ColV Plasmid-Mediated, Colicin V-Independent Iron Uptake System of Invasive Strains of Escherichia coli

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Abstract
Evidence is presented that ColV plasmid-mediated Fe uptake, an important component of the virulence of invasive strains of E. coli, is independent of colicin V synthesis and activity. A mutant of E. coli K-12 deficient in the biosynthesis of enterochelin (strain AN1937) was unable to grow on minimal agar containing the chelating agent .alpha.,.alpha.''-dipyridyl unless it was harboring the plasmid ColV-K30 (strain LG1315). Acquisition of the active plasmid-specific Fe sequestering system was accompanied by marked enhancement of pathogenicity in experimental infections of mice. Mutants of strain LG1315 were isolated that were defective in Fe uptake due to plasmid mutations. They were unchanged with respect to colicin production, but were significantly less virulent than the parent strain. Conversely, mutants isolated as defective in colicin V synthesis were normal for the plasmid-coded Fe uptake mechanism and showed the same lethality for infected mice as did strain LG1315. Mutations in strain AN1937 which render it resistant or tolerant to the bactericidal action of colicin V did not influence the uptake of Fe into plasmid-carrying strains. Cross-feeding tests involving plasmid mutants defective in Fe uptake identified 2 plasmid-specified components of the system, an extracellular Fe-chelating compound and a nondiffusible product allowing transport of Fe across the bacterial cell membrane.

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