Occurrence: Worldwide Age affected: Piglets pre-weaning, weaners, (all ages)
Photo: Vetrifot – Geert Bistervel

Effects: Brown greasy areas of skin, scales, scabs (no itching), weight loss, death

• Detailed causes
• Clinical signs
• Diagnosis
• Treatment and control

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Detailed causes

Greasy pig disease is caused by Staphylococcus hyicus, a skin bacterium which produces an exfoliative toxin which causes loss of skin cells. Six serotypes and a large number of phage types of the organism exist. The organism is resistant to drying but is readily inactivated by heat. It can be cultivated on a wide variety of media and can be identified to species biochemically. It is sensitive in vitro to many antibiotics including penicillins, fluoroquinolones, trimethoprim sulphonamide and cephalosporins. Resistance to these can occur. Infection with S. hyicus often follows abrasions produced by scratches, bites or rough bedding and is most likely in non-immune pigs. The organism rapidly spreads over the entire skin where it form micro-colonies, causes inflammation and produces its exfoliative toxin to cause shedding of epithelial cells, crust formation, formation of vesicles (blisters), pustules and acanthosis. The gross changes of skin reddening are associated with inflammation and excess sebaceous secretion. A neutrophil (white blood cell) response occurs, followed by erosion of the skin down to the basal layers in some areas. Affected piglets die from dehydration and sometimes from loss or protein. Immunity (either passive or active) protects against further infection by the same phage type or serotype.

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Clinical signs

The disease commonly occurs in piglets of between 7 days and 5 weeks of age. The clinical signs begin with listlessness, a dulling of the skin and the appearance of thin, pale brown flecks or scales on the skin surface. There is often scabbing of the cheeks or knees due to fighting or kneeing on rough floors. Within 3-5 days the scabs become darker in colour and extend over much of the back and discolour the abdomen. The skin surface become covered with exudate which gives it a greasy texture and which mats the hair. Affected pigs do not scratch. Affected animals lose weight rapidly and up to 90% of the younger pigs eventually die, often with a grossly thickened, wrinkled skin within 5-10 days. Recovery occurs by healing of the scabs, but takes at least 10 days. Fever is usually absent. Exudative epidermitis usually only affects a few litters on a farm and may not affect all the animals in any one litter. The disease may persist in successive batches of pigs following weaning and 1-2 cm patches of greasy exudate or areas of ulceration can occur on the back or rump or gilts and sows.

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Diagnosis

Diagnosis is based on clinical signs and the age of the affected pigs (7 days to 5 weeks). The presence of a dull skin, and thin, pale brown flecks or scales on the abdominal skin surface suggest early disease. The developed skin lesions are unmistakable when the entire piglet become wrinkled and covered with a greasy exudate which mats the hair. The absence of scratching differentiates the condition from mange. Post-mortem examination adds little to the diagnosis as the main features are restricted to the skin. Diagnosis is confirmed by the isolation of S. hyicus from the skin in profuse culture and microscopical examination of the skin can confirm the absence of other conditions such as parakeratosis and swine pox which might be confused with greasy pig disease. The identification of the disease in adults is more difficult as S. hyicus invades any local lesion of the skin and the underlying cause may be insect bites, injections, abscesses or abrasions.

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Treatment and control

Early cases may be treated successfully using amoxicillin, ampicllin, fluoroquinolone, ceftiofur, trimethoprim sulphonamide and lincomycin, or tylosin by injection or orally in less severe cases. Affected piglets should be given access to water and fluid replacers and washed in a solution of cetrimide or other mild disinfectant. Injections or oral treatment may need to be repeated daily for 2-3 days. Antimicrobial resistance can be present, or arise, after prolonged treatment. The disease may be controlled by clipping the teeth of litters at risk, but providing soft bedding, e.g. chaffed straw and removing sharp wood shavings if present. Hygiene, washing of sows into farrowing houses and local treatment of lesions on sows may all reduce infection. Thorough cleaning and disinfection of accommodation should be carried out between farrowings. Emergency vaccines (autogenous bacterins) have been used to reduce the duration of outbreaks in piglets by sow vaccination and by the vaccination of piglets when infection occurs at weaning, but only protect against the vaccine strain. The disease is introduced by carrier pigs and isolation may protect a herd. The piglets of non-immune gilts introduced to an infected herd are particularly likely to be affected and should be examined frequently.

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