Dissemination and virulence of bacterial gastrointestinal infections
Short description
Enterotoxigenic Escherichia coli (ETEC) is a major cause of diarrhea in children and adults in endemic areas and also a common cause of travellers’ diarrhea and food borne outbreaks of gastroenteritis. We are interested in how ETEC regulate virulence and survival in response to molecules and metabolites present in the human gut, and during dissemination in the environment.
In a second project, we study plasmids carrying antibiotic resistance genes and how they are transferred between bacterial isolates by using a combination of microbiological methods and sequencing techniques. We collect both clinical and environmental isolates and aim to determine factors needed for transmission of antibiotic resistance.
Escherichia coli is a facultative anaerobic gram-negative bacterium that normally inhabits the intestines of mammals, birds and reptiles as a commensal bacterium. Pathogenic E. coli have acquired extrachromosomal genetic properties that enable them to cause disease by colonization of the epithelium, and delivery of toxins or virulence factors.
Enterotoxigenic Escherichia coli (ETEC) is a major cause of diarrhea in children and adults in endemic areas. ETEC is characterized by the production of two toxins (LT and ST) that cause the diarrheal symptoms, and colonization factors (CFs), that mediate adhesion to the epithelium in the small intestine. The toxins and CFs are located on large plasmids that are conserved geographically and over time in different ETEC clones. We study the plasmid genes and how they are regulated in response to environmental and host stress factors. We have identified unique responses to specific bile salt molecules present in the human intestines that induce bacterial aggregation and adhesion in ETEC. Our studies are now focused on gene regulation by transcription factors as well as determination of other protective factors mediated by plasmid-borne genes during dissemination in the environment and in the host.
We hypothesize that pathogenic clones emerge by a perfect match between chromosomal and acquired extrachromosomal genes and regulatory factors that mediate both optimal virulence capacity and ability to spread in the environment. We are also interested in the traits that are acquired when plasmids carrying antibiotic resistance genes are transferred from one bacterium to another. To study this, we collect resistant clinical and environmental isolates of several bacterial species and determine their ability to transfer these plasmids by microbiological methods. We determine the genetic composition of the plasmids by long read sequencing.
