Interactions between Neisseria sicca and viridin B, a bacteriocin produced by Streptococcus mitis

Viridin B, a bacteriocin produced by Streptococcus mitis (mitior), is bactericidal to Neisseria sicca. Oxygen consumption by actively growing N. sicca cultures ceased immediately upon exposure to viridin B. Adenosine triphosphate production was slightly enhanced within 1 h of exposure to the bacteriocin but was subsequently repressed. The uptake and incorporation of glucose was prevented in the presence of viridin B. The bacteriocin also blocked uptake of an amino acid mixture in chloramphenicol-pretreated cells. Pretreatment or concomitant treatment with a variety of antibiotics known to inhibit specific synthetic pathways did not alter the inhibition of macromolecular synthesis produced by the bacteriocin. Although viridin B blocks protein and nucleic acid syntheses, no degradation of such macromolecules was observed. The inhibitory effects of viridin B on macromolecular synthesis and on viability required the presence of sufficient nutrients to allow active metabolism of N. sicca. The bacteriocin did not inhibit viability or macromolecular synthesis in anaerobically incubated N. sicca. Thus, active, oxidative metabolism by N. sicca cells is essential for viridin B action. A model for viridin B action is proposed.