In vitro susceptibility to 17 antimicrobials of clinical Clostridium difficile isolates collected in 1993-2007 in Sweden.

This study investigated the MICs of 17 antimicrobials, for 606 toxigenic clinical isolates of Clostridium difficile collected between 1993 and 2007 in Sweden. Low MIC(90) values were found for metronidazole (0.5 mg/L), vancomycin (1.0 mg/L), teicoplanin (0.125 mg/L), fusidic acid (1.0 mg/L), linezolid (2.0 mg/L), daptomycin (2.0 mg/L) and tigecycline (0.064 mg/L). Three isolates (0.5%) had elevated MICs for vancomycin (4-8 mg/L); however, these isolates originated from the same patient, who was receiving long-term intravenous vancomycin treatment. High-level clindamycin resistant isolates (MIC >256 mg/L) peaked in 1997 with 39 of 95 (41%) and out of these, 36% were also highly resistant to erythromycin. beta-Lactams such as penicillin V and piperacillin displayed MIC(90)s of 8 and 32 mg/L, respectively, whereas MICs of cefuroxime were >256 mg/L for all isolates. Universal resistance to ciprofloxacin and levofloxacin was found, and resistance to moxifloxacin increased from 4% of isolates in 2004 to 23% in 2007. Notably, these moxifloxacin-resistant isolates did not belong to the recent epidemic PCR ribotype 027, but to the pre-existing epidemic type 012 (82%), and these isolates accounted for the majority of isolates that were resistant to clindamycin (70%), tetracycline (84%) and rifampicin (92%) as well. This investigation of susceptibility data on clinical C. difficile isolates showed variations of multiresistance to be due to a specific PCR ribotype 012, emphasizing the importance of genotyping when evaluating emerging resistance over time.

Molecular epidemiology of hospital-associated and community-acquired Clostridium difficile infection in a Swedish county.

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.

Formula diet is a preventive factor in experimentally induced ideal ulcers in rats. A bacteriological study.

We earlier described an experimental model to create recurring chronic ileal inflammation with ulceration in the rat. A 2 cm segment of the distal ileum is excised but left attached to its intact mesentery; the ileum is reanastomosed. The ileal segment will seal off its open ends and a cyst-like structure of varying size will be formed, containing mucus, cell debris and bacteria. Approximately two thirds of the animals develop chronic inflammation with ulceration proximal to the ileal anastomosis. The ileal cyst and the surgical procedure on the distal ileum were shown to be prerequisites of the rat model for the development of lesions. We recently described that, in contrast to rats fed a standard diet, rats fed a hydrolyzed formula diet never developed inflammation or ulceration when subjected to the experimental procedure. In the present study we confirmed these observations and showed that the normal ileal flora (NIF) and the ileal cyst flora (ICF) were significantly influenced by the diets. The bacterial counts of both the aerobic and anaerobic NIF were 2 10log lower, i.e. > or = 99%, in rat fed the formula diet as compared to in those fed standard rat pellets. The NIF of the former group was represented by more aerobic species than the NIF of rats on the standard diet. Compared to the NIF there was a parallel increase in the bacterial counts of the ICF by approximately 2 10log CFU values in both groups of rats. The mean number of anaerobic species, mainly Gram-negative rods of the ICF, increased by approximately 70% in the rats on the standard diet that developed ileal ulceration, whereas identified aerobic species of the ICF decreased by 61% in rats on the formula diet and by 46% in those on the standard diet that did not develop ileal ulceration. The number of anaerobes in those groups of rats remained unchanged. The significant bacteriological differences between the rats that developed ileal ulcers and those which did not indicate that bacteria may be involved, directly or indirectly, in the development of chronic ileal ulceration.