Bacteria utilize bacteriocins as a mechanism to maintain a competitive advantage in their niche. Lantibiotic-producing bacteria have been investigated for their ability to kill opportunistic pathogens such as vancomycin-resistant Enterococcus faecium (VRE). However, not much is known about the impact that lantibiotic-producing bacteria can have on the broader microbiome. We find that lanthipeptide genes, including previously characterized lantibiotics, are common among clinical patient gut microbiomes. Using a mouse model, we show the lantibiotic-producing bacterium, Blautia pseudococcoides SCSK, is capable of preventing recolonization of keystone species in the gut microbiota post antibiotic treatment. This results in prolonged dysbiosis that leave mice susceptible to Klebsiella pneumoniae and Clostrioides difficile infection weeks after antibiotic treatment has been suspended. These findings demonstrate the ability bacteria capable of producing broad-spectrum lantibiotics have in shaping the microbiota and may explain a possible mechanism for prolonged dysbiosis observed by patients in the clinic after taking antibiotics.