Causes of mortality in laying hens in different housing systems in 2001 to 2004

<p>Abstract</p> <p>Background</p> <p>The husbandry systems for laying hens were changed in Sweden during the years 2001 – 2004, and an increase in the number of submissions for necropsy from laying hen farms was noted. Hence, this study was initiated to compare causes of mortality in different housing systems for commercial laying hens during this change.</p> <p>Methods</p> <p>Based on results from routine necropsies of 914 laying hens performed at the National Veterinary Institute (SVA) in Uppsala, Sweden between 2001 and 2004, a retrospective study on the occurrence of diseases and cannibalism, i.e., pecking leading to mortality, in different housing systems was carried out. Using the number of disease outbreaks in caged flocks as the baseline, the expected number of flocks with a certain category of disease in the other housing systems was estimated having regard to the total number of birds in the population. Whether the actual number of flocks significantly exceeded the expected number was determined using a Poisson distribution for the variance of the baseline number, a continuity correction and the exact value for the Poisson distribution function in Excel 2000.</p> <p>Results</p> <p>Common causes of mortality in necropsied laying hens included colibacillosis, erysipelas, coccidiosis, red mite infestation, lymphoid leukosis and cannibalism. Less common diagnoses were Newcastle Disease, pasteurellosis and botulism. Considering the size of the populations in the different housing systems, a larger proportion of laying hens than expected was submitted for necropsy from litter-based systems and free range production compared to hens in cages (<it>P </it>< 0.001). The study showed a significantly higher occurrence of bacterial and parasitic diseases and cannibalism in laying hens kept in litter-based housing systems and free-range systems than in hens kept in cages (<it>P </it>< 0.001). The occurrence of viral diseases was significantly higher in indoor litter-based housing systems than in cages (<it>P </it>< 0.001).</p> <p>Conclusion</p> <p>The results of the present study indicated that during 2001–2004 laying hens housed in litter-based housing systems, with or without access to outdoor areas, were at higher risk of infectious diseases and cannibalistic behaviour compared to laying hens in cages. Future research should focus on finding suitable prophylactic measures, including efficient biosecurity routines, to reduce the risk of infectious diseases and cannibalism in litter-based housing systems for laying hens.</p

Histomorphology of bursa of Fabricius: effects of stock densities on commercial broilers

During the past few years, there has been considerable interest on the effects of stocking density on broiler behavior and immunity. Stress may cause immunodeficiency by affecting cell and humoral responses, as well as body weight decrease, and foot-pad dermatitis. The aim of this study was to study histomorphological changes of the bursa of Fabricius in broilers submitted to three different stocking densities (10, 15, and 20 birds/m²) from one to 42 days of age. Three birds from each group were sacrifieced on days 7 and 42. The bursa was collected, fixed, and processed for histomorphometric assessment using a Kontrom KS 400 image analyzer. Data were analyzed by Biostat 3.0 (Tukey Test). The results of average cortical area percentage in bursal follicles of 6-week-old birds were 45.12a (10 birds/m²), 30.43b (15 birds/m²), and 23.77b (20 birds/m²). Average body weight was 2.58a kg (10 birds/m²), 2.56a Kg (15 birds/m²), and 2.47b Kg (20 birds/m²), respectively. The percentage of foot-pad dermatitis in 6-week-old birds was 3.33a (10 birds/m²), 17.76b (15 birds/m²), and 49.17c (20 birds/m²). These differences were statistically significant at a P<0.05 level. Under these experimental conditions,, it was concluded that the best stocking density to produce broilers is between 10-15 birds per square meter

Rapid environmental effects on gut nematode susceptibility in rewilded mice

Genetic and environmental factors shape host susceptibility to infection, but how and how rapidly environmental variation might alter the susceptibility of mammalian genotypes remains unknown. Here, we investigate the impacts of seminatural environments upon the nematode susceptibility profiles of inbred C57BL/6 mice. We hypothesized that natural exposure to microbes might directly (e.g., via trophic interactions) or indirectly (e.g., via microbe-induced immune responses) alter the hatching, growth, and survival of nematodes in mice housed outdoors. We found that while C57BL/6 mice are resistant to high doses of nematode (Trichuris muris) eggs under clean laboratory conditions, exposure to outdoor environments significantly increased their susceptibility to infection, as evidenced by increased worm burdens and worm biomass. Indeed, mice kept outdoors harbored as many worms as signal transducer and activator of transcription 6 (STAT6) knockout mice, which are genetically deficient in the type 2 immune response essential for clearing nematodes. Using 16S ribosomal RNA sequencing of fecal samples, we discovered enhanced microbial diversity and specific bacterial taxa predictive of nematode burden in outdoor mice. We also observed decreased type 2 and increased type 1 immune responses in lamina propria and mesenteric lymph node (MLN) cells from infected mice residing outdoors. Importantly, in our experimental design, different groups of mice received nematode eggs either before or after moving outdoors. This contrasting timing of rewilding revealed that enhanced hatching of worms was not sufficient to explain the increased worm burdens; instead, microbial enhancement and type 1 immune facilitation of worm growth and survival, as hypothesized, were also necessary to explain our results. These findings demonstrate that environment can rapidly and significantly shape gut microbial communities and mucosal responses to nematode infections, leading to variation in parasite expulsion rates among genetically similar hosts