Potential pathogens persist in every single microbiome community. These pathobionts can act as commensals OR they can change their gene expression to act as pathogens under conditions of imbalance and immunosuppression. This pathobiont behavior helps explain why many microbes + viruses tied to chronic inflammatory disease are also regularly identified in healthy subjects. Here are two excellent 2018 studies on the topic:
Lead author: James Paton, University of Adelaide, Australia
The team found that, in the human body, the bacteria S. pneumoniae can persist as a “highly adapted commensal” or a serious pathogen. This difference hinges on its ability to “evade or take advantage of the host inflammatory and immune responses.”
Lead author: Ami Bhatt, Stanford University
The team used a new bioinformatics software pipeline to identify the source of bloodstream infections in a group of hospitalized + immunocompromised patients. They found that, in many cases, the same strain of a particular bloodstream pathogen was also identified in a patients’ gut microbiome. This suggests that many hospital-acquired infections are not derived from the external environment, but instead represent a change in host pathobiont activity + location of infection + host immunity.
Future research direction: “The results presented are suggestive of a gut microbiota source for both enteric and nonenteric organisms. However, given that the present study sampled only stool microbiota, we cannot exclude the possibility of the same pathogenic strain colonizing multiple body sites from which the infection may have originated instead.”