This condition was first reported in Germany1 and Belgium2 and was recognized in the UK in 1968 and reported later.3 In these cases perineurial fibrosis was a feature and it was thought that the condition resulted from either a neurogenic atrophy or a periarticular fibrosis extending to the peripheral nerves. There is variable asymmetry of the hindquarters which is generally evident during the early grower period and obvious by 80 kg liveweight stage. An asymmetrical distribution of subcutaneous fat is also noted and possibly skin dimpling.4,5 The muscle most frequently affected was the M. semimembranous, followed by the M. semitendinosus, M. biceps femoris, M. adductor femoris, and M. gracilis. The muscles show changes that can be described as myofibre degeneration, interstitial fibrosis, and dystrophic changes. Several breeds, including Landrace, Large White, and Hampshire have been found affected but the problem is generally restricted to certain herds and to certain families within these herds, suggesting that a genetic liability exists for this condition.2 The mechanism of inheritance studied from test matings is not simple.3 Whatever the cause, there is a marked reduction in the number of muscle fibres. Both sexes may be involved and the condition may involve either hindlimb. Despite a marked reduction in muscle mass there is no detectable abnormality in gait. The cause is unknown, although it appears to result from suboptimal muscle growth rather than degenerative loss.6 In the only cases recorded from outside Europe a group of 7 Australian pigs were examined in detail7 and in one of these the affected M. semitendinosus weighed only 41% of the normal unaffected one. Perineural fibrosis and myopathy have been observed in some cases but have not been found consistently.6
This syndrom is also called spraddle leg, but more usually myofibrillar hypoplasia. This may be an erroneous term as this hypoplasia occurs in many normal pigs and may be a normal feature of post-natal muscle growth. This clinical condition of splayleg occurs in newborn piglets in most countries and is characterized by a temporary inability to stand with the hindlimbs.1
The etiology is unknown, but based on epidemiological evidence it is multifactorial.1 The current hypothesis is that the disease is caused by an interaction of genetic and non-genetic factors, a polygenic mode or expression of many genes without dominance.
The studies of Czech workers2,3 have suggested that the pathomorphology of the condition resembles that of glucocorticoid induced myopathy in man and animals.4 Dexamethasone given to minisows from the first to the last days of pregnancy produced in newborn piglets a disorder characterized by the splayleg syndrome with retardation of both muscle growth and myofibillogenesis.3,5 It has also been experimentally produced following the administration of pyrimethamine.6
The prevalence of the disease in the UK is 0–4% and the morbidity in affected herds varies from 2 to 27%. The case fatality rate is approximately 50% and is due to crushing, chilling, and starvation because affected piglets are not able to move around normally. The disease is more common in the Pietrain, Welsh, Landrace, and Large White breeds of swine; Landrace pigs may be especially susceptible. This suggests a genetic basis, but test-matings, with the exception of a few, have not been successful in reproducing the disease.1 On most farms the disease affects both male and female piglets. In a recent retrospective analysis of the incidence of the disease in a swine herd over a period of 5 years, the overall frequency was 1.74 times more in males than females and the birth weight of splayleg piglets tended to be subnormal.7 The environmental factors which have been associated with some outbreaks include slippery floors, a dietary choline deficiency and the ingestion of Fusarium toxin by pregnant sows. Choline deficiency is unlikely to be a factor8 and none of the other factors have been substantiated as etiological factors or epidemiological determinants.1
The pathogenesis of the disease is unclear. In affected pigs there is myofibrillar hypoplasia9,10 but this is also a feature of many muscles in normal pigs. There are simply too few maturing type 1 fibrils in the muscles, particularly of the foreleg, lumbar epaxial group and the hind limb to carry weight. The Mm semitendinosus appears to be the worst affected muscle. However, because myofibrillar hypoplasia may also be present in normal unaffected littermates1 it has been difficult to explain the pathogenesis of the muscular weakness. The use of morphometrics has enabled the detailed determination of the myofibrillar hypoplasia.11 In addition to myofibrillar hypoplasia, in splayleg pigs there is a higher content of sarcoplasmic RNA, reflected ultrastructurally by the presence of numerous ribosomes.12 The extramyofibrillar space was also filled with glycogen in splayleg pigs.13 In myofibrillar hypoplasia induced with glucocorticoids given to the pregnant sow, none of the pigs had splaylegs but the extramyofibrillar space contained little glycogen. There were also many glycogen-filled phagosomes and residual bodies which indicate a difference in the metabolism of glycogen in the first 2 or 3 days after birth. In a study of natural cases there was hypoplasia but there was an increased accumulation of glycogen especially within the large extramyofibrillar spaces in comparison with the normal pigs.14 These authors also found an anomalous distribution of glucose-6-phosphatase in splaylegged muscles in that the activity was concentrated at the periphery of the extremely dilated cisternae of the sarcoplasmic reticulum. In the normal muscles this enzyme activity was normal. This distribution could account for the slower utilization of glycogen in affected muscles and therefore would account for the build up.14 Quantitative image analysis of skeletal muscle revealed that the arrangement of the myofibrils within the fascicles of affected and unaffected pigs was different.
Some studies have found both quantitative (hypoplastic-type) and qualitative (dystrophic-type) insufficiencies in affected pigs which represent a temporary perinatal developmental disturbance. This could explain the muscular weakness and the recovery which occurs.
Larger litters may be more affected possibly because these tend to be born earlier. The clinical signs are usually obvious in 2–3 hours after birth when the litter should be standing and walking around the creep area. Affected piglets are unable to stand, and their hindlimbs are splayed sideways or forwards and the animals are resting in sternal recumbency. Sometimes the fore limbs are also splayed. Most severely affected piglets are unable to move; less severely affected animals are able to move slightly. Many pigs have soiled hindlimbs and perineum as a result of being unable to stand. As a result, the piglets are likely to be crushed or have difficulty gaining access to their source of nourishment. Affected piglets are normal in other respects and have a normal appetite and will suck the sow if placed near a teat. In the experimental induction5 there was hypoplasia but there were no clinical signs, which is further evidence for suggestions15 that the condition has a threshold for clinical signs and has strong maternal influences.
Treatment can be successful.16 If the pigs are able to suck or if they are fed artificially for 2–4 days, recovery will occur within 1 week in about 50% of cases. The ambulatory capacity of affected pigs can be improved, and mortality reduced, by taping or loosely tying together the hindlimbs for a period of up to 1 week. The method of loose tying of the hindlimbs consists of a figure-of-eight bandage (2.5 cm wide adhesive tape) being fixed around the metatarsal bones, leaving a space between the legs of up to 7 cm depending on the size of the piglet. The legs should be tied together within a few hours after the syndrome is obvious; a delay of several hours will decrease the prognosis. The provision of a non-slip floor surface such as a carpet or sack may also be helpful. Many farmers will tell you that repeated massaging of the limbs will also improve the survival rate.
Whether or not to cull the boar depends on the pedigree value of the animal, the incidence of the disease, and the probability that the boar is responsible. There is no evidence that the disease is monogenic. However, the incidence is highest in the Landrace breed, which suggests a hereditary predisposition. In deciding whether to use a suspected carrier animal, there is a need to distinguish between different situations. The consequences of disease are felt differently at the different levels of organization of the pig industry. A boar of high merit for performance traits may be more economical to retain as breeding stock even though some progeny are affected with the disease than a less superior boar whose progeny are unaffected. If stress of the pregnant sow is a factor, control of the disease may be dependent upon the selection of stress-resistant boars and sows.
Concurrent disease should be controlled as producers will tell you that after a period of PRRS infection they had a higher percentage of splayleg piglets. There are also suggestions that induced early farrowing and zearalenone poisoning may also be complicating factors to prevent.
1 Tucek S, Hanzikova V. Physiol Bohemoslav. 1984;33:147.
2 Zelena J. Jirmanova I Zentralbl Vetmed. 1979;26:652.
3 Jirmanova I, Lodja L. Zentralbl Vetmed A. 1985;32:445.
4 Jirmanova I. Vet Res Comm. 1983;6:91.
5 Ducatelle R, et al. J Comp Path. 1986;96:433.
6 Ohnishi N, et al. J Vet Sci. 1989;51:146.
7 Vogt DW, et al. Am J Vet Res. 1984;45:2408.
8 Lax T. J Hered. 1971;62:250.
9 Bradley R, et al. J Comp Path. 1980;90:433.
10 Gilbert FR, et al. Vet Rec. 1967;80:302.
11 Curvers P, et al. Dtsch Tierarztl Wschr. 1989;96:189.
12 Hajek I. Physiol Bohemoslav. 1980;29:145.
13 Lukas Z, et al. Acta Vet Brno. 1978;47:51.
14 Antalikova L, et al. Reprod Nutr Dev. 1996;36:205.
Leg weakness in pigs is a very loose term which includes a wide variety of conditions and is best discarded. In Finland 15% of gilts are culled due to leg weakness.1 Degenerative joint disease would be a much better general term to describe the lameness of young rapidly growing pigs affected with a non-infectious joint disease which includes osteochondrosis (OC), epiphyseolysis, and degenerative osteoarthrosis (OA). The disease is characterized by varying degrees of intermittent but progressive lameness in rapidly growing pigs from 4 to 8 months of age, and pathologically by the presence of OA and OC. The disease is of major economic importance because of the high culling rate of breeding age swine.
Etiology The cause is unknown.
Epidemiology Occurs in majority of breeds of rapidly growing pigs and young breeding females and males. Lesions are commonly present at slaughter. May be related to nutrition and rapid growth rate, genetic predisposition, and type of flooring but no reliable correlations.
Signs These may be no clinical findings or possibly lameness and inability to breed.
Clinical pathology Radiographic evidence of osteochondrosis.
Lesions Osteochondrotic lesions of varying degrees of development, severity and healing.
Diagnostic confirmation Lesions at necropsy.
Other causes of lameness include:
• Polyarthritis due to infectious causes
• Nutritional osteodystrophy due to calcium, phosphorus, and vitamin D imbalance
Control Uncertain. Select breeding stock with sound legs and gait.
The cause of the articular abnormalities is not known. The etiology and factors underlying these syndromes are poorly defined, partly because of the difficulty of definitive clinical examination of affected pigs and the frequent lack of apparent significant pathological changes in necropsy examination of mild cases. There are no specific associations between degenerative joint disease and infectious diseases.2
Recently, a study of 9411 newborn piglets showed that 9.8% were treated for lameness. For parity 3 sows, the level had risen to 11.4%, but by parities 4–7 only 8% were treated. The treatments were in pigs of less than 3 weeks of age in 73% of the cases. Litters with 12 or more pigs had the highest incidences of lameness.3 Osteoarthritic changes are strongly associated with osteochondrotic changes in the humeral and femoral condyles.4 Osteochondrosis has been recorded as early as 1 day of age so the lesions may be congenital. There may be some degree of change in up to 85% of pigs.
The intensification of the swine industry has required that pigs grow rapidly and with high feed efficiency. Under such intensified conditions, rapidly growing pigs develop lesions of the bones and joints, especially the femur. Most pigs near market weight have varying degrees of osteochondrosis (OC). Except for severe lesions, which usually occur in a relatively small proportion of the total population examined, the lesions seen at slaughter often have no detrimental effect on growth rate of pigs up to market weight. An advanced degree of OC however, can result in severe degenerative joint disease and lameness in breeding stock. It is not associated with adventitious bursitis.5
The disease occurs in both male and female pigs and the incidence of lame pigs can be as high as 20–30%. It is a particular problem in gilt and boar testing stations where it may necessitate slaughter of affected animals before the testing period is complete. The lesions develop most commonly in growing pigs, particularly boars from 20 to 30 weeks of age, raised in confinement. The onset occurs when pigs are between 4 and 8 months of age which coincides with a period of maximal growth rate. The peak period of clinical manifestation is from the late grower stage until 18 months of age, although the effect of OA may carry through to the adult period. Extensive multicentric degenerative joint disease in adult sows and boars can cause severe lameness which often warrants euthanasia.6 However, sows ranging in age from 1.5 to 3.0 years and culled for impaired reproductive performance, with no history of lameness may have lesions of the femoral condylar surface.7
Numerous risk factors contribute to the disease. They include nutrition and rate of growth, genetic, and breed predisposition, sex, type and quality of floor, and exercise and confinement. The pig carries 53–51% of its weight on the fore limbs and 46–48% on the hind but the weight supported on the hind is higher at 90 and 105 kg body weight.8 In a study of gilts and sows in Denmark about 12% of gilts showed stiff locomotion but at some point 53% of gilts had at some time showed the same sign. Buck-kneed forelegs, upright pasterns, legs turned out wide, standing under position, and swinging hindquarters were associated with stiff locomotion or lameness. Weak pasterns on the hind feet were associated with stiff locomotion and lameness.9 Weak pasterns on hindlegs and splayed digits on forelegs were associated with brisk movement (freedom from locomotor problems). The following leg weakness signs at the gilt stage were found to have a significant effect on the longevity of the sows: buck-kneed forelegs, swinging hindquarters, and standing under position on the hind legs.
The disease is associated with rapid early growth,10 but it does not appear to be related to protein, vitamins A and D or calcium and phosphorus imbalance in the ration.11 Maximal mineralization of bones is not necessary to prevent leg weakness. Only almost complete absence of calcium and phosphorus causes lameness. Disturbances of the Ca:P ratio below 0.5 or over 3.0 are necessary to produce lameness. Recently, it has been suggested that long-term acidosis may be associated, as bone is not formed as phosphorus is removed from the bone. In this context the acidification of pig diets has been suggested as a contributory cause. It has also been shown that the presence of deformed forelimbs is not associated with low levels of vitamin C in plasma.12 Rapid growth, especially during the early period, was thought to have a significant influence on the occurrence13 and there is also some breed variation in susceptibility. However, in some feeding trials of pigs from weaning to slaughter weight there was no direct effect of rapid growth rate on the incidence and severity of OC. In other feeding trials, average daily gain of gilts was an important factor in the severity of lesions of OC. Decreasing the rate of gain by restricting energy intake appeared to decrease the prevalence and severity of OC when gilts were slaughtered at 110 kg.14 However it was shown that when pigs were fed waste food, and grew more slowly, they had an increased prevalence and score for OC when compared with pigs fed a commercial feed concentrate.15 Decreasing the concentration of protein in the diet of gilts from 16 to 12% resulted in less longitudinal bone growth but did not decrease the incidence of OC.16,17 A simple association between growth rate and the incidence or severity of joint lesions has not been consistently demonstrated and a reduction in growth rate of pigs does not control the disease. A significant favourable association between leg action and daily gain has been noted.18 There has also been speculation that growth hormone could influence the development of lesions of OC by exerting a direct effect on differentiation and colonization of epiphyseal chondrocytes. There is no consistent relationship between the incidence of osteochondrosis and selection of pigs for lean tissue growth rate.19 It may be simply that more feed means more growth which makes stress on developing cartilage worse and therefore predisposes to OC.
Genetic and breed predisposition.
It has been proposed for many years that selection of pigs for increased growth rate resulted in a concomitant increase in the incidence and severity of musculoskeletal disease. Genetic studies indicate that the heritabilities of leg weakness are low to moderate (0.1–0.3).20 A more recent study suggested from 0.01 to 0.42 for leg weakness and OC and that both are associated with production traits (lean% and backfat thickness).14 Genetic analysis of the incidence of OC and leg weakness in the Swedish pig progeny testing scheme revealed a low to moderate heritability. Genetic control of leg weakness has been achieved by various researchers and thus inheritance is probably an important risk factor for this disease complex. The genetics of leg weakness have been described in Finnish Large White and Landrace populations.21 Meaty breeds are worst affected including the Duroc and the Dutch and Swedish Landrace.
Osteochondrosis also occurs in crossbred Wild boar-Yorkshire pigs with a genetically decreased growth rate, raised under the same conditions as finishing pigs.22 The distribution and extent of OC was similar to that of purebred Swedish Yorkshire pigs. This suggests that it is not limited to rapidly growing pigs. Synovial bursae at the hock joints were higher in Large White pigs with straight or bowed hind legs and in Landrace with sickle shaped hind legs.23 There are significant breed differences in the peri-articular and meniscal ossifications seen on X-ray.24 Recently, the quantitative trait loci for locomotion and osteochondrosis-related traits have been identified in Large White x Meishan pigs.25 Correlations between breeding values for longevity and for OC were low but significant, and in a favourable direction. Higher OC scores were associated with a higher risk of being culled.26 It has been seen in wild boar in Slovenia.27
The differences in the incidence and severity of OC between the sexes of different breeds has also been analyzed. The degree of leg weakness and OC of one sex in a breed can neither be translated to the other sex within that breed nor to the same sex of another breed.
Insecure footing because of unfavorable floor surfaces and the presence of foot lesions may change the posture of the animal and cause local overloading of certain joints. The effect of the quality of floor has been examined and there is no clear evidence that hardness of floor contributes to an increased incidence of leg weakness associated with joint disease. However, the incidence and severity of joint lesions may be related to the duration of confinement in pigs confined individually. Exercise will prevent abnormalities such as bow legs, flexion of the carpus and sickle-legs from impairing the mobility of boars, but does not influence the severity of joint lesion. The milder syndromes of poor movement and lameness associated with defects in leg conformation in the grower stage are not necessarily associated with bone or joint lesions and may regress spontaneously or improve if affected pigs are placed on pasture. However, severe lameness at this age, and that which occurs in replacement stock and young adults is frequently associated with severe bone and joint lesions which may be irreversible. A recent study has looked at type of floor (solid floor plus straw, solid floor no straw, and fully slatted).28 The slatted floors were worst for leg weakness and the floors with straw best. The different types of floor affected leg weakness and claw disorders differently.
There is some limited evidence that high lean growth rate may predispose toward leg weakness under confinement rearing. Trauma during handling, penning, and transportation may be associated with a relatively high frequency of OC but the evidence is very limited.29 A high stocking density had an adverse effect on 4 of the leg weakness signs (knock knees, turned out front or hind limbs, standing with the legs under the body).28 A recent study of housing and treadmill training did not show any adverse effects on leg weakness.30 It has even been seen in pigs on grass, on deep litter and in wild boar
In Scandinavia, breeding pigs culled because of lameness had a 100% frequency of OC or OA, and up to 40% of boars in a performance test station had osteochondrosis or osteoarthrosis.6 A conservative estimate suggests that 3% of sows and 10% of boars are culled for unsoundness associated with OC and OA.6 The hidden costs include a reduced pool for selection of high-performance boars and gilts, the maintenance of pigs which cannot be used for breeding, increased mortality among piglets crushed by lame sows, reduced feed intake and growth rate in lame pigs, and transportation costs of replacement stock.
The condition has been seen as early as 1 day and with age the lesions develop. The essential lesion is the necrosis of cartilage canals and surrounding cartilage.31,32 They may be seen to be developing and healing at the same time. In growing animals, the superficial layer of joint cartilage is articular cartilage, and the deeper layer is epiphyseal cartilage which undergoes endochondral ossification as the animal matures. The articular cartilage persists in the mature animal while the epiphyseal cartilage becomes a layer of calcified cartilage and underlying subchondral bone. The cartilage of the physis is known as the growth plate and is involved in metaphyseal growth. The normal growth plate cartilage has a well-ordered structure with the chondrocytes of the proliferative and hypertrophic regions arranged into columns.
Osteochondrosis is a generalized disease in which there are focal areas of failure of endochondral ossification in the physeal (metaphyseal growth) and epiphyseal growth cartilages. The underlying defect may be an abnormality of the chondrocytes which do not undergo normal hypertrophic ossification. They accumulate rough endoplasmic reticulum, lipid droplets and mitochondria. The surrounding matrix contains deposits of electron-dense material which may prevent normal vascularization and therefore ossification. The hypertrophic region is disorganized and greatly extended compared to normal tissue.33 The matrix surrounding the clustered chondrocytes is altered compared to that in normal cartilage.34 The primary abnormality is an increased thickness of the joint cartilages combined with degenerative changes which result in infoldings and erosion of articular cartilages. Defects of the growth plates (physes) result in short deformed bones.
Pathologically, severe clinical cases are characterized by osteochondrosis and secondary degenerative joint disease especially involving the medial aspects of the larger joints, epiphyseolysis and lumbar intervertebral disc degeneration and spondylosis. Osteochondrosis has been used to encompass lesions involving the physes and the articular epiphyseal complexes. However, because of morphological changes that have been observed in growing pigs, dyschondroplasia is now the preferred term to be used generically and then qualified by the location and nature of the morphological description since the causes may be different.
Osteochondrosis occurs commonly in growing pigs at predilection sites of the medical condyle of the humerus and femur, the epiphyseal plates of the distal ulna and the femoral head and the intervertebral joints. The 6th–8th costochondral junctions may also be affected. It may heal spontaneously or it may progress to osteochondritis dissecans and OA. Its progression in either direction is influenced by local loading and by joint stability which depends upon joint shape and muscle and ligamentous support. The age-related changes and OC in the articular and epiphyseal cartilage have been described.35 The cartilage increases with age up to 5 weeks and then begins to decrease in thickness. Deleterious influences such as defects in conformation, heavy muscling with skeletal immaturity, muscular weakness resulting from myofibrillar hypoplasia, myopathies or lack of exercise, inadequate flooring or even simple trauma may adversely affect this progression and lead to severe skeletal change.
Porcine synovial fluid contains both hyaluronic acid and chondroitin sulfate and the chondroitin sulfate-to-hyaluronic acid ratio is not influenced by relatively advanced stages of osteochondrosis. Treatment of lame boars with glycosaminoglycan polysulfate improves leg soundness score and results in an increase in the hyaluronic acid concentration of the cubitus joint synovial fluid, and an increase in the proportion of aggregated proteoglycans in the articular cartilage of the medial femoral condyle. It is suggested that the hyaluronic acid accounts for most of the viscosity of synovial fluid and for efficient lubrication of the joint.
Well-established lesions typical of OC associated with the physes can be found in young pigs between 25 and 30 days of age.6 The earliest change associated with a dyschondroplasia of the physis is a focus of persistent hypertrophied chondrocytes which do progress but heal. Lesions associated with physes and articular epiphyseal complexes develop continuously and regress as pigs grow older. Changes in cartilage canal vessels appear to be important in the pathogenesis.36 There is no evidence that vascular damage is a factor in the pathogenesis of the lesions.
Because foci of dyschondroplastic lesions are associated with physes of pigs between birth and the stage of rapid growth, they could be regarded as part of the usual growth patterns in contemporary commercial swine. However, clinical signs of dyschondroplasias, or degenerative joint disease secondary to dyschondroplasias, usually do not appear until pigs are almost 6 months of age.
Osteochondrosis can be diagnosed radiologically.13 Radiologically the lesions were similar in Yorkshire, and Landrace37 but more severe in the Landrace and similar to the Danish Landrace.
The development of epiphyseal osteochondrosis in pigs from 42 to 147 days of age has been followed radiologically.38 Osteochondrotic lesions were seen radiologically in the articular-epiphyseal (A–E) complexes of the humeral condyles of 42-day-old pigs and in the femoral condyles at 63 days of age in contrast to earlier reports which indicated that lesions were not visible radiologically until 100 days of age. The osteochondrosis lesions of the A–E complexes develop, become progressive, and subsequently become either stable, regressive, or even more progressive as the pigs grows. This supports the observations that the lesions develop and become progressive and regress as the pigs grow. The humeral medial condyles have more pronounced lesions and are more frequent than the lateral ones.
Radiological monitoring of the development and sequelae of physeal osteochondrosis lesions of the growth plate cartilage and A–E complexes of the fore and hind limbs in young breeding swine found that the majority of distal ulna lesions healed by 18–20 months and some started fusing at 18–21 months. The distal ulna healed without complications in most animals and the most severe lesions healed faster than the mild or moderate ones.38 In a recent study peri-articular ossifications at the elbow joint were found in the radiographs at a prevalence of 0.9%.4 Meniscal ossifications were seen as single or multiple foci at the cranial aspect of the joint at a prevalence of 2.6% and had a bilateral occurrence of 20%.4,39 Meniscal ossifications were associated with hind legs turned out and stiff locomotion in the hind leg and negatively associated with growth rate.
The syndrome is called leg weakness and varies in severity from locomotor abnormality that results from conformation and leg defects such as narrow lumbar area and broad hips, hyperflexion of the carpus, bowing of the forelimbs and ‘knock knees’, hyperextension of the phalanges, lateral angulation of the foot and sickle hocks to more severe lameness and, in the extreme, inability to rise and paresis. Nine leg weakness signs were described.28 The signs listed include buck kneed forelegs, steep hock joints, fore and hind limbs turned out, upright pasterns on the hind legs, stiff locomotion, standing under on the hind limbs, swaying hindquarters, goose stepping hind legs, lameness and tendency to slip,4 and the four most common signs were buck knees, small inner claws on forefeet, small inner claws on hind feet, and upright pasterns on the hind legs.4,40
The clinical syndrome is a locomotor disorder usually involving the hindlimbs. Often the most rapidly growing pigs are lame. The lameness may be acute, intermittent, chronic, progressive, or a combination of these. An insidious onset is common, and pigs are unwilling to move, the stride is shortened, and the limbs are held in partial flexion. The carpal joints may be under extended, the metacarpophalangeal joints are overextended, giving the limb an abnormal S-shaped profile.6 The pelvic limbs are commonly held straight and the back is slightly arched. In some cases, affected animals will assume a kneeling position with flexed carpal joints and walk on those joints.
Mild cases show stiffness, especially immediately after a period of lying down and lameness. Slowness to rise and a tendency to walk with short steps on tiptoes frequently in association with a marked inward curve of hindlimb motion during forward progression and side-to-side motion of the buttocks is frequently seen. More severely affected pigs sit on their hindquarters and are reluctant to stand. They carry one or both hindlimbs more forward under the body and walk with a short goose-stepping gait. Wasting is not a feature except in severely affected animals and the locomotor disorder may be minor unless exacerbated by physical exertion.
The syndrome is of particular importance in breeding animals where it may interfere with successful mating. Boars may show initial interest in mounting but subsequently slide off the sow or dummy before mating is complete, presumably due to the pain of the limb lesions. In Europe this problem has been called impotentia coeundi.
There may be no meaningful association between visual scores for physical soundness in the live animal and the degree of joint damage.41 Some pigs with severe lesions are not lame and conversely other pigs are severely lame with minor lesions. Epiphyseolysis of the femoral head produces severe unilateral lameness and if bilateral is usually manifest by marked reluctance to rise and severe locomotor disability. Initial signs are frequently deceptively mild and follow physical exertion such as mating, transport, farrowing, or fighting but they progress to severe lameness over a 7–10-day period.
Epiphyseolysis of the tuber ischii (Apophysiolysis) may also occur following physical exertion but is more common in second or third parity sows and is manifest by ‘paralysis’ with the hindlimbs in forward extension under the body of the sow.42 These animals ‘dog sit’, and are unable to rise. In many instances the injury occurs when the animals arrive on the farm or are first mated.
Because of the pain and muscle contraction, it is frequently difficult to determine the site and severity of the lesion by simple clinical examination, and palpation following general anesthesia or radiography may be required for proper clinical assessment. Physical examination should include complete palpation of all limbs for warmth, swelling, and pain. The palpable parts of the pelvis should be examined with particular emphasis on the ischial tuberosities. Passive flexion, extension and rotation of each limb along with auscultation over the joint may reveal evidence of crepitus or a pain response.
While the lesions of the physes and articular epiphyseal complexes are detectable in pigs under 14 days of age they are not detectable radiographically in live animals until the pigs are over 100 days of age. Only 21% of the lesions associated with the physes and 22% of the lesions associated with the articular epiphyseal complexes were detectable in radiographs of bones of live pigs.
Meniscal ossifications were observed as simple or multiple small smooth firm and irregular swellings in the cranial horn of the lateral meniscus.24 The peri-articular osseus foci were seen as focal firm swellings at the cranio-medial aspect of the elbow joint.24
The carpal, elbow, tarsal, and stifle joints can be radiographed for evidence of joint lesions, and the lesions scored according to a system.38 It is also possible to use ultrasonics for diagnosis.43
The histological, radiological, and angiomicrographical findings of dyschondroplasias of the growth cartilages in crossbred commercial pigs at 1 and 15 days of age have been described. The bone lesions in clinically normal and lame pigs have been described.44,45 The scapulohumeral, humeroradioulnar, carpal, coxofemoral, femorotibial, and tarsal joints should be examined. Typically, in osteochondrosis, the changes are feathery hypertrophy of villi, focal full-thickness cartilage buckles, ulcers of flaps, and no change in the draining lymph node. Joint mice and synovitis may also be seen. Deformation may take place in the long bones or even fractures. Histologically, osseus trabeculae may be seen with clusters of chondrocytes, and between the trabeculae lined by flat osteoblasts there are adipocytes. The osseous center was formed of mineralized cartilage that blended into more or less fibrous cartilage but towards the joint cavity the meniscal ossifications were covered by hyaline cartilage.24
Occasional cases involve the patella in breeding age pigs.16
The ultrastructural characteristics of normal epiphyseal cartilage of the articular epiphyseal cartilage complex in growing swine has been examined and found to be different from the articular cartilage and the cartilage of the physis.46 Histochemical techniques are now used to characterize lesions of osteochondrosis and the lesions associated with articular-epiphyseal cartilage complexes should be considered as different entities.35 Osteopenic lesions have been described.47
The syndrome must be differentiated from other diseases which cause lameness and paralysis in growing and young adult pigs which includes: infectious polyarthritis, laminitis, traumatic foot lesions, foot lesions produced by biotin deficiency and footrot, osteodystrophy resulting from calcium, phosphorus and vitamin D imbalance in rations, vitamin A deficiency and viral encephalomyelitis.
There is no effective treatment. Early cases may recover spontaneously after being placed outside on pasture or housed individually inside on deep straw litter. Recently, it has been suggested that meloxicam at a dosage of 0.4 mg/kg is efficacious and safe for the treatment of non-infectious locomotor disorders in pigs. Treatment with 2,5-D vitamin D had no effect on the incidence and severity of OC/OA lesions.48 Animals that are affected with clinical signs should be removed from the herd quickly and, if necessary, should be humanely destroyed as soon as possible.
Because the etiology is unknown, it is not possible to provide specific control measures. The hereditary nature of the disease suggests that the selection of breeding stock with sound legs and a low incidence of lesions would be an effective long-term control measure. Genetic control of leg weakness has been documented by various researchers.41 Selection of boars for leg soundness has dramatic effects on the structural soundness of their crossbred progeny and therefore selection of structurally sound replacements must be maintained if leg weakness in market or breeding pigs is to be avoided.49 Divergent selection for leg soundness in Duroc pigs has been dramatic.49 Progeny of leg-soundness sires had significantly better measures for all leg traits at 104 kg than did progeny of leg-weakness sires.35 Differences between the two progeny groups indicated that the realized heritability for front leg soundness exceeded 0.50.35
Selection of breeding stock will require careful genetic selection, examination of all pigs which are to be retained for breeding, necropsy of siblings of affected pigs and of the same gender, to identify genetic lines of pigs which have a low incidence of lesions. A recent study showed that the increase in wild boar alleles in crosses with Large White pigs reduced the prevalence of OC.50 It has been suggested that the selection of pigs based on the joint lesion score could lead to a better leg and joint condition both optically and pathologically.51 The reduction of growth rate and exercise may help but are not a real method of control. Increase in calcium and phosphorus in the diet also does not help.
Grondalen T. Osteochondrosis, arthrosis and leg weakness in pigs. Nord VetMed. 1974;26:534.
Hill MA. Economic relevance, diagnosis and counter measures for degenerative joint disease (osteo arthrosis) and dyschondroplasia (osteochondrosis) in pigs. J Am Vet Med Assoc. 1990;197:254-259.
Hill MA. Locomotory Diseases of Swine. Keynote lecture Proceedings of the 15th International Pig Veterinary Society Congress, Birmingham, England, July 1998; Vol 1, p. 181–194.
Ytrehus B, Carlson CS, Lundeheim N, Mathiesen L, Reinholt FP, Teige J, Ekman S. Vascularisation and osteochondrosis of the epiphyseal growth cartilage of the distal femur in pigs-development with age, growth rate, weight and joint shape. Bone, 34:454–465
Orth MW. The replication of growth plate cartilage turnover. J Anim Sci. 1999;77:S183-S189.
Ekman S, Carlson CS. The pathogenesis of articular osteochondrosis. Veterinary Clinics of North America Small Animal Practice. 1998;28:17-29.
1 Kangasniemi R. Proc NJF-Seminar, no 25 Foul UMN. 1996;40:59.
2 Kawrisuk LS, et al. Am J Vet Res. 1987;48:1395.
3 Zoric M, et al. Vet Rec. 2003;153:323.
4 Jorgensen B. Acta Vet Scand. 2000;41:123.
5 Moutttotou N, et al. Prev Vet Med. 1999;39:31.
6 Hill MA. J Am Vet Med Assoc. 1990;197:254.
7 Nakano T, Aherne FX. Am J Anim Sci. 1993;73:1005.
8 Deguchi E. Anim Sci Tech. 1997;68:399.
9 Jorgensen B. Acta Vet Scand. 2000;41:105.
10 Lium B. Norsk Vet Med. 2002;114:209.
11 Kornegay ET, et al. Can J Anim Sci. 1990:70.
12 Armocida A, et al. J Vet Med Sci A. 2001;48:165.
13 Jorgensen B. Live Prod Sci. 1995;41:171.
14 Fukawa K, Kusuhara S, et al. Asian-Aust J Anim Sci. 2001;14:114.
15 Fjetland O, et al. Proc. 15th Int Pig Vet Soc Cong 1998; p. 278.
16 Blowey RW. Vet Rec. 1994;134:601.
17 Woodard JC. Vet Pathol. 1989;24:109.
18 Webb AJ, et al. Anim Prod. 1983;36:117.
19 Stern S, et al. Livestock Prod Sci. 1995;44:45.
20 Jorgensen B, Vestergaard T. Acta Agric Scand. 1990;40:59.
21 Serenius T, et al. Live Prod Sci. 2001;69:101.
22 Uhlorn H, et al. Acta Vet Scand. 1995;36:41.
23 Schulze V, et al. Zuchtungskunde. 1998;70:43.
24 Jorgensen B, Jensen HE. J Vet Med A. 2002;49:353.
25 Lee GJ, et al. Anim Sci. 2003;76:155.
26 Yazdi MH, et al. Anim Sci. 2000;71:1.
27 Stukelj M. Vet Novice. 2002;28:40.
28 Jorgensen B, et al. Anim Sci. 2003;77:439.
29 Nakano T, Aherne FX. Am J Vet Res. 1988;52:154.
30 Petersen JS, et al. Anim Sci. 1998;66:725.
31 Carlson CS, et al. J Orthop Res. 1991;9:317.
32 Carlson CS, et al. Am J Vet Res. 1988;49:396.
33 Wardale RJ, Duance VC. J Cell Sci. 1994;107:47.
34 Ekman S, Heinegard D. Vet Pathol. 1992;29:514.
35 Hill MA, et al. Vet Rec. 1990;127:29.
36 Visco DM, et al. Vet Rec. 1991;128:221.
37 Jorgensen B, Andersen S. J Anim Sci. 2000;71:427.
38 Bittegeko SBP, Arnbjerb J. J Vet Med Assoc. 1994;41:369. 377
39 Jorgensen B, Jensen HE. J Vet Med A. 2002;49:353.
40 Serenius T, et al. Live Prod Sci. 2001;69:101.
41 Boggess MV, et al. J Anim Breed Gen. 1989;106:44.
42 Done SH, et al. Vet Rec. 1979;105:520.
43 Takahara M, et al. Am J Roentgenol. 2000;174:411.
44 Yamasaki K, et al. J Comp Pathol. 1989;100:313.
45 Yamasaki K, Itakura C. J Comp Pathol. 1988;98:415.
46 Farnum CE, et al. Vet Path. 1984;21:141.
47 Hagemoser WA. J Vet Diag Invest. 2000;12:525.
48 Jefferies D, et al. Vet Rec. 2002;23:383.
49 Rothschild MF, Christian LL. Livestock Prod Sci. 1988;19:459. 473
This is a non-contagious disease of horses characterized by acute fever, lymphangitis and severe swelling of one or both hindlegs – forelimbs are rarely, if ever, affected. The disease commences abruptly with fever (40.5–41°C, 105–106°F), shivering and a rapid pulse rate and respiration. Pain in the acute disease can be severe. There is severe pain on palpation of the affected leg and lameness may be so severe that the horse may refuse to put its foot to the ground. The limb is swollen and hot; the swelling extends from the top of the leg and down to the coronet. There is cording of the lymphatics on the medical aspect of the leg and palpable enlargement of the lymph nodes in some horses. The acute disease resolves into a chronic phase with persistent and variable swelling of the leg, intermittent fever, and variable lameness. Occasionally abscesses develop in the lymph nodes and vessels but usually there is no localization of the infection. There is a tendency for the disease to recur and cause chronic fibrotic thickening of the lower part of the limb extending to the level of the stifle in many horses. Swelling of the leg is often exacerbated by late pregnancy.
Sporadic lymphangitis can be associated with superficial wounds and ulcers on the lower parts of the limbs, but often there are no wounds detected. The disease is thought to develop as a lymphangitis and, potentially, lymphadenitis of the deep inguinal nodes as a result of these wounds. The affected lymph nodes and swelling of the limb obstruct lymphatic and venous drainage causing lymphatic obstruction, edema and, in some cases, cellulitis.1 Ultrasonographic examination reveals distended lymph vessels that contain fluid that is not echogenic. Ultrasound guided aspiration of this fluid yeilds fluid with a low total protein concentration and mild neutrophilia (high proportion of the cells present in the fluid are neutrophils, although the absolute count is usually less than 1.0 × 109 cells/L. Culture of the fluid is recommended, and Actinobacillus sp. have been obtained. The clinical significance of results of culture of the fluid is unknown, but results could be used to guide choice of antibiotics. Radiographic examination is usually unremarkable apart from demonstrating the soft tissue swelling. Affected horses, in both the acute and chronic stages, have a mild neutrophilia and hyperfibrinogenemia.
Acutely affected horses should be treated aggressively. The principles of treatment are control of the presumed infection, reduction of inflammation, and reduction of swelling. Penicillin or other antimicrobials should be administered parenterally to control the infection. Non-steroidal antiinflammatory drugs (phenylbutazone, flunixin meglumine, carprofen, or similar) should be administered to control the inflammation and provide pain relief. The limb should be hosed with cold water once to twice daily to reduce heat and provided with gently massage therapy. Manual massage of the limb might be beneficial. Supportive, compressive bandaging of the limb can reduce the swelling. The horse should be exercised as much as is practical and humane.
Horses with chronic disease should be treated with prolonged courses of antimicrobials (penicillin, sulfonamide-trimethoprim combinations, enrofloxacin, or rifampin in combination with sulfonamides-trimethoprim), non-steroidal drugs, and local therapy. Acute exacerbations can be managed by administration of dexamethasone (40 μg/kg orally or parenterally, once daily for 5 days, and then gradually tapering). This dose is not abortifacient in pregnant mares. Exercise and supportive bandaging are important in minimizing the swelling. The chronic disease requires prolonged and intermittent therapy, often for the rest of the horse’s life.
Prevention of the disease necessitates prompt and careful treatment of all wounds of the lower limbs. Provision of daily exercise, restriction of the diet during prolonged rest periods and dry standing in the stable also help to prevent the disease.
Etiology Degeneration of the sensitive laminae of the hoof.
Epidemiology Disease involving single animals. As a sequela to severe systemic disease including colic, diarrhea, metritis, and grain engorgement. Horses or ponies at pasture. Horses worked on hard surfaces. Obese horses and ponies. Horses with unilateral lameness may develop laminitis in the contralateral, supporting limb.
Clinical signs Lameness, ranging from mild to sufficiently severe to cause the horse to be recumbent, involving both front feet, and occasionally all four feet.
Clinical pathology None characteristic of the disease.
Diagnostic confirmation Physical examination. Radiography.
Treatment There is no single effective treatment. Non-steroidal anti-inflammatory drugs, dimethyl sulfoxide, vasodilatory agents, anticoagulants, frog and sole support, and corrective hoof trimming and shoeing are all used with variable success.
Control Prophylaxis for acute, severe diseases. Aggressive treatment of metritis, colic and diarrhea. Prevent unrestricted access to feeds rich in soluble carbohydrates. Maintain optimal body condition.
Laminitis is caused by acute degeneration of the sensitive primary and secondary laminae of the hoof. The cause of this degeneration is unknown although a number of theories have been propounded and are summarized under ‘Pathogenesis’. Situations that are associated with increased risk of laminitis include access to lush pasture (suspected as the cause in 46% of field cases), grain overload (7%), retained placenta (2%), and colic or diarrhea (3%).1 Ingestion of large quantities of soluble carbohydrate, such as grain, bread, calf feed, or exposure to shavings of black walnut (Juglans nigra) causes laminitis.
Single sporadic cases are the rule for horses in which the disease is usually related to individual risk factors such as obesity, systemic illness, or lameness. An estimated 13% of horse operations in the United States have a horse with laminitis at any one time, and laminitis accounts for 7.5 to 15.7% of all lameness in horses.1 Laminitis accounts for up to 40% of hoof problems in horses, depending on the use of the horse.1 Approximately 5% of horses with laminitis die or are euthanized.1 Among cases occurring in the field (as opposed to veterinary hospitals) approximately 74% recover and become sound, with 8% improving but continuing to be lame.1 However, approximately 10% of horses that developed laminitis had a permanent change in their primary use as a result of having developed laminitis.1
With the exception of overweight ponies and horses with systemic disease, there are only a few identified innate factors that predispose individual horses to the development of laminitis:
• Any association between the disease and age, sex or breed is weak, again, with the exception of ponies.2 There is no difference in risk among horses used for pleasure riding, showing, breeding, racing, or farm and ranch work.1
• The disease is more common in the United States during spring and summer (1.3% in spring and 0.4% in winter in the central US).1
• The disease is very uncommon in foals and horses < 8 months of age, and then increases in frequency with increasing age such that horses >20 years of age have an incidence of the disease roughly 3 times that of horses between 5 and 20 years of age.1
• Overweight ponies appear to be most susceptible and the disease occurs four times as commonly in them as in other classes of horse.3 Fat ponies at pasture and getting little exercise commonly develop the chronic form of the disease.
• Laminitis is common in horses with tumors of the intermediate lobe of the pituitary (pars intermedia dysfunction, equine Cushing’s disease).
Trauma and other physical factors such as excessive work on hard surfaces, increased weight bearing on one limb, and persistent pawing contribute to the development of the disease in horses. Standing for periods of days during transport may predispose to laminitis. For horses that are severely lame, and not bearing weight in the affected limb, the risk of developing laminitis in the contralateral limb is related solely to the duration of lameness and not to body weight.4
Laminitis is associated with many systemic illnesses of horses. Horses with illness attributable to colic, diarrhea, pleuropneumonia, and metritis are prone to develop laminitis. Potomac horse fever (equine neorickettsiosis) is frequently a cause of laminitis in horses and laminitis is the major cause of mortality from this disease. Approximately 28% of horses with anterior enteritis (duodenitis/proximal jejunitis) develop laminitis, usually within 2 days of developing enteritis.5 There are anecdotal reports that suggest that administration of corticosteroids (dexamethasone, triamcinolone) causes or exacerbates laminitis, but this association has not been proved. Laminitis is common in horses that engorge on grain or similar feeds containing a high concentration of soluble carbohydrates. Ingestion of large quantities of lush pasture has been anecdotally associated with increased risk of laminitis, especially amongst ponies. It is believed that the presence of a high concentration of soluble carbohydrates fructans in the grass is responsible for the increased risk of laminitis.6 Fructans are metabolized in the large colon and may mimic the situation after ingestion of a large quantity of soluble carbohydrate.
The basic lesion of laminitis is the separation of the sensitive laminae of the third phalanx from the interdigitating laminae lining the internal surface of the hoof, so that the third phalanx drops through the hoof and comes to rest on the sole. Exactly what the mechanism is that links the risk factors listed above to the laminar degeneration, the basis of the separation, is unknown. Briefly, the theories are:
• Ischemia of the laminae with subsequent necrosis. Proposed causes of ischemia include vasoconstriction, development of arterio-venous shunts, interstitial edema, and presence of microthrombi in digital vessels.7-13 Ischemia due to microthrombus formation is considered an unlikely cause of laminitis.7,8 However, there is evidence from experimental laminitis that changes in circulating concentrations of vasoactive amines or contractile activity of vessels in the hoof might contribute to ischemia. Alternatively, increases in capillary filtration pressure, resulting from venoconstriction, might cause edema and increased interstitial pressure with subsequent ischemia of the laminae.13 It is plausible that there is a combination of these mechanisms, beginning with digital venoconstriction and ending in arteriovenous shunting and development of microthrombi.14 There is evidence in horses with gastrointestinal disease treated by emergency celiotomy that endotoxemia after surgery is associated with lower digital blood flow and higher concentrations of endothelin-1, providing evidence for a role of decreased laminar blood flow in the pathogenesis of the natural disease.15
• Inflammation, with subsequent degeneration of sensitive laminae.16-18
• Enzymatic digestion of laminae by matrix metalloproteins (MMPs) induced by circulating factors including products of Streptococcus bovis infection.19,20
• Abnormalities in local (hoof) metabolism of corticosteroid resulting in increased glucocorticoid activity in lamellar tissues.21
There is evidence of each of these mechanisms. The evidence is often based on experimental models of laminitis and the findings differ somewhat with respect to the model used and markedly with the stage of disease studied. More recent studies, focusing on the developmental stage before clinical signs are apparent, have identified evidence of inflammation associated with a marked increase in expression of cycloxygenase-2, an enzyme critical in the metabolism of vasoactive and inflammatory prostaglandins and inhibited by non-steroidal antiflammatory drugs.16
It is speculated that a pain-hypertension-vasoconstriction cycle develops in horses with acute laminitis. The pain associated with the laminar degeneration causes release of vasoconstrictor substances such as the catecholamines, angiotensin II, and vasopressin. These substances then cause peripheral vasoconstriction with a subsequent reduction in blood flow to the foot, and systemic hypertension.
The common thread is that degeneration of the sensitive laminae. Loss of the connection between the third phalanx and hoof allows the third phalanx to rotate within the hoof capsule, likely in response to the torque applied by the deep digital flexor tendon, and to displace ventrally (sink) within the hoof as a result of weight transmitted through the third phalanx; or there may be a combination of these changes. Rotation of the third phalanx causes the sole to be pushed downward or ‘dropped’, and the point of the toe of the third phalanx may actually penetrate the sole. Serum accumulates in the space created by degeneration of the laminae and displacement of the third phalanx and there is breakdown of the white line.
Many of the inciting causes of laminitis are diseases that may be associated with endotoxemia, and in experimental models endotoxin was detectable in the blood of horses that developed laminitis, suggesting that endotoxin may contribute to the development of the disease. However, infusions of endotoxin do not cause laminitis, although endotoxin does impair endothelium-dependent relaxation and augments adrenergic contraction of palmar digital arteries.22
The disease occurs in 3 distinct phases: (1) a developmental stage in which lesions are detectable in the sensitive laminae but during which there are no clinical signs; (2) the acute phase from the development of the first clinical signs through to rapid resolution or to rotation or ventral displacement of the third phalanx; and (3) the chronic stage evidenced by rotation of the third phalanx with or without ventral displacement and characterized by variable but persistent pain.
The disease presents as both an acute disease and as a chronic disease. The severity of the acute disease varies considerably from very mild with rapid (5–7 days) recovery, to severe with progression to the chronic, refractory stage.
The acute disease develops rapidly; apparently normal horses can founder within hours. Signs of the disease are entirely attributable to pain in the feet. All hooves may be affected, but more commonly the fore feet are affected and the hind feet are spared. The disease is rarely unilateral except in cases in which the disease develops because of severe lameness in the contralateral limb or repeated pawing. Mild, or early, disease is apparent as a resistance to movement and repetitive and frequent shifting of weight from one foot to the other. There is a characteristic shuffling gait.
More severe disease is apparent as refusal to move or to lift a hoof. At this stage the horse wears an expression of great anxiety, accompanied by muscle fasciculation, sweating, a marked increase in heart rate to as high as 75/min, rapid, shallow respiration, and a moderate elevation of temperature. There is a characteristic posture with all four feet being placed forward of their normal position, the head held low, and the back arched. There is usually a great deal of difficulty in getting the animal to move and when it does so the gait is shuffling and stumbling and the animal evidences great pain when the foot is put to the ground. The act of lying down is accomplished only with difficulty, often after a number of preliminary attempts. There is also difficulty in getting the animals to rise and some horses may be recumbent for long periods. It is not unusual for horses to lie flat on their sides. In occasional cases the separation of the wall from the laminae is acute and the hoof is shed. There may be exudation of serum at the coronet and this is considered a sign of impending sloughing of the hoof and a poor prognosis.
The diagnostic signs in laminitis include pain on palpation around the coronet and a marked withdrawal response when hoof testers are applied to the hoof. The intensity of the pulse in the palmar digital artery, palpable over the abaxial aspects of the proximal sesamoid, of affected feet is markedly increased over normal. In horses in which the third phalanx is displaced distally (sinks), a concavity may be palpable at the coronary band. Infiltration of the palmar digital nerves at the level of the proximal sesamoid with local anesthetic agents provides marked, but not complete, relief.
In the chronic stages of the disease there is separation of the wall from the sensitive laminae and a consequent dropping of the sole. The hoof wall spreads and develops marked horizontal ridges, and the slope of the anterior surface of the wall becomes accentuated and concave. Horses with chronic or refractory laminitis may continue to feel much pain, lose weight, and develop decubitus ulcers over pressure points because of prolonged recumbency. Loss of integrity of the sole and disruption of the white line may allow infection to develop in the degenerate laminae. The infection may spread to involve the pedal bone, causing a septic pedal osteomyelitis. The lameness may abate but the animal becomes lame easily with exercise and may suffer repeated, mild attacks of laminitis.
Radiographic examination of the feet may not reveal, initially and in mild cases, changes in the position of the pedal bone. Radiographs of more severe or advanced cases will demonstrate rotation of the pedal bone within the hoof, evident as a tilting of the most distal aspect of the third phalanx toward the sole. The space created by rotation of the pedal bone may fill with gas or serum and be evident as a radiolucent line between the pedal bone and the dorsal hoof wall. Displacement of the pedal bone toward the sole will be evident in approximately 25% of cases as a thickening of the dorsal hoof wall and reduction of the distance between the sole and solar aspect of the pedal bone. Chronic or refractory cases may have osteopenia of the pedal bone with proliferation of bone at the toe.
The radiographic examination provides information of prognostic value. Horses that return to their previous level of athletic function after a bout of laminitis have pedal bone rotation of less than 5.5°, whereas horses that can no longer perform as athletes usually have more than 11.5° of rotation.23 However, there is considerable overlap between groups and these values should only be used as rough guidelines. The general rule is that the greater the degree of rotation, the worse the prognosis for return to function and pain-free living.
Objective radiographic variables include the distance between the proximal aspect of the hoof wall (marked on the radiographic image by a piece of wire or strip of metal stuck to the dorsal hoof wall) and the proximal limit of the extensor process of the distal phalanx (the ‘founder’ distance), and the distance between the dorsal hoof wall and the dorsal cortex of the distal phalanx.24 While values for these measures vary among breeds and with the size of the horse, most normal horses will have a ‘founder’ distance of 4.1 ± 2.2 (standard deviation) mm and a wall thickness of 16.3 ± 2.4 mm.24
The disease is not usually fatal but if a necropsy examination is carried out on an acute case, the stomach usually contains excessive amounts of grain, which has a pasty, mealy consistency and an odor suggestive of putrefaction of protein. Retained placenta and metritis may be present in postparturient laminitis in mares. No other reliable gross findings are visible, although the vessels of the sensitive laminae of the digital cushion may appear engorged if the cut surface of the hoof is examined.
In subacute and chronic cases the diagnosis can easily be confirmed by gross examination of sagittal sections of the foot. This permits assessment of the horny, soft, and osseous components of the foot. In some cases the degree of rotation of P3 results in perforation of sole.
Histological examination is required only in acute cases and confirmation of the diagnosis in such instances demands that the foot be cut into slab sections and fixed shortly after the death of the animal, before even moderate autolysis can ensue. Microscopically, the sequence of acute changes in experimentally induced laminitis begins with the loss of some of the keratogenic structures of the epidermal laminae. This is followed by vascular engorgement, edema and some necrosis of laminar tissues.
Acute laminitis is an emergency and treatment should be started without delay, as early and aggressive therapy might enhance the chances of recovery.
The adage ‘where facts are few experts are many’ (Donald R. Gannon) applies well to the treatment of laminitis. There are no well-designed studies of the treatment of naturally occurring laminitis and thus the choice of treatment is based on personal experience, extrapolation from our imperfect understanding of the pathogenesis of the disease, the availability of certain drugs, and current fashion. In general, the treatments can be grouped into several classes, based on the intended intervention. These are:
• Removal of the causative agent or treatment of the inciting disease
• Pain relief and minimization of inflammation
• Vasodilation of blood vessels in the foot
• Prevention of formation of microthrombi in dermal capillaries
• Prevention of rotation or distal displacement of the pedal bone
The efficacy of administration of analgesic, anti-inflammatory, anticoagulant and vasodilatory drugs, local therapy such as ice baths of the hoof or having the horse stand in cold water, and mechanical support of the hoof has never been demonstrated in appropriate clinical trials.
The inciting disease should be treated aggressively and every attempt made to remove any causative agent. Horses with traumatic laminitis should be rested and housed in stalls that are well bedded with sand or soft shavings. Horses suspected of having a tumor of the intermediate lobe of the pituitary gland should have the diagnosis confirmed and appropriate therapy instituted.
A mainstay of the treatment of both acute and chronic laminitis is the use of non-steroidal anti-inflammatory drugs (NSAIDs). Apart from the obvious humane requirement of providing pain relief, the use of NSAIDs is speculated to be beneficial by breaking the pain-hypertension-peripheral vasoconstriction cycle that may be important in the pathogenesis of laminitis. Furthermore, recent evidence suggesting that inflammation mediated by COX-2 plays a role in the developmental phase of laminitis supports the early and aggressive use of NSAIDs.16 Phenylbutazone, at doses of 2.2–4.4 mg/kg intravenously or orally every 12–24 hours, is an effective analgesic in cases of mild to moderate laminitis. Higher doses (6.6 mg/kg every 12–24 hours) may be required in severe cases. However, the potential for phenylbutazone toxicosis, evident as colic, gastrointestinal ulceration, nephrosis, hypoproteinemia, leukopenia, and hyponatremia, is dose related and high doses of phenylbutazone should only be used for at most several days and only in severely painful horses. Flunixin meglumine (1.1 mg/kg, IM or IV every 8–12 hours) and ketoprofen (2.2 mg/kg, IM every 12–24 hours) are also effective analgesics.25 Their concurrent use with phenylbutazone may enhance pain relief but also increases the risk of NSAID toxicosis. The use of aspirin is dealt with under Anticoagulants.
Dimethyl sulfoxide (DMSO), a putative anti-inflammatory drug that is also reputed to scavenge free radicals, has been used in the treatment of acute laminitis, again without clear demonstration of its efficacy. DMSO is administered at a rate of 1 g/kg, intravenously as a 10% solution in isotonic sodium chloride. The treatment can be repeated daily for several days.
Narcotic analgesics such as butorphanol and meperidine (pethidine) provide some pain relief but in general are not as effective as the NSAIDs. Similarly, α-2 agonists such as xylazine and detomidine provide only brief respite from the pain, and may be contraindicated because of the vasoconstriction associated with their use.
Local analgesia of the foot with agents such as lidocaine or bupivacaine provides marked pain relief. However, analgesia is usually only brief, depending on the agent used, and has the disadvantage of causing the horse to bear more weight on the affected limbs. Local analgesia may be useful in facilitating relocation of the horse, hoof trimming, corrective shoeing, or application of sole and frog support but not as a routine treatment.
Because of suspicion that corticosteroids induce or exacerbate laminitis, at this time their use is contraindicated in the treatment of laminitis.
Vasodilatory drugs are used on the premise that vasoconstriction is an important mechanism underlying the development or progression of acute laminitis. Several classes of drugs have been used including α-adrenergic antagonists such as phenoxybenzamine and phentolamine, drugs with multiple mechanisms of action such as acetylpromazine and isoxuprine, and nitric oxide donors including glyceryl trinitrate (nitroglycerine) and l-arginine.26 None of the vasodilatory drugs should be used in horses with compromised cardiovascular function or dehydration.
Phenoxybenzamine and phentolamine are not readily available and have limited use. Phenoxybenzamine causes sedation. Acetylpromazine is a potent vasodilator, principally because of its α-adrenergic antagonist activity, that is currently used frequently in the treatment of acute laminitis. Acetylpromazine increases blood flow to the digit, but its effect on nutritive flow to the laminae is unknown, as is the case for all the vasodilators.27 The effect of acetylpromazine persists for approximately 90 minutes after intravenous administration.27 Acetylpromazine can be administered at dose rates ranging from 0.01 to 0.05 mg/kg, IM, every 6–12 hours. Sedation may be considerable at the higher doses and/or with more frequent administration. Isoxuprine is a combined α-antagonist and β-agonist that increases blood flow to the leg but not to the foot in normal horses.27,28 It has been used at doses of 1–1.5 mg/kg orally every 12 hours. Pentoxyfilline (4.4 mg/kg orally q8 hours) does not increase digital blood flow in normal horses.27
Application of glyceryl trinitrate, a nitric oxide donor, to the palmar digital arteries of affected horses has been reported to increase or not affect blood flow to the dorsal hoof wall.29,30 However, the effect of these substances on the course of the disease is unknown. In spontaneous cases of acute laminitis glyceryl trinitrate has been applied to the skin over both palmar digital arteries of affected feet at a dose of 15–30 mg per artery, once daily. However, because of lack of evidence of efficacy and the potential for systemic hypotension secondary to systemic absorption of the drug, its use is no longer recommended.
Anticoagulant drugs are administered to prevent the development of microthrombi within the hoof. Aspirin and heparin are commonly used. Aspirin is a very poor analgesic in horses but is used because it reduces platelet aggregation in normal horses by blocking formation of thromboxane A2. However, thromboxane may not be an important cause of platelet aggregation in horses.31 Aspirin is administered at a dose of 10 mg/kg orally every 48 hours.
Heparin in sufficient doses prolongs blood clotting, provided that there is adequate antithrombin III in the patient’s blood. Heparin has been reported to prevent or to have no effect on the development of laminitis in horses with anterior enteritis or colic, respectively. Heparin can be administered at 40 to 80 iμ/kg IV or subcutaneously every 8–12 hours for 3–5 days. Anemia may develop during heparin administration, but resolves rapidly when administration of the drug is stopped.
Mechanical support to provide pain relief and in an attempt to prevent rotation or distal displacement of the pedal bone is an important part of the care of horses with acute laminitis.
Support of the frog and/or sole can be achieved using packing material such as dental acrylic or firm plastic that is molded to conform to the shape of the sole. Some clinicians prefer to use wedge pads to elevate the heel and reduce tension in the deep digital flexor tendon with the aim of preventing rotation of the pedal bone.
Housing the horse on sand or other soft bedding is frequently recommended.
Corrective shoeing of horses with chronic laminitis is widely practiced and there are proponents of a wide variety of shoe types (fullered egg-bar, heart bar, glue-on shoes). Appropriate hoof care, which might include shoeing, is important in managing horses with chronic laminitis. Interestingly, there was not a difference among shoe types in efficacy for pain relief in horses with chronic laminitis.32
Methionine has been given to both acute and chronic laminitis cases on the known requirement for methionine in the chondroitin complex of collagen. There is some rationale for the treatment but it seems more appropriate as a supportive than as a principal treatment. The recommended oral dose rate is 10 g/day for 3 days followed by 5 g/day for 10 days.
Antibiotics may be indicated to prevent secondary infection of the degenerate laminae.
Rest is important in the convalescent phase. Horses with no rotation or sinking of the pedal bone should be given 21 days of rest after resolution of the clinical signs. Return to work should be gradual. Horses that develop rotation or sinking of the pedal bone should be monitored both by physical examination and radiographic examination. It will be many months before horses with even mild rotation can be returned to work. Horses with severe rotation will likely never resume active work, although they may become pasture sound.
Summary of treatment of acute laminitis
Depending on the cause, treatment of acute laminitis should include:
• The administration of non-steroidal anti-inflammatory drugs (preferably phenylbutazone)
• Vasodilators (acetylpromazine)
• Support of the frog and/or sole
• Housing on sand or similar soft bedding
• The inciting disease should be treated aggressively
• After the acute phase has passed, likely in 5–7 days, attention should be given to trimming the hoof and corrective shoeing.
The prognosis for chronic or refractory laminitis (laminitis of more than 1 week’s duration) is poor (see above for the use of radiography to determine prognosis). Treatment includes NSAIDs for pain relief, corrective shoeing (egg bar or heart bar shoes), and trimming of the hoof (shortening the toe or complete removal of the dorsal hoof wall). Tenotomy of the deep digital flexor may provide temporary relief but does not affect the long-term prognosis.
The disease is not readily subject to control because of its sporadic nature. Heavily fed or fat horses should be given some exercise when not working; if possible, horses in transit should be removed from the transport vehicle, given light exercise and rested for several hours at the end of each day; retained placenta in mares should be treated promptly. Heavy carbohydrate feeding should be avoided. Susceptible ponies should have limited access to pasture either by limiting the time that they spend at pasture or by application of a grazing muzzle.
1 USDA. Lameness and Laminitis in U.S. Horses. 2000; USDA:APHIS:VS,. #N318.0400.
2 Polzer J, Slater MR. Prev Vet Med. 1996;29:179.
3 Treiber KH, et al. J Am Vet Med Assoc. 2006;228:1538.
4 Peloso JG, et al. J Am Vet Med Assoc. 1996;209:1746.
5 Cohen ND, et al. J Am Vet Med Assoc. 1994;204:250.
6 van Eps AW, Pollitt CC. Equine Vet J. 2006;38:203.
7 Weiss DJ, et al. Am J Vet Res. 1995;56:986.
8 Weiss DJ, et al. Res Vet Sci. 1996;61:157.
9 Elliot J, et al. Am J Vet Res.. 2003;64:1124.
10 Schneider DA, et al. Am J Vet Res.. 1999;60:233.
11 Eaton SA, et al. Am J Vet Res. 1995;56:1338.
12 Morgan SJ, et al. Am J Vet Res. 2003;64:829.
13 Adair HS, et al. Am J Vet Res. 2000;61:853.
14 Moore JN, Allen D. Vet Med. 1996;91:936.
15 Menzies-Gow NJ. Am J Vet Res. 2005;66:630.
16 Waguespack RW, et al. Am J Vet Res. 2004;65:1724.
17 Rodgerson DH, et al. Am J Vet Res. 2001;62:1957.
18 Fontaine GL, et al. Am J Vet Res. 2001;62:714.
19 Pollit CC. Proceedings Am Assoc Equine Pract. 1999;45:188.
20 Mungall BA, et al. Vet Microbiol. 2001;79:209.
21 Johnson PJ, et al. Equine Vet J. 2004;36:41.
22 Baxter GM. Vet Surg. 1995;24:87.
23 Stick JA, et al. J Am Vet Med Assoc. 1982;180:251.
24 Cripps PJ, Eustace RA. Equine Vet J. 1999;31:427.
25 Reed SK, et al. Am J Vet Res. 2006;67:398.
26 Parks AH. Equine Vet Educ. 2003;15:273.
27 Ingle-Fehr JE, Baxter GM. Vet Surg. 1999;28:154.
28 Harkins JD, et al. Equine Vet J. 1998;30:294.
29 Ragle CA. Comp Cont Educ Pract Vet. 1999;21:170.
30 Hoff TK, et al. Am J Vet Res. 2002;63:648.
Etiology Degeneration of the sensitive laminae of the hoof.
Cattle: An endemic disease of some herds of high producing dairy cattle, and in feedlots. Associated with ruminal acidosis, either clinical or subclinical.
Laminitis is caused by acute degeneration of the sensitive primary and secondary laminae of the hoof. The cause of this degeneration is unknown. The disease is less well characterized than that of horses and several conditions are often classified as laminitis.
In cattle the disease may occur as clusters in herds and on farms where a prediposition appears to be inherited or where access to large quantities of soluble carbohydrate are available such as for high producing dairy cows or feedlot cattle. On farms of high-producing dairy cattle the prevalence may be as high as 78%.1 The disease is also reported in calves and first calf heifers.
Subclinical laminitis that predisposes to the development of other diseases of the hoof occurs in calves and first calf heifers and is common in intensively fed feedlot cattle.2 Laminitis, conditioned by the inheritance of an autosomal recessive gene, is recorded in Jersey heifers.3 There may be an association between the disease in feedlot ruminants and ruminal acidosis.
Beef cattle being prepared for shows are often grossly overfed on high grain rations and become affected with a chronic form of the disease which markedly affects their gait and may cause permanent foot deformity. The disease occurs in dairy cattle fed improper rations, and especially first calf heifers and cattle of herds attempting to increase milk production1,4 and it is not uncommon for the disease to present as a herd problem.
Among dairy cattle the heifers are usually worst affected and the disease usually develops soon after calving, with more than 50% of cases occurring in the period 30 days before and 30 days after calving. There may be a relationship between being introduced to the herd, with the frequent harassment by dominant cows, when heavily pregnant and when the surface of the yards is rough. Housing may be important including standing in slurry or having to twist and turn in narrow passageways and races, and there is an association between the prevalence of the disease and rough concrete floors.5,6
Diet is an important risk factor for development of laminitis in heifers. Diets of wet, fermented grass silage are associated with a greater risk of laminitis than are diets rich in dry unfermented straw and a concentrate.7 Furthermore, transition from a low net energy diet to a high net energy diet immediately after calving increases the risk of subclinical mastitis in Holstein dairy cows.8
The disease is also reported to occur after metritis, retained placenta, mastitis, and mammary edema but the incidence is not usually very high.
The pathogenesis of laminitis in cattle, sheep, and pigs is unclear, but likely has some similarity to that in horses (see Laminitis in horses). Subclinical laminitis can predispose to white line disease.
In these species the clinical picture is similar to but less marked than that observed in the horse.
In calves 4–6 months of age, and in heifers, an acute syndrome similar to that seen in the horse has been described. Affected animals lie down much of the time, and are reluctant to rise. When they attempt to rise they remain kneeling for long periods. Their standing posture is with all four feet bunched together and the back is arched; they shift their weight from foot to foot frequently and walk with a shuffling painful gait. The feet are painful when squeezed and later become flattened and enlarged and look as though slippers are being worn. There is severe ventral rotation of the third phalanx.
In adult cows some cases have acute signs, others show only local lesions. These include sole ulcers and patchy changes in the horn including softening, waxy yellow discoloration, and red-brown patches suggestive of previous hemorrhage. The cow is chronically lame.9
Young bulls are very susceptible to laminitis and may develop abnormalities of gait and posture, such as a stilted gait and frequent knuckling of the fetlocks, which may mislead the diagnostician.
Chronic laminitis in adult cows is characterized by a smaller anterior hoof wall-sole angle, down from 558 to 358, a concave anterior wall, and the appearance of horizontal grooves (growth arrest lines) around the entire claw. The sole is usually dropped a little and bruising and sole ulcers may be present. Overgrowth of the sole of the lateral claw may reach the point of creating a false or double sole. The white line is greatly widened and disrupted and stones and other debris may be impacted in it.10
Chronic, traumatic laminitis is most common in heifers when they are first introduced into the milking or dry herds. Housing them on concrete and exposing them to frequent confrontations with bossy cows lead to the development of sole hemorrhages and inflammation of the laminae.
Radiographic signs in cattle include rarefaction of the pedal bone, particularly the toe, and the development of osteophytes at the heel and on the pyramidal process.
Histological findings in the feet of cows affected by laminitis are similar to those in horses.
Although similar principles to those used to determine treatment of laminitis in horses are likely to apply to cattle, treatment in cattle is usually limited to administration of NSAID (aspirin 0.3 grains/kg, orally every 12 hours, phenylbutazone 4.4 mg/kg orally every 48 hours or flunixin meglumine 1.0 mg/kg IV every 12 hours). The inciting cause (metritis, ruminal acidosis) should be treated aggressively.
Cattle and lambs which are brought into feedlots should be gradually introduced to grain feeds and a higher forage:grain ratio provided in the feed. Calves should not be fed intensively on grain until they are 14 months old because of the high frequency of internal hoof lesions at the earlier ages. Some protection against laminitis in dairy cattle in intensive units is gained by careful planning of housing cubicles to make them more comfortable and less damaging to the feet, and by providing more straw in the cubicles. Exercise should be provided around calving time. Vaccination with a Gram-negative bacterin-endotoxoid combination vaccine has provided some protection against laminitis induced by grain overload. Dietary supplementation of biotin (20 mg per head per day) improves hoof health of primiparous dairy cows11 and may be beneficial in reducing the incidence or severity of lameness in a herd. This treatment might not improve objective indicators of hoof health, but it does improve production.12
1 Bass RT, Whittier WD. Vet Med. 1996;91:1033.
2 Greenough PR, et al. Can Vet J. 1990;31:202.
3 Hoyer MJ. J S Afr Vet Assoc. 1991;62:62.
4 Moser EA, Divers TJ. J Am Vet Med Assoc. 1987;190:1575.
5 Bergsten C. Acta Vet Scand. 1994;35:55.
6 Cook NB. J Am Vet Med Assoc. 2003;223:1324.
7 Offer JE, et al. Vet J. 2003;165:221.
8 Donovan GA, et al. J Dairy Sci. 2004;87:73.
9 Greenough PR. Bovine Pract. 1985;20:144.
10 Weaver AD. Bovine Pract. 1988;23:85.
A non-inherited condition has been described in the US and Australia which resembles inherited dwarfism.1 The disease occurs on poor range country and is thought to be due to a maternal nutritional deficiency during the middle trimester of pregnancy. The specific dietary factors involved have not been determined, although supplementary feeding during pregnancy eliminates the condition.
Abnormal osseous development of the head causes it to be either shorter or longer. Shortening of the shafts of the long bones of the limbs is accompanied by bending at the joints, and calves nurse and stand with difficulty. Incoordination, arching of the back and a tendency to bloat, which may cause death, also occur. The dentition is normal. Muscle spasticity, wry neck, circling, falling backwards, and goose-stepping occur rarely.
Most of the calves are born alive and, in badly affected herds, as many as 15% of calves may be affected. The condition derives its name from the common occurrence of acorns in the diet of affected herds, although the acorns are not thought to have any etiological significance.
Congenital joint laxity and dwarfism is a skeletal anomaly which has affected beef calves in Canada,1-3 Australia,4 and Ireland.5 The disease has been recognized in beef cattle ranches in north central British Columbia and Alberta, and northwestern Ontario.1
The etiology is unknown. Epidemiologically, the disease has been associated with feeding clover silage or grass silage without dry feed or grain supplementation to pregnant cows over the winter months.3 The disease is seen almost exclusively in beef herds where pit silage makes up the bulk of the ration. In an outbreak in a beef herd in Prince Edward Island, Canada, feeding spoiled silage to pregnant cattle may have been a risk factor.3 An apparent greater incidence in beef herds in the northern part of the UK may be associated with longer periods of winter feeding in the northern part of the country.6,7 There is no evidence that manganese deficiency is a causative factor.3,5
The problem can be eliminated by supplementation of the silage diet with a combination of hay and rolled barley.2 In one study, calves born to first-calf heifers were 3.2 times more likely to be affected compared to calves born to mature cows.8 In the Australian report, the pregnant dams had experienced severe nutritional deficiency between 3 and 6 months of gestation.4
Controlled feeding trials have supported the epidemiological observations that the disease occurs in calves born to cows fed exclusively grass or clover silage over the winter months.2 Supplementation of the grass and clover silage diet with hay (2.5–4.5 kg/head per day) and rolled barley (0.75–1.5 kg/head per day) eliminated the problem. Supplementation with grain but no hay reduced the risk of abnormal calves to a lesser degree. The period of gestation during which the fetus is susceptible to the abnormality ranges from 107 to 230 days. It is suggested that irreversible injury to the fetus occurs by day 180 of gestation.
Prenatal rickets was considered as a possibility in the early stages of the investigations. The overgrowth of chondrocytes and delayed mineralization of the growth plates of affected calves in previous years were similar to those described for neonatal rickets. In addition, the vitamin D concentration of silage may be low and the wavelengths of ultraviolet light necessary for transformation of the provitamin 7-hydroxycalciferol to vitamin D3 are almost entirely filtered out by the atmosphere during the winter months because of the acute angle of the sun in northern latitudes. In Canada, pregnant beef cows fed exclusively a diet of grass or clover silage during the winter months may have low levels of vitamin D. However, supplementation of pregnant cows with vitamin D3 during one winter season did not reduce the risk of abnormal calves.
The disease resembles ‘acorn calves’ which have occurred in California and Australia. One possible hypothesis suggests that the two conditions may share a common pathway.2 Certain unspecified seasonal and environmental conditions or stressors may convert forage into a teratogenic substance. In areas where acorn calves occur, supplementation feeding of the cows on pasture practically eliminates the problem.
The abnormalities are obvious at birth and characterized clinically by generalized joint laxity, disproportionate dwarfism and, occasionally, superior brachygnathia.2 The anomaly has occurred in some beef herds for several consecutive years and has affected 2–46% of the calf crop.9 In a case reported from Ireland, the affected beef herd consisted of Hereford, Simmental, and Friesien cows bred to a Hereford or Charolais bull. The pregnant cattle were self-fed grass silage preserved with Kofasalt (calcium formate, sodium nitrite, and hexamethylene tetramine). Affected calves, were characterized clinically by disproportionate dwarfism, varying degrees of micromelia, limb rotation, joint laxity, and skull abnormalities.5 Inferior and superior brachygnathia were present. Radiographically, the diaphyses were grossly foreshortened and thickened, the epiphyses were enlarged, misshapen and flared with increased opacity on some radiographs.5 Histologically, there was chondrodystrophic of the metaphysis of the dwarf long bones. Consistent changes in organ weights or in trace element status were not present, and there was no evidence of infectious agents. There was no evidence of an inherited basis for the abnormal calves.
The epiphyses of the long bones are abnormal with overgrowth of chondrocytes and delayed mineralization. The common defect is one of growth plate maturation. The secondary ossification centers are slow to develop. Perinatal mortality is higher in affected calves than for normal calves in the same herd. The joint laxity may cause problems with dystocia. Within a few weeks after birth, the joints in surviving calves become stable, and calves walk normally.
1 Ribble CS, Janzen ED. Aust Vet J. 1987;28:160.
2 Ribble CS, et al. Can Vet J. 1989;30:331.
3 Cebra CK, et al. Vet Rec. 1999;215:519.
4 Peet RL, Creeper J. Aust Vet J. 1994;71:58.
5 Mee JF. Irish Vet J. 1995;48:93.
6 Davies S. Vet Rec. 2000;147:144.
7 Gunn G, et al. Vet Rec. 2000;147:200.
8 Proulx JG, Ribble CS. Aust Vet J. 1992;33:129.
9 Ribble CS, Janzen ED. Proc Am Assoc Bov Pract. 1989;21:96.
This occurs in newborn calves of the well-muscled, rapidly growing European breeds, such as the Charolais, Maine-Anjou, and Simmental. It is characterized by varying degrees of lameness, palpable crepitus over the greater trochanter on passive manipulation of the affected limb, muscle atrophy in longstanding cases, and prolonged recumbency. Some calves carry the affected limb or drag the foot, whereas others tolerate slight weight-bearing during standing or walking. Most calves are lame at birth or within a few days after birth. About 75% of cases are associated with a dystocia and forced traction delivery.1
Laboratory stress testing of calf femurs found that mechanically induced fractures had configurations and locations similar to those found in clinical cases associated with forced extraction.2 The breaking strength of all femurs was within the magnitude of forces calculated to be generated when mechanical devices are used to assist delivery during dystocia. It is suggested that the femur is compressed during force extraction when the pelvis of the calf is wedged in the pelvis of the dam in anterior presentation. Every effort must be employed to avoid premature engagement of the calf’s stifle into the pelvic cavity to avoid or correct a ‘stifle lock’.
Radiographically, there are varying degrees of displacement of the femoral neck from the head. In chronic cases there is partial resorption of the femoral head. Excision arthroplasty has been attempted with some encouraging results.
The disease must be differentiated from perinatal femoral nerve degeneration and neurogenic atrophy of the quadriceps femoris muscle which also occurs most commonly in the same breeds of cattle. The right hindleg is most commonly affected and affected calves are unable to bear weight on the leg; there is obvious neurogenic atrophy of the quadriceps muscle.3 The problem has been treated by stall rest, femoral head and neck excision, and open reduction by use of Knowles pins, multiple intramedullary pins, or interfragmentary compression screws.4
Slipped capital femoral epiphysis has also been reported in cattle 3–5 months and 1.5–2.3 years of age.3 Trauma is the suspected cause. If early diagnosis can be made, intramedullary pinning can provide a good long-term prognosis in cattle when function as a breeding animal is important to their future value.
Tail-tip necrosis occurs in cattle housed in confinement on slatted floors. The disease has occurred in steers, heifers, and bulls being fed for beef production.1,2
The lesion is caused by a traumatic injury of the tail caused by tramping of the tail. The lesion begins at the tip of tail followed by varying degrees of extension proximally. Initially, the tip of the tail is swollen, followed by inflammation and suppuration. Histopathological changes are compatible with cutaneous ischemia as a pathogenetic mechanism.3 Extension of the infection can result in metastases to other parts of the body, resulting in abscesses and osteomyelitis. Affected cattle do not grow normally and deaths from pyemia may occur. The morbidity is about 5%. Approximately 10% of affected animals may be condemned for osteomyelitis and abscessation.
These include slatted concrete floors, close confinement, warm seasons, and a body weight above 200 kg. The risk increases as the space allotment, expressed as kg animal per m2 pen increases from approximately 165 kg/m2. Tail tramping is more frequent in slatted-floor pens with lower space allotment (1.5 m2 per head) than in similar pens with higher space allotment (2.4 m2 per pen head). In an Ontario study, no case of tail-tip necrosis was diagnosed in solid-floor barns, while 1.36% of cattle in slatted-floor barns were either treated or slaughtered for tail-tip necrosis.2 In a mail survey of feedlots in Ontario, 96% of 71 feedlots with slatted floors, but only 5% of 184 feedlots with solid floors, reported a problem with tail-tip necrosis from 1982 to 1986.3 Of 441 tails inspected at slaughter plants, 34.5% were affected, with 3.4% involving skin lacerations and infection, and 4.3% amputated before slaughter.3 Most cases occur from May to September when the temperature is above 18°C. This may be associated with increased contamination due to increased humidity and temperature under confinement conditions.
In slatted-floor barns, abnormal locomotor patterns occur from 20 to 25% of the times animals get up and lie down.2 When animals get up abnormally, they first rise in their front, and consequently assume a dog-like sitting posture. In order to obtain momentum to rise in the rear, they then start to sway back and forth. The tail may become pinched between the hock of the rocking animal and the floor, resulting in blunt trauma to the tip of the tail.
Treatment consists of early amputation combined with intensive antimicrobial therapy. Early detection is important. During warm months, cattle confined on slatted floors and weighing more than 200 kg should be closely inspected at least 2 or 3 times weekly. This includes palpation of all tail tips because early lesions are difficult to see.
A toe ulcer is a defect in the white line at the apex of the sole in adult cattle.1 Lameness does not occur in the early stages but discomfort gradually develops at which stage the animal carries the foot further forward than normal. The etiology is not well understood. In one series of cases, overtrimming using a grinding disc and/or perforation of the sole was considered a major cause (49%), laminitis in 30%, and traumatic injuries in 11%.2
In South America, where dairy herds are pastured and supplemented with concentrate and corn silage, toe ulcers are common lesions in heifers from 15 to 60 days after calving.3 Two types of toe lesions are usually presented. One is a single claw horn defect occurring in Zone 1 which after further examination, granulation tissue is often observed. This lesion responds well to local treatment and the application of an orthopedic block on the healthy claw. The second type of lesion is more severe and includes necrosis of the pedal bone, complicated by secondary infection.
Clinical signs of apical pedal bone necrosis vary widely depending on the severity of the lesions, the number of claws involved and the causative factors. A marked-to-severe lameness may occur in cows with one claw affected, and a severely stilted gait in cows with two or three affected claws. In some cases, the lameness is so severe that the initial impression from a distance was that of a neurological disease because of the severely stilted, convulsive limb movements at rest and walking. The involvement of the pedal bone can be determined by clinical examination, inserting a probe or by direct visualization of the discolored and exposed apex of the distal phalanx.
The gross pathological findings of affected claws vary from moderate topical inflammatory signs of the corium at the toe of the claw, to severe and extensive necrosis and osteomyelitis of the pedal bone.1 Histologically, there are different types of demarcation of the necrotic bone. Mixed infections are common.
Radiographically, the degree of involvement of the distal phalanx can be clearly identified, facilitating the choice of surgical therapy.1
Treatment options include excision of necrotid bone using a bone curette, resection of the necrotic apex of the distal phalanx, and digital amputation in severe cases.2
Diseases characterized by involvement of the skin
Pityriasis rosea is a condition of man. The condition in pigs is not the same because of a prominent component of eosinophils and confluent zones of epidermal necrolysis. Dermatopathological authorities have suggested that the condition be renamed pustular psoriasiform dermatitis of pigs.1
This skin disease of pigs resembles ringworm closely but skin scrapings do not reveal the presence of fungal hyphae or spores, and cultures for fungal growth are usually negative. Treatment with standard preparations used for ringworm is usually ineffective, although spontaneous recovery may occur.
The disease occurs in sucking pigs2 and young pigs in the 10–14 weeks age group. Up to 50% of each litter and herd may be affected and in large groups of feeder pigs there may be only individual pigs or the majority of the group with lesions. The disease is usually innocuous, although digestive disturbances, particularly anorexia and, to a lesser extent, diarrhea and vomiting may accompany the appearance of lesions and affected pigs lose some body weight. There is no fever. Usually the condition resolves spontaneously after 2–4 months.
Lesions occur most commonly on the ventral abdomen but may spread to the rest of the body. They commence as small, red nodules which enlarge to flat plaques and become covered with thin, dry, brown scales. The lesions appear to enlarge centrifugally, leaving a center of normal appearance surrounded by a narrow zone of elevated, erythematous skin covered by typical scales. Individual lesions are generally circular except that they often coalesce to produce a large, irregular lesion. There is little irritation and the skin lesions, although obvious, are superficial. There is no loss of bristles. Histologically, the lesions show a progression from acute to chronic with a dense superficial and deep perivascular infiltrate of eosinophils, lymphocytes, and histiocytes.1
The cause is unknown, although infectious, genetic and allergic causes have been suggested and there is strong evidence of familial susceptibility, either through inheritance or by vertical transmission of an infectious agent.3,4 Transmission experiments have been unsuccessful and the disease has been observed in SPF pigs produced by cesarean section.5 By analogy with a similar condition affecting man, it may be a viral infection. Treatment appears to be completely ineffective but in general consists of the local application of a salve containing 5% salicylic or iodized mineral oil. Affected pigs should be isolated from the group. Spontaneous recovery occurs in 6–8 weeks in most instances.
Reduced ability to sweat affects horses in hot and humid climates. Affected horses are unable to maintain their body temperature within safe limits, especially during or after exercise, and suffer heat stress and a reduction in athletic performance. The only effective treatment is to move the horses to a cooler environment.
The etiology of anhidrosis is unknown, but involves a reduction in the sensitivity of the sweat gland to β-2 adrenergic stimulation, the normal stimulus for sweating in the horse.1 Hypothyroidism does not contribute to anhidrosis.2
The disease occurs in horses, and rarely in cattle, in countries with hot, humid climates including tropical and semitropical regions.1
The overall prevalence is approximately 6% in Florida, with the highest prevalence (25%) in horses in training and the lowest prevalence (1%) in young horses.2 There is no reported sex or color predilection. Both native and imported horses are affected, apparently with similar prevalence.3 Among native horses the age of onset of the condition ranges from 1 year to 10 years.3 Foals, especially of draft breeds, can be affected. Horses imported to endemic areas usually do not develop the disease within 1 year.3 The incidence and severity of the disease are highest in the hotter season.
The disease is rarely fatal unless severely affected horses are exercised in the heat, in which case death from heat stroke can occur. The major importance of the disease is inability of affected horses to exercise and compete in athletic events.
Sweat is produced in horses by apocrine sweat glands that have a single type of secretory cell. The sweat glands are well innervated, and sweating is controlled by a combination of hormonal (β-2 adrenergic) and neural factors.4 Sweat production increases with increasing concentrations of epinephrine in blood up to a peak value, after which sweating rates decline.4 Anhidrotic horses have lower initial and peak rates of sweat production, and lower overall sweat production, than do normal horses during intravenous infusion of epinephrine.5 Suggested, but unproved, mechanisms for decreased sweat production by anhidrotic horses includes diminished glandular sensitivity to epinephrine, failure of secretory function, blocking of sweat gland ducts, fatigue of the gland, and gland atrophy.
Sweating is the predominant means by which horses dissipate heat. Reduction in the capacity to produce sweat results in an inability to effectively control body temperature during exercise and when temperature and humidity are high. The elevation in body temperature results in tachypnea in an attempt to dissipate heat through the respiratory tract. Hyperthermia impairs performance and, if severe, can result in heat shock, a systemic inflammatory response syndrome, and death.
The most apparent clinical sign is lack of sweating in response to an appropriate stimulus, such as exercise. In severely affected horses, sweating may be limited to the perineum, brisket, and areas under the mane and saddle. Less severely affected horses have a diminished sweat response and may not lather during exercise. The skin becomes dry and scurfy and loses its elasticity, and there may be alopecia, especially of the face.
Affected animals become extremely tachypneic when heat stressed, leading to the colloquial term for the disease ‘dry puffer’. The animal’s appetite declines and it loses weight. Athletic performance is severely compromised. High body temperatures are observed after exercise, sometimes reaching 41.5–42°C (107–108°F) and persist for long periods.
The prognosis is poor for athletic function for affected animals that remain in hot and humid environments, but the condition may resolve if the horse is moved to a cool climate.
Plasma epinephrine concentrations are reported to be higher in affected horses than in unaffected horses,6 but this has not been a consistent finding among studies.5
Diagnostic confirmation is achieved by demonstrating reduced sweating in response to intradermal injection of epinephrine, or the β-2 adrenergic agonists, terbutaline and salbutamol.7 A crude test involves the intradermal injection of 0.1 mL of a 1:1000 dilution of epinephrine. If the horse sweats then it is not considered to be completely anhidrotic. A semiquantitative test using epinephrine, terbutaline, or salbutamol may be useful in identifying partially anhidrotic horses.7 Normal horses sweat when 0.1 mL of 1:1000 000 epinephrine is injected, while partially anhidrotic horses sweat only with higher concentrations (1:10 000 or 1:1000). Injections are usually made using small gauge needles (25 g) into the skin over the lateral aspects of the neck.
There are no characteristic gross lesions at necropsy. Histologic examination of the skin of affected horses reveals abnormalities in sweat gland morphology including flattening of cells and loss of luminal microvilli and a reduction in the number of secretory vesicles. These findings are thought to be a consequence, rather than a cause, of the disease.
There is no specific treatment that restores the horse’s ability to sweat, other than movement to a cooler climate. Affected horses for which translocation to a cooler environment is not feasible benefit from housing in air conditioned stables so that exposure to high ambient temperatures is minimized. Exercise of affected horses during the coolest periods of the day is sensible. Affected horses are frequently administered electrolyte supplements, but without demonstrated benefit. However, as with all working horses, an adequate intake of sodium, potassium, and chloride should be insured.
Administration of thyroid hormone supplements is not warranted, and may be dangerous by increasing the metabolic rate, and therefore heat production, of affected horses. Vitamin E administration has no demonstrated efficacy.
Removal of affected animals to cooler climates is often necessary, although air conditioning of stables and maintenance of horses in higher country where they can be returned after a day’s racing may enable susceptible horses to be kept locally.
1 Bijman J, Quinton PM. Am J Physiol. 1984;246:R349.
2 Mayhew IG, Ferguson HO. J Vet Intern Med. 1987;1:136.
3 Warner DE, Mayhew IG. J Am Vet Med Assoc. 1982;180:627.
4 Scott CM, et al. Equine Vet J. 2001;33:605.
5 Marlin DJ, et al. Equine Vet J. 1999;Suppl 30:362.
Ocular squamous-cell carcinoma, often referred to as ‘cancer eye’, is one of the most common neoplasms of cattle.
Etiology Genetic-environmental interaction. Lack of pigmentation around the eye and solar radiation.
Epidemiology One of most common neoplasms of cattle; mostly in beef cattle breeds (Herefords, Simmental) lacking pigment around the eye; animals over 5 years of age.
Solar radiation major risk factor.
Signs Precursor lesions, single or multiple plaques on eyelid or conjunctiva except the cornea or pigmented lid may regress, or lead to carcinomas of sclera resembling papillomas with crumbly, necrotic ulcerated mass attached to the eyelid causing irritation to eye and conjunctiva and excessive lacrimation and pus. Invasion of surrounding tissues of eye and possibly to nearby lymph nodes.
Clinical pathology Histology of lesion.
Lesions Squamous cell carcinoma.
Diagnostic confirmation Biopsy and histology.
Treatment Excision by cryosurgery. Radical surgery may be necessary. Immunotherapy with vaccines has been attempted.
Control Breeding program to increase degree of pigmentation in Hereford cattle.
A genetic-environmental interaction has been proposed as the cause. A relative lack of circumocular and corneoscleral pigmentation, both of which are heritable, increases the probability of lesion development when the animal is exposed to a carcinogenic agent like the ultraviolet component of sunlight. The carcinoma has been regarded as a papilloma-associated tumor because papilloma virus can be found in the precursor lesions, and papillomavirus DNA in the carcinomas. However, advanced virological techniques have failed to reveal any association between the virus and the tumor.1
The p53 gene product is highly expressed in bovine BOSCC, which provides support for its role in BOSCC tumorigenesis.2
Bovine ocular squamous cell carcinoma is a common neoplasm of the eyelids and the eyeball of cattle and one of the most common neoplasms of cattle. The disease is most common in beef cattle which are exposed to more sunlight than dairy cattle. The tumors are uncommon in cattle younger than 5 years and are hardly ever seen in cattle younger than 3 years. The condemnation rate of cattle with ocular squamous cell carcinoma in Canada is about 30% of cases.3 A squamous cell carcinoma of the anal and perianal area of a 15-year-old bull has been recorded.4
The heritabilities, phenotypic, and genetic correlations of lid and corneoscleral pigment and eye lesions associated with eye cancer were investigated in 2831 Herefords from 34 herds in 21 states of the US and one Canadian province. The results indicated that lid and corneoscleral pigment were heritable and genetically correlated.5 These findings lead to the general conclusion that the genetic effect on pigment determines to a large extent the degree to which the eye is susceptible to some carcinogenic agent such as ultraviolet light.
In Zimbabwe, ocular squamous cell carcinoma was frequently observed in five breeding herds of Simmental cattle.6 In these herds, initial signs of the disease were evident in cattle about 3 years of age and gradually the prevalence increased to over 50% in animals over 7 years of age.6 It is suggested that because most cattle in Zimbabwe are slaughtered by 10 years of age, that more than 67% of cattle without periorbital skin pigmentation would develop the tumor. The tumors were multiple and commonly bilateral. Simmental cattle have a complete or partly white face and the lack of facial pigmentation risks exposure to intense solar radiation when they are kept at a high altitude (1500 m) in a sunny and warm climate. The prevalence was much lower in white-faced Friesian cattle in the same environment which suggests a genetic predisposition for the tumors in Simmental cattle. In Zimbabwe, the tumor is not recorded in fully-pigmented cattle breeds.
The association between ocular squamous cell tumors and various measures of solar radiation indicate a significant association between increasing risks of developing eye cancer and increasing levels of radiation.7 Ultraviolet light is generally regarded as an important risk factor. Most tumors are located only in the sun-exposed mucocutaneous areas not protected by hair. Tumors are predominantly localized in the third eyelid and the lateral limbus, and tumor growth usually starts at the outer edge which receives the most sunlight. Cattle exposed to high levels of radiation develop the disease at younger ages.7
The disease results in serious economic consequences through lessened productivity and carcass condemnations. Commercial cattle can be culled early without much loss, because only the head is condemned. Purebred cattle are more of a problem because of the difficulty of deciding when euthanasia must be the humane decision, rather than another attempted extirpation of the eye.
The initial lesion may be on the eyelid or any structure in the conjunctival sac, except the avascular cornea or pigmented eyelid. Lesions can encroach on these tissues from others nearby, carrying a blood supply with them.
The lesions develop through three stages. The first two, a plaque and then a papilloma, are non-malignant and have high regression rates. The third stage is the squamous cell carcinoma which does not regress. The tumor is located in the sclera adjacent to the lateral limbus, in the membrana nictitans (third eyelid), or in the lower eyelid. It is an invasive tumor, metastasizing along the draining lymphatics into cervical lymph nodes. Primary lesions of the lids are most likely to metastasize to these nodes.
Animals do not appear to develop resistance to the cancer; only a few cows with the disease develop measurable antibodies in their sera. It is one of the characteristics of this disease that the carcinomas appear to produce immunosuppressive substances, and removal of tumor mass reduces blood levels of them.
In countries and in herds where ocular carcinoma is common, it is not unusual to encounter lesions on the labia of the vulva especially if there are patches of unpigmented skin.8
Typical precursor lesions are single or multiple plaques of gray-white, smooth or rough, hyperplastic to hyperkeratinized tissue anywhere in the conjunctiva. Plaques may develop into papillomas and acanthomas of the skin of the eyelids, also included as precursor lesions. Squamous-cell carcinomas may develop from any of these precursors which may also regress spontaneously. The proportion that regresses is of the order of 80%.
Classic BOSCC lesions resemble papillomas with a fleshy, sometimes crumbly, often necrotic and ulcerated mass attached to the lid or the orbit by a wide base. They are visible even when the eyelids are closed, and cause obvious irritation to the surrounding conjunctiva, resulting in increased lacrimation and sometimes in the discharge of pus. Invasion of surrounding tissues is common but metastases to nearby lymph nodes and to viscera occur in only a few cases and then only late in the course of the disease.
Differentiation between carcinomas and precursor lesions is difficult clinically and cytological examination or biopsy is recommended for definitive diagnoses. The cytology of squamous cell carcinomas in domestic animals has been described.9
One of the difficulties encountered in the field is the clinical differentiation of benign precursor lesions from the malignant carcinomas; failure to do so may account for the high rates of spontaneous regression recorded, especially in Hereford cattle, where a spontaneous recovery rate of 88% is recorded. To avoid this inaccuracy, exfoliative cytology by the examination of smears of lesions is helpful. Combined with a clinical assessment this is the recommended method of confirming the diagnosis. Differentiation from similar lesions that are not BOSCC can only be achieved by proper laboratory examination of tissues.
Excision, sometimes by cryosurgery, is widely practiced in cattle. Results are good and treatment by the use of radioactive implants has also aroused favorable comment. Recurrence, or the development of new lesions at the same site, is a common sequel. Radical surgery, including removal of the local lymph nodes and parts of the salivary gland, may be desirable in some bovine cases. It is often combined with immunotherapy, e.g. with BCG vaccine injected systemically or into the lesion, or with vaccination with BOSCC tumor material. That there is a significant immune body response at the normal tissue-corneal interface has been demonstrated, but whether this plays any part in the rejection of the tumors is not known. One controlled trial in cattle showed that intralesional injection of BCG vaccine can interrupt neoplastic progression and prevent malignant disease. A permanent regression after BCG vaccination can be expected in 37% of cases, recurrence at the same site in 26%, and continued growth in 37%.10
A favorable response to a single injection of a saline phenol extract of fresh tumor tissue can induce a high rate of regression of ocular tumors with a higher recovery rate after the use of 200 mg of lyophilized tumor extract as compared with an injection of 100 mg. The injection may need to be repeated. Occasional tumors show enhancement of growth after vaccination, especially if it is repeated. The vaccine does not need to be autologous, and only one injection is required. A freeze-dried preparation of tumor antigen has been used successfully. In general, the use of a vaccine seems likely to provide a satisfactory method for controlling an esthetically distressing and financially important disease. Reports on the effect of vaccination with a tumor vaccine on the vulvar form of squamous-cell carcinoma vary.11
Other treatments which have received favorable comment, but need to be evaluated in the light of the known natural recovery rate of the benign precursor lesions, include electrothermal hyperthermia and combinations of the above procedures.
Because of the strong correlation between absence of pigmentation of the eyelids and the occurrence of the disease, and because of the high heritability of this pigmentation in Hereford cattle, it is suggested that a breeding program aimed at increasing the degree of pigmentation of eyelids could quickly reduce the incidence of the disease in this breed.5 A positive approach to the problem would be to crossbreed susceptible Bos taurus cattle with Bos indicus cattle which always have pigmented eyelids and have much less eye cancer. In Ayrshires there is a corresponding predilection for squamous-cell carcinomata of the vulva, but the neoplasm does not occur on both sites in the one cow. Selection on the basis of the occurrence of lesions alone results in only limited reduction in incidence.
1 Rutten VPMG. Am J Vet Res. 1992;53:1477.
2 Carvalho T, et al. Vet Pathol. 2005;42:66.
3 Fisher M. Can Vet J. 1994;35:133.
4 Musser JMB, et al. Cornell Vet. 1993;83:83.
5 Anderson DE. J Hered. 1991;82:21.
6 Otter WDen. Am J Vet Res. 1995;56:1440.
7 Anderson DE, Badzioch M. J Am Vet Med Assoc. 1991;52:784.
8 Omara-Opeyne AL, et al. Kenya Vet. 1984;8:5.
9 Garma-Avina A. J Vet Diagn Invest. 1994;6:238.
Squamous cell carcinoma is one of the most common neoplasms of the horse and is the most common tumor of the eye and orbit but the rate of occurrence is low. The reported frequency has been highest in animals lacking periocular pigmentation and is more common in Appaloosa, albino, and color dilute horses. An increased prevalence for ocular and adnexal SCC has been reported in draft horse breeds, Appaloosas, Paint Horses, Thoroughbreds, and Quarter Horses. A predisposition for the development of ocular and adnexal SCC has also been reported in geldings.1 The risk has been higher in draft breeds than in other pigmented breeds, probably related to the large expanses of white skin on the face and around the eye of the heavy draft breeds. The overall mean age range of affected animals is 8–10 years.2 In a series of limbal neoplasms in horses admitted to the Veterinary Teaching Hospital in the Netherlands, squamous cell carcinoma was the most predominant tumor type and Haflinger horses accounted for 69% whereas their occurrence in the hospital population was 5%.3
In a retrospective study of 50 cases submitted to the University of Florida Veterinary Medical Teaching Hospital, the Appaloosa accounted for the majority of cases4 which may be a reflection of the high level of solar radiation in southeastern US. The average age at which the tumor was diagnosed initially was 11.8 years; males accounted for 64% and females 36% of the cases. The rate of metastasis was 18%.
In the Florida study, higher cure rates were associated with surgical excision followed by radiation therapy for a cure rate of 75%; whereas with only surgical excision the cure rate was 55%.4 Best results with treatment are seen when surgical intervention is early.5 In horses, treatment is largely surgical but all of the immunological techniques developed for cattle have been used including local irradiation therapy with 90Sr or 222Rn.2
The most frequent site for ocular involvement is the nictitating membrane and conjunctiva but the eyelids and cornea are also involved. A case of limbal squamous cell carcinoma with invasion into the cornea and uvea of 12-year-old Haflinger gelding has been described.6 On initial presentation, a light-pink raised mass on the temporal limbus and conjunctiva of one eye was observed. Squamous cell carcinoma was confirmed histologically after keratectomy and cryotherapy. Seven months later, a smooth pink, progressively enlarging mass was observed within the cornea. Ultrasonographically, the mass was found infiltrating the corneal stroma and the anterior chamber. The globe was surgically removed. Histologically, a diagnosis of corneal ocular squamous cell carcinoma with deep stromal invasion, infiltration of the uveoscleral meshwork and iridocorneal angle and resulting intraocular extension was made.
A pigmented squamous cell carcinoma of the conjunctiva of a 17-year-old horse has been described.7
Treatment of ocular and adnexal SCC has included various types of therapy, with and without adjuvant radiation therapy. Types of treatment without adjuvant radiation therapy include excision, cryotherapy, radiofrequency hyperthermia, immunotherapy, chemotherapy with cisplastin, and carbon dioxide laser ablation. Treatment with adjuvant radiation therapy includes use of strontium 90 (90Sr) cobalt 60 (60Co), gold 198, iridium 192 (192Ir), cesium 137, iodine 125 (125I), and radon 222 (222Rn).1 In a series of 157 cases of ocular and adnexa squamous cell carcinoma, those treated with adjuvant radiation therapy had a significantly lower recurrence rate, compared with those treated without adjuvant radiation therapy, independent of anatomic location.1
Superficial keratectomy followed by cryosurgery is a simple and effective procedure for the treatment of small-sized limbal tumors (less than 2 cm) in horses.3 Sophisticated equipment is not required and the legal restrictions associated with the use of radioactive substances in many countries are not a consideration.
Ocular pseudotumors have been described in horses. They are proliferative inflammatory lesions involving the eye, adnexa or orbit, which clinically mimics true neoplasms.8 Cases are characterized by a uniocular, pink proliferative limbal or perilimbal lesion. Affected horses may be from 5 to 9 years of age. Most cases occurred during the summer months and none of the affected animals had a history of trauma or recent deworming. The dorsal bulbar conjunctiva was most commonly affected, followed by the third eyelid. Lesions were relatively flat with indistinct margins or discrete and nodular. Histologically, the lesion is inflammatory characterized by predominantly lymphocytic infiltrates. The cause is unknown but an immune-mediated pathogenesis is suspected based on the preponderance of immunocytes consisting primarily of lymphocytes. Treatment consists of surgical excision alone, partial resection with anti-inflammatory therapy, or anti-inflammatory therapy alone.8
1 Mosunic CP, et al. J Amer Vet Med Assoc. 2004;225:1733.
2 Rebhun WC. Vet Surgery. 1990;19:297.
3 Bosch G, Klein WR. Vet Ophthalmol. 2005;8:241.
4 King TC, et al. Equine Vet. J. 1991;23:447.
5 Schwink IC. Equine Vet J. 1987;19:197.
6 Kaps S, et al. Vet Ophthalmol. 2005;8:193.
A well-differentiated ocular squamous cell carcinoma has been described in twin goats.1 The twin goats, one male and one female, were 3 years of age. Both animals had pigmented eyelids and had been reared at an altitude of 760 m above sea level in Italy. The lesions were very advanced when first examined. There was a history of bilateral ocular disease and impaired vision of 24 months duration. In the affected eyes, a firm mass with a fleshy appearance was evident, covering the entire cornea and protruding through the palpebral fissure. A bilateral ocular mucopurulent discharge, associated with corneal plaques, neovascularization and edema, was also present in both animals.
Histologically, cords and islands of squamous epithelial cells proliferated deeply throughout the cornea and invaded the basal layer, limbus, iris, and cilary body, and other features, characteristic of a well-differentiated ocular squamous cell carcinoma.
Biomolecular studies to the identification of Papillomavirus-related DNA sequences within the neoplastic ocular parenchyma of both animals but immunohistochemical and ultrastructural examinations did not demonstrate viral particles.
This is a superficial nodular dermatitis of sheep recorded only in New Zealand that results in nodules in the skin that are of economic importance to the leather industry. The presence of cockle downgrades the value of the pelt.
Cockle is not usually diagnosed clinically but examination by close inspection of the skin over the upper shoulder region after close shearing has high specificity for detection.1 The lesions are the result of an immune response in some sheep to infestation with the biting louse Bovicola ovis. The occurrence of cockle and its severity is positively correlated with the severity of the louse infestation2 and sheep that develop lesions have B. ovis-specific homocytotrophic antibody. Serum histamine concentrations are significantly higher in louse-infested lambs than louse-naive lambs.3
Lesions commence on the neck and shoulders and may extend over the entire pelt. Widely distributed lesions, ‘scatter cockle’, are attributed to infestation with B. ovis, and this is the most common cause but ‘rib cockle’ may be a hypersensitivity to infestation with the sheep ked Melophagus ovinus. Pelt lesions in the dorsal midline region are usually due to infection with Dermatophilus congolensis.1
This rests with the control of B. ovis. For cockle control sheep should be treated off-shears with pour-on or spray-on insecticide and, as soon as practical after shearing, treated by saturation dipping. Saturation dipping is required to significantly reduce louse populations.4 Prelambing dipping is also recommended to reduce the risk of lambs acquiring louse infestations.
Woolslip is a condition in which housed ewes, shorn in winter, lose part of their fleece and develop bald patches over a large area of the rear half of the back.1 This commonly starts at the base of the tail and progresses to the rump and back and less commonly the neck. There is no systemic disease; the skin is normal. Histological examination of skin biopsies show that in affected sheep the wool follicles are in the active anogen stage rather than the inactive telogen phase of unaffected cohort sheep and the wool regrows immediately following loss.1 The loss of wool starts 2–3 weeks after shearing. All breeds are equally susceptible and there is no effect of age or whether the sheep are carrying single or twin lambs; up to 40% of a flock may be affected. The wool loss occurs because of a premature and synchronized shedding of wool fibers and not because of a pathological process which damages the wool fiber. Wool shedding can be induced experimentally by prolonged treatments with corticosteroids and the current explanation for the wool shedding that occurs with the woolslip syndrome is that blood corticosteroid levels rise after the stress of shearing and are maintained for a long period because of the trauma of being housed and shorn and kept in the cold. Blood zinc concentrations in woolslip affected sheep are within the normal range and there is no epidermal change as occurs in zinc deficiency.
The prevention of the condition is aimed at reducing the severity and length of the stress period by shearing the sheep at the time of entry to winter housing and insuring a good nutritional plane in the post-shearing period.1 This hypothesis as to cause may not be correct as the syndrome has also been seen in the summer in Wiltshire shorn sheep which had little history of stress in the period immediately preceding the woolslip.2
Woolslip should not be confused with the normal shedding of wool that occurs in breeds such as the Wiltshire or Shetland in the spring period. Loss of wool along the backline also occurs in older longwool sheep and may be exacerbated by lambs playing or sleeping on the ewe.3
Impairment of wool growth and a thinning of fiber diameter can occur during the course of any severe disease such as bluetongue, pregnancy toxemia, or foot rot temporarily affecting the growth of the fleece. This results in a segment of the wool fiber that has decreased tensile strength and the condition has the name tender wool. Following recovery from the inciting disease the wool growth is normal but there is a line of wool with poor tensile strength in the staple. This can be observed in the intact fleece as a line of decreased fibre diameter, often with a change in crimp character and discoloration due to entrapment of dust. The wool may break if the staple on either side of this break is sharply snapped between the fingers. The fleece may subsequently be shed in part or in whole at the level of the defect, a condition known as wool break. Tender wool downgrades the value of a fleece and has economic significance in wool-producing sheep.
Zinc deficiency can reduce keratinization, reduce wool growth and occasionally result in fleece loss in sheep.4,5 Wool loss associated with pruritus occurs in association with external parasite infestations (Ch. 27) and with scrapie and pseudorabies in ruminants.
Pelodora dermatitis, characterized by thickening of the skin and complete wool loss in affected skin areas is recorded in winter-housed sheep where there was poor bedding management. The condition affected the majority of the ewes at risk. The parasite, Peladora (Rhabditis) strongyloides is a free living nematode commonly present in decaying organic material but can invade hair follicles to produce an inflammatory response. Histological examination of the skin showed the presence of the parasite in wool follicles and infiltration of eosinophils and mast cells in connective tissue. Affected skin areas were those that had contact with the bedding when the sheep were lying down and large numbers of the nematode were found in the bedding. Clinical signs regressed with the more frequent provision of new bedding and disinfection of the stable.6
Wool eating can occur as a result pica associated with micronutrient deficiency. A condition called shimao zheng, occurring in a region of the Gansu province of China has wool eating as its primary manifestation. The disease has a seasonal occurrence with the peak incidence in January through April. Both goats and sheep are affected but the incidence and severity is much higher in goats where 90% may show signs. Affected animals bite the wool or hair off their own or other animals bodies particularly in the hip, belly, and shoulder areas. Histology on biopsies shows heavily keratinized epithelial cells, a decreased number of hair and aggregated foci of lymphocytes in the dermis. Controlled trials have shown the condition can be corrected by supplementation with sulphur, copper, and iron.7,8 Wool eating is also recorded in Israel possibly associated with trace element copper and zinc deficiency.9 Wool and hair loss in individual sheep and cattle in association with excessive licking is recorded and are postulated as psychogenic dermatoses.10
1 Morgan KL, et al. Vet Rec. 1986;119:621.
2 French NP, et al. Vet Rec. 1990;127:267.
3 Winter AC. Vet Annual. 1995;35:313.
4 White CL, et al. Brit J Nutrit. 1994;71:425.
5 Masters DG, et al. Aust J Biol Sci. 1985;38:355.
6 Ramos JJ, et al. Vet Rec. 1996;138:474.
7 Youde H. Vet Res Communications. 2002;25:585.
8 Youde H. Vet Res Communications. 2002;26:39.