LAUSR

We read with interest the article by Segales et al, “Senecavirus A: An Emerging Pathogen Causing Vesicular Disease and Mortality in Pigs?” The authors postulate that Senecavirus A may cause lesions resembling other vesicular diseases of international importance, including foot-and-mouth disease (FMD). In their introduction, the authors mention a vesiculobullous disease of pigs, porcine idiopathic vesicular disease (PIVD), for which they propose an association to Senecavirus A. PIVD is defined as consisting of “infrequent cases in which swine display erosions and vesicles on the skin, snout, oral cavity, and coronary bands, with unknown cause,” which the authors mention has been reported in multiple countries, including New Zealand. We wish to clearly exclude New Zealand from the list of countries having reported PIVD (and by extension from the list of countries having Senecavirus A presumed present). The authors cite as evidence for the New Zealand inclusion a 1987 article by Montgomery et al. Between 1983 and 1985, a syndrome of acute vesiculobullous disease in pigs occurred within multiple farms in 2 regions in New Zealand. Affected pigs were white-skinned and developed bullae and vesicles on the snout and less frequently the feet. Pigs remained systemically healthy, the lesions developed synchronously in affected pigs, and there was no spread to animals in adjacent pens. Epidemiological investigation found a common exposure to green vegetable material containing celery (Apium graveolens) infected with the fungus Sclerotinia sclerotiorum or parsnips (Pastinaca sativa), combined with exposure to UV light. Subsequent in vivo experimental work confirmed that when parsnip leaves or fungus-infected celery leaves (as in the field outbreak) were fed or rubbed on the snouts and feet of white-skinned pigs and those pigs subsequently exposed to UV light, the pigs developed disease identical to that seen in the outbreak. Furthermore, controls exposed to plant material but not UV light or UV light but not plant material did not develop lesions. Histopathologically, the lesions contained full-thickness degeneration and necrosis of the epidermis. The disease in these New Zealand outbreaks was determined to be phytophotodermatitis, and these cases can therefore not be described as PIVD. In New Zealand, we actively investigate all reported cases of vesiculobullous disease in pigs and ruminants to a point of diagnosis. To date, we are not aware of any reports, published or otherwise, of cases of PIVD in New Zealand pigs despite a high level of awareness of vesicular conditions and the legal requirement to report in our surveillance network of veterinarians, veterinary laboratories, and producers. Thank you for allowing us to correct the record on PIVD in New Zealand pigs. And we are grateful to Segales et al for their important and relevant publication, which illuminates the new and interesting role Senecavirus A might play in vesicular disease in pigs.