Infectivity of bacteria is mediated by several virulent factors that help the bacteria establish an infection. The expression of the virulence factors such as lectin, exotoxin, enterotoxin, fibronectin protein, etc. is regulated by cell–cell communication method, Quorum sensing (QS), which, in turn, help the bacteria invade the host's defense barrier and extend their pathogenicity. The QS is a system of communication of bacterial cells enabling them to coordinate pathogenicity by acting on specific quorum-associated signals. QS is the process of controlling infectivity of bacteria to adapt to the host and environment despite having disadvantages. The QS system is typically identified as bacterial cell synthesizing and subsequently sensing a signaling molecule, that trigger specific response reactions depending on cell population, known to be self-inducing. Biofilm formation is a predominant behavior of bacteria that is driven by QS. This QS control systems are broadly of following types. (1) LuxI/LuxR gene-mediated quorum sensing, where the key signaling molecule is acyl-homoserine lactone (AHL), (2) autoinducing peptide (AIP)–mediated quorum sensing having 5–25 amino acids exported by ABC transporter, and (3) luxS encoding autoinducers 2 (AI-2) quorum sensing for interspecific communication. AHL circuit by LuxI/LuxR type regulation is most common in Gram-negative bacteria. AIP mechanism associated with accessory gene regulator (AGR) is found in Gram-positive bacteria, whereas AI-2 is used by both Gram-positive and Gram-negative bacteria. The serotyping of infectious bacteria is hence categorized according to their quorum sensing. In all these systems, a two component response element has been formed to be pivotal to regulate the reaction cascade ultimately linked to the virulence regulation. In this chapter, a comprehensive approach is made to portray microbial diversity and mode of infectivity along with quorum sensing signaling models.