Abstract

This study was conducted to investigate the impacts of graded severity of Eimeria maxima infection on the growth performance and intestine health of broiler chickens. Four different levels of E. maxima-challenged treatments were used, including a non-challenged control group, a low challenge (12 500 oocysts), a medium challenge (25 000 oocysts), and a high challenge dose (50 000 oocysts). There were eight replicate cages per treatment, with 12 birds in each cage, and chickens in the challenged groups orally received sporulated oocysts on day 14. Gastrointestinal permeability was measured by fluorescein isothiocyanate dextran at 5 days post-infection (dpi), whereas intestinal morphology and gene expression of nutrient transporters and tight junction proteins were determined at 6 dpi. The results demonstrate a linear reduction in growth performance, jejunal villus height, and jejunal integrity with graded challenge doses of E. maxima (P < 0.01). Moreover, linear regulation of nutrient transporters and tight junction proteins was a consequence of increasing Eimeria infection levels (P < 0.01). The linear increase of Claudin 1, cationic amino acid transporter, glucose transporter 1, and L-type amino acid transporter genes was associated with increased severity of coccidiosis (P < 0.01). Furthermore, expression of nutrient transporters located at the brush border membrane were down-regulated (P < 0.01) with increasing E. maxima inoculation dose. In conclusion, growth performance and key intestinal integrity biomarkers in broiler chickens were adversely influenced in a dose-dependent manner by E. maxima infection.

Highlights

  • Coccidiosis, a major parasitic disease of poultry caused by several different species of the genus Eimeria, causing intestine damage, poor nutrient digestion, and diarrhea, costs approximately 14 billion United States dollars per Eimeria infection is known to inhibit the activities of brush border digestive enzymes such as maltase andTeng et al Vet Res (2021) 52:81 sucrase [2,3,4]

  • Simple sugars and amino acids concentrated in the enterocytes are, exported into blood circulation though the nutrient transporters located at the basolateral membrane, such as glucose transporter 1 (GLUT1), glucose transporter 2 (GLUT2), cationic amino acid transporter (CAT1), L-type amino acid transporter 1 (LAT1), and ­Na+-dependent neutral/ cationic amino acid transporter (LAT2)

  • Growth performance and mortality Increasing the inoculation doses of E. maxima linearly and quadratically decreased the body weight (BW), body weight gain (BWG), and feed intake (FI) of birds (P < 0.0001, Table 2)

Read more

Summary

Introduction

Coccidiosis, a major parasitic disease of poultry caused by several different species of the genus Eimeria, causing intestine damage, poor nutrient digestion, and diarrhea, costs approximately 14 billion United States dollars per Eimeria infection is known to inhibit the activities of brush border digestive enzymes such as maltase andTeng et al Vet Res (2021) 52:81 sucrase [2,3,4]. Chickens infected with E. maxima showed down-regulation of gene expression of nutrient transporters in the small intestine [5,6,7]. Simple sugars and amino acids concentrated in the enterocytes are, exported into blood circulation though the nutrient transporters located at the basolateral membrane, such as glucose transporter 1 (GLUT1), glucose transporter 2 (GLUT2), cationic amino acid transporter (CAT1), L-type amino acid transporter 1 (LAT1), and ­Na+-dependent neutral/ cationic amino acid transporter (LAT2). A reduction in the expression of nutrient transporters and endogenous enzymes in Eimeria-infected chickens results in a decrease in the digestibility of amino acids, energy, fat, and minerals [8,9,10,11,12,13]. Given that E. maxima mainly infects the jejunum and impairs the functions of the jejunum, the main focus of this work was on evaluating E. maxima infection on biomarkers associated with intestinal integrity and nutrient transporters of broiler chickens

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call