Molecular Epidemiology of Clostridium difficile over the Course of 10 Years in a Tertiary Care Hospital

• Published in: Clinical infectious diseases 2009-10, Vol.49 (8), p.1141-1147
• Main Authors: Belmares, Jaime, Johnson, Stuart, Parada, Jorge P., Olson, Mary M., Clabots, Connie R., Bettin, Kristine M., Peterson, Lance R., Gerding, Dale N.
• Format: Article
• Language: English
• Subjects: ARTICLES AND COMMENTARIES; Bacterial diseases; Bacterial diseases of the digestive system and abdomen; Bacterial Typing Techniques; Biological and medical sciences; Clostridium difficile; Clostridium difficile - classification; Clostridium difficile - isolation & purification; Cross Infection - epidemiology; Cross Infection - microbiology; Deoxyribonuclease HindIII - metabolism; Diarrhea; Disease outbreaks; DNA Fingerprinting; DNA, Bacterial - genetics; DNA, Bacterial - metabolism; Enterocolitis, Pseudomembranous - epidemiology; Enterocolitis, Pseudomembranous - microbiology; Epidemics; Epidemiology; Genotype; Gram-positive bacteria; Hospitals; Human bacterial diseases; Humans; Infections; Infectious diseases; Medical sciences; Minnesota; Molecular Epidemiology; Polymerase chain reaction; Polymorphism, Restriction Fragment Length; Toxins
• ISSN: 1058-4838; 1537-6591
• DOI: 10.1086/605638

Background. The molecular epidemiology of endemic and outbreak Clostridium difficile strains across time is not well known. Methods. Hin dIII restriction endonuclease analysis (REA) typing was performed on available clinical C. difficile isolates from 1982 to 1991. Results. The annual incidence of C. difficile infection (CDI) ranged from 3.2 to 9.9 cases per 1000 discharges and was significantly higher in 1982, 1983, 1985, and 1991 (high-incidence years) than in other years (mean ± standard deviation number of cases for the high- vs the low-incidence years, 121.8±20.4 and 70.0±15.0 ; P=.002 ). A total of 696 (76.6%) of 908 C. difficile isolates were available for REA typing over the 10-year period. Large clusters (⩾10 CDI cases in consecutive months) were caused by REA types B1 and B2 in 1982 and 1983, F2 and B1 in 1985, and K1 in 1991 (high-incidence years). Small clusters of 4–9 CDI cases in consecutive months were caused by REA types G1 (1984), Y4 and Y6 (1987), Y2 (1988), L1 (1989), Y1 (1990), and K1 (1991). Current epidemic REA group BI (unrelated to type B1) was isolated 6 times, twice in 1984, 1988, and 1990. Conclusions. Years with a high incidence of CDI were associated with large clusters of specific REA types that changed yearly. The molecular epidemiology of CDI in this hospital was characterized by a wide diversity of C. difficile types and an ever-changing dominance of specific C. difficile types over time. The current epidemic BI group was found sporadically on 6 occasions. A changing CDI molecular epidemiology should be expected in the future.