Lameness in Pigs in Nurseries

Causes of polyarthritis in this group of pigs usually include Mycoplasma hyorhinis, Haemophilus parasuis, S suis, or Erysipelothrix rhusiopathiae, and less commonly Streptococcus dysgalactiae subsp equisimilis, Actinobacillus equuli subsp equuli, and other bacteria prone to achieve bacteremia. The birth canal and upper respiratory tract of the sow are often the sources of the organisms for the baby pig, which becomes infected in the farrowing room. M hyorhinis and H parasuis circulation in the sow herd can be predictive of infection levels in growing pigs. Alternatively, older pigs act as carriers and are a source of infection for their peers. Pigs affected by E rhusiopathiae also shed organisms in their feces and urine. Essentially, all are systemic diseases with a septicemic phase, and each may manifest as different clinical syndromes or as 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 an infectious arthritis. Moving and mixing pigs (particularly if all-in, all-out management is not used); overcrowding; cold, damp, poorly ventilated, or cold, drafty environments; and changing rations are all major stresses that can lead to development of infectious arthritides or neurologic diseases that affect movement. It is also likely that active viral infections associated with porcine reproductive and respiratory syndrome virus (see Porcine Reproductive and Respiratory Syndrome) or circovirus 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, in the case of chronic erysipelas (see Erysipelas), runt pigs may be lame with hard, swollen joints.

The clinical signs seen in infections caused by M hyorhinis and H parasuis (Glässer’s disease, see Glasser’s Disease) are similar, because both cause painful polyarthritis and polyserositis. The conditions cannot be differentiated grossly at necropsy. Infection with M hyorhinis usually results in lameness with moderate morbidity and low mortality, but H parasuis can cause infection in 50%–75% of pigs and mortality of up to 10%. Outbreaks of Glässer’s disease have been particularly severe in SPF and other naive herds. H parasuis may also play a part as a primary or concomitant agent in swine respiratory disease complex and cause disease in association with porcine reproductive and respiratory syndrome virus or influenza virus. Fever is associated with mycoplasmosis but can be highest in Glässer’s disease (>107°F [41.7°C]) as pigs become anorexic and lame; sometimes H parasuis causes neurologic signs.

At necropsy, polyarthritis and polyserositis are seen with both mycoplasma infection and Glässer’s disease, 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 Glässer’s disease. Hence, M hyorhinis causes a mild synovitis with villous hypertrophy and hyperplasia; an excess of clear, yellow, or brown synovia; and a serofibrinous pericarditis, pleuritis, and peritonitis. Otitis media has also been reported. With H parasuis, a fibrinopurulent synovitis with periarticular edema, polyserositis with pseudomembranes, and sometimes fibrinopurulent meningitis are seen. The articular surfaces are usually unaffected in either condition.

Diagnosis is based on clinical signs, necropsy findings, and detection of the organism. PCR tests are available to detect M hyorhinis and H parasuis. This is important, because bacterial culture of both bacteria can be challenging if any treatment has been instituted or if the pig has been dead more than a few hours. Treatment for either disease must be aggressive and start soon after the onset of clinical signs if it is to be effective. The effectiveness of treating M hyorhinis infections with tylosin, tetracycline, or lincomycin has been variable. Organisms may be susceptible in vitro and resistant in vivo. Treatment of Glässer’s disease is discussed in the relevant chapter (see Glasser’s Disease). With chronicity, success in treating either disease is unlikely.

Appropriate changes in management to reduce stress, strict all-in/all-out housing, and control of viral infections should all minimize the impact of Glässer’s disease. Herds that maintain an SPF status may be free of both M hyorhinis and H parasuis, but in herds with documented outbreaks of Glässer’s disease, morbidity and mortality were high and productivity was decreased. Some 15 serovars of H parasuis have been identified, with much strain variation. Vaccination with commercial or autogenous H parasuis bacterin may alleviate clinical disease in SPF herds. It is important to vaccinate SPF pigs that are to be shipped to conventional herds with vaccine effective against the serovars present in the recipient herd. There is cross-protection among some serovars. Vaccination of sows against H parasuis reduces the prevalence of the problem in nursery pigs through passive immunity.

The streptococcal disease of main concern to the pig industry is caused by S suis (see Streptococcal Infections in Pigs). Although this organism can cause arthritis, CNS signs and pneumonia are the most common clinical presentations.

Although acute erysipelas can be seen in nursery pigs, it may be more typical of growing/finishing pigs (see Lameness in Pigs in Grower/Finisher Areas). If the acute form of the disease affects nursery pigs and is not treated appropriately, the subsequent progression of the disease to the chronic form is seen in the grower/finisher pigs. Adequate vaccination protocols are essential to controlling erysipelas. (See also Swine Erysipelas.)

Kyphosis or lordosis and cuneiform deformities of vertebrae have been seen in weaned pigs. The condition has been reproduced experimentally using gestation and nursery diets deficient in calcium, phosphorus, and vitamin D. “Humpy back” pigs are seen 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 is usually not seen clinically until the grower phase, but lesions must be initiated earlier, giving time for typical pathologic changes to develop by ~10 wk of age.