Abstract. A disfiguring and debilitating neoplastic condition known as devil facial tumor disease (DFTD) has been discovered in wild Tasmanian Devils (Sarcophilus harrisii) across 51% of its natural range, with population declines of up to 80% in some areas (C. Hawkins, personal communication). Between 2001 and 2004, 91 cases were examined. The tumors presented as large, solid, soft tissue masses usually with flattened, centrally ulcerated, and exudative surfaces. They were typically multicentric, appearing first in the oral, face, or neck regions. Histologically, the tumors were composed of circumscribed to infiltrative nodular aggregates of round to spindle-shaped cells, often within a pseudocapsule and divided into lobules by delicate fibrous septae. They were locally aggressive and metastasized in 65% of cases. There was minimal cytologic differentiation among the tumor cell population under light and electron microscopic examination. The results indicate DFTD to be an undifferentiated soft tissue neoplasm.
An emerging infectious facial cancer threatens Tasmanian devils with extinction. The disease is likely to occur across the range of the devil within 5 years. This urgent time frame requires management options that can be implemented immediately: the establishment of insurance populations, in captivity, wild-living on islands, and aiming for eradication in areas that can be isolated. The long-term options of the spontaneous or assisted evolution of resistance or development of a field-deliverable vaccine are unlikely to be available in time. The disease's characteristic allograft transmission through intimate contact simplifies isolation of insurance populations and breaking transmission in suppression trials. Better knowledge of contact matrices in wild devils will help focus timing and demographic targets of removals. A metapopulation approach is needed that integrates captive and wild-living island and peninsula (disease suppression) populations to minimize the loss of genetic diversity over 50 years until either extinction and reintroduction can occur, resistance evolves or a fielddeliverable vaccine is developed. Given the importance of the insurance populations and the low genetic diversity of devils, a conservative target for retention of 95% genetic diversity is recommended. Encouraging preliminary results of the first disease-suppression trial on a large peninsula show fewer late stage tumors and no apparent population decline. Limiting geographic spread or suppressing the disease on a broadscale are both unlikely to be feasible. Since the synergy of devil decline and impending fox establishment could have devastating consequences for Tasmanian wildlife, it is crucial to manage the dynamics of new and old predator species together.
Nipah virus infection in humans is associated with a higher death rate in Bangladesh than in Malaysia. Additionally, Nipah virus spreads from person to person in Bangladesh but not in Malaysia. To investigate why these differences occur, researchers looked for differences in the virus strains from each country. In experimentally infected ferrets, they examined which tissues each strain infected and how each strain was excreted from the body. They found higher concentrations of the Bangladesh strain in secretions from the mouth. Increased oral excretion of the Bangladesh strain in humans might explain why person-to-person transmission of Nipah virus occurs in that region.
Cases of vomiting and diarrhoea were reported in racing pigeons in Western Australia in May, 2016. Morbidity and mortality rates were high. Similar clinical disease was seen in Victoria in December and by early 2017 had been reported in all states except the Northern Territory, in different classes of domestic pigeon–racing, fancy and meat bird–and in a flock of feral pigeons. Autopsy findings were frequently unremarkable; histological examination demonstrated significant hepatic necrosis as the major and consistent lesion, often with minimal inflammatory infiltration. Negative contrast tissue suspension and thin section transmission electron microscopy of liver demonstrated virus particles consistent with a member of the Reoviridae. Inoculation of trypsin-treated Vero, MDBK and MA-104 cell lines resulted in cytopathic changes at two days after infection. Next generation sequencing was undertaken using fresh liver samples and a previously undescribed group A rotavirus (genotype G18P[17]) of avian origin was identified and the virus was isolated in several cell lines. A q-RT-PCR assay was developed and used to screen a wider range of samples, including recovered birds. Episodes of disease have continued to occur and to reoccur in previously recovered lofts, with variable virulence reported. This is the first report of a rotavirus associated with hepatic necrosis in any avian species.
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