The Infectivity of Exo and Endogenous Stages of Eimeria tenella in Broilers

Abstract

Eimeria tenella is the most prevalent and pathogenic Coccidia causing morbidity, mortality and resulting in serious economic losses to the poultry industry worldwide. The aim of this study was to determine the immune response of broiler chickens to Eimeria tenella developmental stages Four hundred broilers divided into six groups (n=40) were used for the study. Each group was subdivided into two (n=20) as treated and non-treated and infected with different developmental stages (groups I-unsporulated oocysts, II-sporulated oocysts, III-schizonts, IV-merozoites and Vgametocytes respectively) of Eimeria tenella (local isolate), except group VI-control. The molecular identification of the local Eimeria tenella isolate identity was done through polymerase chain reaction (PCR) amplification of the genomic deoxyribonucleic acid (DNA). Clinical signs, gross caecal lesions, humoral and cellular-mediated immune response were determined in the infected broiler chickens with Eimeria tenella developmental stages. The faeces were processed using simple floatation technique and observed at 10x and 40x objectives of the Neiss microscope. Oocysts isolated from the caeca of birds naturally infected in Jos, Nigeria with the local strain were used to obtain the different developmental stages either in vitro or in vivo using bovine monocytes (schizonts), embryonated chicken eggs (gamatocytes) or two weeks old broilers (merozoites). To study the immune response elicited during the primary and secondary infection, each developmental stage was used to infect a group of two, three and half weeks old broilers, twenty of which were treated with the recommended dose of amprolium (250 mg/l (0.025%)) for 5 days at the appearance of clinical signs. At the tertiary infection, all the experimental birds except the control group of forty birds were orally infected with 105 sporulated oocysts of known characterized virulent Eimeria tenella strain. The mean oocysts output or count was 37.07 × 10⁶ in the infected birds non-treated than 25.65 × 106 in the treated groups, although there was a gradual reduction (groups II–8.36 × 10⁶–7.84 × 10⁶–5.10 × 10⁶; III-6.58 × 10⁶–4.83 × 10⁶; IV–7.18 × 10⁶–7.00 × 10⁶–3.83 × 10⁶; V–6.59 × 10⁶–5.87 × 10⁶–4.20 × 10⁶) in oocyst count from primarysecondary- tertiary infections except group I (control). There was a significant difference in oocyst output between the groups (II and IV) (p<0.05).