Clostridium difficile ( C. difficile ) is a Gram-positive, spore-forming, anaerobic bacillus, which is widely distributed in the intestinal tract of humans and animals and in the environment. In the last decade, the frequency and severity of C. difficile infection has been increasing worldwide to become one of the most common hospital-acquired infections. Transmission of this pathogen occurs by the fecal-oral route and the most important risk factors include antibiotic therapy, old age, and hospital or nursing home stay. The clinical picture is diverse and ranges from asymptomatic carrier status, through various degrees of diarrhea, to the most severe, life threatening colitis resulting with death. Diagnosis is based on direct detection of C. difficile toxins in feces, most commonly with the use of EIA assay, but no single test is suitable as a stand-alone test confirming CDI. Antibiotics of choice are vancomycin, fidaxomicin, and metronidazole, though metronidazole is considered as inferior. The goal of this review is to update physicians on current scientific knowledge of C. difficile infection, focusing also on fecal microbiota transplantation which is a promising therapy.

Background: Variations in testing for Clostridium difficile infection (CDI) may hinder patient care, increase

Recent outbreaks of Clostridium difficile-associated diarrhoea (CDAD) with increased severity, high relapse rate and significant mortality have been related to the emergence of a new, hypervirulent C. difficile strain in North America, Japan and Europe. Definitions have been proposed by the European Centre of Disease Prevention and Control (ECDC) to identify severe cases of CDAD and to differentiate community-acquired cases from nosocomial CDAD (http://www.ecdc.europa.eu/documents/pdf/Cl_dif_v2.pdf). CDAD is mainly known as a healthcare-associated disease, but it is also increasingly recognised as a community-associated disease. The emerging strain is referred to as North American pulsed-field type 1 (NAP1) and PCR ribotype 027. Since 2005, individual countries have developed surveillance studies to monitor the spread of this strain. C. difficile type 027 has caused outbreaks in England and Wales, Ireland, the Netherlands, Belgium, Luxembourg, and France, and has also been detected in Austria, Scotland, Switzerland, Poland and Denmark. Preliminary data indicated that type 027 was already present in historical isolates collected in Sweden between 1997 and 2001.

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. ) to clindamycin and erythromycin was found in 39 (49 %) of the C. difficile isolates. Interestingly, 34 (94 %) of macrolide-lincosamide-streptogramin B (MLS B ) 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 MLS B -positive clindamycin/erythromycin-resistant PCR ribotype 017.

Our observations imply that a particular genotype of toxin A(-)B(+) C. difficile has spread extensively, not only in Poland but possibly even worldwide.