Exudative epidermitis

D J TAYLOR

GENERAL INTRODUCTION: GRAM-POSITIVE COCCI Staphylococcus spp. infections

Introduction

Exudative epidermitis occurs most commonly in piglets of one to five weeks of age and is characterized by the sudden onset of excess secretion and exudation from the skin without pruritis, leading to dehydration, growth depression and death. The disease is caused by the infection of susceptible piglets by pathogenic strains of Staphylococcus hyicus. It spreads horizontally within a herd and continues for months or years where susceptible piglets are continuously exposed to the agent or where predisposing factors, such as abrasive pen fittings, affect successive litters. Skin lesions in adults may become infected with the organism which may exacerbate and delay their healing. Staphylococcus hyicus may occasionally initiate skin lesions in non-immune adults.

Infection appears to be worldwide. The condition has been recognized since 1842,⁹ although its aetiological agent was not described until 1953⁸ and was not confirmed as the cause of the disease until 1965.^{5, 10}

Aetiology

Staphylococcus hyicus is Gram-positive and forms nonhaemolytic white colonies 2 mm in diameter on blood agar and pink colonies on MacConkey agar under aerobic conditions. It is coagulase-negative but DNAase positive, and produces a capsule, and Protein A. Pathogenic strains produce an exfoliative toxin of molecular weight 29 to 30 kDa2, 7 of which at least three antigenic types exist (ExhA, ExhB, ExhC). At least six serotypes and a large number of phage types of the organism have been identified. It is resistant to drying but does not form spores and is readily inactivated by heat.

Epidemiology

Exudative epidermitis occurs sporadically. In the UK in 1994 it occurred in 16,5 per cent of pig herds. It can cause losses of up to 35 per cent during the period of the outbreak, and 9 per cent over the year in susceptible herds.⁶Outbreaks are generally self-limiting, lasting two to three months but may persist for 12 to 18 months. The progeny of non-immune recently purchased gilts are susceptible in a herd where the disease is endemic.

The disease is introduced into clean herds by infected carriers and first occurs in litters in contact with those of carrier sows. The latter remain unaffected. Infection may be transmitted to piglets from the vaginal flora of the sow, from other sites on the sow such as the skin of the teats, or from the environment.¹¹ Infection may persist in improperly cleaned farrowing pens and may even persist in older pigs in local lesions caused by mange or harvest mites. In improperly ventilated flat decks, the disease may spread from mildly affected animals; infection may remain on fittings.

Staphylococcus hyicus has been identified in a number of animal species, such as cattle and horses, but their role, as sources of disease for pigs, is as yet unknown. Isolates from these species and from pigs have not yet been compared using the molecular techniques or tested for pathogenicity in pigs.

Pathogenesis

Infection with S. hyicus often follows abrasions or lesions produced by scratches, bites of mange mites, rough bedding, e.g. sawdust or rough concrete flooring. Application of cultures to the skin of gnotobiotic or specific pathogen-free piglets results in infection of the whole skin within a matter of hours. Lesions of exudative epidermitis can be produced by the subcutaneous injection of culture filtrates containing the exfoliative toxin. Pathogenic strains are encapsulated and resist phagocytosis.

Rounding of epidermal epithelial cells occurs within 12 hours of infection and lesions progress with exfoliation of epithelial cells, crust formation, exocytosis, i.e. neutrophil accumulation in the epidermis, formation of vesicles and pustules and acanthosis. The gross change of skin reddening is associated with inflammation and excess secretion.

Microcolonies of S. hyicus are present in the skin. In some areas erosion down to the stratum germinativum occurs. Affected piglets die from dehydration and sometimes from loss of protein.

Immunity (either passive or active) protects against the homologous phage type or serotype.

Clinical signs and pathology

The disease commonly occurs in piglets of between seven days and five weeks of age. The clinical signs begin with listlessness, a dullness of the skin and the appearance of thin, pale brown flecks or scales on the skin surface, particularly in the axillary and inguinal regions. There is often scabbing of the cheeks or knees due to fighting or kneeling on rough floors. Within three to five days the scabs become darker in colour and extend over much of the back and discolour the abdomen and axillae. The skin surface becomes covered with exudate which gives it a greasy texture and which matts the hair. There is no pruritis. Fever is usually absent. Bacterial multiplication and dirt caught in the scabs soon give the skin a black colour. Affected piglets lose weight rapidly and many eventually die, often with a grossly thickened, wrinkled skin. Death generally occurs within five to ten days. The disease affects younger pigs most severely and up to 90 per cent of those affected may die. Recovery occurs by healing of the scabs, but takes at least ten days. Recovered animals are often appreciably smaller than unaffected litter-mates. Exudative epidermitis usually only affects a few litters on a farm and may not...