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Eucalyptus oil: A promising anticoccidial agent with multifaceted protective effects
Jun-Jie Huang1, Jie-Yu Shi1, Kai-Yuan Li1
1College of Veterinary Medicine, Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou 225009, PR China.
Abstract:
In-feed preventive coccidiostat additives are regarded as the primary choice of coccidiosis control, whereas the lasting appearance of drug resistance seriously hampered its application. Eucalyptus oil (EUC) has been evidenced to possess anti-malaria and anti-helminth efficacy. Confronting the urgent requirements for novel anticoccidial remedies, EUC was picked to scrutinize its anticoccidial efficacy with the in vivo coccidiosis model. Birds were orally administrated with 8 × 104 sporulated oocysts and treated with 20 mg/kg EUC in feed during the whole experimental period, diclazuril (DIC) was selected as a positive control. The results manifested that EUC supplementation lessened cecal damage, oocyst shedding and mortality, and recovering body weight gain, so the anticoccidial index (ACI) was up to 160, indicating moderate anticoccidial activity. Additionally, the safeguarding effects of EUC on E. tenella-evoked cecal damage were respectively evidenced on macroscopic, histopathological, and ultrastructural levels. Meanwhile, EUC also exerted an inhibitory effect on redox imbalance and inflammatory response caused by E. tenella. Moreover, EUC treatment remarkably suppressed the invasion-related gene transcriptional level and enhanced the apoptosis mRNA expression level of coccidia. Besides, EUC noticeably decreased the Clostridium perfringens (C. perfringens) proliferation in vivo and in vitro. In conclusion, the EUC additive presented a moderate anticoccidial effect which is associated with the remission activity on E. tenella-induced cecal injury, redox imbalance, and inflammatory response which may be associated with inhibitory effect on Eimeria invasion and C. perfringens proliferation, and activating influence on coccidial apoptosis.
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