Bird immunobiological parameters in the dissemination of the biofilm-forming bacteria Escherichia coli
Background and Aim: With the development of industrial maintenance technology, a group of pathogens called avian pathogenic Escherichia coli (APEC) became very common. The initiation, development, and outcome of the infectious process mediated by virulent APEC strains occur through a decrease in the colonization resistance of the intestine, an immunobiological marker of homeostasis stability in susceptible species. This study focused on the pathogenetic features of colibacillosis and the morphological features of E. coli.
Materials and Methods: Clinical, immunological, bacteriological, and histological studies were conducted on 15-day-old white Leghorn birds (n = 20). The birds were divided into two groups: Control group (Group I; n = 10) with birds intranasally inoculated with 0.5 mL of 0.9% NaCl solution and experimental group (Group II; n = 10) with birds intranasally inoculated with 0.5 mL of an E. coli suspension at 1 billion/mL.
Results: During the biofilm formation, clusters of microcolonies were formed as a gel-like intercellular matrix that accumulated due to cell coagulation. The intercellular matrix “glues” heteromorphic cells together and forms a structure of densely packed heteromorphic cells arranged in an orderly manner and growing in different directions. During the experimental reproduction of E. coli, excessive growth was observed in material isolated from poultry. Pathogenic E. coli strains implementing virulence factors adhered to the receptors of erythrocytes, alveolocytes, and enterocytes. Multicellular heterogeneous biofilms, united by an intercellular matrix, were located at the apical poles of the respiratory tract alveolocytes and enterocytes of the terminal ileum villi. Many bacteria exudate containing desquamated epithelial cells with an admixture of mucus, and polymorphonuclear leukocytes were detected in the lumen of the birds’ abdominal organs. Invasive bacteria damaged the epithelial layer, violated the endothelial layer of blood vessels, and developed inflammatory hyperemia of the lamina propria of the respiratory and digestive systems’ mucous membrane. A correlative dependence of changes developed by the type of delayed hypersensitivity reaction was established. Signs of accidental transformation of the thymus, atrophy of the bursa of Fabricius, disseminated thrombosis, and septic spleen developed. Moreover, toxic cardiomyocyte dystrophy, signs of congestive vascular hyperemia, massive disintegration of lymphocytes, macrophage reactions, perivascular edema resulting from the release of plasma, and shaped blood elements were detected.
Conclusion: The development and outcome of the infectious process in escherichiosis primarily depend on the homeostasis stability of susceptible species and virulence factors of the pathogenic microorganisms. One of the selected strains, E. coli O78:K80 displayed the highest ability to form biofilms. Its strong adhesion ability to bird erythrocytes was demonstrated. Deepening the scientific knowledge of the interaction between eukaryotes and prokaryotes will contribute to a better understanding of the pathogenetic aspects of avian escherichiosis and eventually find promising anti-adhesive drugs that could reduce primary bacterial contamination in vivo and in vitro.
Keywords: avian colibacillosis, biofilm formation, Escherichia coli, intercellular matrix, poultry.