Swinepox in pigs in northern Western Australia Department of Agriculture, CoolibahDrive, Kununm, Western Australia 6743
TFJUBB
Department of Agriculture, Animal Health Laboratories, Baron-Hay Court, South Perth, Western Australia 6151
TM ELLIS RLPEET J PARKINSON
Swinepox is caused by a pox virus, which is highly pathogenic and host specific for pigs. It is immunologically distinct from other pox viruses, and produces a solid immunity. It has not previously been reported in Westem Australia (Seddon and Albiaton 1966). In March and April 1991, swinepox was diagnosed in two backyard pig herds suffering skin eruptions. The herds, one with 20 pigs, the other with 22, were located in the towns of Kununurra and Wyndham in northern Western Australia. To our knowledge this is the f i i t confiied report of swinepox in Western Australia although the disease has previously been suspected. Swinepox outbreaks had recently occuxred in the Darwin area, 440 km to the northeast, in the Northan Taritwy (L Melville personal Communication) and there were other unconfirmed local reports of skin lesions suddenly appearing on pigs. The disease was typical of previously published descriptions of swinepox (Yager and Scott 1985; Blood and Radostits 1989). Most, if not all, pigs in each herd bore
lesions but adult animals tended to be less affected. The lesions on young pigs up to 2 months of age, were more extensive and severe, but no systernic effects were observed. In the worst affectedpigs, face lesionstook up to 3 weeks to disappear,probably becauseof Ongoingtrauma fromfeeding, but most lesions on most pigs had healed by 10 days. Most extemal skin surfaces were affected. Papules, pustules or scabs were mainly concentrated on theface,flanksandlegs(Figurel).Oneseverelyaffectedandlame pig, about 6months old,attracted particular attention when lesions resembling mphmd blisters were found on the curonet and interdigital space but these lesions wem associated with extensive pustular denmititisaffecting the hind limbs generally. The diagnosis of swine pox was c d m e d by laboratory examination of skin biopsy specimens.Focal Superfkial erosions, marked epidermal hyperplasia with acanthosis, ballooning of some epidermal cells, and occasional large eosinophilic intracellularinclusionbodieswerefoundonhistologicalexamination. Eosinqhils and plasma lymphoid cells were visible infitrating the lower epitheliallayers and immediate subcutis. Examination of macerated specimens with negative staining (2% phosphotungsticacid) in a Siemens 102transmission electronmicroscope revealed numerous viral particles approximately 250 to 270nm x 170 to 190 ~I with I I typical pox virus morphology. The virus replicated in primary pig kidney cell monolayers to produce a generalii cytopathiceffect after the thirdpassage. Pox viruses were observedin Supernatantsfrom thesemonolayersby electron mimscopy.
The high morbidity and severity of lesions suggest that these were new infections of non-immune herds. Both were closed herds and materials likely to be contaminated with swinepox virus had not been introduced. Sucking lice, once considered prerequisite to swine pox infections, were not found. Mosquitoes, biting flies and midges are always present in this environment and might have acted as mechanical vectors for the virus (Beveridge 1981). The virus may have originated locally from the few farmed and feral pigs in the area but pox-laden insects could have come from far away, carried by the prevailing easterly winds at the time, but there is only circumstantial evidence that flying biting insects can spread the disease (Beveridge 1981). The identification of swinepox is important because the lesions it produces can resemble those of the exotic vesicular diseases. A costly exotic disease investigation was implemented after the discoveryof swinepox in pigs at Humpty Doo in the Northern Territory in 1983 (D Thomson personal communication). Other differential diagnoses include A c m (Tyroglyphus) spp mite irritation, sarcopticmange, ringworm, pityriasis rosea, hog cholera, dennatosis vegetans, photosensitive dermatitis and sunburn (Yager and Scott 1985;Blood and Radostits 1989).
References Beveridge WIB (1981) Viral Dipeases of Farm Livestock, Aus& Govemcnt PubJishing Service. Canberra,(AnLMlHeobh in Australia, vol I ) p 123 Blood DC rrnd Rad& OM (1989) VeierinaTyMedicine. 7th ed,Bailliere T i n W Loodon.p 571.958 Seddon HR and A I b HE (1966) Disemes OgDomsiic Animals in Australia,Part 4, Proimwn and Virus Diseases, Deparhnent of Health, Commanwerlthof Australia,p 246 YagerJA aadscottDW ( 1 9 ~ ) ~ P a i ~ l o g y ~ D ~ sedited t i c by A ~ s . JubbKW.Kennedy PC and Palmer N. vol 1,3d eQz Acadrmic Press, Lmdon,p470.501 F~ure 1. A young pig affected with swine pox showing lesions on the faw and limb (a)and on the flanks (b).
Australimr VeterinaryJournal, Vol69, No 4,April 1992
(Acceptedfor publication3 Februaq 1992)
99
TFJUBB
Department of Agriculture, Animal Health Laboratories, Baron-Hay Court, South Perth, Western Australia 6151
TM ELLIS RLPEET J PARKINSON
Swinepox is caused by a pox virus, which is highly pathogenic and host specific for pigs. It is immunologically distinct from other pox viruses, and produces a solid immunity. It has not previously been reported in Westem Australia (Seddon and Albiaton 1966). In March and April 1991, swinepox was diagnosed in two backyard pig herds suffering skin eruptions. The herds, one with 20 pigs, the other with 22, were located in the towns of Kununurra and Wyndham in northern Western Australia. To our knowledge this is the f i i t confiied report of swinepox in Western Australia although the disease has previously been suspected. Swinepox outbreaks had recently occuxred in the Darwin area, 440 km to the northeast, in the Northan Taritwy (L Melville personal Communication) and there were other unconfirmed local reports of skin lesions suddenly appearing on pigs. The disease was typical of previously published descriptions of swinepox (Yager and Scott 1985; Blood and Radostits 1989). Most, if not all, pigs in each herd bore
lesions but adult animals tended to be less affected. The lesions on young pigs up to 2 months of age, were more extensive and severe, but no systernic effects were observed. In the worst affectedpigs, face lesionstook up to 3 weeks to disappear,probably becauseof Ongoingtrauma fromfeeding, but most lesions on most pigs had healed by 10 days. Most extemal skin surfaces were affected. Papules, pustules or scabs were mainly concentrated on theface,flanksandlegs(Figurel).Oneseverelyaffectedandlame pig, about 6months old,attracted particular attention when lesions resembling mphmd blisters were found on the curonet and interdigital space but these lesions wem associated with extensive pustular denmititisaffecting the hind limbs generally. The diagnosis of swine pox was c d m e d by laboratory examination of skin biopsy specimens.Focal Superfkial erosions, marked epidermal hyperplasia with acanthosis, ballooning of some epidermal cells, and occasional large eosinophilic intracellularinclusionbodieswerefoundonhistologicalexamination. Eosinqhils and plasma lymphoid cells were visible infitrating the lower epitheliallayers and immediate subcutis. Examination of macerated specimens with negative staining (2% phosphotungsticacid) in a Siemens 102transmission electronmicroscope revealed numerous viral particles approximately 250 to 270nm x 170 to 190 ~I with I I typical pox virus morphology. The virus replicated in primary pig kidney cell monolayers to produce a generalii cytopathiceffect after the thirdpassage. Pox viruses were observedin Supernatantsfrom thesemonolayersby electron mimscopy.
The high morbidity and severity of lesions suggest that these were new infections of non-immune herds. Both were closed herds and materials likely to be contaminated with swinepox virus had not been introduced. Sucking lice, once considered prerequisite to swine pox infections, were not found. Mosquitoes, biting flies and midges are always present in this environment and might have acted as mechanical vectors for the virus (Beveridge 1981). The virus may have originated locally from the few farmed and feral pigs in the area but pox-laden insects could have come from far away, carried by the prevailing easterly winds at the time, but there is only circumstantial evidence that flying biting insects can spread the disease (Beveridge 1981). The identification of swinepox is important because the lesions it produces can resemble those of the exotic vesicular diseases. A costly exotic disease investigation was implemented after the discoveryof swinepox in pigs at Humpty Doo in the Northern Territory in 1983 (D Thomson personal communication). Other differential diagnoses include A c m (Tyroglyphus) spp mite irritation, sarcopticmange, ringworm, pityriasis rosea, hog cholera, dennatosis vegetans, photosensitive dermatitis and sunburn (Yager and Scott 1985;Blood and Radostits 1989).
References Beveridge WIB (1981) Viral Dipeases of Farm Livestock, Aus& Govemcnt PubJishing Service. Canberra,(AnLMlHeobh in Australia, vol I ) p 123 Blood DC rrnd Rad& OM (1989) VeierinaTyMedicine. 7th ed,Bailliere T i n W Loodon.p 571.958 Seddon HR and A I b HE (1966) Disemes OgDomsiic Animals in Australia,Part 4, Proimwn and Virus Diseases, Deparhnent of Health, Commanwerlthof Australia,p 246 YagerJA aadscottDW ( 1 9 ~ ) ~ P a i ~ l o g y ~ D ~ sedited t i c by A ~ s . JubbKW.Kennedy PC and Palmer N. vol 1,3d eQz Acadrmic Press, Lmdon,p470.501 F~ure 1. A young pig affected with swine pox showing lesions on the faw and limb (a)and on the flanks (b).
Australimr VeterinaryJournal, Vol69, No 4,April 1992
(Acceptedfor publication3 Februaq 1992)
99
