Fur animal epidemic necrotic pyoderma: pathology, etiology, and epidemiology

In 2007 Finnish fur farmers detected new kind of signs in farmed mink, foxes and raccoon dogs (Finnraccoon). Mink had severe pyoderma in the head around eyes, mouth or ears or in the feet around the nailbeds. Finnraccoons developed painful abscesses in the paws between the toes. Foxes had severe keratoconjunctivitis that occasionally spread to the eyelids and to facial dermatitis. The disease caused severe symptoms and even increased mortality on the farms. The spread of the disease was typical to an infectious disease. Similar signs have been detected in fur animals in other pelt producing countries as well. Similar signs in mink have been reported for the first time in U.S.A at 1970´s and in Canada 1996. North-American farmers and later researchers linked the onset of the symptoms to the start of feeding mink with feed containing seal byproducts. The University of Helsinki (UH), the Finnish Fur Breeders´ Association (FFBA), and the Finnish Food Safety Authority Evira initiated a collaborative project in 2009 to describe the pathology of the disease, identify the causative organism(s), describe the occurrence of the disease in Finland and to find out possible sources and risk factors for the disease. This thesis includes these studies. Ninety nine fur animals underwent necropsies with complete microbiological examinations, including both diseased and healthy control animals. Due to the common lesions, in diseased animals of all fur animal species, the disease was named Fur animal epidemic necrotic pyoderma (FENP). The bacterium Arcanobacterium phocae was isolated from all diseased animals, but not from healthy controls. The finding of A. phocae is particularly interesting, because this bacterium causes skin inflammations and abscesses in marine mammals such as seals, and there had been found a temporally connection between the onset of the symptoms in mink and the use of seals as feed source in North America. However, the disease occurs also in the countries where seal meat is not used as a feed raw material. Thus, it is probable that there has been a species shift of the bacteria A. phocae from seals to fur animals via feed, and the disease is currently spreading by diseased/carrier animals. The results indicate that the presence of the bacteria A. phocae alone is not enough to cause the disease, as predisposing factors, such as skin or mucosal trauma is needed to evoke the disease. In addition, new Streptococcal species, closely related to Streptococcal species of seals, was detected in these investigations. Furthermore, the infection trial proved that A. phocae caused FENP-like symptoms when mink were experimentally infected. The mail survey study showed that FENP had spread to all areas where fur farming is practiced in Finland and signs of FENP was detected on 40% of responding farms. The results indicated that the disease was introduced to Finland by imported carrier animals and it spread further in the country via domestic purchases. The disease seems to spread on the farms by bird and other wild life contacts. The study revealed also other possible risk factors, such as the farm type; FENP was seen more on larger size farms and on mixed farms (farms farming more than one fur animal species). Also some other predisposing factors were relieved. The results provide a basis for developing preventive methods and treatment of FENP diseased animals to improve animal welfare.