An acute, exudative dermatitis of pigs from a few days to about eight weeks of age characterized by variable to high morbidity and variable mortality.
Exudative epidermitis (EE) occurs in most major swine-raising countries. It is a sporadic disease, one occasionally seen by most swine practitioners. Although acute EE usually occurs in pigs less than eight weeks old, including nursery pigs, the disease also occurs in a less severe form in older pigs. It seldom occurs in adult swine and then is manifested only as a few localized lesions. A similar dermatitis, “greasy heel,” occurs on the pasterns of horses. The same agent that causes EE can be isolated from the pastern lesions. However, there is no proven transmission from horses to pigs.
Exudative epidermitis was described over 150 years ago. Subsequently, it was reported under a variety of names. Staphylococcus hyicus, the etiologic agent, was first identified as a staphylococcus in 1965 and differentiated from nonpathogenic staphylococci in 1978. Despite research, the complete etiology of EE is unclear.
Staphylococcus hyicus, a Gram-positive coccus, is the etiologic agent. At least six serotypes have been identified. There are differences among strains isolated from pigs and other animals. In swine, S. hyicus has been isolated from many sites, including the skin, nasal mucosa, vagina and prepuce. Under experimental conditions certain strains have reproduced the disease. Typical lesions of EE also have been produced by a bacteria-free supernatant from the agent. Five exfoliative exotoxins that target cells of the stratum granulosum in the epidermis have been identified; both toxigenic and non-toxigenic strains exist. EE may be caused by an exotoxin alone although predisposing factors probably play some role.
Many predisposing factors for EE have been suggested. These include vesicular viral diseases (certain strains of parvovirus, poxvirus, perhaps an unidentified virus), nutritional deficiencies (zinc, vitamins), ringworm infection, pityriasis rosea, parasitism (including lice infestation), housing inadequacies, immunologic inadequacy of young pigs (especially in litters from gilts), lack of competing bacterial flora on the skin, poor hygiene, poor ventilation, high humidity, initial abrasions of the skin from trauma, and genetic susceptibility.
The epidemiology is unclear. S. hyicus is present in many herds and yet causes no disease. Under experimental conditions, only certain strains can colonize the skin and cause disease. Some outbreaks have followed the introduction of swine from other herds. Others have not, so that other risk factors (trauma, environmental irritation) are likely involved. The disease is more frequent in new or start-up herds or when a large number of gilts are being introduced into an established herd. One can only speculate that one or more of the predisposing factors listed above precipitate outbreaks.
Initial skin lesions are focal erosions in the stratum granulosum. Lesions extend into hair follicles and lead to a suppurative folliculitis. Sebaceous glands secrete excessively and there is accumulation of greasy exudate over lesions. There soon is severe epidermal erosion and ulceration. Exudate on the surface dries and deep cracks and fissures develop. Lesions enlarge and may coalesce. Degeneration and sloughing of renal epithelium often occurs, possibly the result of dehydration. Deaths are related to dehydration, loss of serum proteins and electrolytes.
Listlessness or depression and anorexia are early signs and may involve part or all of a litter. Body temperatures seldom are elevated. Although the skin is reddened, there is no pruritis. Initial lesions may occur in the axilla or groin but often go unnoticed. Brownish spots, one to two centimeters in diameter and covered by serum and exudate, appear on the skin of the face or head. The lesions later appear as brown to black crusts. In acute cases the lesions enlarge and coalesce, spread from the head posteriorly and may generalize within 24 to 48 hours. Although initial lesions usually affect haired areas, ulcers may develop on the tongue or in the mouth.
Young pigs can die within 3-5 days. Overall morbidity and mortality usually are high in younger pigs. Pigs older than about eight weeks may have only a few lesions, largely confined to the head. They often survive but tend to gain weight slowly. Adult swine occasionally have a few brown exudative lesions on the back and flanks. Lesions on adults are uncommon and often unrelated to known outbreaks in younger pigs.
At necropsy the affected pigs usually are dehydrated and malodorous. The lesions observed clinically may be quite extensive and vary in number and severity among pigs in the same litter. The crusts often are fissured and contain dirt and filth from the environment. In chronic cases there may be inflammation of the external ears. Lesions are predominantly on haired areas, including the feet, but may affect the mouth and tongue. There may be linear streaks on renal papillae, and ureters and kidney pelvises may contain cellular debris. Occasional pigs have pyelonephritis. Lymph nodes draining the skin are swollen.
Microscopically, there is a pustular dermatitis largely in the stratum corneum and a suppurative folliculitis with bacterial colonies often with suppurative lymphadenitis in enlarged lymph nodes.
Few swine diseases resemble typical EE. Signs and lesions usually are adequate for diagnosis. Confirmation can be made by isolation of S. hyicus or by histopathology. In older pigs with only one or a few localized lesions, EE must be differentiated from sarcoptic mange and other microbial skin infections.
In general, treatment has not been very satisfactory. Injectable antimicrobials may be of some benefit. Anecdotal recommendations have included spraying the pigs several times with solutions such as 10% bleach, chlorhexidine, Virkon® (Durvet) or dilute tamed iodine.
Affected litters or individual pigs should be isolated immediately. Mingling of pigs should be avoided if an outbreak has occurred. If an outbreak is well established in small pigs before diagnosis, it may be prudent to euthanize those with advanced lesions. Any that recover will gain inefficiently.
Prevention starts with providing a high standard of sanitation for pregnant sows, especially in housing, and washing of sows may be of value. Control of EE may depend largely on preventing trauma and improving the environment with better ventilation, cleaner and drier pens, controlled humidity and reduced stocking density. For prophylaxis, vaccination with an autogenous bacterin of S. hyicus has been suggested but results are hard to evaluate since EE is sporadic and may not recur, regardless of vaccination. EE often develops so rapidly that an autogenous bacterin cannot be prepared soon enough.