Aquatic wild birds constitute the natural reservoir of influenza A viruses. Under appropriate selection pressure these viruses display a remarkable genetic flexibility which is based on their high mutation rate. At least 16 subtypes of the viral hemagglutinin glycoprotein (HA) und 9 of the viral neuraminidase (NA) are distinguishable as a result of natural evolution. Due to the segmentation of the viral genome, genetic reassortments and, thus, a theoretically unrestricted combination of HA and NA subtypes is possible. Transspecies-specific transmissions of viruses from the natural reservoirs to mammals (horses, swine, humans) led to the establishment of several influenza virus lineages which are circulating stably and independently from the previous reservoir. Introduction of viruses featuring new HA/NA combinations into immunologically naive populations can cause rapid and widespread, even pandemic, dissemination of such viruses. The (highly pathogenic avian influenza, HPAI). These mutants constitute the causative agents of classical fowl plague. HPAI viruses of subtypes H5 and H7 generally share a polybasic endoproteolytical cleavage site in the HA protein which allows for systemic replication in the avian host. Subtype H5 and H7 viruses which are maintained in the natural reservoir hosts, in contrast, are of low pathogenicity (LPAI) and harbour monobasic HA cleavage sites restricting their tissue tropism to epithelia of the respiratory and gastronintestinal tracts. This context forms the basis of all legal measures targeting the monitoring, prevention and eradication of HPAIV and LPAIV of subtypes H5 and H7 in poultry. Results of such measures in Germany in 2008 are presented and discussed.