Erysipelas is an infectious disease caused by Erysipelothrix rhusiopathiae and is one of the oldest known diseases that affect growing and adult swine. Up to 50% of pigs in intensive swine production areas are considered to be colonized with E rhusiopathiae. The organism commonly resides in the tonsillar tissue; nonpathogenic species (E tonsillarum) have been described as residing in the tonsillar tissue also.
Disease outbreaks may be acute or chronic, and clinically inapparent infections are believed to occur. Acute outbreaks are characterized by sudden and unexpected deaths, febrile episodes, painful joints, and skin lesions that vary from generalized cyanosis to the often-described diamond skin (rhomboid urticaria) lesions. Chronic erysipelas tends to follow acute outbreaks and is characterized by low mortality, enlarged joints, lameness, and postmortem evidence of vegetative endocarditis. Pigs with valvular lesions may exhibit few clinical signs; however, when exerted physically they may show signs of respiratory distress and possibly succumb to the infection.
Growth of E rhusiopathiae on non-enriched media produces pinpoint, nonhemolytic colonies after incubation for 24 hr. After 48 hr of incubation, a zone of incomplete hemolysis becomes evident around colonies. At least 28 different serotypes are recognized, and pigs are considered to be susceptible to at least 15.
On farms where the organism is endemic, pigs are exposed naturally to E rhusiopathiae when they are young. Maternal-derived antibodies provide passive immunity and suppress clinical disease. Older pigs tend to develop protective active immunity as a result of exposure to serotypes that do not induce clinical disease. The organism is excreted by infected pigs in feces and oronasal secretions and survives for short periods in soil and water, where it effectively contaminates the environment. The organism can survive passage through the hostile environment of the stomach and intestines and may remain viable in the feces for several months. Recovered pigs and chronically infected pigs may become carriers of E rhusiopathiae. Healthy swine also may be asymptomatic carriers. Infection is by ingestion of contaminated feed, water, or feces and less commonly through skin abrasions. Following ingestion, the organism most likely enters the body via the tonsils or lymphoid tissue of the GI tract.
The acute and chronic forms of swine erysipelas may occur in sequence or separately. Pigs that succumb to the acute septicemic form may die suddenly without previous clinical signs. This form occurs most frequently in growing and finishing pigs. Acutely infected pigs are depressed, febrile (104–108°F [40–42°C]), and are reluctant to stand and move. Affected pigs squeal excessively when handled, require assistance to stand, and prefer to lie down soon after being forced to stand. Affected pigs may also walk stiffly on their toes and shift weight from limb to limb when standing. Anorexia and thirst are common, and febrile pigs will often seek wet, cool areas to lie down. Skin discoloration may vary from widespread erythema and purplish discoloration of the ears, snout, and abdomen, to diamond-shaped skin lesions almost anywhere on the body, but particularly on the lateral and dorsal regions. The lesions may occur as discrete, pink or purple areas of varying size that become raised and firm to the touch within 2–3 days of illness. They may disappear over the course of a week or progress to a more chronic type of lesion such as diamond-skin disease. If untreated, necrosis and separation of large areas of skin can occur, and the tips of the ears and tail may become necrotic and slough.
Clinical disease is usually sporadic and affects individuals or small groups, but sometimes larger outbreaks occur. Mortality is variable (0–100%) and death may occur up to 6 days after the first signs of illness. Acutely affected pregnant sows may abort, probably due to the fever, and lactating sows may show agalactia. Untreated pigs may develop the chronic form of the disease, usually characterized by chronic arthritis, vegetative valvular endocarditis, or both. Such lesions may also be seen in pigs with no previous signs of septicemia. Valvular endocarditis is most common in mature or young adult pigs and is frequently manifest by death, usually from embolism or cardiac insufficiency. Chronic arthritis, the most common form of chronic infection, produces mild to severe lameness. Affected joints may be difficult to detect initially but eventually become hot and painful to the touch and later visibly enlarged. Dark purple, necrotic skin lesions that commonly slough may be seen. Mortality in chronic cases is low, but growth rate is retarded.
At necropsy, acutely infected pigs may exhibit skin lesions, enlarged and congested lymph nodes, edematous and congested lungs, splenomegaly, and hepatomegaly. Petechial hemorrhages may be observed on the kidneys and heart.
In chronic erysipelas, valvular endocarditis is seen as proliferative, granular growths on the heart valves, and embolisms and infarctions may develop. Arthritis may involve joints of one or more legs, and the intervertebral articulations may be involved. Affected joints may be enlarged, with proliferative, villous synovitis and increased viscosity of synovial fluid, inflammatory exudates, and thickening of the joint capsule. Proliferation and erosion of articular cartilage may result in fibrosis and ankylosis of the joint.
Diagnosis of erysipelas is based on clinical signs, gross lesions, and response to antimicrobial therapy. Acute erysipelas can be difficult to diagnose in individual pigs showing only fever, poor appetite, and listlessness. However, in outbreaks involving several animals, the presence of skin lesions and lameness is likely to be seen in at least some cases and would support a clinical diagnosis. Rhomboid urticaria or diamond skin lesions are diagnostic when present. Isolation of E rhusiopathiae from blood of affected pigs is possible in acute cases and aids in establishing a diagnosis. A rapid, positive response to penicillin therapy in affected pigs supports a diagnosis of acute erysipelas because of the sensitivity of the organism to penicillin. A PCR test, if available, augments the diagnosis of acute erysipelas.
Chronic erysipelas can be difficult to definitively diagnose. Arthritis and lameness, coupled with the presence of vegetative valvular endocarditis postmortem, may support a presumptive diagnosis of chronic erysipelas. However, these lesions can be caused by other infectious agents. A positive culture of valvular vegetations is definitive for diagnosing chronic erysipelas. Serologic tests cannot reliably diagnose erysipelas. Complement fixation tests are considered promising as a diagnostic test for erysipelas because they appear to be more accurate and reliable compared with other tests.
Diseases that should be considered as part of the differential diagnosis include conditions that can precipitate gross lesions suggestive of acute septicemia. Septicemic salmonellosis due to Salmonella choleraesuis infection, classical swine fever due to pestivirus infection, and septicemia and endocarditis due to Streptococcus suis infection should be considered, based on similarity of lesions. Glasser's disease due to Haemophilus parasuis infection and Mycoplasma hyosynoviae infection can precipitate similar changes in synovial tissues and joints of affected pigs.
E rhusiopathiae is sensitive to penicillin. Ideally, affected pigs should be treated at 12-hr intervals for a minimum of 3 days, although longer durations of therapy may be necessary to resolve severe infections. On an economic basis, penicillin is the best choice for antibiotic therapy, but ampicillin and ceftiofur also yield satisfactory results in acute cases. Tetracyclines delivered in the feed or water may be useful when injecting large numbers of affected pigs is impractical. Fever associated with acute infections can be managed by administration of NSAID such as flunixin meglumine or by delivery of aspirin in the water. Erysipelas antiserum, where available, is described as an effective adjunct to antibiotic therapy in treating acute outbreaks. Treatment of chronic infections is usually ineffective and not cost effective. Chronically infected pigs should be culled, because they can contaminate the production environment and serve as a source of infectious organisms that may precipitate future outbreaks.
Vaccination against E rhusiopathiae is very effective in controlling disease outbreaks on swine farms and should be encouraged. Cessation of vaccination on some farms has been linked to disease outbreaks. Injectable bacterins and attenuated, live vaccines delivered via the water are available and provide extended duration of immunity. Optimal timing of vaccination may vary from farm to farm. When E rhusiopathiae is endemic in the production environment, vaccination should precede anticipated outbreaks. Susceptible pigs may be vaccinated prior to weaning, at weaning, or several weeks post-weaning. Male and female swine selected for addition to the breeding herd should be vaccinated, with a booster 3–5 wk later. Thereafter, breeding stock should be vaccinated twice yearly. Vaccines should not be administered to animals undergoing antibiotic therapy because antibiotics can interfere with the subsequent immune response to the vaccine.
Vaccination failures may occur in some herds due to management stresses that compromise the immune system of vaccinated pigs. Antigenic differences between serotypes in vaccines and serotypes circulating on farms can also result in incomplete immunity and disease outbreaks.
In addition to vaccination, attention to sanitation and hygiene and elimination of pigs with clinical signs suggestive of erysipelas infection represent other viable methods that may help control the disease on swine farms.
Last full review/revision March 2012 by Darryl Ragland, DVM, PhD