Abstract

Simple SummaryCoccidiosis, which can be induced by Eimeria spp., causes tremendous economic losses in the poultry production. Eimeria tenella (E. tenella) is one of the poultry Eimeria spp. that damage cecal tissue. Broilers infected with E. tenella can have reduced body weight, feed efficiency, and gut health because ceca are the main site for producing volatile fatty acids (VFA; important energy sources) and ceca accommodate diverse pathogens. To find appropriate strategies to cope with E. tenella infection, modes of actions of E. tenella infection on broiler growth and health should be investigated, and experimental infection model should be established. In the study, different levels of sporulated E. tenella oocysts were inoculated to the broilers, and the inoculation dosages induced mild infection in the ceca of broilers. The current study showed that E. tenella infection damaged feed efficiency and small intestinal health in broilers, mainly by reducing cecal volatile fatty acids (VFA) production. Different inoculation levels modulated the tendency of fecal moisture content and fecal oocyst shedding at different time points. Based on the results, energy supplementation and/or modulation of cecal microbiota potentially ameliorates negative effects of E. tenella infection in broilers.The purpose of the study was to investigate effects of different inoculation dosages of E. tenella on growth performance, gastrointestinal permeability, oocyst shedding, intestinal morphology, fecal consistency, ileal apparent digestibility, antioxidant capacity, and cecal VFA profile in broiler chickens. Five different dosages (T0: 0, T1: 6250, T2: 12,500, T3: 25,000, and T4: 50,000) of E. tenella oocysts were inoculated via oral gavage to fourteen-day-old broilers. Inoculation of E. tenella linearly increased FCR (p < 0.05), and feed intake was quadratically increased on 6 days post-infection (dpi; p = 0.08) and 7 dpi (p = 0.09). Cecal lesion score of each treatment was T0: 0; T1: 0.39 ± 0.14; T2: 0.93 ± 0.21; T3: 1.25 ± 0.16; and T4: 1.58 ± 0.2. Cecal total VFA production was linearly reduced due to E. tenella infection on 6 dpi (p < 0.01). E. tenella infection deepened cecal crypts depth on 6 dpi (CD; p < 0.05). Gastrointestinal permeability tended to be linearly increased (p = 0.07). E. tenella infection tended to linearly reduce duodenal VH (p = 0.1) and jejunal VH on 9 dpi (p = 0.09). Different dosages of E. tenella modulated the tendency of fecal moisture content and oocyst shedding. Therefore, E. tenella infection impaired feed efficiency and small intestinal health mainly by reducing cecal VFA production and deepening cecal CD in broilers.

Highlights

  • Coccidiosis causes tremendous economic losses in broiler production by impairing gut health and depressing growth performance and feed efficiency of broiler chickens, and expensive anti-coccidial treatments increase the overall production cost [1,2].Avian coccidiosis are induced by Eimeria spp., which are protozoan parasites, and there are 7 known Eimeria spp. that can infect chickens: Eimeria acervulina, E. maxima, E. tenella, E. brunetti, E. necatrix, E. mitis, and E. praecox [3]

  • This study showed that E. tenella infection deepened crypts depth of the ceca

  • Increased fecal moisture content can result in increased litter moisture, and this can increase the incidence of food pad dermatitis in broilers [41]. This current study showed that mild infection of E. tenella impaired feed efficiency and gut health mainly through reducing volatile fatty acids (VFA) production in broilers

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Summary

Introduction

Coccidiosis causes tremendous economic losses in broiler production by impairing gut health and depressing growth performance and feed efficiency of broiler chickens, and expensive anti-coccidial treatments increase the overall production cost [1,2]. Avian coccidiosis are induced by Eimeria spp., which are protozoan parasites, and there are 7 known Eimeria spp. that can infect chickens: Eimeria acervulina, E. maxima, E. tenella, E. brunetti, E. necatrix, E. mitis, and E. praecox [3]. Each species resides at the different section of the intestinal tract of broiler chickens, and thereby it has different modes of actions to affect growth performance and gut health of broilers [4]. The infection is initiated by ingestion of sporulated (infectious) oocysts, and after the asexual and sexual replications, un-sporulated oocysts are excreted with feces [6]. The oocysts can be sporulated and become infectious, and this life cycle can be repeated with poultry growth cycle

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