Lameness in Nursery Pigs

Causes of polyarthritis in pigs of the nursing age range (3–10 weeks) usually include S suis, Glaesserella parasuis, Mycoplasma hyorhinis, and, less commonly, pyogenic streptococci, staphylococci, actinobacilli, Erysipelothrix rhusiopathiae, or other endemic bacteria prone to bacteremia or sepsis.

The birth canal and upper respiratory tract of the sow are often the sources of these organisms for baby pigs during farrowing and lactation. Variation in dam immunity and demonstrated circulation of these common endemic bacteria and their variants in the sow herd, as well as viral agents that compromise resistance to systemic infections, can be predictive of bacterial infection in growing pigs.

Alternatively, older pigs can act as carriers and sources of infection by these bacteria, as well as of lateral transmission, because of commingling sources or poor biosecurity practices. Essentially all cases of polyarthritis are systemic diseases with a septicemic phase, and each disease may have specific clinical signs or may be characterized by a mix of clinical signs.

As with many infectious diseases, management or environmental factors that stress the pig or depress the immune response can precipitate systemic disease or infectious arthritis. Major stresses that can lead to the development of infectious arthritides or neurological diseases that affect movement or gait include moving and mixing pigs (particularly if all-in all-out management is not used); overcrowding; cold, damp and poorly ventilated, drafty environments; and changing rations.

Active viral infections associated with porcine reproductive and respiratory syndrome virus (PRRSV) or porcine circoviruses may predispose groups of nursery pigs to bacterial polyarthritis.

Initially, shifting-leg lameness occurs, and joints can be warm, swollen, and painful. If pigs are febrile, they may have no interest in standing and become inappetent. Chronic forms of polyarthritis with polyserositis result in unthrifty, runt pigs; and with chronic erysipelas, pigs may be lame with hard, swollen joints.

The clinical signs of disease caused by S suis, G parasuis (Glässer disease), M hyorhinis, and A suis are similar in that all four agents can cause painful polyarthritis and polyserositis. The conditions are not easily differentiated grossly on necropsy, and all of these agents are commonly endemic in swine herds.

Infection with M hyorhinis usually results in lameness with moderate morbidity and low mortality. Disease associated with S suis and G parasuis varies with the strain of the organism, the amount of herd immunity, and the presence of concurrent infections. The morbidity rate is commonly ~5%; the mortality rate is fairly high because of severe polysystemic disease, including neurological signs.

Outbreaks of Glässer disease can be particularly severe in specific pathogen-free or otherwise naive herds. All of these agents may also play a part as a primary or concomitant agent in swine respiratory disease complex and cause disease in association with PRRSV or influenza A virus.

Fever is associated with mycoplasmosis and streptococcosis but is usually higher in Glässer disease and erysipelas (> 41.7°C [107°F]).

Infection due to A suis tends to occur sporadically as septicemia, arthritis, and rapid death.

At necropsy, polyarthritis and polyserositis are common with S suis, G parasuis, M hyorhinis, and A suis, and pneumonia may have developed. The initial, exudative response is usually serous or serofibrinous with a mycoplasmal infection; however, it is fibrinous or fibrinopurulent with other bacterial agents.

M hyorhinis causes a mild synovitis in pigs, with villous hypertrophy and hyperplasia; excess of clear, yellow, or brown synovia; and serofibrinous pericarditis, pleuritis, and peritonitis. Otitis media has also been reported.

With G parasuis, S suis, and A suis, a fibrinopurulent synovitis with periarticular edema, polyserositis, and sometimes fibrinopurulent meningitis occurs. The articular surfaces are usually unaffected.

Diagnosis of infectious arthritis or polyarthritis in pigs is based on clinical signs, necropsy findings, and detection of organisms, along with compatible microscopic lesions. PCR tests are commonly available to detect M hyorhinis, G parasuis, A suis, and Erysipelothrix spp. These tests are particularly valuable because bacterial culture can be challenging if any treatment has been instituted, if the pig is in a chronic stage, or if the pig has been dead more than a few hours, especially for M hyorhinis and G parasuis.

Treatment for infectious arthritis and polyarthritis in pigs must be aggressive and start soon after the onset of clinical signs if it is to be effective. The effectiveness of tylosin, tetracycline, and lincomycin in treating M hyorhinis infections has varied. Treatment selection for other common bacteria relies on actual or historical antibiograms.

Organisms may be susceptible in vitro and resistant in vivo. With chronicity, success in treating either disease is unlikely. Appropriate changes in management to minimize stress, strict all-in all-out housing, and control of viral infections should help mitigate the impact of these agents.

Swine herds may be free of both M hyorhinis and G parasuis; however, outbreaks of infection with these organisms in naive populations result in high morbidity and mortality.

Vaccination with commercial or autogenous bacterins may alleviate disease in some herds. It is important to vaccinate naive pigs that are to be shipped to conventional herds against the serovars present in the recipient herd. Vaccination of sows against these agents can decrease the prevalence of the problem in nursery pigs through passive immunity.

Although acute erysipelas can occur in nursery pigs, it is more common in growing-finishing pigs or adults (see Swine Erysipelas). If the acute form of the disease affects nursery pigs, erysipelas must be treated aggressively with antimicrobials and vaccination, and herd vaccination protocols should be reviewed to ensure sow herd immunity. Adequate vaccination protocols are essential to controlling erysipelas.

Kyphosis, lordosis, and cuneiform deformities of vertebrae have been reported in suckling and weaned pigs. The condition has been reproduced experimentally using gestation and nursery diets deficient in calcium, phosphorus, and vitamin D. “Hump back” pigs occur sporadically in some herds; the spine is curved in the vertical plane such that the lumbar vertebrae are higher than the thoracic vertebrae, and there is a kink between the two segments.

Rickets in pigs is usually not observed clinically until the grower phase; however, lesions can occur in growth plates in the nursery, which may not manifest clinically until > 10 weeks of age.