Foot-and-mouth disease in red deer - experimental infection and test methods performance

Summary: The aim of this study was to evaluate a number of foot-and-mouth disease (FMD) test methods for use in red deer. Ten animals were intranasally inoculated with the FMD virus (FMDV) O UKG 11/2001, monitored for clinical signs, and samples taken regularly (blood, serum, oral swabs, nasal swabs, probang samples and lesion swabs, if present) over a 4-week period. Only one animal, deer 1103, developed clinical signs (lesions under the tongue and at the coronary band of the right hind hoof). It tested positive by 3D and IRES real-time reverse transcription polymerase chain reaction (rRT-PCR) in various swabs, lesion materials and serum. In a non-structural protein (NSP) in-house ELISA (NSP-ELISA-IH), one commercial ELISA (NSP-ELISA-PR) and a commercial antibody NSP pen side test, only deer 1103 showed positive results from day post-inoculation (dpi) 14 onwards. Two other NSP-ELISAs detected anti-NSP serum antibodies with lower sensitivity. It also showed rising antibody levels in the virus neutralization test (VNT), the in-house SPO-ELISA-IH and the commercial SPO-ELISA-PR at dpi 9, and in another two commercial SPO-ELISAs at dpi 12 (SPO-ELISA-IV) and dpi 19 (SPO-ELISA-IZ), respectively. Six of the red deer that had been rRT-PCR and antibody negative were re-inoculated intramuscularly with the same O-serotype FMDV at dpi 14. None of these animals became rRT-PCR or NSP-ELISA positive, but all six animals became positive in the VNT, the in-house SPO-ELISA-IH and the commercial SPO-ELISA-PR. Two other commercial SPO-ELISAs were less sensitive or failed to detect animals as positive. The rRT-PCRs and the four most sensitive commercial ELISAs that had been used for the experimentally inoculated deer were further evaluated for diagnostic specificity (DSP) using 950 serum samples and 200 nasal swabs from non-infected animals. DSPs were 100% for the rRT-PCRs and between 99.8 and 100% for the ELISAs.

Spatial abundance patterns and recruitment of a virus-affected commercial mollusc fishery

 Infectious pathogens figure prominently among those factors threatening marine wildlife. Mass mortality events caused by pathogens can fundamentally alter the structure of wild fish stocks and depress recruitment rates and yield. In the most severe instances, this can precipitate stock collapses resulting in dramatic economic losses to once valuable commercial fisheries. An outbreak of a herpes-like virus among commercially fished abalone populations in the south-west fishery of Victoria, Australia, during 2006-2007, has been associated with high mortality rates among all cohorts. Long-term records from fishery-independent surveys of blacklip abalone Haliotis rubra (Leach) enabled abundance from pre- and post-viral periods to be analysed to estimate stock density and biomass. The spatial distribution of abundance in relation to physical habitat variables derived from high-resolution bathymetric LiDAR data was investigated. Significant differences were observed in both measures between pre- and post-viral periods. Although there was some limited evidence of gradual stock improvement in recent years, disease-affected reefs have remained below productivity rates prior to the disease outbreak suggesting a reduction in larval availability or settlement success. This was corroborated by trends in sublegal sized blacklip abalone abundance that has yet to show substantial recovery post-disease. Abundance data were modelled as a function of habitat variables using a generalised additive model (GAM) and indicated that high abundance was associated with complex reef structures of coastal waters (<15 m). This study highlights the importance of long-term surveys to understand abalone recovery following mass mortality and the links between stock abundance and seafloor variability.

Swine influenza virus PA and neuraminidase gene reassortment into human H1N1iInfluenza Virus is associated with an altered pathogenic phenotype linked to increased MIP-2 expression

Swine are susceptible to infection by both avian and human influenza viruses, and this feature is thought to contribute to novel reassortant influenza viruses. In this study, the influenza virus reassortment rate in swine and human cells was determined. Coinfection of swine cells with 2009 pandemic H1N1 virus (huH1N1) and an endemic swine H1N2 (A/swine/Illinois/02860/09) virus (swH1N2) resulted in a 23% reassortment rate that was independent of α2,3- or α2,6-sialic acid distribution on the cells. The reassortants had altered pathogenic phenotypes linked to introduction of the swine virus PA and neuraminidase (NA) into huH1N1. In mice, the huH1N1 PA and NA mediated increased MIP-2 expression early postinfection, resulting in substantial pulmonary neutrophilia with enhanced lung pathology and disease. The findings support the notion that swine are a mixing vessel for influenza virus reassortants independent of sialic acid distribution. These results show the potential for continued reassortment of the 2009 pandemic H1N1 virus with endemic swine viruses and for reassortants to have increased pathogenicity linked to the swine virus NA and PA genes which are associated with increased pulmonary neutrophil trafficking that is related to MIP-2 expression. IMPORTANCE: Influenza A viruses can change rapidly via reassortment to create a novel virus, and reassortment can result in possible pandemics. Reassortments among subtypes from avian and human viruses led to the 1957 (H2N2 subtype) and 1968 (H3N2 subtype) human influenza pandemics. Recent analyses of circulating isolates have shown that multiple genes can be recombined from human, avian, and swine influenza viruses, leading to triple reassortants. Understanding the factors that can affect influenza A virus reassortment is needed for the establishment of disease intervention strategies that may reduce or preclude pandemics. The findings from this study show that swine cells provide a mixing vessel for influenza virus reassortment independent of differential sialic acid distribution. The findings also establish that circulating neuraminidase (NA) and PA genes could alter the pathogenic phenotype of the pandemic H1N1 virus, resulting in enhanced disease. The identification of such factors provides a framework for pandemic modeling and surveillance.

Avian influenza virus dynamics in Australian wild birds

Understanding avian influenza infection dynamics in wildlife is crucial because of the possibility of virus spill over to livestock and humans. There are still knowledge gaps how different ecological and environmental factors influence infection dynamics in birds. My study highlights the importance of investigating disease dynamics in Australia.

Geographic variation in seasonality and its influence on the dynamics of an infectious disease

Seasonal changes in environmental drivers - such as temperature, rainfall, and resource availability - have the potential to shape infection dynamics through their reverberating effects on biological processes including host abundance and susceptibility to infection. However, seasonality varies geographically. We therefore expect marked differences in infection dynamics between regions with different seasonal patterns. By pairing extensive Avian Influenza Virus (AIV) surveillance data - 65 358 individual bird samples from 12 species of dabbling ducks sampled at 174 locations across North America - with quantification of seasonality using remote sensed data indicative for primary productivity (normalised differenced vegetation index, NDVI), we provide evidence that seasonal dynamics influence infection dynamics across a continent. More pronounced epidemics were seen to occur in regions experiencing a higher degree of seasonality, and epidemics of lower amplitude and longer duration occurred in regions with a more protracted and lower seasonal amplitude. These results demonstrate the potential importance of geographic variation in seasonality for explaining geographic variation in the dynamics of infectious diseases in wildlife.