Epidemic Clostridium difficile (027/BI/NAP1) rapidly emerged in the past decade as the leading cause of antibiotic-associated diarrhea worldwide. However, the key moments in the evolutionary history leading to its emergence and subsequent patterns of global spread remain unknown. Here we define the global population structure of C. difficile 027/BI/NAP1 based on whole-genome sequencing and phylogenetic analysis. We demonstrate that two distinct epidemic lineages, FQR1 and FQR2, not one as previously thought, emerged in North America within a relatively short period after acquiring the same fluoroquinolone resistance mutation and a highly-related conjugative transposon. The two epidemic lineages displayed distinct patterns of global spread, and the FQR2 lineage spread more widely leading to healthcare outbreaks in the UK, continental Europe and Australia. Our analysis identifies key genetic changes linked to the rapid trans-continental dissemination of epidemic C. difficile 027/BI/NAP1 and highlights the routes by which it spreads through the global healthcare system.

Background: High mobility group box-1 (HMGB1) is a newly recognized factor regulating cancer cell tumorigenesis, expansion and invasion. We investigated the correlation between the serum HMGB1 levels and the clinical and pathologic features of gastric cancer and evaluated the validity of HMGB1 as a potential biomarker for the early diagnosis of gastric cancer.

The diarrheal pathogen Clostridium difficile consists of at least six distinct evolutionary lineages. The RT017 lineage is anomalous, as strains only express toxin B, compared to strains from other lineages that produce toxins A and B and, occasionally, binary toxin. Historically, RT017 initially was reported in Asia but now has been reported worldwide. We used whole-genome sequencing and phylogenetic analysis to investigate the patterns of global spread and population structure of 277 RT017 isolates from animal and human origins from six continents, isolated between 1990 and 2013. We reveal two distinct evenly split sublineages (SL1 and SL2) of C. difficile RT017 that contain multiple independent clonal expansions. All 24 animal isolates were contained within SL1 along with human isolates, suggesting potential transmission between animals and humans. Genetic analyses revealed an overrepresentation of antibiotic resistance genes. Phylogeographic analyses show a North American origin for RT017, as has been found for the recently emerged epidemic RT027 lineage. Despite having only one toxin, RT017 strains have evolved in parallel from at least two independent sources and can readily transmit between continents.

The aims of this study were to investigate any change in PCR ribotypes and to determine the antimicrobial resistance of common PCR ribotypes over a 10-year period in a tertiary care hospital. We conducted PCR ribotyping, antimicrobial susceptibility testing and DNA gyrase sequencing to identify changes in 1407 Clostridium difficile non-duplicated isolates obtained between 2000 and 2009. A total of 74 different ribotypes were found. The most prevalent ribotype was ribotype 001 (26.1 %). The prevalence of ribotype 017 was 17 % and that of ribotype 014/020 was 9.6 %. Ribotyping showed that the prevalence of ribotype 001 decreased and the prevalence of ribotypes 017, 014/020 and 018 increased over the 10 years. Antimicrobial resistance rates in prevalent ribotypes were: clindamycin, 81 %; cefotetan, 19 %; moxifloxacin, 42 %; imipenem, 8 %; ciprofloxacin, 100 % and erythromycin, 80 %. Ribotype 018 showed greater antimicrobial resistance than other ribotypes. All ribotype 018 strains showing moxifloxacin resistance had a substitution of a gyrA coding amino acid (Thr82 to Ile). This study will help the understanding of PCR ribotype trends and antimicrobial resistance of C. difficile in Korea.

Carbon supported, Al doped-Li3V2(PO4)3 as a high rate cathode material for lithium-ion batteries