BACKGROUND: On account of the importance of iodine in the synthesis of thyroid hormones, different levels of dietary iodine can affect the occurrence of ascites syndrome in broilers.OBJECTIVES: The current research aimed to investigate the effects of different sources and levels of iodine on performance, carcass traits, ascites mortality, thyroid hormones, and serum biochemical parameters of broiler chickens under cold stress condition.METHODS: This experiment was performed using 375 one-day-old male broiler chickens in a completely randomized design with five treatments, five replications, and 15 birds per replication. To induce ascites, the room temperature was reduced to 15 °C from 14 days and this temperature was maintained until the end of the period. The experimental treatments included: control treatment (basal diet with iodine at the recommended level, 1.25 ppm), basal diet + potassium iodide (KI) with iodine levels (6.25 and 3.75 ppm), and basal diet + calcium iodate [Ca(IO3)2. H2O] with iodine levels (6.25 and 3.75 ppm).RESULTS: The effect of the treatments on the performance indices was not significant throughout the experiment. The lowest percentage of ascites mortality, heart weight, and triiodothyronine (T3) were observed in the treatment (6.25 ppm), which was significantly different from the control treatment (P<0.05). The lowest ratio of right ventricle to total ventricles (RV/TV) was related to potassium iodide treatment (6.25 ppm), which indicated tendency (P<0.10). Chickens receiving higher levels of iodine (6.25 ppm) had higher thyroxine than those receiving lower levels (3.75 ppm) (P<0.05) and showed a lower ratio of triiodothyronine to thyroxine compared to those (P<0.05).CONCLUSIONS: The results of this experiment implied that the use of higher levels of dietary iodine (6.25 ppm), especially as potassium iodide, reduces broiler’s ascites mortality under cold stress conditions.

The relation between average duodenal mast cell count, duodenal mucosal mast cell numbers, duodenal connective tissue mast cell numbers, circulating basophil numbers, heterophil-to-lymphocyte ratio, and lesion score were studied to gain an understanding of the events that may lead to intestinal lesion formation associated with hemorrhagic enteritis virus (HEV) infection. Changes in vascular permeability in the duodenum in birds inoculated with HEV were examined, using colloidal carbon and ferritin as vascular markers. Turkeys inoculated with HEV had significantly (P < 0.05) higher duodenal mast cell counts than did noninfected controls. Birds inoculated with HEV had significantly (P < 0.05) more mucosal mast cells than did phosphate-buffered saline solution-inoculated birds. Connective tissue mast cell and basophil numbers were unaffected by viral inoculation. Thermal stress did not have significant effect on lesion severity, but did increase number of birds that developed the characteristic intestinal lesions. The heterophil-to-lymphocyte ratio was significantly (P < 0.05) higher in HEV-inoculated birds, compared with phosphate-buffered saline solution-inoculated controls. Increase in vascular permeability was only detected in HEV-inoculated birds with intestinal lesions. Results indicate that mast cells, and the vasoactive mediators contained within mast cells, may be important in the early manifestation of HEV infection. They also provide a possible mechanism through which biochemical and physiologic changes characteristic of HEV infection can occur.

Blood samples from sarcoptic mite-infested pigs were evaluated for effects of mite infestation and cold and ambient temperatures on lymphocyte blastogenic responses and for effects of mite infestation on serum cortisol concentrations. In experiment 1, sarcoptic mite-infested and noninfested pigs were housed in cold (5 to 15 C fluctuating) and thermoneural (25 C) environmental chambers for 5 weeks. Differences were not observed (P greater than 0.10) in blastogenic responses to phytohemagglutin or pokeweed mitogen between lymphocytes from infested and noninfested pigs on postinfestation days (PID) 7, 21, 28, and 35 in either environmental chamber. When lymphocytes from noninfested pigs were cultured with sera from infested pigs, alterations of blastogenic responses were not detected. Cortisol values were higher (P less than 0.05) in sera from sarcoptic mite-infested pigs, compared with those from noninfested pigs, at 4 PM on PID 14 and at 4 AM and 10 AM on PID 15. Cortisol values were higher (P less than 0.05) in sera obtained at 10 AM on PID 14 and at 10 AM on PID 15 from pigs housed in cold chambers, compared with those from pigs housed in thermoneutral chambers. Interactive effects between sarcoptic mite infestation and cold ambient temperatures were not observed. At 4 AM on PID 15 (experiment 2), cortisol values were higher (P less than 0.05) in sera of infested pigs, compared with those in noninfested pigs. Seemingly, sarcoptic mange in pigs did not alter mitogen-induced lymphocyte blastogenic responses, but did increase serum cortisol concentrations, indicating that sarcoptic mange may be a stressor in pigs.