The hazel dormouse (Muscardinus avellanarius) population in the UK continues to decline due to habitat loss, despite reintroductions of captive-bred individuals being conducted nationally for over 30 years. Disease surveillance of captive-bred and wild dormice is performed to identify novel and existing disease threats which could impact populations. In this study, we firstly investigated cause of death in seven hazel dormice found dead in England, through next-generation sequencing identifying a virus closely related to a wood mouse encephalomyocarditis virus-2 (EMCV-2). Subsequently, lung tissue samples from 35 out of 44 hazel dormice tested positive for EMCV-2 RNA using a reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) and Sanger sequencing methods developed in this study. Formalin-fixed tissues available for nine hazel dormice which tested positive for EMCV-2 RNA were examined microscopically. Three cases showed moderate interstitial pneumonia with minimal to mild lymphoplasmacytic myocarditis, but no evidence of encephalitis. However, the presence of possible alternative causes of death in these cases means that the lesions cannot be definitively attributed to EMCV-2. Here, we report the first detection of EMCV-2 in hazel dormice and conclude that EMCV-2 is likely to be endemic in the hazel dormouse population in England and may be associated with clinical disease.

Whether an infectious disease threat to wildlife arises from pathogen introduction or the increased incidence of an already-present agent informs mitigation policy and actions. The prior absence of a pathogen can be difficult to establish, particularly in free-living wildlife. Subsequent to the epidemic emergence of the fungus, Batrachochytrium salamandrivorans (Bsal), in mainland Europe in 2010 and prior to its detection in captive amphibians in the United Kingdom (UK), we tested archived skin swabs using a Bsal-specific qPCR. These samples had been collected in 2011 from 2409 wild newts from ponds across the UK. All swabs were negative for Bsal. Bayesian hierarchical modelling suggests that Bsal was absent from, or present at very low levels in, these ponds at the time of sampling. Additionally, surveillance of newt mortality incidents, 2013-2017, failed to detect Bsal. As this pathogen has been shown to be widespread in British captive amphibian collections, there is an urgent need to raise awareness of the importance of effective biosecurity measures, especially amongst people with captive amphibians, to help minimise the risk of Bsal spreading to the wild. Continued and heightened wild amphibian disease surveillance is a priority to provide an early warning system for potential incursion events.

The amphibian chytrid fungus Batrachochytrium salamandrivorans (Bsal) infects newts and salamanders (urodele amphibians), in which it can cause fatal disease. This pathogen has caused dramatic fire salamander population declines in Belgium, the Netherlands and Germany since its discovery in 2010. Thought to be native to Asia, it has been hypothesised that Bsal was introduced to Europe with the importation of infected amphibians for the commercial pet trade. Following the discovery of Bsal in captive amphibians in the United Kingdom in 2015, we used contact-tracing to identify epidemiologically-linked private amphibian collections in Western Europe. Of 16 linked collections identified, animals were tested from 11 and urodeles tested positive for Bsal in seven, including the identification of the pathogen in Spain for the first time. Mortality of Bsal-positive individuals was observed in five collections. Our results indicate that Bsal is likely widespread within the private amphibian trade, at least in Europe. These findings are important for informing policy regarding Bsal control strategies.

Snake fungal disease (SFD) is an emerging disease of conservation concern in eastern North America. Ophidiomyces ophiodiicola, the causative agent of SFD, has been isolated from over 30 species of wild snakes from six families in North America. Whilst O. ophiodiicola has been isolated from captive snakes outside North America, the pathogen has not been reported from wild snakes elsewhere. We screened 33 carcasses and 303 moulted skins from wild snakes collected from 2010-2016 in Great Britain and the Czech Republic for the presence of macroscopic skin lesions and O. ophiodiicola. The fungus was detected using real-time PCR in 26 (8.6%) specimens across the period of collection. Follow up culture and histopathologic analyses confirmed that both O. ophiodiicola and SFD occur in wild European snakes. Although skin lesions were mild in most cases, in some snakes they were severe and were considered likely to have contributed to mortality. Culture characterisations demonstrated that European isolates grew more slowly than those from the United States, and phylogenetic analyses indicated that isolates from European wild snakes reside in a clade distinct from the North American isolates examined. These genetic and phenotypic differences indicate that the European isolates represent novel strains of O. ophiodiicola. Further work is required to understand the individual and population level impact of this pathogen in Europe.

Veterinary RecordVolume 176, Issue 18 p. 468-468 Letter Emerging disease in UK amphibians Andrew A. Cunningham, Corresponding Author Andrew A. Cunningham a.cunningham@ioz.ac.uk Institute of Zoology, Zoological Society of London, Regent's Park, London, NW1 4RYe-mail: a.cunningham@ioz.ac.ukSearch for more papers by this authorKatie Beckmann, Katie Beckmann Institute of Zoology, Zoological Society of London, Regent's Park, London, NW1 4RYSearch for more papers by this authorMatthew Perkins, Matthew Perkins Institute of Zoology, Zoological Society of London, Regent's Park, London, NW1 4RYSearch for more papers by this authorLiam Fitzpatrick, Liam Fitzpatrick Institute of Zoology, Zoological Society of London, Regent's Park, London, NW1 4RYSearch for more papers by this authorRuth Cromie, Ruth Cromie Wildfowl and Wetlands Trust, Slimbridge, Gloucestershire, GL2 7BTSearch for more papers by this authorJay Redbond, Jay Redbond Wildfowl and Wetlands Trust, Slimbridge, Gloucestershire, GL2 7BTSearch for more papers by this authorMichelle F. O'Brien, Michelle F. O'Brien Wildfowl and Wetlands Trust, Slimbridge, Gloucestershire, GL2 7BTSearch for more papers by this authorPria Ghosh, Pria Ghosh Department of Infectious Disease Epidemiology, St Mary's Hospital, Imperial College London, London, W2 1PGSearch for more papers by this authorJennifer Shelton, Jennifer Shelton Department of Infectious Disease Epidemiology, St Mary's Hospital, Imperial College London, London, W2 1PGSearch for more papers by this authorMatthew C. Fisher, Matthew C. Fisher Department of Infectious Disease Epidemiology, St Mary's Hospital, Imperial College London, London, W2 1PGSearch for more papers by this author Andrew A. Cunningham, Corresponding Author Andrew A. Cunningham a.cunningham@ioz.ac.uk Institute of Zoology, Zoological Society of London, Regent's Park, London, NW1 4RYe-mail: a.cunningham@ioz.ac.ukSearch for more papers by this authorKatie Beckmann, Katie Beckmann Institute of Zoology, Zoological Society of London, Regent's Park, London, NW1 4RYSearch for more papers by this authorMatthew Perkins, Matthew Perkins Institute of Zoology, Zoological Society of London, Regent's Park, London, NW1 4RYSearch for more papers by this authorLiam Fitzpatrick, Liam Fitzpatrick Institute of Zoology, Zoological Society of London, Regent's Park, London, NW1 4RYSearch for more papers by this authorRuth Cromie, Ruth Cromie Wildfowl and Wetlands Trust, Slimbridge, Gloucestershire, GL2 7BTSearch for more papers by this authorJay Redbond, Jay Redbond Wildfowl and Wetlands Trust, Slimbridge, Gloucestershire, GL2 7BTSearch for more papers by this authorMichelle F. O'Brien, Michelle F. O'Brien Wildfowl and Wetlands Trust, Slimbridge, Gloucestershire, GL2 7BTSearch for more papers by this authorPria Ghosh, Pria Ghosh Department of Infectious Disease Epidemiology, St Mary's Hospital, Imperial College London, London, W2 1PGSearch for more papers by this authorJennifer Shelton, Jennifer Shelton Department of Infectious Disease Epidemiology, St Mary's Hospital, Imperial College London, London, W2 1PGSearch for more papers by this authorMatthew C. Fisher, Matthew C. Fisher Department of Infectious Disease Epidemiology, St Mary's Hospital, Imperial College London, London, W2 1PGSearch for more papers by this author First published: 02 May 2015 https://doi.org/10.1136/vr.h2264Citations: 10Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume176, Issue18May 2015Pages 468-468 RelatedInformation