SUMMARYThe bacterium Francisella tularensis causes the vector-borne zoonotic disease tularemia, and may infect a wide range of hosts including invertebrates, mammals and birds. Transmission to humans occurs through contact with infected animals or contaminated environments, or through arthropod vectors. Tularemia has a broad geographical distribution, and there is evidence which suggests local emergence or re-emergence of this disease in Europe. This review was developed to provide an update on the geographical distribution of F. tularensis in humans, wildlife, domestic animals and vector species, to identify potential public health hazards, and to characterize the epidemiology of tularemia in Europe. Information was collated on cases in humans, domestic animals and wildlife, and on reports of detection of the bacterium in arthropod vectors, from 38 European countries for the period 1992-2012. Multiple international databases on human and animal health were consulted, as well as published reports in the literature. Tularemia is a disease of complex epidemiology that is challenging to understand and therefore to control. Many aspects of this disease remain poorly understood. Better understanding is needed of the epidemiological role of animal hosts, potential vectors, mechanisms of maintenance in the different ecosystems, and routes of transmission of the disease.
A novel virus was detected in a sample collected from a Swedish moose (Alces alces). The virus was suggested as a member of the Hepeviridae family, although it was found to be highly divergent from the known four genotypes (gt1–4) of hepatitis E virus (HEV). Moose are regularly hunted for consumption in the whole of Scandinavia. Thus, the finding of this virus may be important from several aspects: (a) as a new diverged HEV in a new animal species, and (b) potential unexplored HEV transmission pathways for human infections. Considering these aspects, we have started the molecular characterization of this virus. A 5.1 kb amplicon was sequenced, and corresponded to the partial ORF1, followed by complete ORF2, ORF3 and poly(A) sequence. In comparison with existing HEVs, the moose HEV genome showed a general nucleotide sequence similarity of 37–63 % and an extensively divergent putative ORF3 sequence. The junction region between the ORFs was also highly divergent; however, two putative secondary stem–loop structures were retained when compared to gt1–4, but with altered structural appearance. In the phylogenetic analysis, the moose HEV deviated and formed its own branch between the gt1–4 and other divergent animal HEVs. The characterization of this highly divergent genome provides important information regarding the diversity of HEV infecting various mammalian species. However, further studies are needed to investigate its prevalence in the moose populations and possibly in other host species, including the risk for human infection.
Abstract. Highly pathogenic avian influenza (HPAI) subtype H5N1 is an infectious systemic viral disease that results in high morbidity and mortality in poultry, and has been reported in a wide range of wild bird species during the last few years. An outbreak of HPAI H5N1 occurred in wild birds in Sweden in 2006 that affected several duck species, geese, swans, gulls, and raptors. Tufted ducks (Aythya fuligula) accounted for the largest number of positive cases and, therefore, were selected for more in-depth histologic and immunohistochemical evaluations. The main histologic lesions associated with the presence of avian influenza antigen were found in the brain, pancreas, and upper respiratory tract. Other tissues in which influenza antigen was variably found included liver, lung, adrenal glands, kidneys, and peripheral nerve ganglia. The current study describes the pathology and viral tissue targeting of H5N1 by using histology, polymerase chain reaction, and immunohistochemistry, and highlights the range and variation in the presentation of the natural disease in tufted ducks.
Data on osteochondrosis and femur dimensions from 195 F2 pigs from a wild boar x Large White intercross were analysed with the aim of detecting quantitative trait loci (QTLs) for normal and disturbed bone formation. The information from numerous recorded traits was summarized by principal component analysis and analysed by least-squares interval mapping. An increase in the proportion of wild boar alleles across the genome increased length versus width of femur and reduced the prevalence of osteochondrosis. The presence of QTLs with an impact on femur dimensions was indicated on chromosomes 2, 4, 16 and 17 and on osteochondrosis on chromosomes 5, 13 and 15. A substantial effect of the chromosome 5 QTL calls for further studies within commercial populations to evaluate whether marker-assisted selection could be used to reduce the prevalence of osteochondrosis.
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