Deborah S. Finlaison

Characterization of Virulent West Nile Virus Kunjin Strain, Australia, 2011

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

Influenza Virus Transmission from Horses to Dogs, Australia

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.

Infection of dogs with equine influenza virus: evidence for transmission from horses during the Australian outbreak

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.

Field and laboratory evidence that Bungowannah virus, a recently recognised pestivirus, is the causative agent of the porcine myocarditis syndrome (PMC).

In 2003 an outbreak of sudden deaths occurred in 2-3-week-old piglets on a piggery in New South Wales, Australia. There was a marked increase in the birth of stillborn piglets and preweaning losses associated with a multifocal non-suppurative myocarditis with myonecrosis. The aim of this study was to review existing data and to undertake further investigations of specimens from naturally infected pigs to provide evidence to support the hypothesis that Bungowannah virus, a recently recognised pestivirus, causes the porcine myocarditis syndrome (PMC). Sera collected from gilts and sows from affected and unaffected units were tested for Bungowannah virus antibody by a peroxidase-linked assay and Bungowannah virus RNA by qRT-PCR in selected cases. Stillborn piglets from affected and an unaffected unit were also tested for Bungowannah virus antibody and RNA. Body fluid IgG levels and the incidence of myocardial lesions in these stillborn piglets are summarised. Tissue sections from stillborn piglets with myocarditis/myonecrosis were examined for Bungowannah virus RNA by in situ hybridisation. A clear temporal association between the occurrence of PMC on a unit or module and exposure to Bungowannah virus was identified by serological tests in both breeding aged animals and stillborn pigs. In addition, at the individual animal level on affected units, Bungowannah virus RNA was detected in stillborn piglets in large amounts by qRT-PCR and in association with myocardial lesions by in situ hybridisation. The examination of field material from cases of PMC by serology, qRT-PCR and in situ hybridisation provides strong indirect evidence that Bungowannah virus is the causative agent for PMC.

An epizootic of bovine ephemeral fever in New South Wales in 2008 associated with long‐distance dispersal of vectors

OBJECTIVE To report the rapid transmission of bovine ephemeral fever (BEF) virus from north-western New South Wales south to the Victorian border in January 2008 and to present data that suggests an uncommon meteorological event caused this rapid southward dispersal of vectors. PROCEDURE The locations of reported clinical cases, data from sentinel herds and results from a survey of cattle in the southern affected area were examined to delineate the distribution of virus transmission. Synoptic weather charts for January 2008 were examined for meteorological conditions that may have favoured movement of vectors in a southerly direction. RESULTS Cases of BEF and exposure to BEF virus in NSW were confirmed west of the Great Dividing Range, extending from the Queensland border to Finley, on the far North Coast and around the Hunter Valley. A low-pressure system moved south across the state on 18-19 January 2008, preceding the first cases of BEF in the south of NSW by 1-2 days. CONCLUSION Heavy rainfall in December 2007 provided a suitable environment for vector breeding, resulting in the initiation of and support for continuing BEF virus transmission in north-western NSW. The movement of a low-pressure system south across central western NSW in mid-January 2008 after the commencement of BEF virus transmission in the north-west of the state provided a vehicle for rapid southward movement of infected vectors.

Faecal viruses of dogs — an electron microscope study

Abstract Faecal samples from 112 dogs both with and without diarrhoea were screened for parvovirus by a haemagglutination titration test and then examined by electron microscopy for the presence of viruses and virus-like particles. On the basis of morphology eight distinct viruses or virus-like particles were identified. Particles identified were coronaviruses, coronavirus-like particles, rotavirus-like particles, papovavirus-like particles, torovirus-like particles, picornavirus-like particles, 27 nm virus-like particles with projections and parvovirus-like particles which did not cause haemagglutination.

Application of real-time PCR and ELISA assays for equine influenza virus to determine the duration of viral RNA shedding and onset of antibody response in naturally infected horses.

During the equine influenza (EI) outbreak, two assays were used in parallel to diagnose the disease, to demonstrate freedom from infection in disease control zones and ultimately to demonstrate that EI virus had been eliminated from the Australian horse population. A longitudinal study of a population of naturally infected horses was established to determine the performance characteristics of these assays.

Hendra Virus Infection in Dog, Australia, 2013.

Hendra virus occasionally causes severe disease in horses and humans. In Australia in 2013, infection was detected in a dog that had been in contact with an infected horse. Abnormalities and viral RNA were found in the dog’s kidney, brain, lymph nodes, spleen, and liver. Dogs should be kept away from infected horses.

A prospective longitudinal study of naturally infected horses to evaluate the performance characteristics of rapid diagnostic tests for equine influenza virus.

An outbreak of equine influenza (EI) occurred in Australia in 2007. During the laboratory support for this outbreak, real-time reverse transcriptase polymerase chain reaction (qRT-PCR) assays and a blocking enzyme linked immunosorbent assay (bELISA) were used as testing methods to detect infection with the virus. The qRT-PCR and bELISA tests had not been used for EI diagnosis before, so it was not known how soon after infection these tests would yield positive results, or for how long these results would remain positive. To answer these questions, nasal swabs and blood samples were collected daily from a group of 36 naturally infected horses. EI viral RNA was detected in all horses by qRT-PCR from the first to tenth day after clinical signs were evident, and was detected in some horses for up to 34 days. Antibody was detected in the bELISA in some horses by day 3, with a median time to seroconversion of 5 days. The results from this study indicate that viral RNA can be detected from nasal swabs for much longer than infectious virus is thought to be shed from horses. The bELISA detected antibodies against EI virus in all horses for 139 days following infection, but only detected approximately 50% of horses 12 months following infection. Haemagglutination inhibition testing detected antibodies against H3 antigens in all horses for 28 days following infection, but 2 were negative by 35 days following infection.

Experimental infections of the porcine foetus with Bungowannah virus, a novel pestivirus.

In 2003 an outbreak of sudden deaths occurred in 2-3-week-old pigs on a piggery in New South Wales, Australia. There was a marked increase in the birth of stillborn pigs and preweaning losses associated with a multifocal non-suppurative myocarditis with myonecrosis. The aim of this study was to amplify any infectious agents present in field material to aid the detection and identification of the causative agent of the porcine myocarditis syndrome (PMC). Foetuses were directly inoculated in utero with tissue extracts from field cases of PMC at 56-60, 70-84 or 85-94 days of gestation and euthanased 7-28 days later. The IgG concentration in foetal sera/body fluids was measured, hearts were examined by light microscopy and selected hearts were examined by electron microscopy. An infectious agent was detected in tissues from cases of PMC and its identification as the novel pestivirus Bungowannah virus has recently been reported (Kirkland et al., 2007). Sow sera, foetal tissues and foetal sera/body fluids were tested for Bungowannah virus RNA by qRT-PCR and antibody by peroxidase-linked assay. Bungowannah virus was detected in numerous organs of the porcine foetus. Following direct foetal exposure it is probable that this virus spreads by direct intra-uterine transmission to adjacent foetuses and by trans-uterine transmission to the dam. Data were obtained for both the replication of the virus in the porcine foetus and the humoral immune response in the foetus and sow.