Age affected: Piglets pre-weaning, weaners (all ages).
Causes: Bacterium – Staphylococcus hyicus; wounds; mismanagement; stress.
Effects: Brown greasy areas of skin, scales, scabs (no itching), weight loss, death.
Greasy pig disease is caused by Staphylococcus hyicus, a skin bacterium which produces an exfoliative toxin which causes loss of skin cells. 6 serotypes and a large number of phage types of the organism exist. Other staphylococci (S. sciuri, S. chromogenes and S. aureus) producing one or more of the exfoliative toxins have also been identified in a few cases. 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.
Transmission of infection is by pig to pig contact, usually from piglet to piglet. In some cases, infection can come from the sow at birth. Indirect infection can take place when infection survives on the rough surfaces of pen furniture. Transmission between farms is normally by means of carrier pigs, but can occur from contaminated tools or clothing. Disease may only occur when non-immune pigs are infected by the organism or a strain not previously present on the farm is introduced.
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 kneeling 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 becomes 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 within 5-10 days, often with a grossly thickened, wrinkled skin. 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.
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 suggests 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 and age of onset differentiates the condition from mange. Diagnosis is confirmed by the isolation of S. hyicus from the skin in profuse culture and its toxin and toxin type can be confirmed by PCR. 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.
Affected pigs are dehydrated, emaciated and have the skin changes described above. The superficial lymph nodes are oedematous, the gut is usually empty and there are white precipitates in the kidney. Microscopical changes in the skin include folding of the lower layers of the skin into the dermis and the presence of microabscesses on the surface. These changes distinguish the condition from parakeratosis present in zinc deficiency and from pig pox, both of which might be confused with exudative epidermitis.
Early cases may be treated successfully using amoxicillin, ampicllin, fluoroquinolones, ceftiofur, trimethoprim sulphonamide and lincomycin, or tylosin by injection or orally in less severe cases when allowed. 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 where allowed, but providing soft bedding, e.g. chaffed straw and removing sharp wood shavings if present may also be helpful. 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 so 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.
Animal strains of MRSA may be present in this syndrome and pose a risk to human health.