Lameness in Pigs in Grower/Finisher Areas
Lameness in pigs is of increasing interest in North American swine production. Mycoplasma hyosynoviae in particular has received more attention due, in part, to more intensive diagnostic efforts. Metabolic bone disease has also been an area of focus as problems have arisen after more complex formulations for gestation and grow-finish diets.
Arthritis caused by Mycoplasma hyosynoviae and Erysipelothrix rhusiopathiae emerge as important causes of lameness in pigs that have been moved to the grower/finisher 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 4–8 wk of age, pigs become susceptible to infection. Generally, morbidity is low to moderate, but up to 50% of pigs may be affected; mortality is very low. An acute 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, stifles, and hocks) that may develop soft, fluctuant 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. M hyosynoviae has been isolated at slaughter or necropsy in pigs with degenerative joint disease that is part of the osteochondrosis syndrome, but it is a secondary rather than a causal agent.
Diagnosis is based on the age of onset of clinical disease and clinical signs, including lameness in one or more legs that may be accompanied by fluctuating swelling and puffiness around joints. Typically, pigs are afebrile and there is no evidence of pneumonia, pleuritis, and peritonitis. If a definitive diagnosis is to be made based on detection 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 healthy joints and is not always recovered from affected joints.
Lack of a response to penicillin in acute cases has been used to differentiate this disease from erysipelas. Unlike polyarthritis caused by M hyorhinis, response to treatment with tylosin and lincomycin is generally good if administered promptly, and tiamulin or tetracycline may be effective where allowed. Mycoplasmal arthritis may exacerbate clinical signs associated with degenerative joint disease and osteoarthrosis and vice versa.
Erysipelothrix rhusiopathiae, the cause of erysipelas, is acquired from healthy carrier pigs or the environment, in which the organism can survive for short periods. Erysipelas can be peracute, acute, or chronic. In the peracute form, pigs die without clinical signs. In the acute form, pigs become febrile and may be lethargic and anorectic and unwilling to rise because of painful joints and cyanosis of the extremities; the latter is associated with vasculitis in peripheral vessels. After 2–3 days, the classic “diamond” skin lesions (focal urticaria) develop over the body surface. In some outbreaks, lameness is seen without the skin lesions. In the chronic form, arthritis progresses such that the stifles and hocks become swollen and feel firm on palpation; skin necrosis can result in extensive sloughing of portions of the integument. In chronic cases, discospondylosis also may develop if intervertebral joints are affected. As the arthritis progresses and joints fuse, pain in the lumbar vertebrae may reduce boar libido. Cyanosis in the extremities in chronic cases may be related to heart valve failure. A presumptive diagnosis of acute disease is based on the clinical signs, of which the “diamond” skin lesions are most consistently useful. All three forms of the disease may be seen in the same herd if the problem has not been investigated and treatment has been delayed.
If the chronic form of erysipelas is investigated as a lameness problem and pigs are necropsied, early changes in the disease process will have subsided (eg, hemorrhages in lymph nodes, kidneys, and muscles). 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 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 have sloughed. Vegetative, valvular endocarditis is another finding.
Isolation of the causal organism is important for a definitive diagnosis and is most successful if acutely affected, untreated pigs are necropsied and joint fluid is cultured. PCR testing of chronic lesions (eg, endocarditis) can be used to detect the bacteria in chronic cases. A bacterial culture with an antibiotic sensitivity profile is useful during treatment of the herd. Sometimes, a rapid response of the acute condition to penicillin is a diagnostic aid. Provided the E rhusiopathiae is sensitive to penicillin, this may still be an economic choice for treatments. However, tylosin and lincomycin are also labeled for treatment of erysipelas, and tetracycline may be successful if the organism is susceptible.
Vaccination with either modified-live or killed organisms effectively controls 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 to ensure that sows are regularly vaccinated. Even with sow vaccination, infection is seen in grower/finisher pigs in some herds. On these farms, growers must be vaccinated in addition to the sows. In the face of an outbreak, concurrent use of killed vaccine and antibiotic is likely to be the most effective control measure (see Swine Erysipelas).
Osteomyelitis 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 of 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 a phalangeal bone. Ear and flank biting wounds are other foci of infection. Tail biting can result in local infections that ascend the spinal canal and lead to epidural abscesses that can invade and affect vertebral bodies. Lesions and clinical signs may develop slowly.
Depending on the site of infection, the pig may become ataxic and, ultimately, paralyzed in the pelvic limbs. If bones or joints of a limb are affected, the condition is usually chronic and the pig becomes three-legged lame. Young pigs cease to grow.
At necropsy, cream or green caseous pus is seen at the site of the lesion. If Trueperella pyogenes is involved, there are abundant pockets of green, semiliquid pus. Other organisms isolated from these abscesses may include streptococci, staphylococci, and enterobacteria. Treatment is not usually feasible, and pigs should be culled for humane reasons. However, when applicable, hygiene can be improved, and problems such as tail biting controlled or prevented.
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 Lameness in Pigs in Nurseries). Because there is a hereditary component, the importance of these problems increases if affected replacement breeding stock is brought into a herd that was previously free of either condition.
Although now uncommon, rickets (see Rickets) is occasionally seen, usually associated with a feed formulation or mixing error. 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 can spontaneously fracture so that the pig becomes severely lame and unwilling to move. Ribs may fracture. Some pigs develop posterior paresis and sit on the ground if vertebral bodies fracture and damage the spinal cord.
Absolute deficiencies of calcium, phosphorus, or vitamin D, or an imbalance of the calcium:phosphorus ratio causes cessation of mineralization at the metaphysis and thickening of the growth plate and epiphyseal growth cartilage.
On necropsy, bones should be dissected to determine whether 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 with moderate manual force. Bone remodeling is inadequate and, radiographically, long bones and ribs 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 if slab sections of the ends of long bones are cut on a band saw. In chronic cases, bones can be cut with a knife. A sudden increase in carcass condemnations or partial condemnations because of fractured limb bones, ribs, or vertebrae at slaughter should trigger investigation of rations and their ability to meet the nutritional needs of growing pigs, particularly with some of the fast-growing, lean contemporary hybrids. Ration analysis is useful, but current batches of feed may have been mixed correctly or with different lots of ingredients, thus making it difficult to relate cause and effect. Keeping frozen samples of each batch of feed for retrospective analysis is 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. Culling affected pigs may thus be the most cost-effective alternative.
On occasion, grower/finisher pigs have overgrown claws or bruises and cracks in the wall or sole of the hoof. The floor type and condition is perhaps the single greatest factor in determining whether lesions develop or resolve. Floors with wide slots enable digits to fall between the slats, causing damage. Floors kept too wet can soften the hoof wall, making them more prone to trauma. 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, resulting in abscess formation.
An absolute or intermittent deficiency of biotin results in weak, flaky keratin that makes hoof walls susceptible to cracking; flaky skin accompanies hoof lesion and there is generally poor reproductive performance in the herd. As gilts are prepared for breeding, supplementing biotin may be helpful. Recommended inclusion rates of biotin are 250–400 mcg/kg complete feed. Trace mineral deficiencies or imbalances can also contribute to compromised hoof wall and heel epidermis formation.
Selenium toxicosis can cause coronary band swelling and necrosis in addition to more generalized signs such as anorexia or even paralysis (see Selenium Toxicosis). Selenium and ergot toxicity can result in hoof sloughing in pigs.
In contemporary systems with adequate ration preparation and storage, nutritional myopathy should not be problematic (see Nutritional Myopathy of Pigs). Although unexpected deaths are typical of selenium and/or vitamin E deficiency, sometimes pigs are found recumbent and unable to rise and walk. At necropsy, a variety of pathologic changes may be seen, including pale muscle masses, epicardial hemorrhages (mulberry heart disease), and a pale, scarred liver with an uneven surface (hepatosis dietetica).
Prevention includes supplementation with selenite so that the total ration concentration is 0.3 ppm selenium. If the condition is diagnosed in a batch of pigs, injectable selenium/vitamin E can be given as a stopgap measure until supplemented feed is part of the nutrition program.