It has been widely reported that the incidence and severity of Clostridium difficile infection (CDI) have increased dramatically in North America and Europe. However, little is known about CDI in Mainland China. In this study, we aimed to investigate the incidence of CDI and the main epidemic and drug-resistant strains of C. difficile in Mainland China through meta-analysis of related studies published after the year 2010. A total of 51 eligible studies were included. The pooled incidence of toxigenic C. difficile among patients with diarrhoea was 14% (95% CI = 12–16%). In Mainland China, ST-37 and ST-3 were the most prevalent strains; fortunately, hypervirulent strains, such as ST-1 (BI/NAP1/027) and ST-11 (RT 078), have only occurred sporadically to date. The rates of C. difficile resistance to ciprofloxacin (98.3%; 95% CI = 96.9–99.7%), clindamycin (81.7%; 95% CI = 76.1–87.3%) and erythromycin (80.2%; 95% CI = 73.5–86.9%) are higher than in other counties; however, none of the C. difficile isolates reported in Mainland China were resistant to metronidazole (n/N = 0/960), vancomycin (n/N = 0/960), tigecycline (n/N = 0/41) or piperacillin/tazobactam(n/N = 0/288).

Kaposi's sarcoma-associated herpesvirus (KSHV) is etiologically associated with Kaposi's sarcoma (KS), the most common AIDS-related malignancy. KSHV vIL-6 promotes KS development, but the exact mechanisms remain unclear. Here, we reported that KSHV vIL-6 enhanced the expression of DNA methyltransferase 1 (DNMT1) in endothelial cells,increased the global genomic DNA methylation, and promoted cell proliferation and migration. And this effect could be blocked by the DNA methyltransferase inhibitor, 5-azadeoxycytidine. We also showed that vIL-6 induced up-regulation of DNMT1 was dependent on STAT3 activation. Therefore, the present study suggests that vIL-6 plays a role in KS tumorigenesis partly by activating DNMT1 and inducing aberrant DNA methylation, and it might be a potential target for KS therapy.

PurposeThe emergence and spread of carbapenem-resistant Enterobacteriaceae deserves special concern worldwide. Unlike the epidemiological characteristics reported in other studies, we found that the production of New Delhi metallo-β-lactamase 5 was the main mechanism for the resistance of Escherichia coli to carbapenems.MethodsAll carbapenem-resistant strains were collected from July 2017 to July 2018 of the First Affiliated Hospital of Nanjing Medical University. The presence of carbapenemase-encoding genes was detected using PCR and gene sequencing. Genetic relatedness of the blaNDM-5-positive E. coli strains was determined with PFGE and MLST. Susceptibility profiles were measured with broth microdilution method and E-test strips. Transferability features of blaNDM-5 gene were assessed by conjugation experiments, S1-PFGE, southern blotting and PCR-based replicon typing methods. The genetic structures surrounding blaNDM-5 were acquired by whole genome sequencing and PCR mapping.ResultsAmong the 28 carbapenem-resistant E. coli strains, 18 (64%) were verified as NDM-5 producers. The 18 blaNDM-5-positive E. coli strains showed high resistance to most antibiotics, but 100% were sensitive to colistin and tigecycline. In addition, the 18 blaNDM-5-positive E. coli strains belonged to eight STs, among which ST167, ST410 and ST101 were found to cause clonal spread in the hospital. Further studies found that the blaNDM-5 gene was located on an IncX3-type plasmid, and all plasmids harbored an IS3000-ΔISAba125-IS5-blaNDM-5-bleMBL-trpF-dsbC-IS26 structure.ConclusionThe clonal spread of blaNDM-5-positive E. coli strains and horizontal dissemination via the pNDM-MGR 194-like plasmids should draw more attention. Appropriate infection control operations should be performed to prevent the further spread of blaNDM-5.