Experimental Infection of Mink Enforces the Role of Arcanobacterium phocae as Causative Agent of Fur Animal Epidemic Necrotic Pyoderma (FENP)

• Published in: PLOS ONE
• Main Authors: Nordgren, Heli, Aaltonen, Kirsi, Raunio-Saarnisto, Mirja, Sukura, Antti, Vapalahti, Olli, Sironen, Tarja
• Other Authors: Veterinary Biosciences, Medicum, Department of Virology, Clinicum, Viral Zoonosis Research Unit, Emerging Infections Research Group
• Format: Article in Journal/Newspaper
• Language: English
• Published: PUBLIC LIBRARY OF SCIENCE 2017
• Subjects: 413 Veterinary science; Vulpes lagopus
• Online Access: http://hdl.handle.net/10138/174570

Fur Animal Epidemic Necrotic Pyoderma (FENP) is a severe, often lethal infectious disease affecting all three fur animal species: mink (Neovision vision), foxes (Vulpes lagopus) and finnraccoons (Nyctereutes procyonoides). Previous studies showed an association between Arcanobacterium phocae and FENP. An experimental infection was conducted to confirm the ability of A. phocae to infect mink either alone or concurrently with a novel Streptococcus sp. found together with A. phocae in many cases of FENP. Different inoculation methods were tested to study possible routes of transmission. Typical signs, and gross- and histopathological findings for FENP were detected when naïve mink were infected with the tissue extract of mink with FENP, using a subcutaneous/ intradermal infection route. Edema, hemorrhage, necrosis and pus formation were detected in the infection site. A pure culture preparation of A. phocae alone or concurrently with the novel Streptococcus sp. caused severe acute signs of lethargy, apathy and anorexia and even mortality. The histopathological findings were similar to those found in naturally occurring cases of FENP. In contrast, the perorally infected mink presented no clinical signs nor any gross- or histopathological lesions. This study showed that A. phocae is able to cause FENP. The study also indicated that predisposing factors such as the environment, the general condition of the animals, temperature and skin trauma contribute to the development of the disease. Peer reviewed