Incidence of toxin B producing strains of clostridium difficile and enterotoxigenic strains of clostridium perfringens in patients with antibiotic associated diarrhoea

Isolates (79 in total) of Clostridium difficile obtained over a 2 year period from 785 patients suspected of having C. difficile-associated diarrhoea (CDAD) and being hospitalized in the University Hospital in Warsaw were characterized by toxigenicity profile and PCR ribotyping. Furthermore, their susceptibility to clindamycin and erythromycin was determined. Among the 79 C. difficile isolates, 35 were classified as A+B+, 1 as A+B+CDT+, 36 as A−B+ and 7 as A−B−. A total of 21 different PCR ribotypes was detected. Two main A+B+ strains circulated in our hospital: ribotype 014 and ribotype 046. Unexpectedly, the predominant PCR ribotype was type 017, a known A−B+ strain, and this accounted for about 45·5 % of all isolates cultured from patients with CDAD. Isolates belonging to PCR ribotype 017 were found in cases from epidemics of antibiotic-associated diarrhoea in the internal and surgery units. High-level resistance (MIC⩾256 mg l−1) to clindamycin and erythromycin was found in 39 (49 %) of the C. difficile isolates. Interestingly, 34 (94 %) of macrolide-lincosamide-streptogramin B (MLSB) type resistance strains did not produce toxin A, but produced toxin B and were A−B+ ribotype 017. Thirty-seven of the high-level resistance strains harboured the erythromycin-resistance methylase gene (ermB). C. difficile isolates (2/29) that had high-level clindamycin and erythromycin resistance, and belonged to PCR ribotype 046, were ermB negative. These investigations revealed that the predominant C. difficile strain isolated from symptomatic patients hospitalized in University Hospital in Warsaw was MLSB-positive clindamycin/erythromycin-resistant PCR ribotype 017.

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Epidemic potential and antimicrobial resistance in Clostridium difficile

Microbiology Australia ◽

10.1071/ma07195 ◽

2007 ◽

Vol 28 (4) ◽

pp. 195

Author(s):

Thomas V Riley

Keyword(s):

Clostridium Difficile ◽

Financial Burden ◽

Hospital Environment ◽

Comorbid Conditions ◽

Subsequent Infection ◽

Toxin B ◽

Exposure Age ◽

Hospital Acquired ◽

Hospital Inpatients ◽

Antibiotic Associated Diarrhoea

Clostridium difficile is the most commonly diagnosed cause of infectious hospital-acquired diarrhoea. C. difficile was first isolated in 1935 but not identified as the main causative agent of antibiotic-associated diarrhoea (AAD) and pseudomemranous colitis (PMC) until 1977. The spectrum of disease caused by C. difficile ranges from asymptomatic colonisation to colitis that can progress to more severe PMC. Complications include colonic perforation and death. The term C. difficile-associated diarrhoea (CDAD) is used to describe the symptomatic manifestations of the disease, thus excluding asymptomatic colonisation. Hospital inpatients with CDAD are generally elderly and have several comorbid conditions. The majority of these patients have been exposed to antimicrobials that reduce ?colonisation resistance? of the large intestine allowing subsequent infection with C. difficile. Whether infection progresses to disease is determined by many factors such as antibiotic exposure, age and comorbidities, and others that are as yet unknown. Acquisition of C. difficile is facilitated by its ability to form spores that are resistant to many disinfectants, allowing it to remain viable in the hospital environment for long periods of time. Toxigenic isolates of C. difficile usually produce two toxins, toxin A and toxin B, and these are thought of as the major virulence factors. CDAD is a major financial burden on healthcare systems, with patients spending an extra one?three weeks in hospital costing US$5?10,000 per episode.

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