Stéphane Thibault, DVM, Diplomate ACVP; Richard Drolet, DVM, MSc, Diplomate ACVP; Robert Alain, MSc; Serge Dea, DVM, PhD
ST, RD: Département de Pathologie et de Microbiologie, Faculté de Médecine Vétérinaire, Université de Montréal, C.P. 5000, St-Hyacinthe, Québec J2S 7C6, Canada; RA, SD: Centre de Recherche en Virologie du Québec, Institut Armand-Frappier, Université du Québec, Laval, Québec, Canada (Reprint requests to R. Drolet)
Thibault S, Drolet R, Alain R, et al. Congenital swine pox: A sporadic skin disorder in nursing piglets. Swine Health Prod. 1998;6(6):276-278.
Congenital swine pox infection was identified in 13 piglets with typical gross cutaneous lesions that were present at birth. Characteristic microscopic features of swine pox infection were noted in the more acute cases, whereas chronic cases presented less specific skin lesions. In the four affected herds, disease occurred as a sporadic condition with low morbidity and high case fatality rates. Episodes were of short duration and the economic impact was negligible. Congenital infection was the only manifestation of the disease in these herds.
Received: April 27, 1998
Accepted: August 20, 1998
Swine pox was first reported in North America in 1929.1 The disease occurs worldwide and is usually associated with operations that have poor sanitation. Swine pox virus is the only member of the genus Suipoxvirus in the family Poxviridae. The virus is very resistant and may persist for almost a year in desiccated conditions.2 Infected swine are the reservoir and pig lice (Haematopinus suis) serve as a mechanical vector, although direct transmission may occur.3 Congenital pox infection in swine has been previously described on only a few occasions and presents with low morbidity and high case fatality rates.4-6 This report describes the diagnostic features of sporadic cases of congenital swine pox on four unrelated farms.
There was no history of swine pox or pediculosis in any of the four case herds, and the sows (parity one to six) that farrowed the affected piglets were clinically normal.
Thirteen of the 14 affected piglets from the four case herds were born with cutaneous pox lesions (Table 1). One piglet (Pig 4) developed cutaneous lesions at 1 week of age that were similar to those of its congenitally infected littermate. According to the attending swine specialists, the lesions on the limb extremities made the piglets reluctant to move and decreased their nursing capability. Affected piglets, other than those submitted alive for necropsy, either died or were euthanized in extremis within the first 10 days of life because their condition rapidly deteriorated.
Pathological and microbiological findings
Gross cutaneous lesions were multifocal and distributed over the entire body (Figure 1) except on Pig 3, where lesions were mainly confined to the snout and limb extremities. Skin lesions were generally circular, 1 mm-1.5 cm in diameter, and varied in appearance. Lesions presented as papules (raised, firm, circumscribed lesions); as pustules that evolved into flattened and crusted brown lesions; or as ulcers (Figures 2 and 3). Lesions were often severe and coalesced on the distal part of the limbs, particularly over the coronary band, heel, and sole. Pustular and ulcerative lesions were also found on the tongue and hard palate of four piglets (Pigs 2 and 5-7). Significant lesions were not found in the internal organs of the affected animals.
Microscopic skin lesions included epidermal and infundibular hyperplasia, ballooning degeneration of keratinocytes with intracytoplasmic eosinophilic inclusion bodies and clear intranuclear vacuoles (central nuclear clearing), spongiosis, and hyperkeratosis (Figure 4). In more advanced lesions, intraepithelial pustules formed with necrosis of the keratinocytes progressing to the development of ulcers. Viral inclusion bodies were found in the skin of five of the seven piglets necropsied (Pigs 1 and 4-7) and also in the oral mucosal epithelium of two piglets (Pigs 6 and 7).
Bacterial culture of the skin of these piglets yielded no significant growth and any internal organs cultured were also negative. Poxvirus particles were observed in Pigs 4-7 by transmission electron microscopy in formalin-fixed skin or in skin homogenate preparations following negative staining (Figure 4).
The morbidity and mortality observed in these herds were consistent with those of previous reports of congenital swine pox.4-6 The episodes were minor and of short duration. Typical evolution of pox lesions includes the classical stages of erythematous macules and papules evolving to pustules without a significant vesicular stage. The final stage includes crusts that were eventually shed. The reported time from macule formation to resolution of lesions is 3-4 weeks, with secondary bacterial infection prolonging the resolution of lesions.3 In this report, the lesions found at birth were subacute to chronic in several piglets, suggesting that the infection had occurred some time before birth.
The differential diagnoses of skin disorders similar to these in nursing piglets should include swine pox, vesicular diseases of swine, parvovirus infection, early stages of ringworm, thrombocytopenic purpura, bite wounds, insect bites, allergic skin reactions, and localized streptococcal and staphylococcal epidermitis.3 Among these conditions, only swine pox virus and parvovirus are reported to cause congenital infections. A porcine parvovirus has been associated with a vesicular disease in 1- to 4-week-old pigs, but the lesions were not present at birth and there was no evidence that the infection was congenital.7 Vaccinia virus causes very similar lesions, although smaller and more transient. Intranuclear vacuoles, as seen in Pigs 4-7, are considered in pigs to be specific to swine pox and can be used to differentiate swine pox from vaccinia lesions.3 Virus isolation was not attempted in our cases, but swine pox virus has been successfully isolated on a few occasions in similarly affected piglets.4,6
In this report as in previous cases, there was no evidence of pox infection in the herds other than the congenital disease. It is impossible to determine whether Pig 4, which developed the lesions at 1 week of age, acquired the infection in utero or represented a case of horizontal transmission from its littermate.
The pathogenesis of congenital swine pox virus infection in pigs has not been studied. It has been speculated that infection may occur in fetuses after a low-level viremia in the sow by causing fetal membrane infection.4 Compartmentalization of the placental membranes in swine probably explains why some fetuses are affected and others are not, and why those affected may be at different stages of infection.
We are grateful to the swine specialists who provided some of the farm data and to J. Lagacé, C. Lussier, and L. Wilson for technical assistance.
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