Disparity in the Gut Wall Penetration by Escherichia Coli During Co-Infection with Histomonas Meleagridis in Chickens and Turkeys

Histomonas meleagridis and Escherichia coli exhibit an outstanding interplay in vitro and are well recognized pathogens in poultry causing histomonosis and colibacillosis, respectively. H. meleagridis and E. coli reside in the intestine of birds, thus, to understand their interaction in vivo, gut microbial changes and caecal wall penetration of E. coli were investigated separately in experimentally infected chickens and turkeys (Abdelhamid et al., 2020, 2021). In the first trial, commercial Lohmann Brown layers (23 weeks old) were orally infected with a bioluminescent labelled pathogenic strain of E. coli with or without virulent strain of H. meleagridis (6x105 cells). Infected birds along with mock-inoculated negative controls were sequentially killed at 7, 10, 14 and 28 days post infection (dpi) for sampling. In the second trial, turkeys were inoculated with attenuated and/or virulent strains of H. meleagridis, using the same strain and dose of the parasite as in layers. Negative control birds were left uninfected. Sampling was done in birds killed at 7, 14 and 21 dpi. High throughput amplicon sequencing of 16SrRNA in caecal samples, histopathology, quantification of tagged or total E. coli and immunohistochemistry for the detection of E. coli were performed. Results showed that, infection of layers with E. coli alone did not induce lesions in the gut and had no pronounced effect on the caecal microbial population. In contrast, inoculation of H. meleagridis, both in chickens and turkeys, led to substantial shift in caecal microbiota, coinciding with severity of lesions. In general, bacteria such as Escherichia or Helicobacter were higher and commensals (e.g. Lactobacillus spp.) were lower in their abundance. Typhlitis leading to caecal wall destruction due to H. meleagridis was obvious in chickens and turkeys. However, increased penetration of E. coli from the caecal lumen towards peritoneum was only observed in chickens but not in turkeys. The lack of tendency of intestinal E. coli to penetrate the caecal tissues of turkeys even in the presence of severe mucosal destruction was further confirmed in birds from field cases of histomonosis as well.

In conclusion, H. meleagridis influenced the gut integrity and relative E. coli population in the caeca but the bacterial cells showed different tendency to infiltrate into the caecal wall of chickens and turkeys.