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    Effect of host genotype and Eimeria acervulina infection on the metabolome of meat-type chickens. Aggrey Samuel E,Milfort Marie C,Fuller Alberta L,Yuan Jianmin,Rekaya Romdhane PloS one OBJECTIVE:A study was conducted to identify metabolic biochemical differences between two chicken genotypes infected with Eimeria acervulina and to ascertain the underlying mechanisms for these metabolic alterations and to further delineate genotype-specific effects during merozoite formation and oocyst shedding. METHODS:Fourteen day old chicks of an unimproved (ACRB) and improved (COBB) genotype were orally infected with 2.5 x 105 sporulated E. acervulina oocysts. At 4 and 6 day-post infection, 5 birds from each treatment group and their controls were bled for serum. Global metabolomic profiles were assessed using ultra performance liquid chromatography/tandem mass spectrometry (metabolon, Inc.,). Statistical analyses were based on analysis of variance to identify which biochemicals differed significantly between experimental groups. Pathway enrichment analysis was conducted to identify significant pathways associated with response to E. acervulina infection. RESULTS:A total of 752 metabolites were identified across genotype, treatment and time post infection. Altered fatty acid (FA) metabolism and β-oxidation were identified as dominant metabolic signatures associated with E. acervulina infection. Key metabolite changes in FA metabolism included stearoylcarnitine, palmitoylcarnitine and linoleoylcarnitine. The infection induced changes in nucleotide metabolism and elicited inflammatory reaction as evidenced by changes in thromboxane B2, 12-HHTrE and itaconate. CONCLUSIONS:Serum metabolome of two chicken genotypes infected with E. acervulina demonstrated significant changes that were treatment-, time post-infection- and genotype-dependent. Distinct metabolic signatures were identified in fatty acid, nucleotide, inflammation and oxidative stress biochemicals. Significant microbial associated product alterations are likely to be associated with malabsorption of nutrients during infection. 10.1371/journal.pone.0223417
    Effects of Eimeria acervulina infection severity on growth performance, apparent ileal amino acid digestibility, and plasma concentrations of amino acids, carotenoids, and α1-acid glycoprotein in broilers. Rochell S J,Parsons C M,Dilger R N Poultry science An experiment was conducted to evaluate growth performance, apparent ileal digestibility (AID) of amino acids, and plasma concentrations of amino acids, carotenoids, and α1-acid glycoprotein, an acute-phase protein, in broilers inoculated with graded doses of E. acervulina oocysts. Ross 308 male broilers (400 total) were housed in battery cages from 1 to 21 d post-hatch and received common corn-soybean meal-based diets throughout the experiment. At 9 d post-hatch, birds were individually weighed and allotted to 4 treatment groups with 10 replicate cages of 10 birds per cage. At 15 d post-hatch, all birds were inoculated with 1 mL of distilled water that contained 0, 2.5 × 10(5), 5.0 × 10(5), or 1.0 × 10(6) sporulated E. acervulina oocysts. At 21 d, birds were euthanized for collection of blood and ileal digesta. Body weight gain and feed efficiency decreased linearly (P < 0.05) with increasing E. acervulina dose. With the exception of Trp and Gly, AID values decreased (P < 0.05) linearly or quadratically for all amino acids by an average of 2.6 percentage units for birds inoculated with 1.0 × 10(6) oocysts compared with uninfected birds. Infection with E. acervulina caused a quadratic decrease (P < 0.05) in plasma carotenoid concentrations. Plasma concentrations of Arg and Tyr decreased linearly (P < 0.05) with increasing E. acervulina inoculation dose and plasma Gln and Asn decreased quadratically (P < 0.01). Linear increases (P < 0.05) were observed for plasma Lys, Leu, Ile, Val, Pro, and Orn as E. acervulina inoculation dose increased. Plasma α1-acid glycoprotein of broilers was not influenced (P > 0.05) by E. acervulina infection. In conclusion, E. acervulina challenge adversely impacted growth performance, plasma carotenoids, and AID of amino acids in a dose-dependent manner. However, plasma amino acid responses to graded E. acervulina inoculation doses varied considerably among amino acids. Thus, these results indicated that alterations in amino acid metabolism caused by E. acervulina infection extended beyond reduced amino acid digestibility. 10.3382/ps/pew035
    Isolation and selection of ionophore-tolerant Eimeria precocious lines: E. tenella, E. maxima and E. acervulina. Li G Q,Kanu S,Xiang F Y,Xiao S M,Zhang L,Chen H W,Ye H J Veterinary parasitology Eimeria parasites were isolated from Nanhai Guangdong province (southern China) and studied in chickens in wire cages to evaluate their drug resistance against commonly used ionophores: monensin (100 mg/kg of feed), lasolacid (90 mg/kg), salinomycin (60 mg/kg), maduramicin (5 mg/kg) and semduramicin (25 mg/kg). Chinese Yellow Broiler Chickens were infected with 40,000 crude sporulated Eimeria oocysts at 15 days of age and prophylactic medication commenced a day prior to infection. Drug resistance was assessed for each ionophore drug by calculating the anticoccidial index (ACI) and percentage optimum anticoccidial activity (POAA) based on relative weight gain, rate of oocyst production and lesion values. Results revealed that Nanhai Eimeria oocysts comprising of E. tenella, E. maxima and E. acervulina, were resistant to monensin, sensitive to both salinomycin and lasolacid and partially sensitive to maduramicin and semduramicin. By selection for early development of oocysts during passage through chickens, the prepatent time of E. tenella, E. maxima and E. acervulina were reduced by 49, 36 and 22 h, respectively. The precocious lines are less pathogenic than the parent strains from which they were selected and conferred a satisfactory protection for chickens against coccidiosis. These ionophore-tolerant precocious lines could have wider applications in the development of anticoccidial vaccines for sustainable control of coccidiosis. 10.1016/j.vetpar.2003.12.009