Does the human probiotic bacterium Escherichia coli Nissle (1917) affect growth performance and immune response of Nile tilapia Oreochromis niloticus?

Abstract

Probiotics are used in aquaculture as health and growth promoters as well as prophylaxis to reduce the use of antibiotics. Escherichia coli Nissle 1917 (EcN) is a human probiotic known to outcompete intestinal pathogens and strengthen the tight junctions of the intestinal barrier in mammals. We were not able to find literature that discusses the use of human probiotics as piscine probiotics. The aim of the present work was to determine the best way of incorporating EcN into fish feed as well as to assess the effects of EcN on survival, growth and immune response of Nile tilapia Oreochromis niloticus. EcN was extracted from Mutaflor® capsules, grown in BHI broth and sprayed on the diets of the fish at various concentrations and offered to them for 8 weeks. At the end of the 8 weeks survival, growth, condition index, HSI, VSI and hematological parameters were evaluated. A group of EcN fed fish were also used to test the persistence of EcN in tilapia after reverting to the control diets. Another group of EcN fed fish was challenged with Aeromonas hydrophila and Edwardsiella tarda either by feeding or through injection. Results showed that EcN does not have a significant effect on survival and growth of Nile tilapia (p 0.05). However, EcN has a significant effect on total white blood cell counts, hemoglobin, thrombocytes, lymphocytes, respiratory burst and HSI (p 0.05). Dietary EcN did not affect survival and growth and was not able to permanently colonize the guts of tilapia. Hematological parameters suggest an effect on the immune system of the fish offered EcN and but there was no difference in survival between probiotic offered fish and controls with regards to pathogen challenged individuals. Therefore, we can conclude that EcN was not able to act as a probiotic in tilapia and the immune response observed was probably targeting the EcN itself. The decrease in respiratory burst is probably caused by the iron chelating systems of EcN, whilst the decrease in liver weight is related to intestinal infla