Multicentre study of the prevalence of toxigenic Clostridium difficile in Korea: results of a retrospective study 2000-2005.
The prevalence of toxigenic Clostridium difficile in Korea has been reported to be approximately 60-80%. Although the prevalence of the tcdA(-)tcdB(+) C. difficile strain was less then 5% prior to the year 2000, it has become an emerging nosocomial pathogen in Korea. Therefore, we have attempted to determine the multicentre nationwide prevalence of tcdA(+)tcdB(+) and tcdA(-)tcdB(+) C. difficile for epidemiological purposes. C. difficile strains (n=724, 30 from 2000, 80 from 2001, 74 from 2002, 76 from 2003, 179 from 2004, 285 from 2005) were obtained retrospectively from January 2000 to December 2005 from in-patients at 6 hospitals, all of whom were suspected of having C. difficile-associated disease (CDAD), colitis or pseudomembranous colitis. The numbers of participating hospitals varied yearly (1 in 2000, 2 in 2001-2003, 3 in 2004, 5 in 2005). The hospitals were located in Seoul (n=4), Kyunggi Province (n=1) and Busan (n=1), Korea. PCR assays for tcdA and tcdB genes were conducted using 724 unduplicated C. difficile isolates. The mean prevalence of tcdA(+)tcdB(+) and tcdA(-)tcdB(+) C. difficile strains over the 6 years was 51.8 % (38.4-59.3%) and 25.8%(10-56.0%), respectively. The mean prevalence of tcdA(-)tcdB(+) C. difficile strains was less than 7% until 2002, but began to increase in 2003 (13.2%) and achieved a peak in 2004 (50.3%). In 2005, the mean prevalence of tcdA(+)tcdB(+) and tcdA(-)tcdB(+) C. difficile strains was 47.7% (30.9-60.3%) and 27.0% (17.6-54.8%), respectively. This nationwide epidemiological study showed that tcdA(-)tcdB(+) C. difficile strains have already spread extensively throughout Korea, and our results provide basic data regarding the controversies currently surrounding the toxigenicity of tcdA(-)tcdB(+) C. difficile. The use of enzyme immunoassays capable of detecting both TcdA and TcdB is strongly recommended for the diagnosis of CDAD in microbiology laboratories, in order to control the spread of the tcdA(-)tcdB(+) strains of C. difficile.
Shin
Bo-Moon
BM
Office of Infection Control, Sanggye Paik Hospital, Inje University, Seoul, Republic of Korea.|Department of Laboratory Medicine, Sanggye Paik Hospital, Inje University, Seoul, Republic of Korea.
Kuak
Eun Young
EY
Department of Laboratory Medicine, Sanggye Paik Hospital, Inje University, Seoul, Republic of Korea.
Yoo
Hyeon Mi
HM
Office of Infection Control, Sanggye Paik Hospital, Inje University, Seoul, Republic of Korea.
Kim
Eui Chong
EC
Department of Laboratory Medicine, Seoul National University, Seoul, Republic of Korea.
Lee
Kyungwon
K
Department of Laboratory Medicine, Yonsei University, Seoul, Republic of Korea.
Kang
Jung-Oak
JO
Department of Laboratory Medicine, Hanyang University, Kuri, Republic of Korea.
Whang
Dong Hee
DH
Department of Laboratory Medicine, Seoul Paik Hospital, Seoul, Republic of Korea.
Shin
Jeong-Hwan
JH
Department of Laboratory Medicine, Busan Paik Hospital, Busan, Republic of Korea.
D001426:Bacterial Proteins / Q000235:genetics; D001427:Bacterial Toxins / Q000235:genetics; D016360:Clostridioides difficile / Q000235:genetics / Q000302:isolation & purification*; D003015:Clostridium Infections / Q000453:epidemiology* / Q000382:microbiology*; D003428:Cross Infection / Q000453:epidemiology / Q000382:microbiology; D004761:Enterocolitis, Pseudomembranous / Q000453:epidemiology / Q000382:microbiology; D004768:Enterotoxins / Q000235:genetics; D006801:Humans; D007723:Korea / Q000453:epidemiology; D015995:Prevalence; D012189:Retrospective Studies; D013997:Time Factors
D001426:Bacterial Proteins; D001427:Bacterial Toxins; D004768:Enterotoxins; C041348:tcdA protein, Clostridium difficile; C031815:toxB protein, Clostridium difficile