By the time pigs are weaned, diseases that affected the locomotor system during the nursing phase most likely will have resolved spontaneously, responded to aggressive therapy, or resulted in death. Because pigs that survive episodes of polyarthritis generally remain lame, have ≥1 swollen “knotty” joints, and are in poor condition, they should be culled.
In a recent swine producer survey in the USA, weaned pig deaths amounted to 2.9%. CNS and meningitis problems were considered the second most frequent cause of death, representing 13–19% of losses. In this survey, Streptococcus suis meningitis, Glässer's disease, and edema disease, respectively, were perceived to cause illness or death in one or more pigs in 50%, 17%, and 9% of surveyed herds.
Infectious Arthritis or Polyarthritis
Causes of polyarthritis in this group of pigs usually include Mycoplasma hyorhinis, Haemophilus parasuis, Streptococcus suis, or Erysipelothrix rhusiopathiae. Diseases caused by these pathogens are found sporadically among herds or groups of pigs within herds. The upper respiratory tract of the sow is often the source of the organism for the baby pig, which becomes infected in the farrowing room; 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 the 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 (seesee 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 Glässer's Disease) are similar, because both cause painful polyarthritis and polyserositis. At necropsy the conditions cannot be differentiated grossly. 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) 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.
Stunted pigs in the grower/finisher unit that have been necropsied and in which severe, chronic, fibrinous, fibrinopurulent, or fibrous pleuritis, peritonitis, and arthritis were found could have been affected by either of the above conditions earlier in their lives. It is unlikely that they would have reached market weight and are best culled rather than kept as a source of infection for other pigs.
Diagnosis is based on clinical signs, necropsy findings, and the isolation of the organism; however, if any treatment has been instituted, the chances of finding the organisms are reduced. 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 Glässer'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 documented outbreaks of Glässer's disease in these herds, 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 that is 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 Streptococcus 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, but a cause has not been identified. “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 2 segments. However, grossly, there is not always evidence of incomplete or deformed vertebrae. The condition may have a genetic predisposition, but multiple fractured ribs found in the same pig increase suspicion of an underlying or aggravating, perhaps intermittent, nutritional deficiency, such as that which can cause rickets. 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 about 10 wk of age.
Last full review/revision March 2012 by Michael A. Hill, BVetMed, MS, PhD, MRCVS