An encephalitis outbreak among horses was caused by a pathogenic variant of Kunjin virus.

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In mid-February 2015, a large number of deaths were observed in the sole extant population of an endangered species of freshwater snapping turtle, Myuchelys georgesi, in a coastal river in New South Wales, Australia. Mortalities continued for approximately 7 weeks and affected mostly adult animals. More than 400 dead or dying animals were observed and population surveys conducted after the outbreak had ceased indicated that only a very small proportion of the population had survived, severely threatening the viability of the wild population. At necropsy, animals were in poor body condition, had bilateral swollen eyelids and some animals had tan foci on the skin of the ventral thighs. Histological examination revealed peri-orbital, splenic and nephric inflammation and necrosis. A virus was isolated in cell culture from a range of tissues. Nucleic acid sequencing of the virus isolate has identified the entire genome and indicates that this is a novel nidovirus that has a low level of nucleotide similarity to recognised nidoviruses. Its closest relatives are nidoviruses that have recently been described in pythons and lizards, usually in association with respiratory disease. In contrast, in the affected turtles, the most significant pathological changes were in the kidneys. Real time PCR assays developed to detect this virus demonstrated very high virus loads in affected tissues. In situ hybridisation studies confirmed the presence of viral nucleic acid in tissues in association with pathological changes. Collectively these data suggest that this virus is the likely cause of the mortalities that now threaten the survival of this species. Bellinger River Virus is the name proposed for this new virus.

During the 2007 equine influenza outbreak in Australia, respiratory disease in dogs in close contact with infected horses was noted; influenza (H3N8) virus infection was confirmed. Nucleotide sequence of the virus from dogs was identical to that from horses. No evidence of dog-to-dog transmission or virus persistence in dogs was found.

Cryptococcosis was diagnosed in seven ferrets (five from Australia; two from western Canada) displaying a wide range of clinical signs. Two of the ferrets lived together. One (5-years-old) had cryptococcal rhinitis and presented when the infection spread to the nasal bridge. Its sibling developed cryptococcal abscessation of the right retropharyngeal lymph node 12 months later, soon after developing a severe skin condition. DNA fingerprinting and microsatellite analysis demonstrated that the two strains isolated from these siblings were indistinguishable. Two ferrets (2- to 3-years-old) developed generalised cryptococcosis: one had primary lower respiratory tract disease with pneumonia, pleurisy and mediastinal lymph node involvement, while in the other a segment of intestine was the primary focus of infection with subsequent spread to mesenteric lymph nodes, liver and lung. The remaining three ferrets (1.75 to 4-years-old) had localised disease of a distal limb, in one case with spread to the regional lymph node. Cryptococcus bacillisporus (formerly C. neoformans var gattii) accounted for three of the four infections in Australian ferrets where the biotype could be determined. The Australian ferret with intestinal involvement and the two ferrets from Vancouver had C. neoformans var grubii infections.

Bungowannah virus is a novel porcine pestivirus identified in a disease outbreak in Australia in 2003. The aim of this study was to determine the outcome of infection of the pregnant pig with this virus. Twenty-four pregnant pigs were infected at days 35, 55, 75 or 90 of gestation. Blood, tonsillar and rectal swabs were collected from each pig at birth and then weekly until euthanasia or death. Tissues were sampled at necropsy. Viral load was measured by real-time reverse-transcription polymerase chain reaction (qRT-PCR) and antibody levels in serum by peroxidase-linked immunoassay. Bungowannah virus was detected in the serum and excretions of all infected pigs at birth regardless of the stage of gestation at which infection occurred. Persistent infections occurred following infection prior to the development of foetal immunocompetence. Unexpectedly some animals infected at day 55 of gestation later cleared the virus and seroconverted. Viraemia and viral shedding resolved quickest following infection in late gestation.

During the equine influenza (EI) outbreak, respiratory disease was observed in dogs that were in close proximity to infected horses. Investigations were undertaken to exclude influenza virus infection. Of the 23 dogs that were seropositive in tests using the influenza A/Sydney/2007 virus as the test antigen, 10 showed clinical signs. EI virus appeared to be readily transmitted to dogs that were held in close proximity to infected horses, but there was no evidence of lateral transmission of the virus to other dogs that did not have contact with or were not held in close proximity to horses.

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