The presence of infectious chicken anemia virus (CAV) was detected in a previous study by nested-PCR as a contaminant in seven commercial vaccines, produced in the 1990s by three different manufacturers, prepared against the most relevant virus etiologies. In order to phylogenetically characterize the genome and compare it to CAV isolates from Brazil and other parts of the world, sequences of approximately 675 bp of the gene encoding the hypervariable region of VP1 protein of three CAV vaccine contaminant strains were studied. The CAV genome in contaminated vaccines showed high similarity (> 98.9%) with the Brazilian BR91/99 and Argentinian ArgA001028 (> 99%) strains. However, the comparison with the Cuxhaven-1 vaccine strain showed a lower identity of between 96.8% and 97.7%, and comparing it with the CAV26P4 vaccine strain showed an identity between 97.2% and 98.2%; both are available in Brazil. Such differences might be relevant for the highly conserved CAV genome. CAV contaminants were positioned in the same genetic group (clusters) with the Brazilian strain BR91/99 and Argentinian strain ArgA001028. Results indicated that the contamination of live vaccines by CAV may have influenced CAV epidemiology in the Brazilian and Argentinian poultry industry.
Fifty-four fecal samples taken from broiler chickens from 1 to 45 days of age, and of pullets from 10 to 13 weeks of age, original from eight different poultry regions in the state of Minas Gerais, Brazil, were collected from March 2008 to January 2010 for avian Orthoreovirus (ARV) and avian Rotavirus (AvRV) analyses. For the assay of ARV, RNA was immediately extracted (Trizol) and transcribed into cDNA for assaying in a nested-PCR with ARV-specific primers. For AvRV, polyacrylamide gel electrophoresis (PAGE) was performed with RNA extracts obtained by phenol-chloroform extraction. CAV was additionally investigated through a nested-PCR of thymus and spleen. Results found 5.55% positive for ARV and 9.25% for AvRV. Also, CAV and ARV genomes were detected in co-infection, in a highly prostrated and claudicating chicken flock. No ARV or AvRV infections were detected in pullets. Material of a clinically affected flock was inoculated into SPF embryos, resulting in embryonic hemorrhage, whitish foci in the chorio-allantoic membrane and death. Sequencing of ARV amplicons and isolate cDNA grouped local strains with the ARV S1133 strain, historically used in live vaccines, suggesting the continued circulation of this vaccine virus strain in intensive poultry regions. Detection rates for ARV and AvRV, as well as the presence of CAV, were additionally indicative of failing biosecurity strategies for the intensive poultry regions examined.Keywords: Broiler, layer, chicken anemia virus, CAV, avian reovirus, ARV, avian rotavirus, AvRV, nested-PCR, PAGE.
RESUMO
Avaliou-se a ocorrência de Orthoreovirus (ARV) e Rotavirus (AvRV) aviários na avicultura industrial de
The occurrence of CAV in backyard chickens in the metropolitan area of Belo Horizonte, Brazil, was evaluated. The spleen and thymus of chickens from different origins were collected for DNA extraction and nested-PCR. CAV genome was detected in 30% of the flocks (n=20) examined. CAV origin for backyard chickens is speculated, taking into consideration its widespread incidence in the chicken industry, the contamination of live vaccines with CAV prior to its eradication from SPF flocks, and the use of attenuated CAV vaccines.
Three experiments were carrie out to evaluate the influence of cage density on the performance of 25-to 84-week-old laying hens. Forty hundred Lohmann-LSL layers were distributed in cages (100x40x 45x50cm) according to a completely randomized experimental design with split plot in time.Three treatments (10, 12, or 14 hens per cage, corresponding, to 450, 375, and 321cm 2 /bird, respectively), with 15 assessment periods (four weeks each), and eight replicates per treatment were applied. Considering that layer`s production cycle is affected by age, three experimental trials (25 to 44; 45 to 64 and 65 to 84 weeks of age) were carried out, and the data collected in each trial was individually analyzed. Increasing cage density significantly reduced feed intake in all phases studied. Increasing birds/cm 2 significantly decreased feed intake and improved feed conversion at all stages of study, and egg production was only affected in 45-week-old birds. The number of birds per cage should be reduced as birds age in order not to affect their performance. Birds with more cage space in the presented higher feed intake; however, this did not result in higher egg production or lower mortality. These results suggest that up to 45 weeks of age, 375 cm 2 per layer results in the best performance, and from then on, 450 cm 2 per bird is required to maintain egg production and to reduce hen mortality.
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