After reproductive failure, lameness is typically the most important reason for removal of breeding stock from the herd. Lameness in breeding swine can result in the following: 1) higher rate of breeding stock replacement with attendant increased risk of disease introduction; 2) an inability to maintain a breeding schedule due to an unreliable pool of breeding pigs and, ultimately, an impact on pig flow in the grower/finisher area; 3) increased cost of maintaining additional breeding stock; 4) poorer reproductive performance due to regular replacement of lame sows with gilts; 5) poorer growth and feed efficiency in progeny pigs due to a higher proportion of pigs produced by first-parity sows; 6) reduced pigs born alive because of higher stillborn rates in lame sows and reduced subsequent litter size due to poor lactation feed intake; 7) increased preweaning mortality due to clumsy, lame sows that tread or lie on baby pigs; 8) reduced weaning weights of pigs due to reduced feed intake of sows in lactation; 9) reduced salvage value of cull sows due to increased lactation weight loss and sow mortality; and 10) reduced fertility in sound boars that are overworked while others are lame or being replaced. In sum, the impact of breeding herd lameness on the biologic and economic performance of a farm can be substantial.
Many diseases that affect grower/finisher pigs (see Lameness in Pigs in Grower/Finisher Areas) can also affect young gilts and boars selected as breeding stock. Arthritis caused by Mycoplasma hyosynoviae or acute or chronic erysipelas can cause an incapacitating lameness. Polyarthritis and polyserositis caused by M hyorhinis are seen occasionally in these older pigs. Susceptible, stressed adult pigs can succumb to M hyorhinis with a higher fever and a more severe lameness than is seen in nursery pigs. Likewise, Haemophilus parasuis can develop as an acute epidemic disease in gilts sourced from herds free of the bacteria after entering a herd endemically infected. High morbidity and even mortality that is quite refractory to treatment can result.
If rickets or skeletal weakness was a problem in the growing phase, pigs that could have been affected should not be retained as breeding stock. Ambulation should be assessed as a component of breeding stock selection. Pigs with conformational abnormalities of their limbs or restricted or abnormal ambulation should be culled. Feet should be evaluated for uniformity among and angulation of the digits and for integrity of the wall, sole, and heel. If any problems are identified, including abnormal traits such as overgrowth of the major or secondary digits in a particular line of pigs, these pigs also should be culled.
These syndromes can affect older age groups of pigs, with various clinical outcomes. Most pigs, including breeding stock, are slaughtered before their skeleton has fully matured; some growth plates are functional up to 3.5 yr of age and, therefore, are susceptible to rachitic or other changes.
Osteomalacia is characterized by an excess of unmineralized or poorly mineralized osteoid that forms as bone remodeling occurs (or does not occur). Hence, osteomalacia is the component of rickets (see Rickets) that affects the growth plate and is described in younger pigs. In contrast, osteoporosis develops when established bone loses mineral and mass by a process of osteolysis, a different pathogenesis from that of either rickets or osteomalacia.
Gilts that have normal skeletal development and are selected as breeding stock must continue to have their nutritional needs met, both for their own growing skeleton and, once pregnant, that of the growing fetuses. This may precipitate as osteomalacia if amounts of calcium, phosphorus, or vitamin D are inadequate or, in the case of the minerals, inappropriately balanced. The problem is further compounded once the sow farrows, due to secretion of calcium in the milk. A first-parity sow may soon draw on her skeletal reserves and become osteoporotic. Because sows can become pregnant within 7 days of weaning, there is little time for recovery of skeletal mass between one breeding cycle and the next, so the skeleton becomes progressively weaker. Limited exercise may also exacerbate calcium mobilization and bone loss. Consequently, in sows late in gestation, during lactation, or soon after weaning, bones that have become weak are susceptible to fractures. It is not surprising that considerable numbers of first- and second-litter sows are culled because of fractures and lameness.
Factors that may lead to bone fractures include entrapment of a limb in or under the bars of a farrowing crate, activity as sows are moved from their farrowing crates, and fighting as new groups of weaned sows reestablish a social order in the breeding or gestation area in group housing conditions. Sows mounted by other sows that are in estrus are also prone to injury. The most frequent sites of fractures are femurs, humeruses, lumbar vertebrae, and occasionally ribs. Whatever the factors that precipitate the fractures, affected sows are in pain and are either severely lame and unwilling to move or paraplegic.
Diagnosis is based on a history of acute lameness or paraplegia in pregnant, lactating, or recently weaned gilts or sows. Sometimes, crepitus can be detected in affected limbs. A neurologic examination can help locate spinal lesions if a sow is paralyzed in the pelvic limbs. Affected sows should be culled or euthanized after an early diagnosis. Prevention through adequate nutrition and exercise for gilts and sows curtails the problem.
In addition to the causes discussed under grower/finisher pigs, osteomyelitis may also develop secondary to a vertebral fracture or an epiphyseal separation. It is reasonable to assume that occasional “showering” with organisms from superficial wounds, abscesses, or the respiratory or GI tracts can be a source of infection. Trueperella pyogenes seems to be a frequent cause of the suppuration and abscessation. Osteomyelitis of the ulnar epiphysis in young boars and sows has been reported.
Vertebral osteomyelitis and epidural abscesses can cause a variety of signs, including nonspecific lameness, hypermetria, ataxia, or bilateral flaccid paralysis of the pelvic limbs. Except for the temporal nature of the infectious process, clinically it is difficult to differentiate a destructive or space-occupying abscess from a fracture. Regardless of underlying cause, recovery is unlikely, and the pigs should be culled.
Degenerative joint disease (DJD) and leg weakness syndrome are generic terms for a clinical syndrome that is a major cause of lameness and culling for lameness in swine breeding stock. Although the conditions are more often investigated in purebred stock, they can cause major losses in commercial pig herds. Given the increased scale of production in many herds and the shift toward pigs that grow faster, are more muscular, and finish heavier, DJD and leg weakness are critical issues.
Osteochondrosis is a specific developmental condition that represents the major cause of DJD. Osteochondrosis is a defect in the development of cartilage of the growth plates or articular cartilage in growing pigs. The pathogenesis of osteochondrosis is increasingly but still incompletely understood. In osteochondrosis, growth plates are more prone to fracture because of areas of retained hypertrophic cartilage that focally thicken and weaken the cartilage. Lesions develop when articular cartilage on the interior aspect of the joint surface becomes necrotic, ostensibly due to loss of vascular supplies. The necrotic cartilage interferes with the advancing ossification front, and the resulting irregular ossification underlying the weight-bearing cartilage surfaces is prone to clefting (displaced cartilage “chips,” or osteochondrosis dissecans), exposing the endochondral bone and causing pain and lameness. The developmental lesions have a very high prevalence in young pigs but mostly resolve with age and further development.
Osteochondrosis is apparently seen in all the major breeds of purebred and commercial hybrid pigs. Dyschondroplasia results in deformed long bones, particularly the ulna. Pigs that have valgus deformity or permanently flexed carpi tend to be unsuitable for sale as breeding stock and may be lame. In addition, epiphyseolysis and epiphyseal separation may be precipitated by weakening of underlying growth plates and cause an incapacitating lameness.
Although lesions that precede or develop into DJD or result in limb deformities begin to develop in younger pigs, clinical problems are not usually seen until pigs are >4–8 mo old. Frequently, the fastest growing, most muscular, and heaviest pigs are affected. Given time, some pigs (if not culled) recover from episodes of lameness, but deformities remain. Clinical signs vary with the site and extent of lesions and can range from stiffness and a shortened stride or a stride affected by an angular limb deformity to a three-legged lameness or an inability to stand. Most commonly, these animals have a weight-bearing, shifting lameness because of bilateral lesions that affect multiple joints in the same pig. Pigs that “walk” on flexed carpi usually have severe DJD in the elbows, and pigs that tuck their pelvic limbs under their abdomen in a stance that resembles a "circus elephant balancing on a ball" often have DJD that affects stifles, tibial tarsal bones, or joints on intervertebral processes.
If epiphyseal separation of the femoral head has occurred, the pig has difficulty standing and initially will not use the affected limb. A pig that has unilateral separation of the ischiatic tuberosity also has difficulty standing and a tendency to slip; if both tuberosities are affected, the pig has a hopping gait for a few steps after being lifted and then collapses. The severity of clinical signs in any of these conditions varies, and joints with less extensive lesions appear to be protected by the gait if they are more painful than other degenerating joints. Severe joint lesions also have been seen in pigs that did not appear to be lame.
In pigs that have limb deformities (eg, dyschondroplasia affecting the distal ulnar growth plate), thickened, irregular growth plates are seen on radiographs or at necropsy. In degenerating joints, there is an excess of yellow synovia, and synovial villi may have proliferated. There are various irregularities of the articular surface, including folds in the cartilage, clefts into the cartilage, flaps of cartilage, and in severe cases, craters and exposed subchondral bone. In chronic cases, osteophytes develop, detached fragments of cartilage become embedded in the synovium and start to ossify, and craters fill with fibrocartilage. If vertebral joints are affected, vertebrae eventually fuse. Growth plates that are most severely affected by dyschondroplasia are those of the distal part of the ulna and the ribs, whereas joints most often affected by DJD include the elbow, stifle, and hock, or the intervertebral synovial joints.
Many potential causes of DJD or osteochondrosis have been investigated. There is evidence of a genetic component, because within breeds, specific boars have been identified to have progeny with a higher incidence of osteochondrosis. Breeds and lines of pigs that are heavy and well muscled, particularly in the hams, are commonly affected; therefore, crossbreeding for hybrid vigor (ie, to create faster growing, muscular hybrids) does not solve the problem. The fastest growing pigs in a group seem to have a greater propensity for lesions to develop in either growth plates or joints, but once slower-growing pigs reach the body weight of their faster-growing peers, lesions are comparable. Growth hormone may affect chondrocyte metabolism and thereby influence the onset of articular lesions.
Research into manipulating the energy, protein, and mineral concentrations of the ration in an attempt to influence the development of lesions has been inconclusive, even contradictory. None of the imbalances or deficiencies of nutrients that typically are associated with lesions of cartilage or bone (calcium, phosphorus, and vitamins A, C, and D) seemed to exacerbate osteochondrosis. Deficient or excess zinc and manganese may be causal factors in osteochondrosis, but there is a paucity of evidence from research.
The stress of mixing pigs appears to have little impact on the frequency of osteochondrosis, but trauma from handling or housing conditions have been found to affect clinical osteochondrosis. The culling rate due to lameness for sows kept on solid floors is less than that for those kept on slats, but the benefits of placing pigs with DJD on dirt lots or pasture is equivocal. Although such pigs usually become clinically sound within 6 wk, they are potential carriers of the syndromes.
Because osteochondrosis and DJD interfere with production efficiency, the prognosis for affected pigs is poor. At best, the following practices are recommended: selecting against replacement pigs that are lame or have poor conformation, providing adequate rations for the growth of a strong skeleton, housing gilts in pens with ≥12 sq ft (1.1 sq m) per animal, and promoting exercise on nonslip floors. In problem herds, providing a “hardening off” period for gilts is encouraged. This includes purchasing gilts at <75 kg live weight, restricting their feed intake to slow their growth rate, providing ≥1.1 sq m per animal in pens with solid or only partially slatted floors, waiting to breed gilts until they are 8–10 mo old, and housing gilts in pens until they farrow. If replacements are purchased, suitable breeding stock must be found and inferior pigs rejected at the time of arrival at the farm.
Foot lesions can be quite prevalent and severe among sows and boars and have been shown to cause lameness and reduce productivity and longevity of breeding stock. Specific lesions particularly associated with lameness include white line lesions, heel-sole cracks, and heel overgrowth with erosions, but any of the lesions can be significant in individual cases.
As with finishing pigs, floor type and condition are important with respect to lesion development. Housing type and management are also important risk factors for various types of foot lesions. Nutrition, including water quality, can affect the growth rate and quality of the horn wall and heel epithelium.
Bacterial infections of the foot can develop in any age pig but cause serious losses in breeding pigs. Bacterial infections are often a sequelae of foot lesions that allow penetration of bacteria into underlying sensitive foot structures. Foot infections are seen in both confinement and semiconfinement systems, with morbidity of 20%–68%. Often a single limb is affected, and the lameness progresses to the point that the pig is three-legged lame.
Lesions usually develop gradually, and the foot becomes swollen. Lesions vary in severity and can include heel erosions, separation along the white line, toe erosions, sole erosions, vertical hoof wall cracks, deep necrotic ulcers, sinuses at the coronary band, and chronic fibrosis. A mix of organisms has been isolated from the lesions or identified in smears from lesions and tissue sections. These included Trueperella pyogenes, Fusobacterium necrophorum, Borrelia suilla, and a mixture of gram-negative and gram-positive cocci and rods.
A diagnosis is made from the clinical signs and a thorough evaluation of the feet. Ideally, the whole foot should be examined in a recumbent or suitably restrained pig. If there is a herd problem, all sows in crates or pens should be examined. Whenever possible, feet of pigs from affected herds should be evaluated at the slaughterhouse. Superficial examination of some less extensive lesions may lead to inappropriate cause-effect conclusions. Therefore, to ensure that lesions are severe enough to be the cause of the lameness, some pigs can be culled for diagnosis of the problem and their feet sectioned or claws removed after immersing the foot in 140°F water for 60 min to determine whether the soft tissues and bones within the foot are infected.
Treatment of apparent foot infections with penicillin has been commonly practiced (200,000 U into the lesion or 600,000 U, IM), but effectiveness has not been proved and success decreases with chronicity of the lesion. Prevention is a more productive longterm strategy, and it involves improving the nature and cleanliness of the flooring, reducing moisture, resurfacing rough, abrasive areas, and ensuring nutritional adequacy for hoof health. As replacement gilts mature, biotin and trace mineral supplementation enhances the quality and strength of the hoof, and use in breeding sows is recommended.
Trauma associated with overexertion can cause detachment of muscle tendons and a proliferative osteitis on the medial humeral epicondyle and the greater trochanter of the femur in sows. Mixing gilts or sows before or after breeding or at weaning commonly results in pigs becoming injured as they reestablish a social order. This can lead directly to fractures of long bones or skin abrasions that may cause secondary bacterial infections.
Traumatic injuries can also result from movement of groups to and from farrowing facilities, especially movements of gilts into farrowing. Gilts typically are more anxious and flighty than older sows. Carrying a heavy, gravid uterus over potentially slippery flooring over some distance poses a high enough risk of injury without adding other stressors. Movement should be calm and deliberate, with small groups of gilts and sows moved at a time to reduce potential injuries.
Sows housed in stalls with concrete slats may tear their dewclaws when they attempt to stand. Treatment with appropriate antibiotics, protection of the wound with a dressing, and isolation in a hospital pen that has clean, deep bedding should enable a lesion to heal. Prevention by trimming elongated dewclaws is a prudent and simple management practice.