The emergence and spread of finch trichomonosis in the British Isles.

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 greenfinch, 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.

Evidence of spread of the emerging infectious disease, finch trichomonosis, by migrating birds.

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.

Acute necrotising pneumonitis associated with Suttonella ornithocola infection in tits (Paridae).

Suttonella ornithocola, first isolated from the lungs of British tit species in 1996, was found to be a novel bacterium belonging to the family Cardiobacteriaceae. Comprehensive surveillance of garden bird mortality across Great Britain between April 2005 and April 2009 involved post mortem and microbiological examination of 82 tits (Paridae; multiple species) and six long-tailed tits (Aegithalidae; Aegithalos caudatus). S. ornithocola was isolated from six birds submitted from six incidents of morbidity and mortality involving Paridae and Aegithalidae species with a wide geographical distribution. The mortality incidents occurred sporadically at low incidence throughout the study period, which suggested that the infection is endemic in native bird populations, with a seasonal peak during early spring. Histopathological examination showed multiple foci of acute pulmonary necrosis associated with gram-negative cocco-bacillary bacteria. These findings supported the hypothesis that S. ornithocola is a primary pathogen of tits in Great Britain.

Emerging infectious disease leads to rapid population declines of common British birds.

Emerging infectious diseases are increasingly cited as threats to wildlife, livestock and humans alike. They can threaten geographically isolated or critically endangered wildlife populations; however, relatively few studies have clearly demonstrated the extent to which emerging diseases can impact populations of common wildlife species. Here, we report the impact of an emerging protozoal disease on British populations of greenfinch Carduelis chloris and chaffinch Fringilla coelebs, two of the most common birds in Britain. Morphological and molecular analyses showed this to be due to Trichomonas gallinae. Trichomonosis emerged as a novel fatal disease of finches in Britain in 2005 and rapidly became epidemic within greenfinch, and to a lesser extent chaffinch, populations in 2006. By 2007, breeding populations of greenfinches and chaffinches in the geographic region of highest disease incidence had decreased by 35% and 21% respectively, representing mortality in excess of half a million birds. In contrast, declines were less pronounced or absent in these species in regions where the disease was found in intermediate or low incidence. Also, populations of dunnock Prunella modularis, which similarly feeds in gardens, but in which T. gallinae was rarely recorded, did not decline. This is the first trichomonosis epidemic reported in the scientific literature to negatively impact populations of free-ranging non-columbiform species, and such levels of mortality and decline due to an emerging infectious disease are unprecedented in British wild bird populations. This disease emergence event demonstrates the potential for a protozoan parasite to jump avian host taxonomic groups with dramatic effect over a short time period.

Analysis of feces samples collected from a wild-bird garden feeding station in Scotland for the presence of verocytotoxin-producing Escherichia coli O157.

Composite wild bird feces collected at regular intervals from a garden feeding station in southwest Scotland over a 3-year period were examined for verocytotoxin-producing Escherichia coli O157. One sample was positive for Escherichia coli O157. The isolate belonged to phage type 21/28 and possessed vtx2, eaeA, and enterohemorrhagic E. coli hlyA genes.