Clostridioides difficile
[Display omitted] Clostridioides difficile is a spore-forming, anaerobic, intestinal pathogen that causes severe diarrhea that can lead to death. In 2011, C. difficile infected ∼500000 people in the USA and killed ∼29000 people. C. difficile infection (CDI) is the most common healthcare-related infe...
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| Veröffentlicht in: | Trends in microbiology (Regular ed.) 2018-12, Vol.26 (12), p.1049-1050 |
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| container_title | Trends in microbiology (Regular ed.) |
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| creator | Sandhu, Brindar K. McBride, Shonna M. |
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Clostridioides difficile is a spore-forming, anaerobic, intestinal pathogen that causes severe diarrhea that can lead to death. In 2011, C. difficile infected ∼500000 people in the USA and killed ∼29000 people. C. difficile infection (CDI) is the most common healthcare-related infection in the USA, leading to increased healthcare costs of $4.8 billion. This pathogen transmits via the oral–fecal route as a highly contagious and resilient spore. Upon exposure to primary bile acids in the intestine, C. difficile germinates, and in the absence of colonization resistance from the normal microbiota, the bacterium colonizes the colon and produces toxins. These toxins inhibit actin polymerization in host cells, leading to cell death. C. difficile cells can then sporulate in the intestine and exit the body via diarrheal shedding. In culture, sporulation is induced at stationary phase in a nutrient-limiting environment, but the intestinal triggers of sporulation are still unknown. |
| doi_str_mv | 10.1016/j.tim.2018.09.004 |
| format | Article |
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Clostridioides difficile is a spore-forming, anaerobic, intestinal pathogen that causes severe diarrhea that can lead to death. In 2011, C. difficile infected ∼500000 people in the USA and killed ∼29000 people. C. difficile infection (CDI) is the most common healthcare-related infection in the USA, leading to increased healthcare costs of $4.8 billion. This pathogen transmits via the oral–fecal route as a highly contagious and resilient spore. Upon exposure to primary bile acids in the intestine, C. difficile germinates, and in the absence of colonization resistance from the normal microbiota, the bacterium colonizes the colon and produces toxins. These toxins inhibit actin polymerization in host cells, leading to cell death. C. difficile cells can then sporulate in the intestine and exit the body via diarrheal shedding. In culture, sporulation is induced at stationary phase in a nutrient-limiting environment, but the intestinal triggers of sporulation are still unknown.</description><identifier>ISSN: 0966-842X</identifier><identifier>EISSN: 1878-4380</identifier><identifier>DOI: 10.1016/j.tim.2018.09.004</identifier><identifier>PMID: 30297117</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Anti-Bacterial Agents - therapeutic use ; Bile Acids and Salts - metabolism ; Clostridiales - drug effects ; Clostridiales - physiology ; Clostridium difficile - drug effects ; Clostridium difficile - pathogenicity ; Clostridium difficile - physiology ; Clostridium Infections - drug therapy ; Clostridium Infections - microbiology ; Feces - microbiology ; Humans</subject><ispartof>Trends in microbiology (Regular ed.), 2018-12, Vol.26 (12), p.1049-1050</ispartof><rights>2018 Elsevier Ltd</rights><rights>Copyright © 2018 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-201414d92a7745ad8d70fccf50905a93964f138739870d80e144ac40d5ccea483</citedby><cites>FETCH-LOGICAL-c451t-201414d92a7745ad8d70fccf50905a93964f138739870d80e144ac40d5ccea483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0966842X18302002$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30297117$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sandhu, Brindar K.</creatorcontrib><creatorcontrib>McBride, Shonna M.</creatorcontrib><title>Clostridioides difficile</title><title>Trends in microbiology (Regular ed.)</title><addtitle>Trends Microbiol</addtitle><description>[Display omitted]
Clostridioides difficile is a spore-forming, anaerobic, intestinal pathogen that causes severe diarrhea that can lead to death. In 2011, C. difficile infected ∼500000 people in the USA and killed ∼29000 people. C. difficile infection (CDI) is the most common healthcare-related infection in the USA, leading to increased healthcare costs of $4.8 billion. This pathogen transmits via the oral–fecal route as a highly contagious and resilient spore. Upon exposure to primary bile acids in the intestine, C. difficile germinates, and in the absence of colonization resistance from the normal microbiota, the bacterium colonizes the colon and produces toxins. These toxins inhibit actin polymerization in host cells, leading to cell death. C. difficile cells can then sporulate in the intestine and exit the body via diarrheal shedding. In culture, sporulation is induced at stationary phase in a nutrient-limiting environment, but the intestinal triggers of sporulation are still unknown.</description><subject>Animals</subject><subject>Anti-Bacterial Agents - therapeutic use</subject><subject>Bile Acids and Salts - metabolism</subject><subject>Clostridiales - drug effects</subject><subject>Clostridiales - physiology</subject><subject>Clostridium difficile - drug effects</subject><subject>Clostridium difficile - pathogenicity</subject><subject>Clostridium difficile - physiology</subject><subject>Clostridium Infections - drug therapy</subject><subject>Clostridium Infections - microbiology</subject><subject>Feces - microbiology</subject><subject>Humans</subject><issn>0966-842X</issn><issn>1878-4380</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtLAzEQx4Motj7uehGPXnadbJJNgiBI8QUFLwreQkyymrK7qcm24Lc3pbXoxdMc5v-Y-SF0iqHEgOvLWTn4rqwAixJkCUB30BgLLgpKBOyiMci6LgStXkfoIKUZADBWsX00IlBJjjEfo5NJG9IQvfXBW5fOrW8ab3zrjtBeo9vkjjfzEL3c3T5PHorp0_3j5GZaGMrwUORyiqmVleacMm2F5dAY0zCQwLQksqYNJoITKThYAQ5Tqg0Fy4xxmgpyiK7XufPFW-escf0Qdavm0Xc6fqmgvfq76f2Heg9LVdeEU1gFXGwCYvhcuDSozifj2lb3LiySqvKfRGYgMkvxWmpiSCm6ZluDQa2IqpnKRNWKqAKpMtHsOft939bxgzALrtYClyktvYsqGe9646yPzgzKBv9P_DdYNoWj</recordid><startdate>20181201</startdate><enddate>20181201</enddate><creator>Sandhu, Brindar K.</creator><creator>McBride, Shonna M.</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20181201</creationdate><title>Clostridioides difficile</title><author>Sandhu, Brindar K. ; McBride, Shonna M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-201414d92a7745ad8d70fccf50905a93964f138739870d80e144ac40d5ccea483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Anti-Bacterial Agents - therapeutic use</topic><topic>Bile Acids and Salts - metabolism</topic><topic>Clostridiales - drug effects</topic><topic>Clostridiales - physiology</topic><topic>Clostridium difficile - drug effects</topic><topic>Clostridium difficile - pathogenicity</topic><topic>Clostridium difficile - physiology</topic><topic>Clostridium Infections - drug therapy</topic><topic>Clostridium Infections - microbiology</topic><topic>Feces - microbiology</topic><topic>Humans</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sandhu, Brindar K.</creatorcontrib><creatorcontrib>McBride, Shonna M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Trends in microbiology (Regular ed.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sandhu, Brindar K.</au><au>McBride, Shonna M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clostridioides difficile</atitle><jtitle>Trends in microbiology (Regular ed.)</jtitle><addtitle>Trends Microbiol</addtitle><date>2018-12-01</date><risdate>2018</risdate><volume>26</volume><issue>12</issue><spage>1049</spage><epage>1050</epage><pages>1049-1050</pages><issn>0966-842X</issn><eissn>1878-4380</eissn><abstract>[Display omitted]
Clostridioides difficile is a spore-forming, anaerobic, intestinal pathogen that causes severe diarrhea that can lead to death. In 2011, C. difficile infected ∼500000 people in the USA and killed ∼29000 people. C. difficile infection (CDI) is the most common healthcare-related infection in the USA, leading to increased healthcare costs of $4.8 billion. This pathogen transmits via the oral–fecal route as a highly contagious and resilient spore. Upon exposure to primary bile acids in the intestine, C. difficile germinates, and in the absence of colonization resistance from the normal microbiota, the bacterium colonizes the colon and produces toxins. These toxins inhibit actin polymerization in host cells, leading to cell death. C. difficile cells can then sporulate in the intestine and exit the body via diarrheal shedding. In culture, sporulation is induced at stationary phase in a nutrient-limiting environment, but the intestinal triggers of sporulation are still unknown.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>30297117</pmid><doi>10.1016/j.tim.2018.09.004</doi><tpages>2</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Trends in microbiology (Regular ed.), 2018-12, Vol.26 (12), p.1049-1050 |
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| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Anti-Bacterial Agents - therapeutic use Bile Acids and Salts - metabolism Clostridiales - drug effects Clostridiales - physiology Clostridium difficile - drug effects Clostridium difficile - pathogenicity Clostridium difficile - physiology Clostridium Infections - drug therapy Clostridium Infections - microbiology Feces - microbiology Humans |
| title | Clostridioides difficile |
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