The avian colibacillosis outbreak is a disease that threatens public health, poultry production, and economic interests, even after antibiotic feed addition. It is known that avian pathogenic E. coli is a major pathogenic factor; however, the systemic characteristics of gut flora in disease samples and how pathogens grow remain unknown. To study these issues in depth, we used the whole microbial genome shotgun sequencing technique to compare entire microbes in diseased and healthy broiler chickens. We found that it was not only E. coli that increased substantially, but most pathogenic flora also increased significantly in diseased samples. Subsequently, we proved that aminoglycoside antibiotic resistance genes were mainly found in non-E. coli strains. This suggests that E. coli survival under antibiotic stress was due to the cooperative resistance from non-E. coli strains. Among all these increasing strains, attaching and effacing pathogens could damage host intestinal epithelial cells to release oxygen in the gut to make the microenvironment more adaptable for E. coli strains. Furthermore, we observed that the functions of the T4SS/T6SS secretion system were dramatically enhanced, which could help E. coli to compete and enlarge their living spaces. Ultimately, pathogenic E. coli accumulated to cause avian colibacillosis. This study provides a new insight into intestinal microecology in diseased individuals, which would propose new treatment options for avian colibacillosis from a metagenome perspective.
Keywords: Antibiotic resistance; Avian colibacillosis; Dynamics balance; Gut microbiome; Intestinal microenvironment.
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