Pigs in Grower/Finisher Areas - The Merck Veterinary Manual

Pigs in Grower/Finisher Areas

Arthritis

Erysipelas

Osteomyelitis

Osteochondrosis and Osteoarthrosis

Rickets

Foot Disorders

Arthritis:

Arthritis caused by Mycoplasma hyosynoviae and Erysipelothrix rhusiopathiae emerge as important causes of lameness in pigs that have been moved to the growing and finishing areas. Again, mixing and moving groups of pigs; overcrowding; cold, drafty environments; or changes in management and feed may precipitate outbreaks of lameness.

In the case of M hyosynoviae , the upper respiratory tract of sows and older pigs in peer groups is the likely source. As colostral immunity wanes at 6-8 wk of age, pigs become susceptible to infection. Morbidity may be low to moderate, but mortality is very low. An acute, afebrile lameness, lasting up to 10 days, develops in groups of grower/finisher pigs or selected replacement stock. Arthritis may be exacerbated by trauma or stress, and pigs exhibit pain in major joints (eg, elbows and stifles) that may develop fluctuating swellings. On necropsy, lesions are restricted to the joints, especially the stifles, and include an excess of clear, yellow synovial fluid that may have fibrin flakes, and yellow synovium with obvious villous hypertrophy. Articular surfaces and periarticular tissues usually are unaffected.

Diagnosis is based on the age of onset of clinical disease and clinical signs that exclude fever or evidence of pneumonia, pleuritis, and peritonitis. If a definitive diagnosis is to be made based on isolation of the organism, samples of synovium and synovial fluid should be collected from untreated pigs within 3-4 days of the onset of clinical signs. However, M hyosynoviae can be cultured from normal joints and is not always recovered from affected joints. Unlike polyarthritis caused by M hyorhinis , response to treatment with tylosin and lincomycin is generally good, and tiamulin, tetracycline, and enrofloxacin may be effective. (Of these, only lincomycin is labeled for use against arthritis in swine.) Concurrent treatment with corticosteroids may be used to curtail the inflammatory response and to alleviate the discomfort. Isoflupredone is labeled for use in food-producing animals. Reduction of any stresses such as mixing and moving batches of pigs helps prevent the problem, and SPF herds can be kept free of the condition. Mycoplasmal arthritis may exacerbate clinical signs associated with degenerative joint disease and osteoarthrosis and vice versa.

Erysipelas:

Erysipelothrix rhusiopathiae is acquired from healthy carrier pigs or the environment, in which the organism can survive for weeks. Erysipelas can be peracute, acute, or chronic. In the peracute form, pigs are found dead without prior clinical signs. In the acute form, pigs become moderately febrile, lethargic, unwilling to rise because of painful joints, anorectic, and cyanotic in their extremities; after 2-3 days, the classic “diamond” (focal, urticarial) skin lesions develop over the body surface. In some outbreaks, lameness is seen without the skin lesions. In the chronic form, the arthritis progresses such that the carpuses and hocks become swollen and firm, and skin necrosis can result in extensive sloughing of portions of the integument. In chronic cases, diskospondylosis also may develop. As the arthritis progresses and joints fuse, pain in the lumbar vertebrae may reduce the libido of a boar.

If the chronic form of erysipelas is investigated as a lameness problem and pigs are necropsied, early changes in the disease process (eg, hemorrhages in lymph nodes, kidneys, and muscles) may be less obvious. An excess of synovial fluid accumulates during the acute phase, but in chronically affected joints, there is villous hypertrophy and hyperplasia, hyperemia, and periarticular fibrosis. If a pannus has formed, the articular surface becomes disrupted. Raised, focal skin lesions progress to sloughed areas and, in extreme cases, the ears and tail may also slough. Vegetative endocarditis is a frequent change.

Diagnosis is based on the clinical signs, of which the “diamond” skin lesions are most consistently useful. All 3 forms of the disease may be seen in the same herd if the problem has not been investigated and treatment has been delayed. Isolation of the causal organism is important for a definitive diagnosis and is most successful if acutely affected, untreated pigs are necropsied. A bacterial culture with an antibiotic sensitivity pattern is useful during treatment of the herd. Sometimes, a rapid response of the acute condition to penicillin is a diagnostic aid.

Vaccination with either modified live or killed organisms is effective in controlling erysipelas in a herd, and outbreaks may be related to noncompliance with vaccination protocols rather than to changes in the virulence of the causal organism or the nature of the disease. Therefore, any investigation of the problem should begin with a detailed vaccination history. However, in some herds, sow vaccination is not sufficient to control the infection in grower/finisher pigs. On these farms, growers must be vaccinated as well as the sows. In the face of an outbreak, concurrent use of killed vaccine and antibiotic is likely to be the most effective control measure. Affected pigs are individually treated with penicillin IM. (See also Swine Erysipelas.)

Osteomyelitis:

This can be seen in pigs of any age. If the integument is damaged, sepsis develops and a suppurative lesion extends to the periosteum and bone. Alternatively, organisms can invade bone from the synovium and infected joints. Poor processing or injection techniques can initiate abscesses that can extend into adjacent bone. Disruption of the integrity of the hoof wall initiates cellulitis and osteomyelitis of one or more phalanges. Ear and flank biting wounds are other foci of infection. Tail biting leads to spinal abscesses that either affect vertebral bodies directly or start as epidural abscesses. Lesions and clinical signs may develop slowly.

Clinical signs vary with both the site and nature of the lesion. If bones or joints of a limb are affected, the condition is usually chronic and the pig becomes 3-legged lame. Young pigs cease to grow. With tail biting, the pig becomes lame or paralyzed in the hind end.

At necropsy, cream or green, caseous pus is seen at the site of the lesion. If Arcanobacterium (Actinomyces) pyogenes is involved, there are abundant pockets of green, semiliquid pus. Other organisms isolated from the abscesses include streptococci, staphylococci, and enterobacteria. Treatment is not usually feasible, and pigs should be culled for humane reasons. However, when applicable, hygiene should be improved and vices such as tail biting controlled or prevented.

Osteochondrosis and Osteoarthrosis:

Lameness associated with these problems may become clinically relevant by the time the pigs are 4-6 mo old, but the major ramifications are in gilts, sows, and boars (see below). The importance of these problems increases if affected replacement breeding stock is brought into a herd that was previously free of either condition.

Rickets:

Although now uncommon, rickets ( Rickets) is occasionally seen. Rickets affects rapidly growing young pigs with a clinical onset at ~10 wk of age. Morbidity is high, and affected pigs become crippled, anorectic, and unthrifty. Limbs are stunted and bowed, joints are swollen, and the head may seem disproportionately large. Long bones of the limbs or ribs can spontaneously fracture so that the pig becomes immobile. Some pigs develop posterior paresis and sit on the ground. Absolute deficiencies of calcium, phosphorus, or vitamin D, or an imbalance of the calcium:phosphorus ratio cause cessation of mineralization at the metaphysis and thickening of the growth plate and epiphyseal growth cartilage.

On necropsy, bones should be dissected to determine if there are any fractures or healing fractures, particularly in the ribs, humeruses, and femurs. The costochondral junctions of most ribs are enlarged to form a rachitic rosary, and ribs may bend. Bone remodelling is inadequate and, radiographically, bones are poorly mineralized. Failure of calcification and endochondral ossification results in thickened, irregular growth plates and epiphyseal growth cartilages in which hemorrhages may be seen grossly. A generalized dietary fibrous osteodystrophy may develop, and bones are easily cut with a knife. Ration analysis is useful, but current batches of feed may have been mixed correctly or with different batches of ingredients, thus making it difficult to relate cause and effect. Keeping samples of each batch of feed for retrospective analysis may be a good practice.

Although rations can be corrected and vitamin D given parenterally, there is no effective treatment, and attempts to rear large numbers of affected pigs have been economically disastrous.

Foot Disorders:

On occasion, grower/finisher pigs have overgrown claws or bruises and cracks in the wall or sole of the hoof. The type of the floor is perhaps the single greatest factor in determining if lesions develop or resolve. Floors with wide slots enable feet to fall between the slats, causing damage. If the floor is too smooth, the balance between growth and wear of the horn is lost; if it is too rough, the hoof wall, coronary band, or skin above the hoof is damaged so that infectious agents can penetrate the foot or adjacent joints. Footrot then develops.