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Characterization of a nosocomial Clostridium difficile outbreak by using plasmid profile typing and clindamycin
C R Clabots1, L R Peterson, D N Gerding
1Department of Medicine, Veterans Administration Medical Center, Minneapolis, Minnesota.
Abstract:
The mean number of cases of Clostridium difficile diarrhea at the Minneapolis Veterans Administration Medical Center increased to 17.3 per month in June-August 1985, compared with 7.1 per month in the previous 17 mo. Plasmid profiles and clindamycin susceptibility were used as markers to evaluate the increase in cases. Ninety clindamycin-resistant and 22 clindamycin-susceptible isolates of C. difficile from 1985 were examined for plasmids. A clindamycin-resistant organism contained a cryptic plasmid of 3.1 kilobases (kb). None of the clindamycin-susceptible isolates contained the 3.1-kb plasmid, as compared with 40 of 90 clindamycin-resistant isolates (P less than .005). Restriction endonuclease digestion and Southern blot hybridization were used to confirm the identity of the 3.1-kb plasmid between strains. Isolates retained clindamycin resistance after plasmid curing. It could not be determined if the organism responsible was an indigenous C. difficile strain that acquired a plasmid or was a new strain introduced from outside the hospital.
Insights
Clostridium difficile diarrhea cases surged in 1985, linked to a specific 3.1-kilobase plasmid in resistant strains. This plasmid was associated with increased clindamycin resistance in C. difficile infections.
Area of Science:
- Microbiology
- Infectious Diseases
- Molecular Biology
Background:
- Clostridium difficile diarrhea cases significantly increased at the Minneapolis VA Medical Center in mid-1985.
- The rise in cases prompted an investigation into potential molecular markers associated with Clostridium difficile strains.
Purpose of the Study:
- To investigate the role of plasmids and clindamycin resistance in the increased incidence of Clostridium difficile diarrhea.
- To identify specific genetic markers, such as plasmids, associated with resistant C. difficile isolates.
Main Methods:
- Plasmid profiling and clindamycin susceptibility testing were performed on 112 C. difficile isolates from 1985.
- Restriction endonuclease digestion and Southern blot hybridization were used to analyze plasmid characteristics and confirm plasmid identity between strains.
- Plasmid curing experiments were conducted to assess the stability of clindamycin resistance.
Main Results:
- A 3.1-kilobase (kb) cryptic plasmid was identified in 40 of 90 clindamycin-resistant C. difficile isolates.
- None of the clindamycin-susceptible isolates contained the 3.1-kb plasmid (P < .005).
- Clindamycin resistance was retained in isolates even after plasmid curing, suggesting complex resistance mechanisms or stable integration.
Conclusions:
- The 3.1-kb plasmid is strongly associated with clindamycin-resistant Clostridium difficile strains and may contribute to the observed increase in infections.
- The origin of the resistant strain remains unclear: it could be an existing C. difficile strain that acquired the plasmid or a newly introduced strain.
- Further research is needed to elucidate the precise role of this plasmid in C. difficile pathogenesis and transmission.