Impact of dietary modification on aflatoxicosis in poultry
Aflatoxin contamination in feed and feed ingredients is of high worldwide prevalence, posing serious risks to the livestock industry. A series of studies were conducted to better understand the comprehensive impact of aflatoxicosis and its interrelationships with dietary modifications in broiler chicks and ducks. Results of these studies emphasize the many factors that the severity of aflatoxicosis depends on, including animal species, age, presence of mycotoxin adsorbent, and concentration of major dietary nutrients. Exposure to 2 mg/kg cultured AFB1 led to reduced feed intake, BW gain, depressed feed efficiency, increased relative liver weight, negatively affected serum measures and complement activity, as well as affected hepatic gene expression in 21 d broiler chicks. Additionally, impaired gut barrier, increased endogenous N loss, and reduced energy, N, and amino acid digestibility, and altered mRNA expression of intestinal tight junction proteins and transporters are also consequences of AFB1 exposure at 1.5 mg/kg in broilers. Disparately, as low as 0.1 mg/kg AFB1 led to significantly impaired growth, liver functions, and innate immune dynamics in 14 d Pekin ducklings, while effects of AFB1 on the gastrointestinal tract are less noticeable in ducks, with partial changes in jejunum morphology, digestive enzyme activity, and apparent energy digestibility. This suggests that while broilers may be more resistant, ducks are extremely sensitive to AFB1, and that the negative effects from AFB1 primarily result from reduced feed intake for ducks. Although total protection was not observed, supplementing HSCAS at 0.05% was effective to partially prevent aflatoxicosis in both broilers and ducks, as shown by improved performance (weekly but not cumulative in both species), restoring the negatively affected serum measures, and increased relative liver weight. Whether this is a direct effect on the liver and/or indirect result from reduced AFB1 absorption awaits further verification. Notably, the tested HSCAS was able to increase the mRNA expression and protein activity of major hepatic anti-oxidant activity, suggesting stimulated anti-oxidant function of the animal and likely a better ability to relieve the oxidative stress during aflatoxicosis. Thus, this may be a direct cause for the relieved liver damage by HSCAS. In addition to non-nutritive adsorbents, dietary nutrients can also influence the response and extent of the animal’s response to AFB1 exposure. A significant interaction of dietary crude protein and AFB1 was found in broilers, where the growth performance and health impairment (including serum measures, gut permeability, and N and amino acid digestibility) from aflatoxicosis were augmented when birds were fed a lower CP diet, and were completely eliminated by a higher CP diet. Higher dietary protein also improved BW gain and G:F ratio in ducks during aflatoxicosis, but no interaction was observed. Nevertheless, in both species, feeding low protein diets exacerbated the negative effects of AFB1, thus extra caution is needed when low CP diets are being fed. In addition, higher dietary branched chain amino acids (BCAA), key regulators in protein synthesis, improved all performance measures in broilers during aflatoxicosis, but no interaction was observed and higher BCAA negatively affected nutrient digestibility and serum measures. These observations reveal the complexity of the dynamic relationship between aflatoxicosis and dietary nutrients. On the other hand, the question remains whether in vitro response can be used to predict in vivo toxicity with sufficient accuracy. Good in vitro estimation of the toxicity potential of sample may be useful in initial screening of feed and feed ingredients. By exploring the response of fresh primary duck embryonic fibroblasts to various cytotoxins and mycotoxins, we showed that primary DEF had a higher sensitivity to toxins compared to HepG2 cells, and thus great potential in serving as a cytotoxicity screening model in vitro. Further attention should be given to the understanding of additive, synergistic, and antagonistic effects of multiple mycotoxins in in vitro systems and implications for animal responses in vivo.
Applegate, Purdue University.
Animal sciences|Animal Diseases
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