A spatial assessment of Culicoides spp. distribution and bluetongue disease risk areas in Austria.

Bluetongue disease (BT) was introduced into Central Europe in the summer of 2006 and has since affected most European countries. In this study we analysed the distribution of the biting midge vector Culicoides spp. in Austria and modelled Bluetongue disease risk zones. Culicoides spp. abundance data was collected from weekly catches of 14 months from 54 trapping locations. The corresponding weather data mean temperature (p < 0.001), wind (p < 0.001), relative humidity (p = 0.019) and altitude (p = 0.059) were identified as predictors on Culicoides spp. distribution in a regression model (R 2.8.0). The majority of catches were detected at temperatures above 10 degrees C and at relative humidities between 65-80%. The point data of these parameters originating from 186 meteorological stations were interpolated using the Geostatistical Analyst Kriging tool (ESRI ArcGIS 9.3). To create seasonal risk maps we overlaid regions with optimal temperature and humidity conditions with domestic ruminants density data. Our results show that the summer season holds the greatest risk of a BT epidemic with 25.9% of the analysed area providing optimal conditions for vector abundance and 12.4% showing contact risk with ruminant hosts. This project (1) provides fundamental data on the Culicoides spp. distribution in Austria, (2) determines limiting climatic parameters on vector abundance and (3) identifies risk areas by including areas of possible host-parasite-interactions. These high-risk areas can subsequently be given special attention for precautionary monitoring and surveillance measures.

Bluetongue virus RNA detection by RT-qPCR in blood samples of sheep vaccinated with a commercially available inactivated BTV-8 vaccine.

In 2008, a country-wide bluetongue virus 8 (BTV-8) vaccination campaign has been initiated in Austria, using a single commercial inactivated BTV-8 vaccine. Based on preliminary data, we hypothesised that vaccine-derived BTV RNA is transiently detectable by reverse transcription quantitative real-time PCR (RT-qPCR) in the blood of vaccinated animals. Thus BTV-8 vaccine was administered to five BTV-naïve adult sheep and blood samples were taken at various time-points post-vaccination. BTV RNA was detectable by several RT-qPCR methods in all five animals, mainly within the first 9 days post-vaccination. These results show that RT-qPCR based testing for BTV-infection may be influenced by vaccination with certain inactivated BTV-8 vaccines.

Geographical spread of highly pathogenic avian influenza virus H5N1 during the 2006 outbreak in Austria.

In spring 2006, highly pathogenic avian influenza virus (HPAIV) of subtype H5N1 was detected in Austria in 119 dead wild birds. The hemagglutinin cleavage site showed that the amino acid sequence motif was identical to that of the Qinghai lineage. For detailed analysis, the hemagglutinin (HA) and neuraminidase (NA) genes of 27 selected Austrian H5N1 viruses originating from different regions and wild bird species were analyzed phylogenetically, which revealed two clearly separated Austrian subclusters, both belonging to European cluster EMA-1. Subcluster South (SCS) contains virus isolates from the south of Austria as well as from Slovenia, Turkey, Egypt, and Nigeria. The second subcluster, Northwest (SCN), covered a larger group of viruses originating from different locations and wild bird species in the northern and very western parts of Austria, as well as from Bavaria and Switzerland. Surprisingly, virus isolates originating from two mute swans and one wild duck found on the north side of the Alps did not cluster with SCN but with SCS. Together with isolates from Bavarian, the Czech Republic, Italy, and Slovakia, they form a genuine subgroup, named subgroup Bavaria (SGB). This subgroup forms a link to SCN, indicating a spread of the virus from south to north. There has been a general assumption that the generic HPAI introduction route into Europe was from Russia to north Germany, introducing cluster EMA-2 into Europe. Interestingly, our findings support the assumption of an alternative introduction of the HPAI H5N1 virus from Turkey to central Europe, where it spread as cluster EMA-1 during the outbreak of 2006.