Interaction of dietary vitamin E with Eimeria maxima infections in chickens

In two trials, broiler chickens, processed similarly to those placed in commercial operation, were fed, from 1 d of age, a range (13 to 200 ppm) of DL-alpha-tocopheryl acetate (VE-AC) levels, and the effects on the pathology of Eimeria maxima infections were assessed at 6 d postinoculation (PI). In Trial 1, dietary levels of VE-AC had little significant effect on variables characterizing pathology except for the number of oocysts shed, which was significantly increased in chicks treated with higher VE-AC levels. The infection was judged to be mild based on moderate lesion scores (2.2 ± 0.2), lack of significant effects on weight gain (7 ± 1.6% decrease), moderate reduction in plasma carotenoids (21 ± 2%) and small increases in plasma NO2−+NO3− (141 ± 12%). In uninfected and infected chickens, plasma alpha-tocopherol (AT) increased with dietary levels of VE-AC; however, E. maxima infection caused a fairly constant decrease in AT of 35.3 ± 3.2% across these levels. Plasma γ-tocopherol (GT) levels were unaffected by dietary VE-AC or E. maxima infection. In Trial 2, pathology, again, was relatively unaffected by dietary VE-AC level. The infection was judged to be severe based on lesion scores (3.5 ± 0.1), reduction in weight gain (30.7 ± 3%), plasma carotenoids (72.4 ± 1.5%), uric acid (16.3 ± 3.4), albumin (37.8 ± 2.8%), large increases (261 ± 8%) in plasma NO2−+NO3−, and high numbers of oocysts shed per chick (4.12 ± 0.4 × 107). Plasma AT again increased with increasing dietary VE-AC levels in uninfected and infected chicks, but the mean decrease across VE-AC levels caused by E. maxima infection was 73.14 ± 3.3%. GT levels were erratic and unrelated to dietary VEAC or infection. Thus, in processed broiler chickens, high dietary VE-AC did not prevent or lessen the pathology caused by mild or severe infections with E. maxima. The main effect of E. maxima infection appeared to be reduction in plasma AT levels. We postulate that this reduction may be due to malabsorption of AT, which results from physical damage to the absorptive mucosa, reduction in esterases required to hydrolyze the VE-AC, and a generalized lipid malabsorption, preventing movement of the free AT to circulating blood and infected tissues.