J. Paul Duff

Wildlife Disease Surveillance and Monitoring

Emerging diseases of human or veterinary importance are a major challenge to human society. As previously discussed, infectious diseases of wild mammal populations can have significant economic impact, may threaten human and livestock health (Artois et al. 2001), and can affect the welfare and conservation of game (Gortazar et al. 2006) and species of high conservation value (Cleaveland et al. 2002). Wild mammals are also implicated as sources of emerging diseases (Daszak et al. 2000a; Cleaveland 2003; Cunningham 2005). Comprehensive epidemiological investigations and disease surveillance of wild mammal populations will enhance our capaCity to detect and control infectious diseases that may emerge in the future in human and domestic animal populations. Given that the majority of diseases that have emerged in the last couple of decades had a wildlife origin (see Chapter 1), surveillance for wildlife diseases may be seen as an essential tool for the protection of human health. For these reasons, the development of effective programmes for the surveillance of disease in wildlife populations is becoming increasingly important. Epidemiological investigations in wildlife are similar in many respects in terms of their objectives, concepts and methodology to those undertaken for domestic animal health surveillance and monitoring. However, there are also substantial differences, owing to the zoological, behavioural and ecological characteristics of wildlife populations. Consequently, definitions, methods and procedures must often be adapted to suit the unique conditions of wildlife disease surveillance.

Epidemiological Evidence That Garden Birds Are a Source of Human Salmonellosis in England and Wales

The importance of wild bird populations as a reservoir of zoonotic pathogens is well established. Salmonellosis is a frequently diagnosed infectious cause of mortality of garden birds in England and Wales, predominantly caused by Salmonella enterica subspecies enterica serovar Typhimurium definitive phage types 40, 56(v) and 160. In Britain, these phage types are considered highly host-adapted with a high degree of genetic similarity amongst isolates, and in some instances are clonal. Pulsed field gel electrophoresis, however, demonstrated minimal variation amongst matched DT40 and DT56(v) isolates derived from passerine and human incidents of salmonellosis across England in 2000–2007. Also, during the period 1993–2012, similar temporal and spatial trends of infection with these S. Typhimurium phage types occurred in both the British garden bird and human populations; 1.6% of all S. Typhimurium (0.2% of all Salmonella) isolates from humans in England and Wales over the period 2000–2010. These findings support the hypothesis that garden birds act as the primary reservoir of infection for these zoonotic bacteria. Most passerine salmonellosis outbreaks identified occurred at and around feeding stations, which are likely sites of public exposure to sick or dead garden birds and their faeces. We, therefore, advise the public to practise routine personal hygiene measures when feeding wild birds and especially when handling sick wild birds.

Epidemiology, control and management of an EBHS outbreak in captive hares.

Here we describe an outbreak of European brown hare syndrome (EBHS) in a captive hare population. The EBHS outbreak occurred in March 2009, at the beginning of the breeding season. Overall mortality was 53% out of an original population of 61 animals. Animals between five and eleven months showed a significantly higher mortality rate than other age classes. Pregnant females either aborted their foetuses and survived or died pregnant. All foetuses (n=10) of the pregnant hares were PCR positive for EBHSV. Only one offspring born during the outbreak survived. Shortly after the outbreak, the surviving hares developed a specific anti-EBHSV titre between 1:80 and 1:2560, which dropped to 1:10-1:160 nine months later. Hares between one and three years of age developed a significantly higher titre than hares younger than one year or older than four years. Offspring born after the outbreak showed a lower titre of 1:10, indicating passive antibody transfer via placenta and milk. After two months, the titre was not detectable any longer. In December 2009, the captive population was vaccinated against EBHS virus with inactivated virus prepared from the organs of infected hares. The titres after the first vaccination ranged from 1:10 to 1:640, and after the second vaccination from 1:10 to 1:320. To estimate the effect of EBHS on reproduction, we compared the breeding seasons 2008 and 2009. Several possible sources of infection of the colony are discussed, but the definite cause could not be determined.

Haemorrhagic disease in cattle with genotype 1 bovine viral diarrhoea virus infection.

Bovine viral diarrhoea virus (BVDV), which exists as two genotypes (BVDV1 and BVDV2), has been associated with a complex of disease syndromes in cattle (Brock 2004). BVDV causes acute (transient) and persistent infections in cattle. Cattle persistently infected with BVDV often develop, as a late sequel to foetal infection, a syndrome termed mucosal disease (Brownlie and others 1984). Persistent infection occurs in animals that are specifically immunotolerant as a result of early gestational infection (Radostits and others 2007a), and is characterised by widespread distribution of BVDV antigen including CNS neurones (Hewicker and others 1990, Montgomery 2007, Bielefeldt-Ohmann and others 2008, Montgomery and others 2008), in contrast with later gestational and postnatally acquired infections in which the distribution of BVDV antigen is more limited and does not include CNS neurones (Ellis and others 1998, Bielefeldt-Ohmann and others 2008, Montgomery and others 2008). Most acute BVDV infections in cattle are subclinical, but there are a number of reports of acute infections causing severe disease (Corapi and others 1989). Acute uncomplicated BVDV2 infection has been reported as the cause of a haemorrhagic syndrome in cattle in North America (Ridpath and others 2000), which has been reproduced experimentally (Corapi and others 1989). BVDV-induced haemorrhagic syndrome in calves is characterised by pyrexia, diarrhoea, leukopaenia, thrombocytopenia and haemorrhages (Corapi and others 1989). BVDV1 has also been isolated from cases of haemorrhagic disease in cattle in Europe, although experimental infection with these isolates did not result in clinical illness or thrombocytopenia (Hamers and others 2000), and the relationship between these observations of haemorrhagic disease and BVDV1 isolation is unclear. Induction of a sporadic haemorrhagic syndrome by BVDV1 may require the presence of a number of cofactors (Hamers and others 2000), for example, host and environmental factors may be involved (Odeon and others 1999). This short communication …

Mass mortalities in gulls associated with eating livestock fodder

AS part of the Defra-supported Great Britain Wildlife Disease Surveillance Partnership, the Veterinary Laboratories Agency (VLA) Diseases of Wildlife Scheme undertakes investigations into unusual wildlife mortality incidents. VLA - Preston has dealt with two incidents involving gulls that died as a

RECENT CHANGES IN INFECTIOUS DISEASES IN EUROPEAN WILDLIFE

Abstract: Many infectious diseases originating from, or carried by, wildlife affect wildlife conservation and biodiversity, livestock health, or human health. We provide an update on changes in the epidemiology of 25 selected infectious, wildlife-related diseases in Europe (from 2010–16) that had an impact, or may have a future impact, on the health of wildlife, livestock, and humans. These pathogens were selected based on their: 1) identification in recent Europe-wide projects as important surveillance targets, 2) inclusion in European Union legislation as pathogens requiring obligatory surveillance, 3) presence in recent literature on wildlife-related diseases in Europe since 2010, 4) inclusion in key pathogen lists released by the Office International des Epizooties, 5) identification in conference presentations and informal discussions on a group email list by a European network of wildlife disease scientists from the European Wildlife Disease Association, or 6) identification as pathogens with changes in their epidemiology during 2010–16. The wildlife pathogens or diseases included in this review are: avian influenza virus, seal influenza virus, lagoviruses, rabies virus, bat lyssaviruses, filoviruses, canine distemper virus, morbilliviruses in aquatic mammals, bluetongue virus, West Nile virus, hantaviruses, Schmallenberg virus, Crimean-Congo hemorrhagic fever virus, African swine fever virus, amphibian ranavirus, hepatitis E virus, bovine tuberculosis (Mycobacterium bovis), tularemia (Francisella tularensis), brucellosis (Brucella spp.), salmonellosis (Salmonella spp.), Coxiella burnetii, chytridiomycosis, Echinococcus multilocularis, Leishmania infantum, and chronic wasting disease. Further work is needed to identify all of the key drivers of disease change and emergence, as they appear to be influencing the incidence and spread of these pathogens in Europe. We present a summary of these recent changes during 2010–16 to discuss possible commonalities and drivers of disease change and to identify directions for future work on wildlife-related diseases in Europe. Many of the pathogens are entering Europe from other continents while others are expanding their ranges inside and beyond Europe. Surveillance for these wildlife-related diseases at a continental scale is therefore important for planet-wide assessment, awareness of, and preparedness for the risks they may pose to wildlife, domestic animal, and human health.