RESUMO
Resilient animals can cope with environmental disturbances in life with minimal loss of function. Resilience can be enhanced by optimizing early-life conditions. In poultry, eggshell temperature (EST) during incubation and early feeding are two early-life conditions that are found to alter neonatal chick quality as well as immune response in later life. However, whether these early-life conditions affect disease resilience of chickens at later ages has never been studied yet. Hence, we studied the effects of EST [(37.8°C (control) or 36.7°C (lower)] during late incubation (≥embryonic days 17-19.5) and feeding strategy after hatch [immediately (early feeding) or 51-54 h delayed (delayed feeding)] on later-life broiler resilience in a 2 × 2 factorial arrangement. At hatch, 960 broilers of both sexes from a 54-week-old Ross breeder flock were equally divided over 32 pens (eight replicate pens per treatment combination) and grown for 6 weeks. Necrotic enteritis was induced by a single inoculation of Eimeria spp. at d 21 and repeated Clostridium perfringens inoculation (3×/d) during d 21-25. Mortality and body weight (BW) gain were measured daily during d 21-35 as indicators of resilience. Additionally, disease morbidity was assessed (gut lesions, dysbacteriosis, shedding of oocysts, footpad dermatitis, and natural antibody levels in blood). Results showed a lack of interaction between EST and feeding strategy for the vast majority of the variables. A lower EST resulted in lower BW gain at d 5 and 8 post Eimeria inoculation (P = 0.02) and more Eimeria maxima oocysts in feces at d 8 post Eimeria inoculation compared to control EST (P < 0.01). Early feeding tended to lower mortality compared to delayed feeding (P = 0.06), but BW gain was not affected by feeding strategy. Morbidity characteristics were hardly affected by EST or feeding strategy. In conclusion, a few indications were found that a lower EST during late incubation as well as delayed feeding after hatch may each impair later-life resilience to necrotic enteritis. However, these findings were not manifested consistently in all parameters that were measured, and conclusions are drawn with some restraint.
RESUMO
Predators and competitors of vertebrates can in theory reduce the density of infected nymphs (DIN)-an often-used measure of tick-borne disease risk-by lowering the density of reservoir-competent hosts and/or the tick burden on reservoir-competent hosts. We investigated this possible indirect effect of predators by comparing data from 20 forest plots across the Netherlands that varied in predator abundance. In each plot, we measured the density of questing Ixodes ricinus nymphs (DON), DIN for three pathogens, rodent density, the tick burden on rodents and the activity of mammalian predators. We analysed whether rodent density and tick burden on rodents were correlated with predator activity, and how rodent density and tick burden predicted DON and DIN for the three pathogens. We found that larval burden on two rodent species decreased with activity of two predator species, while DON and DIN for all three pathogens increased with larval burden on rodents, as predicted. Path analyses supported an indirect negative correlation of activity of both predator species with DON and DIN. Our results suggest that predators can indeed lower the number of ticks feeding on reservoir-competent hosts, which implies that changes in predator abundance may have cascading effects on tick-borne disease risk.
