Factors Associated with Owner-Reported Euthanasia in Equids in France.

There is limited evidence regarding the proportion of dead equids in France that were euthanized and the factors influencing the decision-making of euthanasia. The better understanding of which could facilitate research on improvement of welfare, especially on end of life issues. The aim of this study was to estimate the proportion of euthanasia and identify associated factors in equids in France. A web-based survey was created and distributed by the French horse and riding institute to owners who reported an equine death between April 2017 and April 2018 (n = 5 158). Factors associated with euthanasia were identified using a multivariable logistic regression model. The percentage of responses was 10.6% (n = 548/5 158; 95% CI 9.8% to 11.5%). The proportion of euthanasia was 71.0% (n = 389/548; 95% CI 67.2% to 74.8%). The factors "age category", "cause of natural death or reason for euthanasia" and "the length of time during which the animal was reported to be ill by the owner" were significantly associated with euthanasia (P <0.001). The results highlighted that a large majority of owners faced euthanasia decisions and our findings could support veterinarians and owners to better prepare for such an eventuality.

Identification of levers for improving dead equine traceability: A survey of French equine owners' perception of regulatory procedures following their animal's death.

The core of the French equine traceability system is the census database (SIRE) managed by the French horse and riding institute (IFCE). Following the death of an equine, owners are legally obliged to take charge of cadaver removal by contacting a rendering company directly or after registration on the national ATM-équidés ANGEE association (ATM) website, which proposes negotiated prices for removal and recording of the death in the SIRE database. Despite these offers, ATM notes few users. Owners are also legally obliged to return the equine's passport to the IFCE, but only 30-40 % of owners comply with the regulation. Rendering companies register data on equine mortality in the fallen stock data interchange database (FSDI), but it is difficult to cross-reference these data with SIRE data. Consequently, the death of equines is not well registered in the SIRE database. The objective of the present study was to identify levers that could be used to improve dead equine traceability by i) investigating the level of satisfaction of equine owners with ATM and rendering company services; and ii) investigating the drawbacks of owners having to return the passport to the IFCE. An online survey was designed and distributed by email to the 5 158 owners who used ATM services between April 2017 and April 2018. The response rate was 16.4 %. Most owners were satisfied by ATM and rendering company services. The lack of simple and quick removal procedures and the lack of any connection between ATM and the rendering companies were among the main drawbacks identified. Regarding the return of the passport to the IFCE, most responding owners returned it through the rendering company (65 %) or directly (2 %). The passport was returned significantly more frequently when requested by the renderers. The main reason for not providing the passport was the owner wanted to keep it as a souvenir. These results suggest that ATM and the rendering companies are key players in dead equine traceability. ATM services should be developed through the establishment of a direct connection with rendering companies to accelerate the cadaver removal request and to allow the cross-referencing of data between the ATM, FSDI and SIRE databases for a better dead equine traceability. Rendering companies need regulatory support to help them ask owners for the equine's passport, formalizing their contribution to equine traceability. Finally, effective communication has to be established to inform owners about the removal procedures and the regulations.

The Molecular Basis for Antigenic Drift of Human A/H2N2 Influenza Viruses.

Influenza A/H2N2 viruses caused a pandemic in 1957 and continued to circulate in humans until 1968. The antigenic evolution of A/H2N2 viruses over time and the amino acid substitutions responsible for this antigenic evolution are not known. Here, the antigenic diversity of a representative set of human A/H2N2 viruses isolated between 1957 and 1968 was characterized. The antigenic change of influenza A/H2N2 viruses during the 12 years that this virus circulated was modest. Two amino acid substitutions, T128D and N139K, located in the head domain of the H2 hemagglutinin (HA) molecule, were identified as important determinants of antigenic change during A/H2N2 virus evolution. The rate of A/H2N2 virus antigenic evolution during the 12-year period after introduction in humans was half that of A/H3N2 viruses, despite similar rates of genetic change.IMPORTANCE While influenza A viruses of subtype H2N2 were at the origin of the Asian influenza pandemic, little is known about the antigenic changes that occurred during the twelve years of circulation in humans, the role of preexisting immunity, and the evolutionary rates of the virus. In this study, the antigenic map derived from hemagglutination inhibition (HI) titers of cell-cultured virus isolates and ferret postinfection sera displayed a directional evolution of viruses away from earlier isolates. Furthermore, individual mutations in close proximity to the receptor-binding site of the HA molecule determined the antigenic reactivity, confirming that individual amino acid substitutions in A/H2N2 viruses can confer major antigenic changes. This study adds to our understanding of virus evolution with respect to antigenic variability, rates of virus evolution, and potential escape mutants of A/H2N2.

Identification of a Lineage D Betacoronavirus in Cave Nectar Bats (Eonycteris spelaea) in Singapore and an Overview of Lineage D Reservoir Ecology in SE Asian Bats.

Coronaviruses are a diverse group of viruses that infect mammals and birds. Bats are reservoirs for several different coronaviruses in the Alphacoronavirus and Betacoronavirus genera. They also appear to be the natural reservoir for the ancestral viruses that generated the severe acute respiratory syndrome coronavirus and Middle East respiratory syndrome coronavirus outbreaks. Here, we detected coronavirus sequences in next-generation sequence data created from Eonycteris spelaea faeces and urine. We also screened by PCR urine samples, faecal samples and rectal swabs collected from six species of bats in Singapore between 2011 and 2014, all of which were negative. The phylogenetic analysis indicates this novel strain is most closely related to lineage D Betacoronaviruses detected in a diverse range of bat species. This is the second time that coronaviruses have been detected in cave nectar bats, but the first coronavirus sequence data generated from this species. Bat species from which this group of coronaviruses has been detected are widely distributed across SE Asia, South Asia and Southern China. They overlap geographically, often share roosting sites and have been witnessed to forage on the same plant. The addition of sequence data from this group of viruses will allow us to better understand coronavirus evolution and host specificity.

Transmission of influenza A/H5N1 viruses in mammals.

Highly pathogenic avian H5N1 influenza A viruses occasionally infect humans and cause severe respiratory disease and fatalities. Currently, these viruses are not efficiently transmitted from person to person, although limited human-to-human transmission may have occurred. Nevertheless, further adaptation of avian H5N1 influenza A viruses to humans and/or reassortment with human influenza A viruses may result in aerosol transmissible viruses with pandemic potential. Although the full range of factors that modulate the transmission and replication of influenza A viruses in humans are not yet known, we are beginning to understand some of the molecular changes that may allow H5N1 influenza A viruses to transmit via aerosols or respiratory droplets among mammals. A better understanding of the biological basis and genetic determinants that confer transmissibility to H5N1 influenza A viruses in mammals is important to enhance our pandemic preparedness.

Predicting 'airborne' influenza viruses: (trans-) mission impossible?

Repeated transmission of animal influenza viruses to humans has prompted investigation of the viral, host, and environmental factors responsible for transmission via aerosols or respiratory droplets. How do we determine-out of thousands of influenza virus isolates collected in animal surveillance studies each year-which viruses have the potential to become 'airborne', and hence pose a pandemic threat? Here, using knowledge from pandemic, zoonotic and epidemic viruses, we postulate that the minimal requirements for efficient transmission of an animal influenza virus between humans are: efficient virus attachment to (upper) respiratory tissues, replication to high titers in these tissues, and release and aerosolization of single virus particles. Investigating 'airborne' transmission of influenza viruses is key to understand-and predict-influenza pandemics.

Pandemic 2009 H1N1 influenza virus causes diffuse alveolar damage in cynomolgus macaques.

The pathogenesis of lower respiratory tract disease from the pandemic 2009 H1N1 (H1N1v) influenza A virus is poorly understood. Therefore, either H1N1v virus or a seasonal human H1N1 influenza A virus was inoculated into cynomolgus macaques as a nonhuman primate model of influenza pneumonia, and virological, pathological, and microarray analyses were performed. Macaques in the H1N1v group had virus-associated diffuse alveolar damage involving both type I and type II alveolar epithelial cells and affecting an average of 16% of the lung area. In comparison, macaques in the seasonal H1N1 group had milder pulmonary lesions. H1N1v virus tended to be reisolated from more locations in the respiratory tract and at higher titers than seasonal H1N1 virus. In contrast, differential expression of messenger RNA transcripts between H1N1v and seasonal H1N1 groups did not show significant differences. The most upregulated genes in H1N1v lung samples with lesions belonged to the innate immune response and proinflammatory pathways and correlated with histopathological results. Our results demonstrate that the H1N1v virus infects alveolar epithelial cells and causes diffuse alveolar damage in a nonhuman primate model. Its higher pathogenicity compared with a seasonal H1N1 virus may be explained in part by higher replication in the lower respiratory tract.