Pathogen leptospires are responsible for the zoonotic disease leptospirosis. The clinical manifestations of this infection range from a febrile state to a severe life-threatening form characterized by multiple organ hemorrhages and failure. More than one million cases of leptospirosis are currently reported annually in the word, with 10% of mortality.
Pathogen leptospires penetrate host organisms through skin abrasion or mucous membranes, are able to escape innate immunity and rapidly disseminate through the bloodstream to target organs, including liver and kidneys.
The strategies used by pathogenic leptospires for successful host colonization and virulence are not fully understood. Cultivating leptospires in vitro in culture media does not accurately reproduce the complexity of the host environment. To gain a comprehensive understanding of the host-pathogen interaction upon Leptospira infection, we will determine gene expression changes simultaneously in Leptospira and infected hamsters, the animal model that reproduces acute human leptospirosis. This should allow to identify Leptospira factors that allow host colonization and the host cellular pathways that are altered upon infection.
