Beyond Rabies: Are Free-Ranging Skunks (Mephitis mephitis) in British Columbia Reservoirs of Emerging Infection?

Wild animal reservoirs are an important source of emerging and zoonotic infection. Skunks (Mephitis mephitis) are a reservoir of skunk strain rabies virus in Canada, with the exception of some areas including the province of British Columbia (BC). Beyond rabies, the reservoir status of skunks for emerging and zoonotic pathogens in BC is unknown. From March 2011 to February 2015, 50 free-ranging skunks were necropsied and tested for 4 pathogens: influenza A, Aleutian disease virus (ADV), Leptospira spp. and Salmonella spp. Two skunks (4%) with respiratory disease caused by influenza A (H1N1) pdm09 were detected during the human flu season suggesting that skunks may represent a target population for reverse zoonosis of this strain of influenza A virus. High prevalence of ADV infection was detected (43/50, 86%). Two of the infected skunks exhibited Aleutian disease (AD) suggesting that skunks act as both a reservoir and a target population for the virus. Most studies of ADV have focused on the potential for infection of free-ranging species living near mink farms. Our study suggests that urban skunks may be a primary host for the virus independent of domestic mink. Whether skunks act as a reservoir of ADV infection for other peridomestic species will depend on host specificity of the viral strains. Leptospira interrogans was detected in 18% (9/49) of the skunks. Identification of the serovar(s) detected is needed to determine any public health risk of leptospirosis following exposure to infected skunks. Salmonella spp. was isolated from three of 43 skunks (7%), specifically S. Typhimurium, S. Muenchen and S. Enteritidis. These serotypes cause disease in humans, but the low prevalence of infection suggests there is a low risk for zoonotic transmission.

Piscine reovirus in wild and farmed salmonids in British Columbia, Canada: 1974-2013.

Piscine reovirus (PRV) was common among wild and farmed salmonids in British Columbia, western Canada, from 1987 to 2013. Salmonid tissues tested for PRV by real-time rRT-PCR included sections from archived paraffin blocks from 1974 to 2008 (n = 363) and fresh-frozen hearts from 2013 (n = 916). The earliest PRV-positive sample was from a wild-source steelhead trout, Oncorhynchus mykiss (Walbaum), from 1977. By histopathology (n = 404), no fish had lesions diagnostic for heart and skeletal muscle inflammation (HSMI). In some groups, lymphohistiocytic endocarditis affected a greater proportion of fish with PRV than fish without PRV, but the range of Ct values among affected fish was within the range of Ct values among unaffected fish. Also, fish with the lowest PRV Ct values (18.4-21.7) lacked endocarditis or any other consistent lesion. From 1987 to 1994, the proportion of PRV positives was not significantly different between farmed Atlantic salmon, Salmo salar L. (44% of 48), and wild-source salmonids (31% of 45). In 2013, the proportion of PRV positives was not significantly different between wild coho salmon, Oncorhynchus kisutch (Walbaum), sampled from British Columbia (5.0% of 60) or the reference region, Alaska, USA (10% of 58).

Parasites and hepatic lesions among pink salmon, Oncorhynchus gorbuscha (Walbaum), during early seawater residence.

Juvenile pink salmon, Oncorhynchus gorbuscha (Walbaum), in the Broughton Archipelago region of western Canada were surveyed over 2 years for sea lice (Lepeophtheirus salmonis and Caligus clemensi), gross and microscopic lesions and evidence of infections with viruses and bacteria. The 1071 fish examined had an approximate ocean residence time no longer than 3 months. A high prevalence of degenerative liver lesions, renal myxosporean parasites and a low prevalence of skin lesions and sea lice were observed. No indications of viral or bacterial diseases were detected in either year. The monthly prevalence of sea lice in 2007 (18-51%) was higher than in 2008 (1-26%), and the infestation density exceeded the lethal threshold in only two fish. Degenerative hepatic lesions and renal myxosporean parasites occurred in approximately 40% of the pink salmon examined in June of both years, and the peak monthly prevalence of hepatocellular hydropic degeneration was greater in 2007 (32%, in May) than in 2008 (12%, in June). Logistic regression analysis found skin lesions and hepatocellular hydropic degeneration significantly associated with sea lice. Most parasites and lesions occurred during both years, but the prevalence was often higher in 2007. Fish weight was 35% less in June 2007 than in June 2008, but condition factor was not different. Further research is required to monitor inter-annual variations and aetiology of the liver lesions and to assess their potential role on pink salmon survival.

Virus characterization, clinical presentation, and pathology associated with H7N3 avian influenza in British Columbia broiler breeder chickens in 2004.

Low-pathogenicity avian influenza (LPAI) subtype H7N3 was diagnosed on a two-age broiler breeder farm in Abbotsford, British Columbia (BC), in early February 2004. The presenting complaint in the older index flock was feed refusal, with 0.5% mortality over 72 hr that resolved over the following week Ten days after the initial complaint in the index flock, a younger flock in an adjacent barn experienced an abrupt spike in mortality (25% in 48 hr). The gross lesions of tracheal hyperemia and hilar pulmonary consolidation were subtle and nonspecific, and the diagnosis of avian influenza required laboratory confirmation. Two different viruses were isolated from the index farm: a LPAI (H7N3) was isolated from the older flock and a high-pathogenicity avian influenza (HPAI) (H7N3), which had an additional 21 base insertion at the hemagglutinin-cleavage site, was isolated from the younger flock. The presence of this insertion sequence and the similarity of adjacent sequences indicate that the LPAI had mutated into HPAI at some point between the first and second barn. Despite enhanced on-farm biosecurity measures, the virus was not contained on the index farm and eventually spread to over 40 commercial poultry facilities before massive depopulation efforts enabled its eradication.