Coinfection with Eimeria spp. decreases bacteremia and spinal lesions caused by pathogenic Enterococcus cecorum

• Published in: Animal feed science and technology Vol. 250; pp. 59 - 68
• Main Authors: Borst, L.B., McLamb, K.A., Suyemoto, M.M., Chen, L.R., Levy, M.G., Sarsour, A.H., Cordova, H.A., Barnes, H.J., Oviedo-Rondón, E.O.
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01.04.2019
• Subjects: Coccidiosis; Enterococcus cecorum; Gut health; Kinky-back; OCD; Kinky-back; BWG; FI; FCR; BW; Cocci; FTV; Coccidiosis; EC; Enterococcus cecorum; Gut health
• ISSN: 0377-8401; 1873-2216
• DOI: 10.1016/j.anifeedsci.2018.09.014

•Pathogenic strains of Enterococcus cecorum (EC) cause a paralytic disease of chickens known as ‘kinky-back’.•Pathogenic EC escape the gut and infect the spleen (bacteremia) independent of gut damage.•Co-infection with coccidian parasites increases gut inflammation and decreases bacteremia due to EC.•Infection with either EC alone or dual infection had a negative impact on live performance parameters.•Undesirable live performance parameters were significantly increased in groups fed nicarbazin compared to zoalene. Pathogenic strains of Enterococcus cecorum (EC) escape the gut niche to infect the spine of broilers at the free thoracic vertebra (FTV) causing the disease enterococcal spondylitis or ‘kinky-back’. Intestinal barrier damage caused by coinfection with Eimeria spp. has been suggested to play a role in potentiating EC bacteremia and FTV lesion development. To test this hypothesis, 1440 broilers were experimentally infected with EC only, EC and a coinfection of E. acervulina, E. maxima and E. tenella (EC:Cocci), and a saline only control (Sham). Birds were grown for 35 days, spleen cultures, histologic lesions in the FTV and live performance parameters were compared among groups. Coccidian coinfection significantly decreased the prevalence of EC bacteremia and histologic lesions in the FTV. Histologic evaluation of the ceca revealed significantly increased cecal mucosal height and mean inflammatory scores in the EC:Cocci group compared to EC only and sham inoculated controls. These findings indicate that the decrease in pathogenic EC bacteremia observed with coccidia coinfection may be due to increased intestinal epithelial turnover or increased immune surveillance of the intestine. In both infection groups, body weights, body weight gain and feed intake were significantly decreased and feed conversion ratios were significantly increased. These undesirable alterations in live performance parameters were exacerbated by nicarbazin treatment but not zoalene or bacitracin treatment. Further work is needed to determine the mechanism for the observed benefit of coccidian coinfection in decreasing bacteremia and FTV lesions due to pathogenic EC.