In the early 2000s researchers in Quebec, Canada noticed an increase in the number of colectomies being performed as a result of an increase in the frequency and severity of CDAD. At around the same time, doctors at the CDC were receiving reports of increased frequency and severity of disease in the United States. There were also reports of more disease and more severe forms of C. difficile infection in other areas of the world, suggesting that the experience was very widespread and possibly global.
In 2004, analysis of this hypervirulent strain showed a very characteristic strain that had previously been rare but was responsible for the majority of the more serious outbreaks. This strain – BI/NAP1/027 – has several designations depending on which biological property was examined:
- BI: Restriction Endonuclease Analysis (USA)
- NAP1: North American PFGE Type 1 based on polyacrylamide gel electrophoresis (USA)
- 027: Ribotype 027 by polymerase chain reaction (Europe)
There are five unique features associated with this strain:
- It produces the classic toxins A and B, but faster and at much higher levels than other strains.
- It is Toxinotype III in contrast to the more typical clinical isolates, which tend to be Toxinotype 0.
- The toxin regulatory gene tcdC is deleted from the PaLoc locus, possibly explaining the observed increase in toxin production.
- It produces the binary toxin CDT, but its role is still unclear.
- It exhibits a high level of in vitro resistance to fluoroquinolones.
