Gilts, Sows, and Boars - The Merck Veterinary Manual

Gilts, Sows, and Boars

Degenerative Joint Disease (Osteochondrosis Dissecans, Osteoarthritis, Osteo- arthrosis), Dyschondroplasia (Osteochondrosis), and Leg Weakness

Footrot or Septic Laminitis

Trauma

Many diseases that affect grower/finisher pigs (see Pigs in Grower/Finisher Areas) can also affect young gilts and boars that have been selected as breeding stock. Lameness 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. 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 should be culled. Gilts with buck-kneed forelegs, swaying hindquarters, or a ‘‘standing-under” position of the hindlegs are likely to be culled for lameness early in their reproductive life. Feet should be evaluated for uniformity among and angulation of the digits and for integrity of the wall, sole, and heel.

Lame breeding pigs 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; 3) increased cost of maintaining additional breeding stock; 4) poorer reproductive performance due to regular replacement of lame sows; 5) increased preweaning mortality due to clumsy, lame sows; and 6) reduced fertility in sound boars that are overworked.

Rickets, Osteomalacia, and Osteoporosis:

These syndromes can affect one or more age groups of pigs with various clinical outcomes. Most pigs, including breeding stock, are slaughtered before their skeleton has fully matured; however, some growth plates are functional up to 3.5 yr of age and, therefore, are susceptible to rachitic and other changes.

Osteomalacia is characterized by an excess of unmineralized or poorly mineralized osteoid that forms as bone remodeling occurs (or does not occur). Rickets (see above) is the component of osteomalacia that affects the growth plate. The pathogenesis of osteoporosis is different from that of either rickets or osteomalacia. Established bone loses mineral and mass by a process of osteolysis. Consequently, particularly in sows late in gestation, during lactation, or soon after weaning, bones become weaker and are susceptible to fractures.

A gilt selected for breeding stock that has had clinically normal skeletal development must meet the needs of her own skeleton and that of the growing fetuses. This may result in development of osteomalacia, which is compounded by secretion of mineral in her milk when lactation begins. The gilt 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. Therefore, 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 reestablish 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 the humerus, femur, lumbar vertebrae, and occasionally ribs. Multiple vertebral body fractures have been described in gilts that were considered to have been exposed to stray electrical voltage ( Stray Voltage in Animal Housing: Introduction). 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. 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 is the best (and only) way to curtail the problem.

Osteomyelitis and Spinal Abscesses:

In addition to the causes discussed under grower/finisher pigs (above), 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 (Actinomyces) 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 lameness or bilateral flaccid paralysis of the pelvic limbs, and hypermetria or ataxia. 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 pig should be culled.

Degenerative Joint Disease (Osteochondrosis Dissecans, Osteoarthritis, Osteo- arthrosis), Dyschondroplasia (Osteochondrosis), and Leg Weakness:

These syndromes are the most important causes of lameness and culling for lameness in breeding stock animals and cause major losses in commercial pig herds. They are more important than ever 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 osteoarthritis are seen in all the major breeds of commercial pigs; they are particularly important and common because they are not eliminated by crossbreeding. In addition, epiphyseolysis and epiphyseal separation may be precipitated by weakening of underlying growth plates if they are affected by osteochondrosis. Degenerative joint disease (DJD) can also decrease growth rate in lame finishing pigs, and there is a risk of partial carcass condemnations if affected joints are swollen.

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, 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 due to the bilateral lesions that affect multiple joints in the same pig. Lesions of the ischial tuberosity cause a tendency to slip. Pigs that “walk” on flexed carpuses 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; if both tuberosities are affected, the pig has a hopping gait for a few steps and then collapses. The severity of clinical signs in any of these conditions varies individually, and seemingly less severely affected joints may be protected by the gait if they are more painful than other degenerating joints. Severe joint lesions have been seen in pigs that did not appear to be lame.

In pigs that have limb deformities (eg, osteochondrosis 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, 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 sites most often affected by DJD include the elbow, stifle, hock, and 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 in the middle region 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.

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 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. Overgrown claws predispose gilts to osteochondrosis. Mechanical stress to joints also leads to an increased prevalence of this condition in breeding stock. This occurs during transport or when animals are housed on slippery floors.

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.

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. Pigs with DJD placed on dirt lots or pasture usually become clinically sound within 6 wk.

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. 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. When these practices are not followed, suitable breeding stock must be selected and inferior pigs rejected at the time of arrival at the farm.

Footrot or Septic Laminitis:

This can develop in any age pig but causes serious losses in breeding pigs. Footrot is 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 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 sandcracks, 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 (Actinomyces) 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. If there is a herd problem, all sows in crates should be examined and their feet evaluated at the slaughterhouse. To ensure that lesions are severe enough to be the cause of the lameness, it is advisable to section feet 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 removing abrasive areas. As replacement gilts mature, biotin supplementation seems to enhance the quality of the hoof wall. Foot baths that include copper sulfate, formalin, or oxytetracycline and paraffin help to prevent or alleviate lesions. Success in increasing longevity of pigs with amputated digits has been variable.

Trauma:

Trauma associated with overexertion 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 after breeding or at weaning is a common source of trauma. This can lead to osteochondrosis (see above), epiphysiolysis, fractures, 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. Affected animals must be moved to a pen to avoid repeated trauma to the injured foot. Treatment with a broad-spectrum antibiotic and penned housing enable the lesion to heal.