growing foals and these are considered to be traumatic in origin. Failure of chondrogenesis of the growth plate may be the result of crush injuries in heavy, rapidly growing foals with interruption of the vascular supply to the germinal cells of the growth plate. Asymmetric pressures due to abnormal muscle pull or joint laxity may slow growth on the affected side and result in limb angulation.

Femoral fractures occur in newborn calves during the process of assisted traction during birth.⁵ Laboratory compression of isolated femurs from calves revealed that the fracture configurations and locations are similar to those found in clinical cases associated with forced extraction. The breaking strength of all femurs fell within the magnitude of forces calculated to be created when mechanical devices are used to assist delivery during dystocia. It is suggested that the wedging of the femur in the maternal pelvis and resulting compression during forced extraction accounts for the occurrence of supracondylar fractures of the femur of calves delivered in anterior presentation using mechanical devices in a manner commonly used by veterinarians and farmers.

Tumors

Osteosarcomas are highly malignant tumors of skeletoblastic mesenchyme in which the tumor cells produce osteoid or bone. Osteosarcomas are the most common type of primary bone tumor in animals such as dogs and cats but are rare in horses and cattle. Most tumors of bone in large animals occur in the skull. A periosteal sarcoma on the scapula has been recorded in the horse⁶ and an osteosarcoma of the mandible in a cow.⁷

Rickets

Rickets is a disease of young growing animals in which there is a failure of provisional calcification of the osteoid plus a failure of mineralization of the cartilaginous matrix of developing bone. There is also failure of degeneration of growing cartilage, formation of osteoid on persistent cartilage with irregularity of osteochondral junctions and overgrowth of fibrous tissue in the osteochondral zone. Failure of provisional calcification of cartilage results in an increased depth and width of the epiphyseal plates, particularly of the long bones (humerus, radius and ulna and tibia) and the costal cartilages of the ribs. The uncalcified, and therefore soft, tissues of the metaphyses and epiphyses become distorted under the pressure of weightbearing, which also causes medial or lateral deviation of the shafts of long bones. There is a decreased rate of longitudinal growth of long bones and enlargement of the ends of long bones due to the effects of weight causing flaring of the diaphysis adjacent to the epiphyseal plate. Within the thickened and widened epiphyseal plate there may be hemorrhages and minute fractures of adjacent trabecular bone of the metaphyses. and in chronic cases the hemorrhagic zone may be largely replaced by fibrous tissue. These changes can be seen radiographically as ‘epiphysitis’ and clinically as enlargements of the ends of long bones and costochondral junctions of the ribs. These changes at the epiphyses may result in separation of the epiphysis, which commonly affects the femoral head. The articular cartilages may remain normal or there may be subarticular collapse resulting in grooving and folding of the articular cartilage and ultimately degenerative arthropathy and osteochondrosis. Eruption of the teeth in rickets is irregular and dental attrition is rapid. Growth of the mandibles is retarded and is combined with abnormal dentition. There may be marked malocclusion of the teeth.

Osteomalacia

Osteomalacia is a softening of mature bone due to extensive resorption of mineral deposits in bone and failure of mineralization of newly formed matrix. There is no enlargement of the ends of long bones or distortions of long bones but spontaneous fractures of any bone subjected to weightbearing is common.

Osteodystrophia fibrosa

Osteodystrophia fibrosa may be superimposed on rickets or osteomalacia and occurs in secondary hyperparathyroidism. Diets low in calcium or that contain a relative excess of phosphorus cause secondary hyperparathyroidism. There is extensive resorption of bone and replacement by connective tissue. The disease is best known in the horse and results in swelling of the mandibles, maxillae and frontal bones (the ‘bighead’ syndrome). Spontaneous fracture of long bones and ribs occurs commonly. Radiographically there is extreme porosity of the entire skeleton.

Osteoporosis

Osteoporosis is due to failure or inadequacy of the formation of the organic matrix of bone; the bone becomes porous, light and fragile, and fractures easily. Osteoporosis is uncommon in farm animals and is usually associated with general undernutrition rather than specifically a deficiency of calcium, phosphorus, or vitamin D. Copper deficiency in lambs may result in osteoporosis due to impaired osteoblastic activity. Chronic lead poisoning in lambs also results in osteoporosis due to deficient production of osteoid. In a series of 19 lactating or recently weaned sows with a history of lameness, weakness or paralysis, 10 had osteoporosis and pathological fractures while six had lumbar vertebral osteomyelitis. Bone ash, specific gravity of bone and the cortical to total ratio were significantly reduced in sows with osteoporosis and pathological fractures.

Ovariectomized sheep that are fed a calcium-wasting diet develop osteoporosis, which is being used as a model to study the disease in humans.⁸

Osteodystrophy of chronic fluorosis

Osteodystrophy of chronic fluorosis is characterized by the development of exostoses on the shafts of long bones due to periosteal hyperostosis. The articular surfaces remain essentially normal but there is severe lameness because of the involvement of the periosteum and encroachment of the osteophytes on the tendons and ligaments.

Congenital defects of bone

These include complete (achondroplasia) and partial (chondrodystrophy) failure of normal development of cartilage. Growth of the cartilage is restricted and disorganized and mineralization is reduced. The affected bones fail to grow, leading to gross deformity, particularly of the bones of the head.

Osseous sequestration in cattle

Osseous sequestration is a common orthopedic abnormality in cattle and horses.⁶ In most cases, the lesions develop in the bones of the distal portion of the limbs. Sequestration is associated with trauma that results in localized cortical ischemia and bacterial invasion secondary to loss of adjacent periosteal and soft-tissue integrity and viability. The soft tissues covering the bones that comprise the distal portions of the limbs fail to provide adequate protection and collateral blood supply to the bone.

Osteomyelitis secondary to trauma

In horses, osteomyelitis is a frequent sequela to wounds of the metacarpal and metatarsal bones and the calcaneus. These bones have limited soft tissue covering, which may predispose them to osteomyelitis following traumatic injury. Similarly, a portion of the lateral aspect of the proximal end of the radius has limited soft-tissue covering. Penetrating and nonpenetrating wounds in this region, therefore, may result in serious consequences even though they may initially appear to be minor. Because lesions may be an extension of septic arthritis, a thorough examination of the wound area is necessary.

Osteomyelitis of the sustentaculum tali in horses has been described.⁷

Inflammation of bone marrow

Inflammation of bone marrow in animals has been described.^8,9 Acute inflammation commonly accompanies bacterial sepsis, resulting in either multifocal microabscesses or perivascular infiltrates of neutrophils, fibrin, edema, and hemorrhage. The most common abnormality associated with fibrinous inflammation is disseminated intravascular coagulopathy. Discrete granulomas may occur in the marrow of animals with systemic mycotic disease, idiopathic granulomatous disease and serous atrophy of fat.

Nutritional causes

Poisonings

Steroid-induced

The intra-articular injection or prolonged parenteral administration of corticosteroids in horses may lead to degenerative joint disease.

Biomechanical trauma

Growth rate, body size, and genetic predisposition

Degenerative coxofemoral arthropathy occurs in young beef bulls as early as 9 months of age. A congenital shallow acetabulum may predispose. It may be secondary to hip dysplasia, but in some cases there is no evidence of this. The large, weightbearing joints subjected to the greatest movement and concussion appear to be most susceptible. Rapidly growing bull calves appear to be most susceptible and some of them have an inherited susceptibility.

Osteochondrosis

Osteochondrosis is an important cause of lameness in horses. It is usually seen in young rapidly growing animals, and affects males more commonly than females. The predilection sites of osteochondrosis in the horse and their general order of incidence are hock, stifle, shoulder, fetlock, and cervical spine. The stifle, hock, and shoulder joints are more commonly affected, but many other joints may also be affected, including the metatarsal and metacarpal bones and rarely the acetabula of young foals.

The epidemiology, heritability and body measurements and clinical findings of osteochondrosis of hock and fetlock joints in Standardbred trotters have been examined.¹ The incidence of the disease is high in the Swedish Standardbred population and well developed by the age of 1.5 years. The incidence of osteochondrosis is higher in horses born later in the foaling season than earlier and the incidence was related to body size: affected horses were taller at the withers and had a greater circumference of the carpus.¹ This suggests that differences in body size at birth and the first few months of the foal’s life are of major importance in the development of osteochondrosis. The heritability estimates of osteochondrosis in the hock and fetlock joints of 753 Standardbred trotters 6–21 months of age was 0.52 and 0.21, respectively.²

Aging process

Degenerative arthropathy in aged dairy cows and bulls may be a manifestation of the normal aging process. Osteochondrosis, degenerative joint disease and vertebral osteophysis occur in middle-aged bulls.

Osteoarthrosis of the antebranchial joint of riding horses has been described.³ Affected animals were aged mares that developed osteoarthrosis and ankylosis. The cause was unknown.

Conformation and intensive animal production

Osteoarthropathy occurs in rapidly growing cattle and pigs raised in confinement on hard, usually concrete, floors and with minimal exercise. Osteochondrosis in feedlot cattle may be associated with a high-caloric diet and rapid growth rate. It is thought that weight-bearing trauma in these rapidly growing animals is sufficient to cause degenerative lesions of certain joints, especially in animals with a skeletal conformation that results in abnormal stress on certain weightbearing condyles of long bones.

In a series of 42 cases of stifle lameness in cattle, 18 had evidence of subchondral bone cyst and ranged in age from 6–18 months. It is suggested that the subchondral bone cyst is an indicator of osteochondrosis. In a series of osteochondrosis in cattle, male, purebred cattle of a mean age of 21 months were affected.⁴

Osteochondrosis may occur in rapidly growing bull beef calves fed a diet lacking adequate calcium, sodium, copper and vitamins A, D, and E,^5,6 grazing beef cattle on improved native pasture in which a common ancestral sire and gender (all males) may have been contributing factors.⁷ Severe osteochondrosis of multiple joints but with remarkable changes in the humeral head and glenoid of both shoulder joints in 10-month-old beef calves has been described.⁸

Osteochondrosis similar to that seen in pigs has been recorded in purebred Suffolk lambs raised in a system designed to produce rapidly growing, high-value rams.⁹ The disease has been recorded in a single pedigree Suffolk ram.¹⁰

Osteochondrosis and arthrosis are considered to be major causes of ‘leg weakness’ in rapidly growing pigs.¹¹ Restricting the energy intake appears to decrease the prevalence and severity of osteochondrosis when gilts are examined at 100 kg. The prevalence and severity of osteochondrosis in growing pigs is probably not related to floor type.¹¹ Recent work has shown a significant relationship between body conformation and the presence of joint lesions. Pigs with a narrow lumbar region, broad hams and a large relative width between the stifle joints were highly susceptible to poor locomotor ability due to lesions in the elbow and stifle joints, the lumbar intervertebral joints and the hip joint.

This excellent work represents real progress in understanding the relationship between skeletal conformation and bone and joint lesions. It is postulated that inherited weakness of muscle, ligaments, cartilage and exterior joint conformation results in local overloading in the joint and the development of osteochondrosis and arthrosis. Some breeds, such as the Duroc, have more problems of structure and movement in the front legs than in the rear legs, but osteochondrosis is not responsible for the leg weakness. Osteochondrosis has been recorded in wild boar–Swedish Yorkshire crossbred pigs in which the growth rate was low.¹²

Osteoarthrosis of the distal tarsal joints of the horse (bone spavin)

Osteoarthrosis of the distal tarsal joints (hock), commonly known as bone spavin, is common in Icelandic horses and strongly related to age.^13,14 In Icelandic horses aged 6–12 years and used for riding, the prevalence of radiographic signs of osteoarthrosis in the distal tarsus increased from 18% in horses 6 years of age up to 54% in 12-year-old horses. The age onset of radiographic signs reflect a predisposition to bone spavin indicating a trait with medium–high heritability.¹³ There is a high prevalence of chondronecrosis in young Icelandic horses, indicating an early onset and slow progression of disease.¹⁴ The disease is the most common cause of culling due to disease in riding horses in the age group 7–17 years.¹⁵

Primary osteoarthropathy

This is due to normal aging processes and ordinary joint usage. The initial lesions occur in the superficial layers of the articular cartilages where, with increasing age, there is loss of the normal resilience of the cartilage, a lowering of the chondroitin sulfate content and reduction in the permeability of the cartilaginous matrix, which results in progressive degeneration of the articular cartilage. There is grooving of the articular cartilage, eburnation of subchondral bone and secondary hypertrophy of marginal cartilage and bone, with the formation of pearl-like osteophytes. In experimentally induced arthritis in the horse the major changes include synovitis, increased synovial effusion and superficial fibrillation with chondrocyte necrosis in the articular cartilage. These are comparable to the early changes in naturally occurring degenerative joint disease.

Secondary osteoarthropathy

This appears to be initiated by injuries or congenital conformational defects that create greater shearing stresses on particular points, in contrast to the intermittent compressive stresses typical of ordinary weightbearing. These irregular stresses result in cartilaginous erosion, increased density of subchondral bone at points of physical stress and proliferation of bone and cartilage at the articular margins.

Following acute trauma, the initial changes are often characterized by acute synovitis and capsulitis. As a result of the inflammatory response, leukocytes, prostaglandins, lysosomal enzymes and hyaluronidase enter the synovial fluid, which becomes less viscous and affects the nutrition of the cartilage. There is some evidence of immune complexes associated with collagen-type-specific antibodies in horses with secondary osteoarthritis. Cytokines can be detected in the synovial fluid after racing in horses with degenerative joint disease.¹⁸ The cartilage matrix undergoes a variety of changes, possibly because of chondrocyte damage with lysosomal enzyme release, or to collagen fiber injury. There is an increase in water content and loss of orientation of the collagen fibers. Proteoglycans are lost and, while increased chondrocyte activity synthesizes proteoglycans, they are of lower molecular weight and altered glycosaminoglycan composition. This leads to loss of elasticity and surface integrity of the cartilage, resulting in increased friction, blistering and ulceration. There is additional lysosomal enzyme release from the chondrocytes, resulting in matrix destruction and further proteoglycan destruction. The degrading enzymes enter the altered matrix and cause further degradation.

The first stage of matrix degradation involves discoloration, softening and blistering of the tangential layer of the cartilage surface, a process known as early fibrillation. As the fissuring extends to the radial layer, microfractures occur, with loss of cartilage fragments (detritus) into the synovial fluid. As the cartilage is destroyed the underlying bone is exposed and becomes sclerotic. Bony proliferation occurs in the floor of the cartilage lesions, while at the joint margins osteophyte formation occurs. The pathogenesis of degenerative joint disease indicates that the ideal treatment would be the use of a substance that would promote synthesis of matrix components and retard catabolic processes.

The major proteoglycan in cartilage is a high-molecular-weight aggrecan that contains chondroitin sulfate and keratin sulfate chains located on specific regions of the core protein. These macromolecules are continuously released into the synovial fluid during normal cartilage matrix metabolism. Cartilage proteoglycans are degraded early in the course of joint disease and released from the cartilage into the synovial fluid, where they can be identified.¹⁹

In horses with degenerative joint disease, proteoglycan fragments – glycosaminoglycans – have been determined in equine synovial fluid as indicators of cartilage metabolism in various types of arthritides.¹⁹ The presence of high-molecular-weight proteoglycans and high concentrations of hyaluronate in horses with various arthritides – acute or chronic traumatic arthritis, intra-articular fracture and infectious arthritis, with and without abnormal radiographic and/or arthroscopic findings – compared with control joints has been investigated.¹⁹

The intra-articular injection of corticosteroids depresses chondrocyte metabolism, alters the biochemical composition and causes morphological changes in the articular cartilage, which remains biochemically and metabolically impaired for several or more weeks.

In femoral–tibial osteoarthrosis of bulls the secondary degenerative joint lesions are due to rupture of the attachments of the lateral meniscus resulting in mechanical instability in the joint with unusual mechanical stresses on the articular cartilage leading to degeneration. The cranial cruciate ligament becomes progressively worn and eventually ruptures, resulting in loss of all joint stability and the development of gross arthrosis. In cattle with severe degenerative joint disease of the coxofemoral joints, an acetabular osseous bulla may develop at the cranial margin of the obturator foramen.

Osteochondrosis

Osteochondrosis (dyschondroplasia) is characterized by disturbance of the normal differentiation of the cells in the growing cartilage. Both the metaphyseal growth plate (the growth zone of the diaphysis) and immature joint cartilage (the growth zone of the epiphysis) are affected. The loss of normal differentiation of the cartilage cells results in failure of provisional calcification of the matrix and endochondral ossification ceases. Degeneration and necrosis of blood vessels in cartilage canals results in ischemia of an area of growing cartilage followed by chondrocyte degeneration and death. The initial lesion occurs in growing cartilage and dyschondroplasia is a more appropriate term. The primary lesion of osteochondrosis directly affects the differentiation and maturation of the cartilage cells and the surrounding matrix that are destined to become replaced by bone. This can occur at the two sites of endochondral ossification in long bones – the articular/epiphyseal cartilage complex and the metaphyseal growth plate. In osteochondrosis, the capillary buds fail to penetrate the distal region of the hypertrophic zone, which leads to a failure of the final stages of cartilage maturation and modification of the surrounding matrix. These changes lead to retention and thickening of cartilage with subsequent weakening of the articular/epiphyseal cartilage complex.

Typical lesions in the horse involve extensive cartilaginous and subchondral bone degeneration with flap formation and, ultimately, loose pieces in the joint. This is usually referred to as osteochondritis dissecans and is associated with synovial effusion and varying degrees of synovitis. Osteochondral fracture associated with severe pathological changes to the subchondral bone occurs most commonly on the trochlear ridges and the lateral or medial malleoli of the hock. In some instances, cartilage damage weakens underlying bone and causes a bone cyst to form, usually at a site of biomechanical stress or weightbearing.¹¹

It is suggested that osteochondrosis lesions in horses develop prior to 7 months of age and that ischemic necrosis of cartilage secondary to a defect in vascular supply is an important factor in the pathogenesis of the disease in horses.²⁰ An osteochondrotic lesion in the metaphyseal growth plate may disturb growth to such a degree that the whole shape of the bone is altered. Epiphyseolysis may also occur. Osteochondrosis of joint cartilage may lead to osteochondritis dissecans and secondary osteoarthrosis. The lesion may heal and only the sequelae are present once the period of growth is over.

In rapidly growing pigs raised in confinement with minimal exercise, osteochondrosis and arthrosis are seen as degeneration of the deep layer of the articular cartilage and adjacent subchondral bone with degenerative lesions of the epiphyseal plate. Lesions in the epiphyseal plate may result in epiphysiolysis, which occurs most commonly in the femoral head. The typical lesions are usually symmetrical and commonly involve the elbow, stifle and hip joints and the distal epiphyseal plate of the ulna. Lesions also occur in the intervertebral articulations. The lesions are common in pigs when they are examined at slaughter (90–100 kg BW) and there may have been no evidence of clinical abnormality or a proportion of the pigs with severe lesions may have been affected with the leg-weakness syndrome. Osteochondrosis and Erysipelothrix rhusiopathiae are the most common causes of nonsuppurative joint disease of pigs examined at the abattoir. Thus not all lesions are clinical.

Joint fluid

The changes in the synovial fluid of joints affected with degenerative arthropathy are usually unremarkable and can be distinguished from the changes in infectious arthritis. A summary of the laboratory evaluation of synovial fluid in diseases of the joints is set out in Table 13–2. The isolation of an infectious agent from the synovial fluid of a diseased joint suggests the presence of an infectious arthritis but failure to isolate an organism must not be interpreted as the presence of a noninfectious arthritis. In well advanced cases of infectious arthritis the number of organisms may be small or they have been phagocytosed by neutrophils in the joint fluid.

Table 13.2 Laboratory evaluation of synovial fluid in diseases of the joints

Total protein concentration and viscosity of synovial fluid of horses can be determined. Normal values are available²¹ and the concentration and molecular weight distribution of hyaluronate in synovial fluid from clinically normal horses and horses with diseased joints have been compared.^19,22 Synovial fluid viscosity is reduced in horses with infectious and chronic arthritides and with radiographic evidence of cartilage degeneration. The synovial fluid hyaluronate concentration can be used as a diagnostic marker for chronic traumatic arthritis. However, high-molecular-weight proteoglycans or other markers in the synovial fluid cannot be used for diagnosing or monitoring degenerative joint disease.¹⁹

Hematology and serum biochemistry should be combined with appropriate hematology and serum biochemistry where indicated. The concentration of hyaluronic acid in synovial fluid can be determined using an assay technique. The determination of serum calcium and phosphorus may reveal the existence of a dietary deficiency or imbalance of minerals.

Radiography

Radiography of the hock joints in a craniomedial–caudolateral oblique view and of the fetlock joints in lateromedial view are standard techniques for the diagnosis of osteochondrosis in the horse. Those joints with abnormal radiographs may be radiographed from additional perspectives. Horses with bony fragments or defects at the cranial edge of the intermediate ridge of the distal aspect of the tibia or defects at the lateral trochlea of the talus can be classified as having osteochondrosis.² The radiographic progression of femoropatellar osteochondrosis in horses under 1 year of age at the onset of clinical signs has been examined.²² The full extent of the radiographic lesions may take several weeks to develop.

Arthroscopy

Arthroscopic examination and surgery of affected joints of horses with osteochondrosis can provide considerably more information than is possible from clinical and radiographic examination alone.²³

Nonsteroidal anti-inflammatory agents

Several nonsteroidal anti-inflammatory drugs (NSAIDs), such as phenylbutazone, flunixin meglumine, ketoprofen, naproxen, and carprofen, are available treatment options. Each has associated toxicities. They are now the most commonly used drugs because of their analgesic, antipyretic and anti-inflammatory properties.²⁵ They inhibit some component of the enzyme system that converts arachidonic acid into prostaglandins and thromboxanes. All cells, including chondrocytes and synoviocytes, possess arachidonic acid as a fatty acid constituent of phospholipids. Once released, arachidonic acid is oxidized by either cyclooxygenase (COX) or 5-lipooxygenase. COX oxidation leads to prostaglandin production, while lipoxygenase oxidation leads to leukotriene formation. The effect of NSAIDs is primarily from inhibiting COX, which blocks arachidonic acid conversion to prostaglandin.

Intra-articular steroids

Various steroidal formulations for intra-articular administration are available and correct dosage, frequency of administration, indications and toxicity are factors to consider for each drug. They include methylprednisolone acetate, betametasone, and triamcinolone acetonide.²⁵

Chondroprotective agents

Various chondroprotective drugs such as hyaluronic acid, polysulfated glycosaminoglycan, and oral glucosamine-chondroitin sulphate are also used to control inflammation and provide viscosupplementation.²⁵

There is a notable lack of treatment information based on randomized, blinded placebo-controlled clinical trials in the horse to identify the efficacy of therapeutic agents for both symptomatic and disease-modifying activity in degenerative joint disease.²⁵ Until there are validated outcome measures that can be used practically in clinical trials, there will always be uncertainty about whether these therapeutic agents have any real disease-modifying action.²⁶

Other treatments

Surgical therapy includes curettage of articular cartilage, removal of osteophytes and surgical arthrodesis.²⁹ In a retrospective study of stifle lameness in 42 cattle admitted to two veterinary teaching hospitals over a period of 6 years, 18 had radiographic evidence of subchondral bone cyst without radiographic evidence of degenerative joint disease. The prognosis in those with a subchondral bone cyst was favorable, 75% returning to their intended function, while in septic arthritis only 22% returned to normal.

Chemical arthrodesis using the intra-articular injections of monoiodoacetate (MIA) has been described as an alternative to surgical arthrodesis for the treatment of degenerative joint disease of the distal tarsal joints.³⁰ MIA causes an increase in intracellular concentration of adenosine triphosphate resulting in inhibition of glycolysis and cell deaths. It causes dose-dependent cartilage degeneration characterized by cartilage fibrillations, chondrocyte death and glycosaminoglycan and proteoglycan depletion. MIA produces reliable radiographic and histological ankylosis of the distal tarsal joints. Resolution of the lameness required 12 months and occasionally longer. Soundness was achieved in 82% and 85% of horses at 12 and 24 months, respectively. Complications of the injections were uncommon and were probably related to peri-articular injection or leakage of MIA, or to use of higher concentrations or volumes. Postinjection pain was marked in a small number of horses but was transient and managed effectively with analgesic drugs. The procedure is controversial.³¹ Some clinicians argue that arthrodesis should only be used where lameness is localized to the tarsometatarsal and centrodistal joints with objective means such as local analgesic techniques, and when other more conservative treatments have failed.

Experimental infectious arthritis in calves

Septic arthritis induced by E. coli is a reliable and reproducible model of infectious arthritis in laboratory animals, horses and calves.⁶ The inoculation of E. coli into the tarsal joint of newborn colostrum-fed calves resulted in septic arthritis in all calves. Clinical signs of septic arthritis appeared on day 2 after infection and persisted until day for all calves. E. coli was cultured from synovial fluid on day 2 for one calf and until day 4 for five other calves. Polymerase chain reaction (PCR) for E. coli was positive in the synovial fluid of all calves. Synovial fluid neutrophil and white blood cell counts were increased on days 2–4. All bacterial cultures were negative on day 8, although clinicopathological signs of inflammation persisted until day 20. Rapid recovery occurred within 1 week when an appropriate treatment was begun early in the course of the disease.

Foals with septicemia

Septicemic foals may develop infectious arthritis and a concurrent polyosteomyelitis because of the patency of transphyseal vessels in the newborn foal; this allows spread of infection across the physes with the development of lesions in the metaphysis, epiphysis and adjacent to the articular cartilage. The syndrome is classified according to the location of the lesions:

Horses

Septic arthritis has been reproduced experimentally in horses and the sequential synovial fluid changes monitored. Following intra-articular inoculation of S. aureus, clinical signs are evident as early as 8 hours after infection. A high and persistent neutrophilia is one of the earliest and most accurate diagnostic abnormalities. The total white blood cell count rises within 12–24 hours to a mean value of 100 × 10⁹/L. Total protein also increases. Synovial fluid acidosis also occurs in infectious arthritis, which may interfere with the antibacterial activity of some antimicrobials. In experimental arthritis, the synovial pH declined from a mean value of 7.43 to 7.12. Bacteria could be detected in 40% of the smears of infected synovial fluid samples and primary cultures of the fluid were positive in 70%. The intra-articular inoculation of E. coli into horses induces a reliable, reproducible and controlled model of infectious arthritis consistent with the naturally occurring disease and has been used to evaluate the efficacy of gentamicin for treatment. The injection of E. coli lipopolysaccharide into various joints of horses can cause clinical signs of endotoxemia, and the synovial fluid total nucleated cell count and total protein are linearly responsive in increases in endotoxin.⁷

Endothelin (ET)-1, a 21-amino-acid polypeptide, is locally synthesized in the joints of horses with various forms types of joint disease.⁸ It induces a potent and sustained vasoconstriction. Synovial fluid concentrations of ET-1 varies among horses with joint disease, with higher concentrations in animals with joint sepsis suggesting a pathogenetic role in septic arthritis.

Synovial fluid in infectious arthritis in the horse may contain the proteolytic enzymes collagenase and caseinase which may derive from both synovial cells and neutrophils.⁹ These enzymes are involved in the degradation of connective tissue and loss of cartilage matrix. Lavage of affective joints is intended to remove these enzymes.

Infectious arthritis may occur following traumatic injury to a joint but the pathogenesis is obscure. Traumatic injury of the joint capsule resulting in edema and inflammation may allow latent organisms to localize, proliferate and initiate an arthritis.

Arthrocentesis

Aspiration of joint fluid for culture and analysis is necessary for a definitive diagnosis. Careful disinfection of the skin and the use of sterile equipment is essential to avoid the introduction of further infection.

Analysis of joint fluid

Total and differential cell count, total protein concentration and specific gravity are determined.

In infectious arthritis the volume of joint fluid is increased and the total leukocyte count is increased, with a high percentage (80–90%) of neutrophils. The severity of infectious arthritis may be manifested systemically by a leukocytosis with a marked regenerative left shift. In degenerative joint disease, the volume may be normal or only slightly increased and the total and differential leukocyte count may be manifested within the normal range. In traumatic arthritis there may be a marked increase in the number of erythrocytes. Special biochemical examinations of joint fluid are available that measure for viscosity, strength of the mucin clot and concentrations of certain enzymes. The laboratory findings in examination of the joint fluid are summarized in Table 13.2. The synovial fluid analysis of 130 cases in cattle compared the characteristics of animals with infectious and noninfectious arthritis.¹⁰

Culture of joint fluid

Joint fluid must be cultured for aerobic and anaerobic bacteria and on specific media when Mycoplasma sp. is suspected. It is often difficult to isolate bacteria from purulent synovial fluid. The rates of recovery of organisms vary from 40–75%. In one study of suspected infectious arthritis in 64 horses admitted to a veterinary teaching hospital over a period of 8.5 years, positive cultures were obtained from 55% of the joints sampled.¹¹ The most common organisms were S. aureus, E. coli and Pseudomonas aeruginosa, accounting for more than half the isolates obtained.

There is no single test that is reliable for the diagnosis of septic arthritis. Failure to isolate organisms on culture does not exclude the a bacterial cause, and organisms are often not observed in synovial fluid smears. Poor collection, storage and laboratory techniques, prior administration of antibiotics or partial success of the immune system in containing the infection may explain the failure to detect organisms. Arthrocentesis should be done before antibiotics are given and a blood culture bottle should be inoculated immediately, a Gram stain made and culture for anaerobes included.¹² Positive cultures from synovial fluid can be expected in only about 65% of cases.

A biopsy sample of synovial membrane may be more reliable than synovial fluid for culture but there is little evidence based on comparative evaluations to support such a claim. PCR has been examined in in-vitro studies to detect selected bacterial species in joint fluid compared with microbial culture.¹³ The benefits would include rapid and accurate diagnosis infectious arthritis, ability to detect bacteria in synovial fluid in the presence of antimicrobial drugs and diagnosis of infectious arthritis when culture results are inconclusive. However, initial studies found no difference between microbial culture and PCR analyses.

Serology of joint fluid

Serological tests may be of value in determining the presence of specific infections with Mycobacterium mycoides, Salmonella spp., Brucella spp., and E. insidiosa. Radiographic examination may aid in the detection of joint lesions and can be used to differentiate between inflammatory and degenerative changes. In foals with arthritis and suspected osteomyelitis there may be radiographic evidence of osteolysis of the metaphysis or epiphysis.

Radiography

Radiography of the affected joint will often reveal the nature and severity of the lesions. Typical radiographic findings of septic arthritis include osteolytic lesions of the articular cartilage, increased width of intra-articular joint space, and soft tissue swelling. Osteomyelitic changes are seen in some cases. Because radiographic changes usually appear after 2–3 weeks when destruction of subchondral bone has become extensive, it may be necessary to take a series of radiographs several days apart before lesions are detectable.

Ultrasonography

Arthrosonography is an effective, fast and noninvasive complement to traditional diagnostic techniques for comprehensive evaluation of the pathology of joints of cattle.¹⁴ Distension of the joint cavities can be imaged; assessing echogenicity, acoustic enhancement and ultrasonographic character of the exudate correlates well with findings by arthrocentesis, arthrotomy or at necropsy. Joint effusion, which is the earliest indication of septic arthritis, can usually be detected with ultrasound by an experienced operator in the early stages. The synovial membrane, synovial fluid, ligaments, tendons and periarticular soft tissue, only inadequately imaged by radiography, can be imaged with ultrasonography. In advanced septic arthritis, ultrasonography provides accurate information on the location of the soft-tissue swelling, the extent and character of the joint effusion and involvement of concurrent periarticular synovial cavities.

Arthroscopy

Endoscopy is now used widely to define joint abnormalities more clearly and to gain access to the joint cavity as an aid in the treatment of septic arthritis.¹⁵

Parenteral antimicrobials

Acute septic arthritis should be treated as an emergency to avoid irreversible changes in the joint. The conservative approach is the use of antimicrobials given parenterally daily for several days and up to a few weeks in some cases. The selection of the drug of choice will depend on the suspected cause of the arthritis. The antimicrobial sensitivities of bacterial isolates from horses with septic arthritis/synovitis or osteomyelitis after fracture repair vary widely. A combination of cephalosporin and amikacin is recommended before culture and sensitivity results are available.

The antimicrobials that perfuse into the joint in therapeutic concentrations include the natural and synthetic penicillins, tetracycline, trimethoprim-potentiated sulfonamides, neomycin, gentamicin, and kanamycin.

Cloxacillin, methicillin, or penicillin have been used successfully for the treatment of staphylococcal septic arthritis in the horse.

Amphotericin B given intravenously daily for up to 30 days combined with joint drainage has been used for the treatment of Candida sp. arthritis in the horse.¹⁶

The relative efficacies of antimicrobials administered parenterally versus by intra-articular injections has been uncertain. Trimethoprim–sulfadiazine, given to calves parenterally, results in therapeutic concentrations of the drug in the synovial fluid of calves and penetrability was not enhanced nor restricted by experimental joint inflammation. Oxytetracycline and penicillin given parenterally readily penetrate the synovial membrane of both normal neonatal calves and those with experimental arthritis. Since peak synovial joint fluid levels of oxytetracycline and penicillin exceeded the minimum inhibitory concentrations for organisms such as A. pyogenes, the use of parenteral antimicrobials for the treatment of infectious arthritis in calves is appropriate. Ceftiofur at 1 mg/kg BW intravenously every 12 hours for 20 days, along with joint lavage, was successful in treating experimental septic arthritis associated with E. coli.⁶ The duration of antibiotic therapy is empirical; 3 weeks is recommended. Cephapirin administered parenterally to normal calves or those with arthritis resulted in synovial fluid levels approximately 30% of serum levels. The use of ampicillin trihydrate in calves with suppurative arthritis, at a dose of 10 mg/kg BW intramuscularly, resulted in a peak serum concentration of 2.5 μg/mL, 2 hours after injection; the highest concentration in normal synovial fluid was 3.5 μg/mL at 4 hours and the highest concentration in suppurative synovial fluid was 2.7 μg/mL at 2 hours.

Marbofloxacin at 4 mg/kg BW intramuscularly daily for 10 days was effective for the treatment of infectious arthritis in calves.¹⁷ Amoxicillin at 40 mg/kg BW intravenously is effective for the treatment of infectious joint disease in horses.¹⁸

The administration of trimethoprim– sulfadiazine at 30 mg/kg BW orally once daily to horses with experimentally induced S. aureus arthritis was ineffective in maintaining adequate levels of both drugs in infected synovial fluid. The use of the same drug at 30 mg/kg BW orally given every 12 hours was effective in maintaining therapeutic concentrations of both drugs in the serum and in the joint fluid.

In piglets at 2 weeks of age, streptococcal arthritis is most likely and it will respond quickly to penicillin given parenterally. Likewise, acute arthritis associated with erysipelas in pigs will respond beneficially if treated early before there is pannus formation.

Synovitis due to Histophilus somni infection responds quickly to systemic treatment. However, in other specific types of infectious arthritis the response is poor and recovery, if it does occur, requires several days or a week. Mycoplasmal arthritis in cattle is relatively nonresponsive to treatment and affected cattle may be lame for up to several weeks before improvement occurs and complete recovery may not occur. Chronic arthritis due to infection of pigs with E. insidiosa will commonly develop into a rheumatoid-like arthritis and be refractory to treatment.

Failure to respond to conservative therapy has been attributed to:

It is often not possible to determine which situation is responsible.

If conservative treatment is not providing sufficient improvement and the value of the animal warrants extended therapy, a joint sample should be obtained for culture and sensitivity. The most suitable antimicrobial may then be given parenterally and/or by intra-articular injection. Strict asepsis is necessary to avoid introduction of further infection.

Intra-articular antimicrobials

The combined intra-articular and intravenous administration of gentamicin to normal horses can result in concentrations 10–100 times greater than after intravenous administration alone. In addition, gentamicin concentration in synovial fluid remained above the minimum inhibitory concentration for many common equine bacterial pathogens for at least 24 hours after treatment. The intra-articular administration of gentamicin is advantageous for the treatment of infectious arthritis in animals in which the systemic administration of the drug may be contraindicated, especially in the presence of impaired renal function or endotoxemia. Continuous infusion of gentamicin into the tarsocrural joint of horses for 5 days is an acceptable method of treating septic arthritis.¹⁹

Antimicrobial-impregnated polymethylmethacrylate beads have been used for the treatment of orthopedic infections involving bone, synovial structures and other soft tissues.^20-22 The antimicrobials diffuse from the beads in a bimodal fashion. There is a rapid release of 5–45% of the total amount of antimicrobial within the first 24 hours after implantation and then a sustained elution that persists for weeks to months, depending on the antimicrobial used. For effective diffusion, the antimicrobials must be water-soluble, heat-stable and available in powder form. Aminoglycosides and the cephalosporins have been incorporated most commonly into the beads.

Regional limb perfusion with antimicrobials has been used for the treatment of experimentally induced septic arthritis. The antimicrobial is infused under pressure to a selected region of the limbs through the venous system. The concentration of the antimicrobial in the septic synovial fluid will usually exceed those obtained by intravenous administration. However, there are insufficient data available to evaluate the procedure in naturally occurring cases. Therapeutic concentrations of cefazolin are achieved in the synovial fluid of clinically normal cows when injected intravenously distal to a tourniquet and the technique could be used as an alternative to systemic administration of antimicrobials to provide adequate concentrations in a joint cavity.

Lavage of joint

Drainage of the affected joint and through-and-through lavage of the joint is also desirable along with the systemic administration of antimicrobials. Aspiration and distension–irrigation of the joint cavity using polyionic electrolyte solutions buffered to 7.4 is recommended.⁶ The irrigation removes exudates and lysozymes that destroy articular cartilage. A through-and-through lavage system may also be used with drainage tubes. General or local anesthesia should be provided. The distended joint is identified by palpation, the hair is clipped short and the skin is prepared with appropriate surgical disinfection. A 2 cm 16-gauge needle is inserted into the joint cavity, avoiding direct contact with the bones of the joint. A second needle is inserted into the joint as far as possible from the first needle to cause any fluid perfused into the joint to pass through as much of the joint cavity as possible. 0.5–1 L of Ringer’s solution warmed to 37°C is flushed through the joint using a hand-pumped pressure bag to keep a steady fluid flow into the joint.⁶

Arthroscopy

Arthroscopy provides excellent visualization of most parts of an affected joint and can be used to access the joint for the treatment of septic arthritis.¹⁵ The endoscope can be used to explore and debride the affected joint during the same intervention. Purulent exudate can be removed and necrotic areas within the synovial membrane can be debrided.

Surgical drainage and arthrotomy

Failure to respond to parenteral and intra-articular medication may require surgical opening of the joint capsule, careful debridement and excision of synovium and infected cartilage and bone. This may be followed by daily irrigation of the joint cavity with antimicrobials and saline. A lavage system can be established and the joint cavity infused with an antimicrobial and saline daily for several days.²³ Arthrotomy with lavage was more effective in eliminating joint infections by providing better drainage than arthroscopy, synovectomy and lavage. However, with arthrotomy the risk of ascending bacterial contamination is greater and the major difficulty is to eliminate the infection from the joint and incision site.²⁴ Infected sequestra and osteomyelitis of subchondral bone will prevent proper healing. Curettage of septic physeal lesions in foals may be necessary.

Open drainage and intra-articular and parenteral antimicrobials has been used to treat persistent or severe septic arthritis/tenosynovitis. While joint lavage through needles is still effective in many horses with acute infectious arthritis or tenosynovitis, in those with chronic or recurring septic arthritis, open drainage is indicated to remove the inflammatory exudate from the synovial space. Infected synovial structures are drained through a small (3 cm) arthrotomy incision left open and protected by a sterile bandage. Joint lavage using antimicrobials is done daily and parenteral antimicrobials are given intensively.

Septic pedal arthritis in cattle may be treated successfully by the creation of a drainage tract to promote adequate drainage. In cattle with septic arthritis of the digit, placement of a wooden block under the unaffected digit decreases weightbearing on the affected digit and provides for earlier, less painful ambulation.²⁵

Arthrodesis or artificial ankylosis

Surgical arthrodesis can be used for the treatment of chronic septic arthritis in horses and calves.^26,27

Septic arthritis of the distal interphalangeal joint is a common complication of diseases of the feet of cattle. Facilitated ankylosis of the joint is a satisfactory alternative to amputation of the affected digit in valuable breeding animals.²⁸ In a series of 12 cases of septic arthritis of the distal interphalangeal joint treated by use of facilitated ankylosis, the success rate was 100%.

Physical therapy

The local application of heat, by hot fomentations or other physical means, is laborious but, if practiced frequently and vigorously, will reduce the pain and local swelling. Analgesics are recommended if there is prolonged recumbency. Persistent recumbency is one of the problems in the treatment of arthritis, particularly in foals. The animal spends little time feeding or sucking and loses much condition. Compression necrosis over bony prominences is a common complication and requires vigorous preventive measures.

Anti-inflammatory agents

NSAIDs are used parenterally to decrease the inflammatory response and to provide analgesia. In experimental synovitis in the horse, similar to septic arthritis, phenylbutazone was more effective than ketoprofen in reducing lameness, joint temperature, synovial fluid volume and synovial fluid prostaglandin.²⁹

Prognosis for survival and athletic use in horses with septic arthritis

The factors affecting the prognosis for survival and athletic use in 93 foals treated for septic arthritis have been examined.¹² The femoropatellar and tarsocrural joints were most commonly affected. Osteomyelitis or degenerative joint disease were detected in 59% of the foals. Failure of transfer of passive immunity, pneumonia and enteritis were common. Treatment consisted of lavage, lavage and arthroscopic debridement with or without partial synovectomy, or lavage and arthrotomy to debride infected bone and parenteral antibiotics. Seventy-five foals survived and were discharged from hospital, and approximately one-third raced. Isolation of Salmonella from synovial fluid was associated with an unfavorable prognosis for survival, and multisystemic disease was associated with an unfavorable prognosis for survival and ability to race. The key to successful outcome for septic arthritis is rapid diagnosis and initiation of treatment.

In a series of 507 horses treated for joint disease at one equine hospital during a period of 7 years, the risk factors affecting discharge from the hospital, of ever being sound, or of being alive after a 3-month followup were examined;³⁰ 58% of foals, 78% of yearlings and 94% of racing adults were discharged. Foals with a less severe lameness, duration of less than 1 day and infectious arthritis had increased odds of discharge.