Clinical signs and progression of lesions in the gizzard are not influenced by inclusion of ground oats or whole wheat in the diet following experimental infection with pathogenic fowl adenovirus serotype 1.

In the present study the effects of dietary gizzard stimulation on the development and severity of adenoviral gizzard erosion were investigated. For this purpose, specific pathogen-free broilers were divided into six groups, investigating the influence of an oat-containing diet with higher fibre content, a whole wheat-containing diet and a control diet of nearly identical composition, but containing ground wheat. For each feed administered, one group of birds was experimentally infected on the 10th day of age by the oral route with virulent fowl adenovirus serotype 1 (FAdV-1), recently proven to induce gizzard erosions, while the respective negative control groups remained uninfected. Experimental feed was administered from 2 days post-infection onwards. No significant differences on gizzard health or in weight gain could be detected between uninfected control groups or between FAdV-1 infected groups that received different experimental feed. However, independent of the supplied diet, a significantly reduced weight gain was noted from 7 days post-infection onwards in FAdV-1 infected broilers compared to uninfected birds that received the same diet. Macroscopically, discolouration and erosion of the koilin layer and inflammation of the gizzard mucosa were observed in all FAdV-1 infected groups. Histologically, necrosis, degeneration of gizzard epithelial cells and multiple basophilic intranuclear inclusion bodies were observed. In summary, after experimental infection with FAdV-1 development of gizzard erosion in chickens was not influenced by the feeding regimes investigated. Therefore, it is unlikely that dietary gizzard stimulation influences the outcome of adenoviral gizzard erosion in vertically infected broilers.

Identification of a new reovirus causing substantial losses in broiler production in France, despite routine vaccination of breeders.

Numerous cases of tenosynovitis appeared in France causing high morbidity in free-range and standard broilers. The main clinical findings were lameness, stunting and non-uniform bodyweights. Although the natural mortality was low, the economic losses due to birds that had to be removed from the flock prematurely, downgrading of carcases and lower average weights at slaughter were substantial. Postmortem examinations, bacteriological, virological and serological examination confirmed the aetiology of avian orthoreovirus (ARV)-induced tenosynovitis. The isolated ARVs were analysed serologically and genetically. Sequencing of σC RT-PCR products and phylogenetic analysis revealed a new type of ARV. The virus was not neutralised in serum neutralisation test using monovalent sera from vaccinated chickens. Together with the flock data, epidemiology of these recent reovirus outbreaks in France was reconstructed. It is concluded that these reovirus isolates differ serologically and genetically from the well described reovirus isolates used in commercial vaccines which were not capable of preventing the disease. The outbreaks resulted in substantial losses in broilers from vaccinated breeders.

Safety of avirulent histomonads to be used as a vaccine determined in turkeys and chickens.

In the present work, chickens and turkeys were infected with virulent or attenuated Histomonas meleagridis to investigate and compare the effect of both isolates on birds. Thereby, histomonads of a clonal culture were propagated in vitro either for a short period of time (21 passages) to preserve virulence or for 295 passages to achieve attenuation. On the first day of life birds of each species were infected with either virulent or attenuated parasites. Throughout the experiment, all birds were examined daily for clinical signs attributable to the infection. Furthermore, the excretion of viable parasites was determined after in vitro reisolation from cloacal swabs. For the investigation of pathological changes of organs a defined number of infected birds were killed on d 4, 7, 10, 14, and 21 postinfection (PI) and necropsy was performed. By this routine, changes in livers and ceca were classified by a scoring system to evaluate the severity of lesions. Samples of cecum, liver, and lung were generated and screened for the presence of parasites by PCR and immunohistochemistry. Turkeys infected with virulent histomonads showed first clinical manifestation of histomonosis on d 10 PI, whereas the remaining birds did not express clinical signs. Positive reisolations of virulent and attenuated histomonads were obtained intermittently from individual chickens and turkeys from d 2 PI until the end of the experiment. Both species of birds displayed lesions in the ceca and the liver following infection with virulent parasites, whereas no changes occurred in birds inoculated with attenuated histomonads. The PCR revealed the dissemination of virulent histomonads in ceca, livers, and lungs of some chickens and turkeys in contrast to attenuated parasites, which were exclusively found in cecal samples. The attenuated isolate of H. meleagridis did not induce clinical signs or pathological changes and offers high safety after infection of chickens and turkeys. Therefore, the in vitro attenuation and the use of avirulent histomonads represent a viable tool for vaccination against histomonosis.

Phylogenetic analysis of avian hepatitis E virus samples from European and Australian chicken flocks supports the existence of a different genus within the Hepeviridae comprising at least three different genotypes.

Using PCRs that amplify regions of helicase and capsid genes, the presence of avian hepatitis E virus (avian HEV) was determined in samples from European and Australian chicken flocks (collected from 2005 to 2007 and 1986 to 1995, respectively). A total of 27 virus samples from 9 countries were analysed to determine the phylogenetic relationship following PCRs and nucleic acid sequencing of the helicase and capsid regions of 18 avian HEV samples. For comparison, helicase and capsid sequences of completely sequenced avian HEVs from Europe, Australia and the USA were used. In addition, available helicase and capsid sequences of other avian HEVs and four mammalian HEVs were included. At least three genotypes within the avian HEV were revealed. These genotypes tend to be differentiated geographically. Altogether, the present investigation is of importance to understand the epidemiology of avian HEV infections in chickens and gives new insight into the phylogenetic relationships between isolates. Furthermore, we would like to propose that avian HEV represent a separate genus within the Hepeviridae consisting of different genotypes.