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 18 January 2018

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News

Toxin gene-variant strain of C difficile causes epidemic

A previously uncommon strain of C difficile with variations in toxin genes has become more resistant to fluoroquinolones, reports this week's New England Journal of Medicine.

News image

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Recent reports suggest that the rate and severity of Clostridium difficile-associated disease in the United States are increasing.

This increase may be associated with the emergence of a new strain of C difficile with increased virulence, resistance, or both.

Dr Clifford McDonald and colleagues collected a total of 187 C difficile isolates between 2000 and 2003.

The isolates were collected from 8 health care facilities in 6 states in which outbreaks of C difficile-associated disease had occurred.

The research team characterized the isolates by restriction-endonuclease analysis, pulsed-field gel electrophoresis, and toxinotyping.

The results were then compared with those from a database of more than 6000 isolates obtained before 2001.

The polymerase chain reaction was used to detect the recently described binary toxin CDT.

The team also used the polymerase chain reaction to detect a deletion in the pathogenicity locus gene, tcdC, that increases production of toxins A and B.

Isolates that belonged to a restriction-endonuclease analysis group, and had the same pulsed-field gel electrophoresis type were identified.

The research team noted that these specimens accounted for at least half of the isolates from 5 facilities.

Gatifloxacin resistance is more common in current isolates with restriction-endonuclease analysis
New England Journal of Medicine

Restriction-endonuclease analysis was first identified in 1984, and was found to be uncommon among 14 isolates from the historic database.

Both historic and current restriction-endonuclease analysis with the same pulsed-field gel electrophoresis type isolates were of toxinotype III.

The researchers found that these were positive for the binary toxin CDT, and contained an 18-bp tcdC deletion.

The team observed that resistance to gatifloxacin and moxifloxacin was more common in current isolates with restriction-endonuclease analysis with the same pulsed-field gel electrophoresis type.

The rate of resistance to clindamycin was the same in isolates both with and without restriction-endonuclease analysis and gel electrophoresis type.

All of the current but none of the historic restriction-endonuclease analysis with the same pulsed-field gel electrophoresis type isolates were resistant to gatifloxacin and moxifloxacin.

However, none of the historic restriction-endonuclease analysis with the same gel electrophoresis type isolates were resistant to gatifloxacin and moxifloxacin.

Dr McDonald's team concluded, “A previously uncommon strain of C difficile with variations in toxin genes has become more resistant to fluoroquinolones.”

“This has emerged as a cause of geographically dispersed outbreaks of C difficile-associated disease.”

NEJM 2005: 353(23):2433-41
13 December 2005

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