Production, purification and characterization of Clostridium difficile toxic proteins different from toxin A and from toxin B

Author(s):  
Javier F. Torres ◽  
Ivar Lönnroth
1992 ◽  
Vol 60 (10) ◽  
pp. 4192-4199 ◽  
Author(s):  
S P Borriello ◽  
B W Wren ◽  
S Hyde ◽  
S V Seddon ◽  
P Sibbons ◽  
...  

1992 ◽  
Vol 60 (11) ◽  
pp. 4633-4639 ◽  
Author(s):  
D M Lyerly ◽  
L A Barroso ◽  
T D Wilkins ◽  
C Depitre ◽  
G Corthier

2000 ◽  
Vol 38 (7) ◽  
pp. 2706-2714 ◽  
Author(s):  
Michelle J. Alfa ◽  
Amin Kabani ◽  
David Lyerly ◽  
Scott Moncrief ◽  
Laurie M. Neville ◽  
...  

Clostridium difficile-associated diarrhea (CAD) is a very common nosocomial infection that contributes significantly to patient morbidity and mortality as well as to the cost of hospitalization. Previously, strains of toxin A-negative, toxin B-positive C. difficile were not thought to be associated with clinically significant disease. This study reports the characterization of a toxin A-negative, toxin B-positive strain ofC. difficile that was responsible for a recently described nosocomial outbreak of CAD. Analysis of the seven patient isolates from the outbreak by pulsed-field gel electrophoresis indicated that this outbreak was due to transmission of a single strain of C. difficile. Our characterization of this strain (HSC98) has demonstrated that the toxin A gene lacks 1.8 kb from the carboxy repetitive oligopeptide (CROP) region but apparently has no other major deletions from other regions of the toxin A or toxin B gene. The remaining 1.3-kb fragment of the toxin A CROP region from strain HSC98 showed 98% sequence homology with strain 1470, previously reported by M. Weidmann in 1997 (GenBank accession number Y12616), suggesting that HSC98 is toxinotype VIII. The HSC98 strain infecting patients involved in this outbreak produced the full spectrum of clinical illness usually associated with C. difficile-associated disease. This pathogenic spectrum was manifest despite the inability of this strain to alter tight junctions as determined by using in vitro tissue culture testing, which suggested that no functional toxin A was produced by this strain.


2010 ◽  
Vol 67 (2) ◽  
pp. 198-201 ◽  
Author(s):  
Sue Jung Kim ◽  
Heejung Kim ◽  
Younghee Seo ◽  
Dongeun Yong ◽  
Seok Hoon Jeong ◽  
...  

2000 ◽  
Vol 38 (8) ◽  
pp. 3072-3075 ◽  
Author(s):  
J. Scott Moncrief ◽  
Limin Zheng ◽  
Laurie M. Neville ◽  
David M. Lyerly

Toxin-specific enzyme immunoassays, cytotoxicity assays, and PCR were used to analyze 48 toxin A-negative, toxin B-positiveClostridium difficile isolates from various geographical sites around the world. All the isolates were negative by the TOX-A TEST and positive by the TOX A/B TEST. A deletion of approximately 1.7 kb was found at the 3′ end of the toxA gene for all the isolates, similar to the deletion in toxinotype VIII strains (e.g.,C. difficile serotype F 1470). Additional PCR analysis indicated that the toxin B encoded by these isolates contains sequence variations downstream of the active site compared to the sequence of reference strain VPI 10463. This variation may extend the glucosylation spectrum to Ras proteins, as observed previously for closely related lethal toxin from Clostridium sordellii and toxin B from toxin A-negative, toxin B-positive strain F 1470. Toxin A-negative, toxin B-positive isolates have recently been associated with disease in humans, and they may be more common than was previously supposed.


2015 ◽  
Vol 53 (11) ◽  
pp. 3702-3704 ◽  
Author(s):  
Grace O. Androga ◽  
Julie Hart ◽  
Niki F. Foster ◽  
Adrian Charles ◽  
David Forbes ◽  
...  

Large clostridial toxin-negative, binary toxin-positive (A−B−CDT+) strains ofClostridium difficileare almost never associated with clinically significantC. difficileinfection (CDI), possibly because such strains are not detected by most diagnostic methods. We report the isolation of an A−B−CDT+ribotype 033 (RT033) strain ofC. difficilefrom a young patient with ulcerative colitis and severe diarrhea.


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