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Over 200 million people are estimated to have acute or chronic giardiasis, with infection rates approaching 90% in areas where\n                    <jats:named-content content-type=\"genus-species\">Giardia<\/jats:named-content>\n                    is 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.\n                    <jats:named-content content-type=\"genus-species\">Giardia<\/jats:named-content>\n                    colonization 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 of\n                    <jats:named-content content-type=\"genus-species\">Giardia<\/jats:named-content>\n                    infection 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 with\n                    <jats:named-content content-type=\"genus-species\">Giardia<\/jats:named-content>\n                    . We discovered that\n                    <jats:named-content content-type=\"genus-species\">Giardia<\/jats:named-content>\n                    's colonization of the small intestine causes a systemic dysbiosis of aerobic and anaerobic commensal bacteria. Specifically,\n                    <jats:named-content content-type=\"genus-species\">Giardia<\/jats:named-content>\n                    colonization is typified by both expansions in aerobic\n                    <jats:named-content content-type=\"genus-species\">Proteobacteria<\/jats:named-content>\n                    and decreases in anaerobic\n                    <jats:named-content content-type=\"genus-species\">Firmicutes<\/jats:named-content>\n                    and\n                    <jats:named-content content-type=\"genus-species\">Melainabacteria<\/jats:named-content>\n                    in the murine foregut and hindgut. Based on these shifts, we created a quantitative index of murine\n                    <jats:named-content content-type=\"genus-species\">Giardia<\/jats:named-content>\n                    -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.\n                  <\/jats:p>","DOI":"10.1128\/iai.00948-16","type":"journal-article","created":{"date-parts":[[2017,4,10]],"date-time":"2017-04-10T20:30:30Z","timestamp":1491856230000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":132,"title":["Giardia Alters Commensal Microbial Diversity throughout the Murine Gut"],"prefix":"10.1128","volume":"85","author":[{"given":"N. R.","family":"Barash","sequence":"first","affiliation":[{"name":"Department of Microbiology and Molecular Genetics, UC Davis, Davis, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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