Pathogenic bacteria encounter hostile environments and experience diverse stresses from their initial moment of contact with the host. To survive within the host, bacteria improved metabolic fitness and altered virulence character. As in the case of respiratory pathogens, bacteria respond against an array of host-derived antimicrobial mediators, nitrosative stress, hyperosmolarity, and oxygen limitation. Further, in case of enteric pathogens, after ingestion, they must survive the acidic pH. Moreover, enteric pathogens living within the intestinal lumen encounter host-generated antimicrobial peptides, reactive oxygen radicals, bile salts, and free fatty acids and enhanced osmolality. Subsequently, inflammatory responses against pathogen recruit macrophages, neutrophils, and other phagocytic cells. These defense mechanisms increase oxidative and nitrosative stresses as well as sequestration of essential metals and nutrients. Bacteria respond to these by developing exquisite systems that sense these stresses and trigger appropriate mechanism for successful survival. Different environmental stimuli not only trigger adaptive responses but also modulate virulent genes at particular condition. An array of stress responses and their mechanism is consequently critical and necessary to understand bacterial pathogenesis.

In an effort of emphasizing the complexity of bacterial adaptation during the host infection, this chapter will focus on different stress-sensing and stress response mechanisms that finally improvise the bacterial metabolic fitness.