Type IV Pili, Transient Bacterial Aggregates, and Virulence of Enteropathogenic <i>Escherichia coli</i>

TLDR

Type IV bundle‑forming pili of enteropathogenic Escherichia coli mediate localized adherence and autoaggregation. The study examined whether these pili are required for virulence by inactivating the pilus subunit gene bfpA or the transcriptional activator bfpT (perA) in volunteers. The authors disrupted bfpA or bfpT, encoding the pilus subunit and the bfp operon transcriptional activator, to assess virulence. Both mutants caused significantly less diarrhea, and the bfpF mutant, which exhibited increased piliation and adherence but lacked dispersal motility, colonized the intestine yet was about 200‑fold less virulent, demonstrating that BfpF is essential for aggregate dispersal and full virulence.

Abstract

Type IV bundle-forming pili of enteropathogenic Escherichia coli are required for the localized adherence and autoaggregation phenotypes. Whether these pili are also required for virulence was tested in volunteers by inactivating bfpA or bfpT ( perA ) encoding, respectively, the pilus subunit and the bfp operon transcriptional activator. Both mutants caused significantly less diarrhea. Mutation of the bfpF nucleotide-binding domain caused increased piliation, enhanced localized adherence, and abolished the twitching motility–dispersal phase of the autoaggregation phenotype. The bfpF mutant colonized the human intestine but was about 200-fold less virulent. Thus, BfpF is required for dispersal from the bacterial aggregate and for full virulence.