ABSTRACT
Asiatic cholera is an acute and often fatal diarrheal disease afflicting humans infected with the Gram-negative bacterium Vibrio cholerae. Although toxin production is directly responsible for the manifestation of diarrhea, cholera pathogenesis relies on numerous elements acting synergistically to promote vimlence. Electron microscopic observation of strains grown on CFA (colonization factor agar) revealed that, in addition to the TCP (Toxin Coregulated Pilus) pilus, V. cholerae strains expressed at least two other fimbrial types The most extensively characterized fimbria expressed by V. cholerae is the TCP pilus, identified as being coexpressed with cholera toxin. An initial understanding of the regulation of TCP expression along with the phenotypes described allowed identification of the pilin structural gene, tcp A, through TnphoA mutagenesis. Amino acid sequencing of gel-purified TcpA reveals an antino-terrninal region that bears striking homology with a group of pilins that have been termed type 4 on the basis of major subunit homology, similar morphology, and putative function.
