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Lawson B.,UK Institute of Zoology | Robinson R.A.,British Trust for Ornithology | Colvile K.M.,UK Institute of Zoology | Peck K.M.,Royal Society for the Protection of Birds | And 5 more authors.
Philosophical Transactions of the Royal Society B: Biological Sciences | Year: 2012

Finch trichomonosis, caused by the protozoal parasite Trichomonas gallinae, was first recognized as an emerging infectious disease of British passerines in 2005. The first year of seasonal epidemic mortality occurred in 2006 with significant declines of greenfinch Carduelis chloris and chaffinch Fringilla coelebs populations. Here, we demonstrate that large-scale mortality, principally of green-finch, continued in subsequent years, 2007-2009, with a shifting geographical distribution across the British Isles over time. Consequent to the emergence of finch trichomonosis, the breeding greenfinch population in Great Britain has declined from ca 4.3 million to ca 2.8 million birds and the maximum mean number of greenfinches (a proxy for flock size) visiting gardens has declined by 50 per cent. The annual rate of decline of the breeding greenfinch population within England has exceeded 7 per cent since the initial epidemic. Although initially chaffinch populations were regionally diminished by the disease, this has not continued. Retrospective analyses of disease surveillance data showed a rapid, widespread emergence of finch trichomonosis across Great Britain in 2005 and we hypothesize that the disease emerged by T. gallinae jumping from columbiforms to passeriforms. Further investigation is required to determine the continuing impact of finch trichomonosis and to develop our understanding of how protozoal diseases jump host species. © 2012 The Royal Society.

Lawson B.,UK Institute of Zoology | Lawson B.,University of Liverpool | Robinson R.A.,British Trust for Ornithology | Neimanis A.,National Veterinary Institute | And 15 more authors.
EcoHealth | Year: 2011

Finch trichomonosis emerged in Great Britain in 2005 and led to epidemic mortality and a significant population decline of greenfinches, Carduelis chloris and chaffinches, Fringilla coelebs, in the central and western counties of England and Wales in the autumn of 2006. In this article, we show continued epidemic spread of the disease with a pronounced shift in geographical distribution towards eastern England in 2007. This was followed by international spread to southern Fennoscandia where cases were confirmed at multiple sites in the summer of 2008. Sequence data of the ITS1/5.8S/ITS2 ribosomal region and part of the small subunit (SSU) rRNA gene showed no variation between the British and Fennoscandian parasite strains of Trichomonas gallinae. Epidemiological and historical ring return data support bird migration as a plausible mechanism for the observed pattern of disease spread, and suggest the chaffinch as the most likely primary vector. This finding is novel since, although intuitive, confirmed disease spread by migratory birds is very rare and, when it has been recognised, this has generally been for diseases caused by viral pathogens. We believe this to be the first documented case of the spread of a protozoal emerging infectious disease by migrating birds. © 2011 International Association for Ecology and Health.

Lawson B.,UK Institute of Zoology | De Pinna E.,Public Health England | Horton R.A.,Animal Health and Veterinary Laboratories Agency | Macgregor S.K.,Zoological Society of London | And 8 more authors.
PLoS ONE | Year: 2014

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. © 2014 Crown Copyright.

Richards N.L.,Anglia Ruskin University | Cook G.,Anglia Ruskin University | Simpson V.,Wildlife Veterinary Investigation Center | Hall S.,Anglia Ruskin University | And 2 more authors.
European Journal of Wildlife Research | Year: 2011

The pervasiveness of pharmaceuticals such as nonsteroidal anti-inflammatory drugs (NSAIDs) in the aquatic ecosystem through the discharge of wastewater, and their potential to biomagnify within this ecosystem, is now recognised. Residues of diclofenac and ibuprofen are currently being detected in surface waters and aquatic organisms throughout the UK and Europe. However, the levels of these residues in fish and other aquatic organisms, particularly lower trophic level prey species, have not yet been determined. While exposure to diclofenac is known to adversely affect fish, the degree to which other aquatic organisms are exposed and impacted through continuous ingestion of contaminated prey and interaction with the aquatic habitat remains unknown. The extent and effects of exposure to ibuprofen also remain largely unknown. As an exploratory subset of a broader study to investigate the detectability of diclofenac in alternative biological matrices, we analysed hair samples from Eurasian otters (Lutra lutra, n = 28) for residues of the two NSAIDs using GC-MS. The otters were collected from six counties in England as part of an ongoing otter health monitoring project at the Wildlife Veterinary Investigation Centre in Chacewater, UK. Diclofenac was qualitatively detected in five hair wash and 15 extract samples, and ibuprofen was determined to be present in at least two of the hair extract samples. Here, we provide preliminary evidence that otters are exposed to both NSAIDs and argue for further studies to identify residue loads in the otters and their prey to fully assess the pervasiveness of these compounds and potential risks of ongoing exposure to them. © 2011 Springer-Verlag.

Harrington L.A.,University of Oxford | Gelling M.,University of Oxford | Simpson V.,Wildlife Veterinary Investigation Center | Harrington A.,University of Oxford | Macdonald D.W.,University of Oxford
European Journal of Wildlife Research | Year: 2012

Haematological and serum biochemistry values were determined for 13 adult, free-living American mink, Neovison vison, in southern England live trapped as part of a longer term research project. Serum samples were tested for the presence of antibodies against Toxoplasma gondii, Aleutian disease virus (ADV) and canine distemper virus (CDV). Animals were examined to assess ectoparasite burden; faecal samples were examined for the presence of gut parasites and bacteria (identified via culture). Post-mortem examinations were carried out on four individuals shot during on-going control operations. Haematological and serum biochemistry values for most individuals were similar to published values for captive mink. Neutrophil/lymphocyte ratios were high in two animals (possibly due to trap-associated stress). Three individuals had high levels of creatinine, urea and the liver enzymes, alanine transaminase, aspartate transaminase, alkaline phosphatise and gamma-glutamyl transpeptidase. Six of 12 mink tested positive for antibodies to T. gondii and 8 of 12 tested positive for antibodies to ADV; none tested positive for antibodies to CDV. No significant bacteria or parasites were detected in faecal samples. Post-mortem examinations in three cases showed no significant lesions but the fourth animal had Skrjabingylus nasicola nematodes in the nasal passages, lung lesions suggestive of adiaspiromycosis, cholangiohepatitis possibly indicative of Pseudamphistomum truncatum infection and tubulointerstitial nephritis associated with renal calculi. © 2012 Springer-Verlag.

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