Diamond Skin Disease (Erysipelas)

The Diamond Skin Disease (Erysipelas) causes a sudden death with high fatality in pigs and a characteristic diamond shaped skin lesions, arthritis and endocarditis.

Diamond Skin Disease is an important zoonotic disease.

Etiology

Erysipelothrix rhusiopathiae (insidiosa) is a pathogenic organism where as E. tonsillarum is non-pathogenic. Around 32 serotypes have been identified, among which 15 serotypes are found affecting pigs. Serotype 1 and 2 are more common and isolated from swine. Smooth strain is used to produce antigen.

The non pathogenic E. tonsillarum (serotype-7) is found in tonsil but morphologically similar to E.rhusiopathiae. Cattle strains are pathogenic for pigs. Serotypes, 1a, 3, 5, 6, 8, 11, 21 and N have been isolated from pigs suffering from chronic arthritis and lymphadenitis.

The 64-68 kda proteins are found to be more immunogenic. The organism able to withstand at 60° C for 15 minutes and resistant to normal chemical disinfectants including 0.2% phenol. It is resistant to oxy-tetracycline and diyhydro-streptomycin. It can survive for long time in frozen or refrigerated media and in alkaline soil.

Epidemiology

Prevalence of infection

Both vaccinated and un-vaccinated pigs are affected and has the prevalence of 3-9.8% but it may varies between the places and countries. About 20-40% pigs are acting as carriers. The organism is also isolated from both clinically ill and clinically healthy pigs.

There has been a geographical variation in morbidity (30%) and case fatality rate(7.5%) and it also varies depends on the factors. Finisher pigs are affected by chronic arthritis and extensive acute septicemia during outbreaks. Sudden diet changes may predisposes the condition.

Predisposing factors

Inter-current diseases are risk factors. Poorly constructed floors and cohabitation with other carrier species such as birds.

Source of Infection

Clinically normal pigs are becoming the good.

Transmission

Skin abrasions and alimentary mucosa are considered a portal of entry. Birds, flies and other animals also favours the spread of infection.

Host affected

Un vaccinated pigs greater than 3 months and adults are most commonly affected with high case fatality rate. Wild boars act as reservoirs. Pigs of all ages and furrowed pigs are susceptible. Adult pigs are affected mainly by low virulent strains but young piglets are affected by virulent strains. The organism from bovine tonsils is pathogenic for mice, pigs, and to other animals and humans.

Pathogenesis

Hot and humid weather condition favors the entry of organism into farm premises. The pathogenic serotype produces capsule and resists phagocytosis.

The organism which is producing neuraminidase cleaves the mucopolysaccharides of cell walls and causes vascular damage which results in haemorrhage and thrombosis. Initially, the organism invade the blood stream of all infected animals and develops septicemia in 1-7 days.

Coagulase activity is a virulent factor which is in association with hog cholera may increase the susceptibility of the host. In chronic form, localization is commonly seen in skin, joints and heart valves.

Lesions in cartilage develops in 8 months may continue to progress up to 2 years. Organism attaches to the heart valves leading to endocarditis. In the early stages, there is an accumulation of fluid in joints and synovial membrane.

Hyperaemia of the mucous membrane followed by proliferation of synovial villi, thickening of the joint capsule and enlargement of the local lymphnodes. Disc spondylitis in association with poly arthritis occurs.

The increased levels of IgG and IgM in the synovial fluid in polyarthritis pigs. Microscopic lesion such as vasculitis in capillaries and venules and in many sites including glomeruli, pulmonary capillaries and the skin occurs.

Clinical Signs

Peracute form

High temperature 42 ° C, depression and death observed in affected finisher pigs.

Acute form

Incubation period is 1-7days. Sudden onset of high fever, severe prostration, complete anorexia, thirst, occasional vomiting, reluctant to rise, in-coordination during walking, dyspnoea, conjunctivitis with ocular discharge.

Affected animals may be active and continue to eat during the beginning of the infection
but severely affected pigs show-marked red to purple discolouration of the skin of jowl and ventral surface of the whole body and become cyanotic.

Skin form

Lesions are pathognomonic: Classical diamond shaped, red urticarial plaque, about 2.5-5 cm2 or more diffuse edematous eruption present.

Mostly, lesions seen in belly, inside the thigh, throat, neck and ears. After 2-4 days, the pig recovers or dies as a result of diarrhoea, dyspnoea, and cyanosis.

Chronic form

A non-suppurative proliferative arthritis involving limb and inter-vertebral joint is characteristic.

Synovitis with a serous, serofibrinous amber colored intra-articular effusion seen first and degenerative changes in the sub-endochondral bone cartilage and ligaments follows in later stage.

Joint capsule and villi are thickened if the synovial changes are prominent.

Enlarged dark patches of vascular granulation tissue which spread as a pannus on to the articular surface.

In the bony predominant cases, the articular cartilage is detached from the underlying bone and cause abnormal motility.

Ulceration of articular cartilage fibrosis ankylosis and lymphnode enlargement seen.

In Erysipelas, a characteristic intense erythema, indurations, and a sharply demarcated border which differentiates it from other skin infections.

Reproductive form

In late pregnancy shows septicaemia and death in sucklers are the first indication of the disease in specific pathogen free herds. Abortion occurs due to fever but there is a direct congenital infections.

Circulatory form

Large, friable, vegetation on the heart valves. Rapid heart rate, loud murmur is audible on auscultation if the valves are badly damaged.

Internally, petechial and echymotic haemorrhage mainly on the pleura, peritoneum, beneath the renal capsule, heart, liver and spleen.

Venous infarction of stomach is accompanied by swollen haemorrhagic mesenteric lymphnodes.

Congestion of lung and liver, Infarcts in spleen, Infarcts of kidney yields lot of pure culture, Enlargement of kidney and spleen.

Cauliflower like growths in heart valves is called Vegetative Endocarditis.

Arthritic form

Joint lesions in elbow, hip, hock, stiffle, lameness and stiffness.

Enlargement of the joint is obvious, later become hard and allow healing to occurs Paraplegia due to involvement of inter-vertebral joints or gross distortion of limb joints

Zoonotic implications

Human beings exposed to vaccination with virulent culture develops swollen finger known as Erysipeloid. Mortality rate reach 75 % More prominent localization in skin and low mortality.

Skin lesion disappear in 10 days with no residual signs Serious cases of plague spread and coalesce often over the neck to form a continuous, deep purple area, extending over a greater part of skin surface.

Affected skin become black, hard, edges curl up and separate from an underlying raw surface. Alopecia, sloughing of tail, tip of ears, dermatitis in the form of hyperkeratosis of the skin of back, shoulders, legs and retarded growth The dry skin may hang on and rattle while pig walking or it may slough off. If skin is pink to light purple resolution occur in 4-7days and if dark, angry looking, black/purple prognosis is grave.

Necropsy Findings

Whole carcass may be congested with discoloration of skin.

Classic diamond skin lesions present, diffuse purplish discoloration of the belly and cyanosis of extremities.

Chronic form: Widespread echymotic haemorrhages (kidney, pleura, peritonium, venous infarction of stomach non-suppurative proliferative arthritis and vegetative endocarditis.

Diagnosis

• Based on clinical signs and necropsy findings. Isolation and identification of organism. Smears from heart blood 1-2 days in acute disease.
• The organism is slender, facultative anaerobe, gram positive, rod shaped, single short chain or as a palisade.
• Acute leucocytosis followed by a leukopenia and monocytosis. Leukopenia is moderate, 40% drops in total leukocyte count seen.
• Monocytosis is quiet marked varies from five fold to a ten fold increase (2.5-4.5% normal level rise to 25% ).
• Toxaemia, thrombosis.
• Detection of antibody and antigen done by Fluorescent Antibody test and PCR respectively.
• Enzyme Immunoassay is quicker, easier and more economic to perform.
• The 65 kda antigen is an diagnostic agent and CFT may be of more reliable test.

Sample collection

Culture swabs, joints, synovial fluid, heart valve, spleern, kidney, bone marrow, and particularly long blood. Smears from heart blood.

Differential diagnosis

• Septicemic salmonellosis
• Arthritides of pigs
• Glassers disease
• Mycoplasma anthritis
• Chronic Zinc poisoning
• Rickets
• Foot rot in pigs

Treatment

• Procaine penicillin 50,000 IU/kg bw i/m for 3 days.
• Enrofloxacin 2mg/kb bw i/m for 5days.
• Amoxycillin 10mg/kg bw for 5 days.
• Anti-erysipelas serum.
• Chronic cases does not respond well.
• Most strains are resistant to aspramycin, neomycin, streptomycin, spectinomycin and polymyxins.

Prevention

Vaccine with sero-types 2 and 10 give protection. Single vaccine between 6 and 10 weeks and booster 2-4 weeks intervals behind axilla region can be followed. Crystal violet vaccine can be used very widely.

Control

Control depends on hygiene, bio-security, quarantine, rapid diagnosis and reduction of stress. Adaptation of vaccination policyParental administration of 5-20 ml of serum give protection for 1-2 weeks to 6 weeks during outbreaks.

Suckling piglets in endemic areas are given serum 10 ml/day during first week at monthly intervals until vaccination is done.

Slaughter of reactors based on agglutination reaction can be done Disposal and incineration of carcass, disinfection of premises with hypochlorite.