Molecular Epidemiology of Hospital-Associated and Community-Acquired Clostridium difficile Infection in a Swedish County

Abstract

All episodes of Clostridium difficile associated diarrhea (CDAD) diagnosed in a defined population of 274,000 including one tertiary and two primary hospitals and their catchment areas were studied during 12 months. The annual CDAD incidence in the county was 97 primary episodes per 100,000, and 78% of all episodes were classified as hospital associated with a mean incidence of 5.3 (range, 1.4 to 6.5) primary episodes per 1,000 admissions. The incidence among hospitalized individuals was 1,300-fold higher than that in the community (33,700 versus 25 primary episodes per 100,000 persons per year), reflecting a 37-fold difference in antibiotic consumption (477 versus 13 defined daily doses [DDD]/1,000 persons/day) and other risk factors. Three tertiary hospital wards with the highest incidence (13 to 36 per 1,000) had CDAD patients of high age (median age of 80 years versus 70 years for other wards, P < 0.001), long hospital stay (up to 25 days versus 4 days), or a high antibiotic consumption rate (up to 2,427 versus 421 DDD/1,000 bed days). PCR ribotyping of C. difficile isolates available from 330 of 372 CDAD episodes indicated nosocomial acquisition of the strain in 17 to 27% of hospital-associated cases, depending on the time interval between index and secondary cases allowed (2 months or up to 12 months), and only 10% of recurrences were due to a new strain of C. difficile (apparent reinfection). In other words, most primary and recurring episodes were apparently caused by the patient's endogenous strain rather than by one of hospital origin. Typing also indicated that a majority of C. difficile strains belonged to international serotypes, and the distribution of types was similar within and outside hospitals and in primary and relapsing CDAD. However, type SE17 was an exception, comprising 22% of hospital isolates compared to 6% of community isolates (P ‫؍‬ 0.008) and causing many minor clusters and a silent nosocomial outbreak including 36 to 44% of the CDAD episodes in the three high-incidence wards.

Predictors of Clostridium difficile colitis infections in hospitals

“…The analysis of hospital characteristics is particularly useful, since most CDAD cases are acquired while patients are hospitalized [15]. Significant correlations between ' high CDAD ' hospitals and facilities that admit large numbers of patients with other bacterial pathogens and other common infections was noted.…”

“…A recent county-level evaluation in Sweden revealed that hospital-acquired CDAD is 1300 times more common than community-acquired infections [15]. Thus, effective prevention and control measures are needed to reduce acquisition of CDAD.…”

Geographical clustering of cases of infection with moxifloxacin-resistant Clostridium difficile PCR-ribotypes 012, 017 and 046 in Sweden, 2008 and 2009

“…[23]). From previous geographically localised studies in Sweden in 1999 to 2001, the six most common types were 014/SE21, 012, 001, 020, 002 and 005 [2][3][4]. All these were still among the most common types in 2009.…”

“…We found decreased susceptibility mainly in types 012, 017, 046 and 231/SE37. Type 012 is related to serogroup C [29] and has been reported as a common type in Sweden, Greece and Hungary [2,19] while toxin A-negative, toxin B-positive type 017 has been found to be associated with outbreaks in, for example, Poland, Canada and the Netherlands [6,30]. Regarding type 231/SE37, the proportion of this type was 0.8 % at the Karolinska University Hospital, Huddinge, Sweden, in 1999 [4], but there is no information on whether this type has caused any outbreaks in other countries.…”

“…C. difficile is typically isolated from faeces of 1-5% of healthy individuals, but colonisation increases upon admission to hospitals. Hospital-based studies performed in 1999 to 2001 showed that nosocomial spread of C. difficile was rare in Swedish hospitals in which infection control routines were implemented, although there were small outbreaks associated with multiresistant PCR-ribotype 012/SE17 [2][3][4]. Many outbreaks involving other C. difficile types have been reported in Europe and the rest of the world [5][6][7][8], particularly those caused by moxifloxacin-resistant PCR-ribotype 027/PFGE NAP1 [9][10][11][12][13][14][15][16][17] …”