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Rabbit hemorrhagic disease (RHD) was detected in European rabbits ( Oryctolagus cuniculus) for the first time ever in Finland in 2016. Reports of dead feral rabbits in Helsinki started to accumulate from April 2016. The Finnish Food Safety Authority Evira received the first animals in late April, and the main necropsy finding was severe, acute necrotizing hepatitis. Genetic material from RHD virus (RHDV) was detected in the liver and was further characterized as RHDV2. The Finnish virus did not group with RHDV strains from a concurrent outbreak in neighboring Sweden, suggesting another origin. The outbreak peaked in May and lasted until August, after which sightings of both live and dead rabbits became rare. No major outbreaks in domestic rabbits were observed, although infection in one pet rabbit was confirmed.

Brucella infection in seals was reported for the first time in 1994 around the coast of Scotland. Since then, marine mammal Brucella infections were found to be widely distributed in the northern hemisphere. Two Brucella species affect marine mammals: Brucella pinnipedialis in pinnipeds and Brucella ceti in cetaceans. We examined the livers of Baltic grey seals (Halichoerus grypus) from the Finnish coast (n=122) hunted, found dead, or killed as by-catch in fishing gear in 2013-15 as part of population health monitoring. We detected B. pinnipedialis in the livers of three grey seals. The bacterium was isolated from livers displaying parasitic cholangitis. We also detected Brucella DNA in liver flukes (Pseudamphistomum truncatum) obtained from a Brucella-infected grey seal, suggesting that flukes might be possible vectors of this pathogen in the marine environment.

Influenza A viruses (IAVs) of the subtypes H13 and H16 are primarily found in gulls ( Larus spp., order Charadriiformes). Although the gull-adapted subtypes replicate efficiently during infection, gulls usually remain apparently healthy during infection. Avian influenza virus isolates are generally separated into two distinct populations, North American and Eurasian, because of the limited gene flow between the continents. Reassortment between these lineages does occur occasionally; however, direct intercontinental transmission of all eight gene segments is rare. Extensive research has been done to understand the ecology of IAV subtypes that naturally circulate in ducks (order Anseriformes), but the ecology of H13 and H16 IAVs in gulls remains far less studied. In Finland, gulls were screened for IAVs for passive (dead and diseased gulls) and active (clinically healthy gulls) surveillance purposes during the years 2005-10. During that period, 11 H13, two H16 viruses, and one H3N8 IAV were detected. We sequenced partial and full-length hemagglutinin genes of these gull-origin IAVs for phylogenetic assessments. All but one of the H13 genes clustered together with northern European and northeastern Asian viruses, whereas one virus clustered with North American viruses. Interestingly, a high rate (10/14) of these low-pathogenic IAVs was detected in dead or diseased gulls. The atypical clinical status of the IAV-positive gulls and previous observations of circovirus-like inclusion bodies in diseased gulls during autopsies, led us to screen for concurrent circovirus infections in our samples. The DNA of circovirus, an immunosuppressive pathogen of both birds and mammals, was detected in 54% (7/13) of the tested IAV-positive gulls, whereas only 25% (14/56) of our panel of IAV-negative gulls tested positive by circovirus PCR.

In material examined postmortem in Finland from May 2006 to April 2009, acute generalized toxoplasmosis was the immunohistochemically confirmed cause of death in 14 (8.1%) of 173 European brown hares (Lepus europaeus) and four (2.7%) of 148 mountain hares (Lepus timidus). Sera from 116 of the European brown hares and 99 of the mountain hares were screened with a commercial direct agglutination test for Toxoplasma gondii-specific IgG antibodies at a dilution of 1:40. All sera from cases of fatal toxoplasmosis had high titers of antibodies reactive to T. gondii. In contrast, none of 107 European brown hares and four (4%) of 96 mountain hares that died of other causes were antibody-positive. The proportional mortality rates and the T. gondii antibody prevalences among noncases differed significantly between the two host species (P<0.05). Direct genetic characterization of the causative agent was performed on DNA extracted from formalin-fixed, paraffin-embedded tissue of the hares with fatal toxoplasmosis. Based on the results with six microsatellite markers (B18, TUB2, TgM-A, W35, B17, and M33; all six in 15 cases and four in three cases), all the cases were caused by T. gondii genotype II; the size of the PCR product at the seventh marker (M48) varied (213-229 base pairs). The presence of T. gondii genotype II, which is endemic in Europe, is now confirmed in Finnish wildlife: Natural infections with T. gondii parasites belonging to this widespread genotype caused fatal generalized toxoplasmosis in the two species of wild hares.