Erysipelas - Pig

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Also known as: Diamond Skin Disease


An infectious disease caused by Erysipelothrix rhusiopathiae. The disease is characterised by sudden death, septicaemia, arthritis, endocarditis, diamond shaped skin lesions, laminitis and abortion in pregnant sows. Infection occurs via ingestion of contaminated food and water, or through skin abrasions. Swine Erysipelas is commonly called "Diamond skin disease".


Affects pigs of all ages but is most common in pigs kept in poor conditions and also in batches of newly bought gilts. Often occurs during hot humid weather or in particular buildings or fields.


Development of the typical diamond shaped lesion on the skin is pathognomic for this disease. Erysipelas should be considered in any cases where fever and lameness occur together, or in pregnant sows struggling to farrow in combination with a fever.

Clinical Signs

Clinical outcome depends on the susceptibility of the pig and the virulence of the strain of Erysipelas. Pigs are susceptible after maternal antibody has waned (after 3 months) and before protective immunity is acquired (3 years). Changes in diet, extremes of temperature and fatigue are thought to predispose to infection. 3 forms of disease occur: Hyperacute, Acute and Chronic.

The hyperacute form is more common in younger pigs, who may present dull, collapsed or pyrexic with a scarlet tinge to the skin. This form can also present with cases of sudden death.

In the acute form, anorexia and pyrexia are the two most common clinical signs in younger pigs. Affected animals still die but normally after a day during which time they become dyspnoic. Older pigs tend to be pyrexic, anorexic and polydypsic. All pigs show, pink/purple raised areas or extensive diamond-shaped plaques over the skin within 24-48 hours of developing clinical signs. If pregnant sows are infected at this time they may abort.

Following the chronic form of the disease, affected animals can completely recover, lesions often resolve within a week however they can become necrotic and slough. The bacteria localises in joints causing destruction of the synovial membrane lining, hyperaemia, villus formation and lymphocyte and plasma cell infiltration resulting in chronic serofibrinous polyarthritis. Initially joints are hot and swollen leading to stiffness, lameness, non-weight bearing on the affected limbs and eventual ankylosis. Discospondylitis can also occur if animals are chronically affected. Additionally valvular lesions may develop in the heart causing chronic valvular endocarditis, vegetative thrombosis of mitral valves and asymptomatic or congestive heart failure sometimes resulting in sudden death following stress.

Laboratory Tests

Slender Gram-positive rods can be seen on microscopy of acute lesions and filamentous forms in chronic lesions and on smears. High levels of antibody may be found in joint fluid and so may aid diagnosis.

ELISA and Polymerase Chain Reaction tests are also available which can be used directly on tissue or following culture.


Post mortem diagnosis may be needed for definitive diagnosis, in particular the, liver, spleen, heart valves, kidney, a long bone and synovial tissues should be submitted for bacterial examination.


For hyperacute cases, typically no specific lesions are found except general congestion of the carcass and a change in skin colour.

For acute cases there is often congestion of the carcass, in particular the spleen. The lungs are oedematous and petechiae may be found below the kidney, peritoneum and on the heart. Lymph nodes will also be swollen and haemorrhagic. Skin discolouration is also often present.

For chronic cases, growths on heart valves may be evident as well as changes in joint architecture. Joint capsules will be thickened in the presence of granulation tissue and in some cases erosion of articular surfaces may have progressed to ankylosis. Necrotic skin lesions may also be present.


Vegetative lesions on the heart valves consist of connective and granulation tissue. Synovial lesions consist of macrophages and lymphocytes and short gram positive rods may be seen in smears made from blood in the heart.


A 3 day course of Penicillin or a tetracycline is the treatment of choice and the response is normally rapid. Hyperimmune serum is also available however this is an expensive treatment option.


Hygiene is very important to control Erysipelas including good sanitation and regular disinfection of pens. It is advisable to cull chronic cases which will be acting as carrier pigs infecting other animals. Additionally, any pigs being treated should be isolated to reduce the spread of disease. Live attenuated or inactivated vaccines are also available. Immunity lasts for six months and the vaccine is normally given to recently weaned pigs and gilts or sows prior to service.


Varies from sudden death to recovery depending on the virulence of the strain and age and immune status of the affected pig.

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Swine erysipelas and human erysipeloid - a veterinary public health concern. Neelu Gupta; Vikas Gupta; Intas Pharmaceuticals Ltd, Ahmedabad, India, Intas Polivet, 2006, 7, 2, pp 341-347, 21 ref.


Taylor D.J. (2006) Pig Diseases. 8th edition published by the author.