title: Giardia Alters Commensal Microbial Diversity throughout the Murine Gut.
abstract: Giardia lambliais the most frequently identified protozoan cause of intestinal infection. Over 200 million people are estimated to have acute or chronic giardiasis, with infection rates approaching 90% in areas whereGiardiais endemic. Despite its significance in global health, the mechanisms of pathogenesis associated with giardiasis remain unclear, as the parasite neither produces a known toxin nor induces a robust inflammatory response.Giardiacolonization and proliferation in the small intestine of the host may, however, disrupt the ecological homeostasis of gastrointestinal commensal microbes and contribute to diarrheal disease associated with giardiasis. To evaluate the impact ofGiardiainfection on the host microbiota, we used culture-independent methods to quantify shifts in the diversity of commensal microbes throughout the gastrointestinal tract in mice infected withGiardiaWe discovered thatGiardia's colonization of the small intestine causes a systemic dysbiosis of aerobic and anaerobic commensal bacteria. Specifically,Giardiacolonization is typified by both expansions in aerobicProteobacteriaand decreases in anaerobicFirmicutesandMelainabacteriain the murine foregut and hindgut. Based on these shifts, we created a quantitative index of murineGiardia-induced microbial dysbiosis. This index increased at all gut regions during the duration of infection, including both the proximal small intestine and the colon. Giardiasis could be an ecological disease, and the observed dysbiosis may be mediated directly via the parasite's unique anaerobic fermentative metabolism or indirectly via parasite induction of gut inflammation. This systemic alteration of murine gut commensal diversity may be the cause or the consequence of inflammatory and metabolic changes throughout the gut. Shifts in the commensal microbiota may explain observed variations in giardiasis between hosts with respect to host pathology, degree of parasite colonization, infection initiation, and eventual clearance.
authors.affiliation: Department of Microbiology and Molecular Genetics, UC Davis, Davis, California, USA.
authors.forename: N R
authors.initials: NR
authors.lastname: Barash
authors.affiliation: Departments of Biology and Microbiology & Immunology, Georgetown University, Washington, DC, USA.
authors.forename: J G
authors.initials: JG
authors.lastname: Maloney
authors.affiliation: Departments of Biology and Microbiology & Immunology, Georgetown University, Washington, DC, USA.
authors.forename: S M
authors.identifier: http://orcid.org/0000-0001-5719-7535
authors.initials: SM
authors.lastname: Singer
authors.affiliation: Department of Microbiology and Molecular Genetics, UC Davis, Davis, California, USA scdawson@ucdavis.edu.
authors.forename: S C
authors.identifier: http://orcid.org/0000-0002-0843-1759
authors.initials: SC
authors.lastname: Dawson
mesh_terms: D000818:Animals; D064806:Dysbiosis / Q000469:parasitology*; D005260:Female; D000069196:Gastrointestinal Microbiome; D016829:Giardia lamblia; D005873:Giardiasis / Q000503:physiopathology*; D054884:Host-Pathogen Interactions; D007421:Intestine, Small / Q000382:microbiology / Q000469:parasitology*; D051379:Mice; D008810:Mice, Inbred C57BL; D059208:Parasite Load
keywords: Giardia; microbiome; parasite; pathogenesis