Disease Risk Analysis and Post-Release Health Surveillance for a Reintroduction Programme: the Pool Frog Pelophylax lessonae.

There are risks from disease in undertaking wild animal reintroduction programmes. Methods of disease risk analysis have been advocated to assess and mitigate these risks, and post-release health and disease surveillance can be used to assess the effectiveness of the disease risk analysis, but results for a reintroduction programme have not to date been recorded. We carried out a disease risk analysis for the reintroduction of pool frogs (Pelophylax lessonae) to England, using information gained from the literature and from diagnostic testing of Swedish pool frogs and native amphibians. Ranavirus and Batrachochytrium dendrobatidis were considered high-risk disease threats for pool frogs at the destination site. Quarantine was used to manage risks from disease due to these two agents at the reintroduction site: the quarantine barrier surrounded the reintroduced pool frogs. Post-release health surveillance was carried out through regular health examinations of amphibians in the field at the reintroduction site and collection and examination of dead amphibians. No significant health or disease problems were detected, but the detection rate of dead amphibians was very low. Methods to detect a higher proportion of dead reintroduced animals and closely related species are required to better assess the effects of reintroduction on health and disease.

Neuropathology of scrapie: a study of the distribution patterns of brain lesions in 222 cases of natural scrapie in sheep, 1982-1991.

Detailed neuropathological findings in 222 cases of naturally occurring scrapie from Great Britain are described. The material consisted of formalin-fixed brain from eight breeds of sheep submitted between 1982 and 1991. Paraffin-embedded histological sections were made from several specified brain areas, including the medulla oblongata, cerebellum, pons, mesencephalon, diencephalon, septal area, basal ganglia and frontal cortex. Sections were examined by conventional and polarised light microscopy and the type and distribution of the lesions were recorded. Histologically, the lesions included vacuolation of neuronal perikarya and grey matter neuropil, neuronal degeneration (especially "dark' neurons) and loss, a reactive glial (predominantly astrocytic) response and amyloidosis. Vacuolar lesions were present in the cerebral cortex of 37 per cent of cases, centred around the superior frontal gyrus. Vacuolar lesions were detected in the neocortex for as long as sections have been taken from the superior frontal gyrus and are thus probably not a new feature of the disease. The distribution of vacuolation in the grey matter neuropil could be classified into seven patterns. Data from individual breeds of sheep showed that in some breeds there were significant differences in the age at which animals with different patterns of vacuolation died from scrapie.

Neuropathological findings in cattle with clinically suspect but histologically unconfirmed bovine spongiform encephalopathy (BSE).

Neuropathological observations were made in 200 clinically suspected cases of bovine spongiform encephalopathy (BSE) in which pathognomonic vacuolar changes were absent. Routine histological and immunocytochemical techniques were applied to formalin-fixed, paraffin-embedded sections of the central nervous system. Significant neuropathological findings were detected in 85 (42.5 per cent) cases. The most frequent lesion, detected in 46 (23 per cent) cases, was a focal white matter vacuolation principally affecting the substantia nigra, but its clinical significance was unclear. Listeriosis was diagnosed in 17 (8.5 per cent) cases. In three of seven cases of non-suppurative encephalitis, lesions suggested sporadic bovine encephalomyelitis, a disease not previously reported in the UK. Suppurative thromboembolic or granulomatous lesions accounted for other inflammatory changes. Neuroectodermal tumours were present in five cases (2.5 per cent); three were identical in form and considered to be atypical ependymoma. Cerebrocortical necrosis, oedema or both were detected in four cases. The remaining cases (4.5 per cent), comprised those in which the changes were minor and of doubtful significance. Incidental pathological findings included occasional degenerating or vacuolated neurones, which occurred in the red nucleus in 105 brains, in the habenular nucleus in 71 brains, and singly at other sites in 17 brains. In sections of 37 brains immunostained with antiserum to prion protein (PrP), no evidence of PrP accumulation was found, providing some evidence that the series did not contain bovine prion disease cases which, based on the histological diagnosis, had given a false negative result. It is suggested that, of 115 cases (57.5 per cent) which lacked significant histological lesions, some were suffering from metabolic disorders. The study identified diseases and lesions which feature in the differential diagnosis of BSE. Their more accurate diagnosis may become particularly important if, as predicted, the BSE epidemic declines.

Prion protein immunocytochemistry helps to establish the true incidence of prion diseases.

Creutzfeldt-Jakob disease (CJD) and Gerstmann-Strüssler-Scheinker disease (GSSD) are transmissible spongiform encephalopathies or prion diseases affecting man. It has been reported that prion diseases may occur without the histological hallmarks of spongiform encephalopathies: vacuolation of the cerebral grey matter, neuronal loss and astrocytosis. These cases without characteristic neuropathology may go undiagnosed and consequently the true incidence of transmissible dementias is likely to have been under-estimated. Immunocytochemistry using antibodies to prion protein gives positive staining of these cases, albeit the pattern of immunostaining differs from that seen in typical forms. Accumulation of prion protein is a molecular hallmark of prion diseases, and thus a reproducible, speedy and cost-efficient immunocytochemical screening of unusual dementias may help to establish the true incidence of prion diseases.

Recently described scrapie-like encephalopathies of animals: case definitions.

Since 1986, naturally occurring scrapie-like encephalopathies have been described in the United Kingdom in domestic cattle, in five species of captive exotic bovids and in domestic cats. The disease in domestic cattle, bovine spongiform encephalopathy, has been characterised by all currently available diagnostic criteria as a transmissible spongiform encephalopathy or 'prion' disease, and has been shown to have a dietary origin. The pathology in the other species is also entirely consistent with the scrapie-like diseases. The contemporaneous occurrence in the UK of such disease in these species suggests a close epidemiological association. The diagnostic criteria of the scrapie-like encephalopathies of animals are reviewed in the light of experience with the recent extension of their natural host range.

Bovine spongiform encephalopathy: a neuropathological perspective.

The occurrence of bovine spongiform encephalopathy (BSE), recognition that it is a new scrapie-like disease epidemic in domestic cattle in the United Kingdom and concern of a remote zoonotic potential has, in four years, produced a plethora of documented information. While much of this information has been communicated outwith the scientific literature, this review attempts to summarise, from a neuropathological viewpoint, the main findings to emerge. The initial studies established the nosological homology of BSE with the subacute spongiform encephalopathies or "prion" diseases of animals and man. Epidemiological data are consistent with an extended common source epidemic originating from an abrupt change, commencing in 1981-82, in the exposure of domestic cattle to a scrapie-like agent in meat and bone meal incorporated into commercial animal feedstuffs. It is currently proposed that the method of production of meat and bone meal has contributed vital factors to the change in exposure. Invariability of the distribution pattern of vacuolar pathology in the natural disease and on primary transmission to cattle suggests a uniformity of the pathogenesis of BSE. Studies in mice suggest uniformity also of the biological properties of different BSE isolates but indicate that the properties differ from those of sheep scrapie isolates. Human health risks, although perceived to be negligible, have been addressed by various strategies including statutory measures and long term monitoring.