The Clostridium difficile spo0A Gene Is a Persistence and Transmission Factor

被引：268

作者：

Deakin, Laura J. ^{[2
]}

Clare, Simon ^{[2
]}

Fagan, Robert P. ^{[3
]}

Dawson, Lisa F. ^{[4
]}

Pickard, Derek J. ^{[2
]}

West, Michael R. ^{[2
]}

Wren, Brendan W. ^{[4
]}

Fairweather, Neil F. ^{[3
]}

Dougan, Gordon ^{[2
]}

Lawley, Trevor D. ^{[1
]}

机构：

[1] Wellcome Trust Sanger Inst, Bacterial Pathogenesis Lab, Hinxton, England

[2] Wellcome Trust Sanger Inst, Microbial Pathogenesis Lab, Hinxton, England

[3] Univ London Imperial Coll Sci Technol & Med, Ctr Mol Microbiol & Infect, London, England

[4] Univ London London Sch Hyg & Trop Med, Dept Pathogen Mol Biol, London WC1E 7HT, England

来源：

INFECTION AND IMMUNITY | 2012年 / 80卷 / 08期

基金：

英国惠康基金;

关键词：

DIFFICILE-ASSOCIATED DIARRHEA; CLOSTRIDIUM-DIFFICILE; ESCHERICHIA-COLI; SEVERE DISEASE; NORTH-AMERICA; EPIDEMIOLOGY; SPORULATION; EMERGENCE; VECTORS; STRAINS;

D O I：

10.1128/IAI.00147-12

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Clostridium difficile is a major cause of chronic antibiotic-associated diarrhea and a significant health care-associated pathogen that forms highly resistant and infectious spores. Spo0A is a highly conserved transcriptional regulator that plays a key role in initiating sporulation in Bacillus and Clostridium species. Here, we use a murine model to study the role of the C. difficile spo0A gene during infection and transmission. We demonstrate that C. difficile spo0A mutant derivatives can cause intestinal disease but are unable to persist within and effectively transmit between mice. Thus, the C. difficile Spo0A protein plays a key role in persistent infection, including recurrence and host-to-host transmission in mice.

引用

页码：2704 / 2711

页数：8

共 39 条

[1]

Barbut F, 2000, J CLIN MICROBIOL, V38, P2386

[2] Clostridium difficile infection in Europe: a hospital-based survey [J].

Bauer, Martijn P. ;

Notermans, Daan W. ;

van Benthem, Birgit H. B. ;

Brazier, Jon S. ;

Wilcox, Mark H. ;

Rupnik, Maja ;

Monnet, Dominique L. ;

van Dissel, Jaap T. ;

Kuijper, Ed J. .

LANCET, 2011, 377 (9759) :63-73

[3] Improved broad-host-range RK2 vectors useful for high and low regulated gene expression levels in gram-negative bacteria [J].

Blatny, JM ;

Brautaset, T ;

WintherLarsen, HC ;

Karunakaran, P ;

Valla, S .

PLASMID, 1997, 38 (01) :35-51

[4] Pathogenesis of Clostridium difficile infection [J].

Borriello, SP .

JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY, 1998, 41 :13-19

[5] Hypervirulent Clostridium difficile PCR-Ribotypes Exhibit Resistance to Widely Used Disinfectants [J].

Dawson, Lisa F. ;

Valiente, Esmeralda ;

Donahue, Elizabeth H. ;

Birchenough, George ;

Wren, Brendan W. .

PLOS ONE, 2011, 6 (10)

[6] Clostridium difficile colitis causing toxic megacolon, severe sepsis and multiple organ dysfunction syndrome [J].

Dobson, G ;

Hickey, C ;

Trinder, J .

INTENSIVE CARE MEDICINE, 2003, 29 (06) :1030-1030

[7] Clostridium difficile toxin synthesis is negatively regulated by TcdC [J].

Dupuy, B. ;

Govind, R. ;

Antunes, A. ;

Matamouros, S. .

JOURNAL OF MEDICAL MICROBIOLOGY, 2008, 57 (06) :685-689

[8]

Engelkirk PG, 2010, BURTONS MICROBIOLOGY

[9] The transcriptional profile of early to middle sporulation in Bacillus subtilis [J].

Fawcett, P ;

Eichenberger, P ;

Losick, R ;

Youngman, P .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (14) :8063-8068

[10] Measures to control and prevent Clostridium difficile infection [J].

Gerding, Dale N. ;

Muto, Carlene A. ;

Owens, Robert C., Jr. .

CLINICAL INFECTIOUS DISEASES, 2008, 46 :S43-S49

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