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

Cytopathic bovine viral diarrhea viruses (BVDV): emerging pestiviruses doomed to extinction

Bovine viral diarrhea virus (BVDV), a Flaviviridae pestivirus, is arguably one of the most widespread cattle pathogens worldwide. Each of its two genotypes has two biotypes, non-cytopathic (ncp) and cytopathic (cp). Only the ncp biotype of BVDV may establish persistent infection in the fetus when infecting a dam early in gestation, a time point which predates maturity of the adaptive immune system. Such fetuses may develop and be born healthy but remain infected for life. Due to this early initiation of fetal infection and to the expression of interferon antagonistic proteins, persistently infected (PI) animals remain immunotolerant to the infecting viral strain. Although only accounting for some 1% of all animals in regions where BVDV is endemic, PI animals ensure the viral persistence in the host population. These animals may, however, develop the fatal mucosal disease, which is characterized by widespread lesions in the gastrointestinal tract. Cp BVD virus, in addition to the persisting ncp biotype, can be isolated from such animals. The cp viruses are characterized by unrestrained genome replication, and their emergence from the persisting ncp ones is due to mutations that are unique in each virus analyzed. They include recombinations with host cell mRNA, gene translocations and duplications, and point mutations. Cytopathic BVD viruses fail to establish chains of infection and are unable to cause persistent infection. Hence, these viruses illustrate a case of “viral emergence to extinction” – irrelevant for BVDV evolution, but fatal for the PI host

The Outcome of Porcine Foetal Infection with Bungowannah Virus Is Dependent on the Stage of Gestation at Which Infection Occurs. Part 2: Clinical Signs and Gross Pathology

Bungowannah virus is a novel pestivirus identified from a disease outbreak in a piggery in Australia in June 2003. The aim of this study was to determine whether infection of pregnant pigs with Bungowannah virus induces the clinical signs and gross pathology observed during the initial outbreak and how this correlates with the time of infection. Twenty-four pregnant pigs were infected at one of four stages of gestation (approximately 35, 55, 75 or 90 days). The number of progeny born alive, stillborn or mummified, and signs of disease were recorded. Some surviving piglets were euthanased at weaning and others at ages up to 11 months. All piglets were subjected to a detailed necropsy. The greatest effects were observed following infection at 35 or 90 days of gestation. Infection at 35 days resulted in a significant reduction in the number of pigs born alive and an increased number of mummified foetuses (18%) and preweaning mortalities (70%). Preweaning losses were higher following infection at 90 days of gestation (29%) and were associated with sudden death and cardiorespiratory signs. Stunting occurred in chronically and persistently infected animals. This study reproduced the clinical signs and gross pathology of the porcine myocarditis syndrome and characterised the association between the time of infection and the clinical outcome