scholarly journals Identification of Clostridium difficile Immunoreactive Spore Proteins of the Epidemic Strain R20291

2018 ◽  
Vol 12 (5) ◽  
pp. 1700182 ◽  
Author(s):  
Marjorie Pizarro-Guajardo ◽  
María Cristina Ravanal ◽  
Maria Daniela Paez ◽  
Eduardo Callegari ◽  
Daniel Paredes-Sabja
2014 ◽  
Vol 20 (6) ◽  
pp. 380-383 ◽  
Author(s):  
Itaru Nakamura ◽  
Tetsuo Yamaguchi ◽  
Ayaka Tsukimori ◽  
Akihiro Sato ◽  
Shinji Fukushima ◽  
...  

2013 ◽  
Vol 57 (11) ◽  
pp. 5266-5270 ◽  
Author(s):  
Kristin J. Nagaro ◽  
S. Tyler Phillips ◽  
Adam K. Cheknis ◽  
Susan P. Sambol ◽  
Walter E. Zukowski ◽  
...  

ABSTRACTNontoxigenicClostridium difficile(NTCD) has been shown to prevent fatalC. difficileinfection in the hamster model when hamsters are challenged with standard toxigenicC. difficilestrains. The purpose of this study was to determine if NTCD can preventC. difficileinfection in the hamster model when hamsters are challenged with restriction endonuclease analysis group BIC. difficilestrains. Groups of 10 hamsters were given oral clindamycin, followed on day 2 by 106CFU of spores of NTCD strain M3 or T7, and were challenged on day 5 with 100 CFU of spores of BI1 or BI6. To conserve animals, results for control hamsters challenged with BI1 or BI6 from the present study and controls from previous identical experiments were combined for statistical comparisons. NTCD strains M3 and T7 achieved 100% colonization and were 100% protective against challenge with BI1 (P≤ 0.001). M3 colonized 9/10 hamsters and protected against BI6 challenge in the colonized hamsters (P= 0.0003). T7 colonized 10/10 hamsters, but following BI6 challenge, cocolonization occurred in 5 hamsters, 4 of which died, for protection of 6/10 animals (P= 0.02). NTCD colonization provides protection against challenge with toxigenic BI group strains. M3 is more effective than T7 in preventingC. difficileinfection caused by the BI6 epidemic strain. Prevention ofC. difficileinfection caused by the epidemic BI6 strain may be more challenging than that of infections caused by historic BI1 and non-BIC. difficilestrains.


Anaerobe ◽  
2016 ◽  
Vol 37 ◽  
pp. 85-95 ◽  
Author(s):  
Chandrabali Ghose ◽  
Ioannis Eugenis ◽  
Adrianne N. Edwards ◽  
Xingmin Sun ◽  
Shonna M. McBride ◽  
...  

2010 ◽  
Vol 31 (8) ◽  
pp. 867-868 ◽  
Author(s):  
Amy L. Pakyz ◽  
Norman V. Carroll ◽  
Spencer E. Harpe ◽  
Michael Oinonen ◽  
Ronald E. Polk

Clostridium difficile infection (CDI) is a potentially serious disease for which the epidemiology has recently changed, because of an emerging drug-resistant strain of the pathogen. Metronidazole and oral vancomycin are the primary treatment agents.2 Metronidazole has been historically favored as the first-line agent, partly to reduce the selection pressure for vancomycin-resistant enterococci (VRE), although metronidazole can also select for VRE. Vancomycin was traditionally reserved for metronidazole treatment failure or life-threatening disease. In a study conducted before emergence of the epidemic strain, vancomycin was reported to be superior for the initial treatment of severe CDI and for treatment of CDI that does not respond to metronidazole. Expert opinion calling for the use of vancomycin as first-line therapy, especially for severe CDI emergence of the epidemic strain, and reports of decreased metronidazole efficacy may have impacted CDI treatment practices. The purpose of this study was to characterize trends in CDI treatment in US hospitals.


2014 ◽  
Vol 52 (9) ◽  
pp. 3264-3270 ◽  
Author(s):  
Pengcheng Du ◽  
Bo Cao ◽  
Jing Wang ◽  
Wenge Li ◽  
Hongbing Jia ◽  
...  

2007 ◽  
Vol 28 (2) ◽  
pp. 198-201 ◽  
Author(s):  
Priscilla Biller ◽  
Beth Shank ◽  
Leah Lind ◽  
Meghan Brennan ◽  
Lisa Tkatch ◽  
...  

An outbreak ofClostridium difficile-associated disease (CDAD) caused by the epidemic North American pulsed-field gel electrophoresis type 1 (NAP1) strain began after a formulary change from levofloxacin to moxifloxacin. Cases of CDAD were associated with moxifloxacin use, but a formulary change back to levofloxacin failed to reduce rates of disease. Substituting use of one fluoroquinolone with use of another without also controlling the overall use of drugs from this class is unlikely to control outbreaks caused by the NAP1 strain ofC. difficile.


1994 ◽  
Vol 15 (11) ◽  
pp. 697-702 ◽  
Author(s):  
Kris Bettin ◽  
Connie Clabots ◽  
Pamela Mathie ◽  
Keith Willard ◽  
Dale N. Gerding

AbstractObjective:To compare liquid soap versus 4% chlorhexidine gluconate in 4% alcohol for the decontamination of bare or gloved hands inoculated with an epidemic strain ofClostridium difficile.Design:C difficile(6.7 log10colony-forming units [CFU], 47% spores), was seeded onto bare or latex gloved hands of ten volunteers and allowed to dry. Half the volunteers initially washed with soap and half with chlorhexidine, followed by the other agent 1 week later. Cultures were done with Rodac plates at three sites on the hand: finger/thumbtips, the palmar surfaces of the fingers, and the palm. Statistical comparison was by paired Student’sttest.Results:On bare hands, soap and chlorhexidine did not differ in residual bacterial counts on the finger/thumbtips (log10CFU, 2.0 and 2.1, P= NS) and fingers (log10CFU, 2.4 and 2.5,P=NS). Counts were too high on bare palms to quantitate. On gloved hands, soap was more effective than chlorhexidine on fingers (log10CFU 1.3 and 1.7, P<.01) and palms (log10CFU 1.5 and 2.0, P<.01), but not finger/thumbtips (log10CFU 1.6 with each, P=NS). ResidualC difficilecounts were lower on gloved hands than bare hands (P<0.01 to <0.0001).Conclusions:The two agents did not differ significantly in residual counts of Cdifficileon bare hands, but on gloved hands residual counts were lower following soap wash than following chlorhexidine wash. These observations support the use of either soap or chlorhexidine as a handwash for removal ofC difficile,but efficacy in the prevention ofC difficiletransmission must be determined by prospective clinical trials.


2015 ◽  
Vol 2 (suppl_1) ◽  
Author(s):  
Stanley Giddings ◽  
Michaela Gazdik ◽  
John Burke ◽  
Bert K. Lopansri

2007 ◽  
Vol 51 (8) ◽  
pp. 2674-2678 ◽  
Author(s):  
Daniel A. Adams ◽  
Michelle M. Riggs ◽  
Curtis J. Donskey

ABSTRACT Several recent outbreaks of Clostridium difficile-associated disease (CDAD) have been attributed to the emergence of an epidemic strain with increased resistance to fluoroquinolone antibiotics. Some clinical studies have suggested that fluoroquinolones with enhanced antianaerobic activity (i.e., gatifloxacin and moxifloxacin) may have a greater propensity to induce CDAD than ciprofloxacin and levofloxacin do. We examined the effects of subcutaneous fluoroquinolone treatment on in vitro growth of and toxin production by epidemic and nonepidemic C. difficile isolates in cecal contents of mice and evaluated the potential for these agents to inhibit fluoroquinolone-susceptible isolates during treatment. When C. difficile isolates were inoculated into cecal contents collected 2 days after the final antibiotic dose, gatifloxacin and moxifloxacin promoted significantly more growth and toxin production than ciprofloxacin and levofloxacin did. During treatment, gatifloxacin and moxifloxacin inhibited growth of fluoroquinolone-susceptible but not fluoroquinolone-resistant isolates. Ciprofloxacin and levofloxacin promoted growth of C. difficile when administered at higher doses (i.e., 20 times the human dose in mg/kg of body weight), and levofloxacin inhibited growth of fluoroquinolone-susceptible, but not fluoroquinolone-resistant, C. difficile isolates when administered in combination with ceftriaxone. Thus, fluoroquinolones with enhanced antianaerobic activity (i.e., gatifloxacin and moxifloxacin) promoted C. difficile growth to a greater extent than did ciprofloxacin and levofloxacin in this model. However, our findings suggest that fluoroquinolones may exert selective pressure favoring the emergence of epidemic fluoroquinolone-resistant C. difficile strains by inhibiting fluoroquinolone-susceptible but not fluoroquinolone-resistant isolates during treatment and that agents such as levofloxacin or ciprofloxacin can exert such selective pressure when administered in combination with antibiotics that disrupt the anaerobic microflora.


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