Background: Fresh produce such as leafy green salads have recently become recognized as a potential source of food-borne infection by enteric pathogens This study investigated whether compounds released from damaged salad leaves were recognized by Listeria monocytogenes strain EGD and if they impacted its growth and virulence. Methods: The effects of extracts of salad leaves or salad bag fluids were tested on the growth, biofilm formation, and colonization of salad leaves and host cell virulence. Results: The presence of salad extract at a concentration of less than 0.5% v/v and salad bag fluids at a concentration of 10% v/v enhanced the growth in water and serum-based medium by more than 10,000 times over un-supplemented control cultures. Light and scanning electron microscopy, as well as eukaryotic Caco-2 and Galleria mellonella models of infection, showed that leafy green extracts from rocket, lettuce, spinach, and their salad bag fluids significantly increased the ability of Listeria to establish biofilms and infect host cells. Conclusions: This investigation showed that salad leaf extracts can markedly enhance bacterial virulence, which has implications for bagged salad leaf consumer safety if the leaves become contaminated with pathogenic bacteria such as Listeria.

Streptococcus pneumoniae is an asymptomatic colonizer of the nasopharynx, but it is also one of the most important bacterial pathogens of humans, causing a wide range of mild to life-threatening diseases. The basis of the pneumococcal transition from a commensal to a parasitic lifestyle is not fully understood. We hypothesize that exposure to host catecholamine stress hormones is important for this transition. In this study, we demonstrated that pneumococci preexposed to a hormone released during stress, norepinephrine (NE), have an increased capacity to translocate from the nasopharynx into the lungs compared to untreated pneumococci. Examination of NE-treated pneumococci revealed major alterations in metabolic profiles, cell associations, capsule synthesis, and cell size. By systemically mutating all 12 two-component and 1 orphan regulatory systems, we also identified a unique genetic regulatory circuit involved in pneumococcal recognition and responsiveness to human stress hormones. IMPORTANCE Microbes acquire unique lifestyles under different environmental conditions. Although this is a widespread occurrence, our knowledge of the importance of various host signals and their impact on microbial behavior is not clear despite the therapeutic value of this knowledge. We discovered that catecholamine stress hormones are the host signals that trigger the passage of Streptococcus pneumoniae from a commensal to a parasitic state. We identify that stress hormone treatment of this microbe leads to reductions in cell size and capsule synthesis and renders it more able to migrate from the nasopharynx into the lungs in a mouse model of infection. The microbe requires the TCS09 protein for the recognition and processing of stress hormone signals. Our work has particular clinical significance as catecholamines are abundant in upper respiratory fluids as well as being administered therapeutically to reduce inflammation in ventilated patients, which may explain why intubation in the critically ill is a recognized risk factor for the development of pneumococcal pneumonia.