Many diseases that affect grower/finisher pigs (see Lameness in Pigs: 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. Boars may develop scrotal edema and discomfort, potentially rendering them temporarily unfit for breeding.
If rickets or skeletal weakness has been a problem, 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.
Lameness in breeding pigs can result in the following: 1) continuous replacement of breeding stock and 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) increased preweaning mortality due to clumsy, lame sows that tread or lie on baby pigs; and 6) reduced fertility in sound boars that are overworked while others are lame or being replaced. With greater use of artificial insemination in pigs, the overall boar stud does not have to be as large. However, lameness among boars and an unwillingness to mount, combined with reliance on fewer boars, may ultimately affect reproductive success in a herd or reduce income for a boar stud.
In a recent Swedish survey, 8.6% of sows were culled because of lameness or foot lesions. In a Finnish survey of sows and gilts, 8.8% were lame, with clinical diagnoses of osteochondrosis, skin lesions, or claw lesions; more than twice as many lame pigs were on slatted floors compared to those on solid floors.
In another study of sows in the USA, the removal rates associated with conformational issues over a 1-yr period were, respectively, 16.1% and 12.9% for fore- and hindlimbs. Risk of removal due to lameness increased with severity of the hindlimb conformation score. Over a 10-year survey of sow mortality in herds in Denmark, 72% of sows were culled because of locomotor problems.
Rickets, Osteomalacia, and Osteoporosis
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 (p 1051) that affects the growth plate and is described in younger pigs. The pathogenesis of osteoporosis is different from that of either rickets or osteomalacia. Established bone loses mineral and mass by a process of osteolysis.
Gilts that have normal skeletal development and are selected as breeding stock must continue to meet the needs of their own growing skeleton and, once pregnant, that of the growing fetuses. This may precipitate 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 due to 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 re-establish a social order in the breeding or gestation area. 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 aid in locating spinal lesions if a sow is paralyzed in the pelvic limbs. Affected sows should be culled after an early diagnosis, but they have little salvage value. Prevention through adequate nutrition and exercise for gilts and sows curtails the problem.
Osteomyelitis and Spinal Abscesses
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. Arcanobacterium 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.
Osteochondrosis and Leg Weakness (Degenerative Joint Disease, Dyschondroplasia)
Osteochondrosis and leg weakness are generic terms for a clinical syndrome that is perhaps the most important 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, osteochondrosis and leg weakness are a critical issue.
Osteochondrosis is apparently seen in all the major breeds of purebred and commercial hybrid pigs. Degenerative joint disease (DJD) can decrease growth rate in lame finishing pigs that are less inclined to stand and eat, ultimately affecting pig flow. There is a risk of partial carcass condemnations if affected joints are swollen at the time of slaughter. 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 3-legged lameness or an inability to stand. Most commonly, these animals have a weightbearing, 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 or develop kyphosis 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 in 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.
The pathogenesis of lesions is poorly understood, but foci of poorly mineralized cartilage persist in the metaphyses and epiphyses (and may be points of weakness), or foci of necrotic chondrocytes develop at the interface of the articular-epiphyseal cartilage complex. It is postulated that there is failure of the vasculature that supplies or penetrates the sites where lesions develop or that chondrocytes are not functioning normally to maintain the homeostasis of the cartilage or to promote endochondral ossification. Based on research in horses that develop lesions similar to those in pigs, investigators currently favor failure of vascular supply to areas where lesions are initiated.
Many potential causes of DJD or osteochondrosis have been investigated. 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 developing 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 and protein concentrations of the ration in an attempt to influence the development of lesions has been inconclusive. 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 DJD or osteochondrosis. Deficiencies of zinc and manganese may be causal factors in DJD, but there is a paucity of evidence from research.
The stress of mixing pigs appears to have little impact on the frequency of DJD. 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. Downgrading carcass characteristics by using genetic selection or reducing growth rates by controlling protein and energy intake is counter to the goals of modern swine production for providing quality pork. The use of drugs may alleviate clinical signs but mask the real incidence and create a false sense of security if affected stock is used in the breeding herd.
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, and housing gilts in pens with ≥12 sq ft (1.1 sq m) per animal, 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 of age, 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.
Footrot or Septic Laminitis
Footrot can develop in any age pig but causes serious losses in breeding pigs. Footrot is seen in both confinement and semi-confinement systems, with morbidity of 20–68%. Often a single limb is affected, and the lameness progresses to the point that the pig is 3-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, false sand cracks, deep necrotic ulcers, sinuses at the coronary band, and chronic fibrosis. A mixture of organisms has been isolated from the lesions or identified in smears from lesions and tissue sections. These included Arcanobacterium 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. Wherever 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 parallel with the sole to determine if the soft tissues and bones within the foot are infected.
Treatment with penicillin has proved effective (200,000 U into the lesion or 600,000 U, IM), but success decreases with chronicity of the lesion. Prevention involves improving the nature and cleanliness of the flooring, reducing moisture, and resurfacing rough, abrasive areas. As replacement gilts mature, biotin supplementation seems to enhance the quality and strength of the hoof, and its use in breeding sows is recommended. Foot baths that include copper sulfate or zinc sulfate help to prevent or alleviate lesions. Success in increasing longevity of pigs by amputating severely affected digits has been variable. If amputation is practiced, appropriate wound dressing and a clean, deeply bedded pen are essential to the well-being of the pig.
Trauma associated with over-exertion was considered to have caused 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 re-establish a social order. This can lead directly to fractures of long bones or skin abrasions that may cause secondary bacterial infections.
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.
Last full review/revision March 2012 by Michael A. Hill, BVetMed, MS, PhD, MRCVS