VIRULENCE MECHANISMS OF AVIAN FIMBRIATED ESCHERICHIA-COLI IN EXPERIMENTALLY INOCULATED CHICKENS

Virulence mechanisms of avian pathogenic Escherichia coli were investi gated by inoculating commercial broiler chickens via the left caudal t horacic air sac with three highly pathogenic and three less pathogenic E., coli isolates. At 6 h postinoculation, all isolates had colonized the respiratory tract (trachea, lungs, and air sacs) and internal org ans (liver, spleen, and kidney) of inoculated birds, but bacteria were recovered from pericardial fluid and blood only of birds inoculated w ith the more pathogenic isolates. Fl fimbriae were expressed on a high proportion of bacteria colonizing the trachea and to a lesser extent on bacteria in the lungs of birds inoculated with each of the isolates . Fl fimbriae were also expressed on bacteria in air sacs only for the less pathogenic isolates. P(F11) fimbriae were expressed on bacteria present in air sacs, lungs, kidney, blood, and pericardial fluid of bi rds inoculated with one of the more virulent isolates, On electron mic roscopy, bacteria of the more pathogenic isolates but not of the less pathogenic isolates were observed often associated with or within macr ophages, which appeared to be viable, in the air sacs and lungs. In in vitro assays, the more pathogenic but not the less pathogenic isolate s, were resistant to opsonization and phagocytosis in the absence of F l fimbriae, whereas bacteria of all isolates were rapidly killed by av ian macrophages when they expressed Fl fimbriae. These results suggest that resistance to phagocytosis may be an important mechanism in avia n colisepticemia. They also suggest that Fl fimbrial phase variation t o the nonfimbriated phase is favored in the avian lower respiratory tr act, is more marked for the more pathogenic isolates, and may be a vir ulence mechanism. (C) 1997 Elsevier Science B.V.