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Erysipelas is an infectious disease mostly of growing or adult swine. It may be clinically inapparent, may cause acute illness involving many animals, or be a chronic disease characterized by enlarged joints, lameness, and endocarditis. Rhomboid skin (diamond-skin) lesions are an inconsistent feature only associated with acute cases.


Erysipelas occurs in swine, lambs and turkeys. It occurs occasionally in other poultry and many kinds of wild birds. Seasonal distribution has not been documented but losses may be greater during warm summer months. Sporadic outbreaks are seen in most kinds of livestock, wild mammals (including rodents), reptiles and amphibians. Erysipeloid, a localized skin infection, occasionally occurs in people who work with infected animals or process meats, poultry, fish or animal by-products. In humans, the disease referred to as “erysipelas” is actually caused by a streptococcal infection.

Historical information

In 1885, Dr. Theobald Smith isolated an organism from swine in the US that was similar to one Pasteur had isolated 3 years earlier from swine with rouget du porc; both were eventually identified as Erysipelothrix rhusiopathiae, the causative agent of swine erysipelas (SE). In 1886 Dr. Friedrich Löffler, a German bacteriologist, published the first accurate description of SE.

In the US, SE did not assume importance until 1928 when several outbreaks were reported in South Dakota. Within a few years, erysipelas began to be reported frequently from many geographic regions. Prevalence of SE decreased after introduction of bacterins but remains a constant threat, unaffected by widespread adoption of confinement rearing.


Erysipelothrix rhusiopathiae is a Gram-positive, aerobic, slightly bent, thin bacillus. It is resistant to many environmental influences and survives for long periods of time in pork meats, cured hams, contaminated fish meal and decaying animal carcasses. There are at least 26 serotypes of which swine are susceptible to at least 15. In the United States, most isolates from sick pigs are serotype 1a, followed by 2, 5, and 1b. Nonpathogenic species (E. tonsillarum) have been isolated from normal swine. The organism is sensitive to penicillin and usually to tetracyclines. It resists many antibiotics and sulfonamides. It can be destroyed by many disinfectants, including caustic soda and hypochlorites.


Erysipelothrix rhusiopathiae is thought to be spread among swine by carriers in the herd. Many healthy swine are carriers of pathogenic and/or nonpathogenic Erysipelothrix and disseminate the organism in their feces and oronasal secretions. Pigs affected with erysipelas also shed large numbers that contaminate feed, water, soil and bedding. Contaminated soil probably does not remain infective for more than 35 days. The resistant organisms can flow in surface water to adjacent premises. A wide range of wild mammals, poultry, wild birds and pets can disseminate the bacteria. There is empirical evidence that biting flies and ticks can sometimes transmit E. rhusiopathiae between swine. The many carriers of E. rhusiopathiae make eradication of SE unlikely.


Ingestion of contaminated feed and water usually allows E. rhusiopathiae to gain access to the body, probably through the tonsils or other lymphoid tissue of the digestive tract (the organism often can be cultured from tonsils of normal swine). Less often, contaminated skin wounds may permit entry. In acute erysipelas, and perhaps in other forms of the disease, a bacteremia develops and leads to spread of organisms throughout the body.

The precise mechanism by which E. rhusiopathiae causes disease is speculative. The organism produces neuraminidase, an enzyme that cleaves mucopolysaccharides in cell walls which may mediate the widespread vascular damage that accompanies SE. Vascular damage leads to thrombosis and interference with microcirculation in capillaries and venules at many sites.

In chronic arthritic cases, there is a vasculitis with exudation of fibrin into perivascular tissues and joint(s). There also is marked villous proliferation of the synovial membrane. Joint lesions are more proliferative than exudative. Pannus may develop and eventually result in destruction of articular cartilage and ankylosis of adjacent bones. Connective tissue formation around joints is stimulated, apparently by perivascular fibrin, and the joint capsule may be thickened. Persistence of inflammation around an affected joint may be from a few living bacteria in the joint or it may be the result of hypersensitivity to remaining bacterial antigens.

Vegetative, valvular endocarditis, another manifestation of chronic erysipelas, is less common than joint involvement. Emboli of E. rhusiopathiae are believed to cause inflammation of blood vessels within heart valves. In the inflammatory process, the endocardium is breached and bacterial colonies are established at the site. Fibrin is deposited there and slowly organized to form nodular vegetations. Emboli that arise from vegetations can cause sudden death. Interestingly, outbreaks of vegetative endocarditis can occur in the absence of other clinical signs.

Susceptibility to infection is not well understood. Many swine known to have been exposed to organisms do not sicken with the disease. Lactogenic immunity protects piglets for several weeks. In older, susceptible swine, various stresses (heat, aflatoxin, poor nutrition) have been suspected of playing a role in precipitating outbreaks.

Clinical signs

Swine erysipelas will be discussed as acute or chronic erysipelas. However, clinically inapparent erysipelas probably occurs and may precede acute or chronic SE.

Many acute outbreaks of SE occur in animals approaching market weight. Acute outbreaks often begin with the sudden and unexpected death of one or a few thrifty pigs. Careful observation then reveals other sick pigs with very high temperatures (104-108°F), usually without respiratory signs or diarrhea. Sick pigs often have reddened or cyanotic skin, especially about the ears, snout, jowls, throat and ventral abdomen. On a few of the animals there may be discrete, raised, and red to purple areas of skin. These often have a rhomboid or diamond shape and are more obvious on white pigs. On dark skinned pigs, the lesions may be visible or palpable as slightly raised patches of hair. Leg joints are painful but may or may not be swollen. Affected pigs resist getting on their feet but are alert. When forced to arise, they often have to be assisted, squeal with pain, stand with their feet close together and soon lie down again. Pregnant sows may abort.

Classic cutaneous rhomboid urticaria (diamond skin) occurs in a percentage of pigs shortly after the acute febrile stages. Cutaneous lesions may coalesce over the rump, back or shoulders. Large patches of skin may have sloughed or still be attached to underlying, healing areas. Sloughing of the tip of the tail or tips of the ears can occur with chronic erysipelas but can have other causes. In younger pigs (suckling, nursery, grower) with acute erysipelas, signs are similar, with cyanosis of extremities, ears and snouts pronounced and urticaria less common.

The chronic forms of SE may follow acute outbreaks or develop insidiously. SE frequently is manifested by enlargement of joints in an increasing number of pigs, often with little mortality. Chronic SE, when manifested by cutaneous lesions, more often follows acute outbreaks. Pigs with valvular lesions in the heart often present few signs unless exerted. They then may show respiratory distress, perhaps collapse and die.


Pigs which die of acute erysipelas may present as “sudden deaths” and may not have discrete gross lesions. The cyanosis or diamond-shaped skin lesions will remain apparent. Necropsy may reveal congested lymph nodes, often quite edematous; there may be subcapsular hemorrhage if the animal lived a few days after onset. Petechial hemorrhages may be present on the kidneys, epicardium and endocardium. The liver is swollen and the capsule tense. The lungs frequently are congested and edematous. The spleen may be markedly enlarged, especially in cases that lived a few days; it occasionally may contain infarcts.

Chronic, arthritic cases have a proliferative, villous synovitis in one or more swollen joints (hocks or carpal). Synovial fluid is viscous and only modestly increased in amount. The joint capsule may or may not be visibly thickened. An organized inflammatory exudate (pannus) may be present in affected joints, sometimes with ulceration of the articular cartilage or ankylosis of adjacent bony surfaces.

Chronic cutaneous lesions may be apparent as one or more patches of dry, necrotic skin. Sometimes there are granulating, healing areas where patches of necrotic skin have sloughed.

Vegetative, valvular endocarditis of chronic cases usually affects the mitral valve and may appear as irregular masses of considerable size. Such cases often have infarcts in the spleen, kidneys or other sites, the result of embolism from valvular lesions.

Microscopic lesions include vasculitis in capillaries and venules at many lesion sites, including glomerular tufts, pulmonary alveolar walls and skin. E. rhusiopathiae bacteria may be apparent within microthrombi in blood vessels.


Clinical diagnosis is based on signs, typical lesions in several pigs and favorable response of acute cases to high doses of penicillin and/or hyperimmune serum. Pigs in the early stage of acute erysipelas often respond favorably; severe or chronic cases do not. In acute cases, signs of special value in diagnosis include exceptionally high temperatures, evidence of marked pain in multiple joints and typical skin lesions. Diagnosis can be confirmed by bacterial culture of kidney, spleen, lymph nodes, blood, or other tissues and, where available, polymerase chain reaction (PCR). Culture of E. rhusiopathiae is more likely from acute cases; failure to recover the organism should not rule-out a diagnosis of erysipelas. Acute erysipelas must be differentiated from acute hog cholera and acute septicemia (salmonellosis, streptococcal infection). Actinobacillus suis is also reported to cause cutaneous lesions that resemble those of acute SE.

A firm diagnosis is more difficult with chronic cases. Culture attempts on multiple joints often fail. However, the appearance of many cases of arthritis in growing pigs is more typical of erysipelas than of other diseases. Vegetative, valvular endocarditis can be caused by many different organisms, most notably Streptococcus suis.

E. rhusiopathiae should be cultured from those vegetations before diagnosing chronic SE.


Acute outbreaks of SE usually can be controlled by administering penicillin and/or erysipelas antiserum to affected pigs along with antimicrobials added to the drinking water until no sick pigs have been observed for at least three days. Vaccination in the face of an outbreak is warranted.

A vaccination program is advisable for premises on which outbreaks have occurred or where exposure is expected. Attenuated vaccines and bacterins are available with recent products improved, having duration of immunity of 26 weeks and efficacy across a broad spectrum of serotypes. Killed vaccines may be given by injection and attenuated live vaccines via injection or in drinking water. Two doses of most bacterins usually will protect growing pigs to market weight but may have to be boostered later in grow-finish stages in some herds, especially those with a history of repeated exposure to the organism. Booster vaccination at least 1-2 times per year is recommended for breeding stock.

A combination of regular vaccination, good sanitation, the elimination of carriers with skin and joint lesions, and appropriate quarantine measures for purchased stock usually will aid control of SE.