Influence of incubation temperature on chorio-allantoic membrane vascularization heart size and ascites incidence in broilers (Gallus domesticus)

Abstract

Ascites or pulmonary arterial hypertension (PAH) syndrome is a significant cause of mortality in modern fast-growing broilers that are raised at high altitude. Damage caused by temperature to the cardio-vascular system during embryo development is often overlooked as an important predisposing factor to ascites experienced on the farm. Eggs from a 38 week-old Ross 308 flock were exposed to three temperature treatments. One group was exposed to 36.8oC (cool), the second group to 37.5oC (control) and the third group to 38.2oC (hot). Relative humidity ranged from 55-59% in all groups. These treatments were used throughout the incubation period. Vascularisation of the chorio-allantoic membrane (CAM) was used as an indirect measure of embryonic blood vessel reaction to temperature insult. Vascular fraction (VF), density and fractal dimension (FD) and branching of blood vessels were assessed using a stereo microscope. The control had significantly lower (p<0.001) VF and FD compared to both hot and cool groups suggesting that high and low temperatures in incubators and hatchers trigger vascular compensation. High temperature during embryonic development resulted in significantly lower heart mass in both the control (p<0.002) and the hot (p<0.001) groups compared to the cool treatment. A smaller heart will limit the ability of the fast growing broiler to compensate for low oxygen levels at high altitude and thus be prone to ascites. Formation of the embryo muscle mass was significantly reduced in hot (p<0.001) and the control (p<0.007) groups compared to the cool treatment. In this study embryo mass was reported as yolk-free body mass (YFBM). The hot treatment had significantly (p<0.001) lower (1 843g) body mass at 35 days of age when slaughtered compared to the cool and control groups that averaged 2 107g and 2 130, respectively. There was, however, no statistical difference (p<0.178) on heart mass (HM) to YFBM ratio amongst all three temperature treatment groups. Mortality due to ascites was double (53%) in the hot group compared to the control and cool treatments which were similar. The difference in mortality was significant at p<0.001. This very high mortality in the hot group is likely to have skewed the right ventricle to total ventricular (RV: TV) ratio which was the same to that of the cool treatment at 0.26. This falls within the range of a normal fowl. Birds in the control group had higher (0.28) RV: TV ratio which indicated susceptibility to ascites. Feed conversion for the control group was 2.94% better (1.517) than the cool group (1.563) and 5.2% better than the hot treatment (1.601), the differences were not significant between the hot and control group and slaughter. The combined farm performance variables expressed in terms of an efficiency factor (PEF) showed that the control group (292) performed 4.8% better than the cool group (278) and 47.6% better than the hot group (153). Bacterial growth in yolks from eggs in the hot treatments was recorded in 19.2% of the samples, with 12% being gram-negative bacteria. Only 3% and 3.7% of samples from the control and cool groups, respectively, had bacterial growth. Of the bacteria isolated in the cool treatment group, all were gram-negative isolates. As the incubation and setter temperature increased, so has the number of positive samples. Statistically, bacterial growth was significantly (p<0,024) higher in the hot treatment compared to the cool and control groups combined.