Whole genome sequence of carbapenem-resistant hypermucoviscous Klebsiella pneumoniae K2-ST375 with blaNDM-harbouring conjugative IncX3 and pLVPK-like virulence plasmids from a patient in China.

OBJECTIVES: Carbapenem-resistant hypermucoviscous Klebsiella pneumoniae (CR-HMKP) poses unprecedented public health challenges. However, genomic information regarding the CR-HMKP K2-ST375 strain is scarce. The aim of this study was to characterize the whole genome sequence of the CR-HMKP K2-ST375 strain Kp0179 isolated from a male patient in China. METHODS: The whole genome of Kp0179 was sequenced using the DNBSEQ and Pacific Biosciences RSII platforms. The capsular serotype, multilocus sequence typing (MLST), antimicrobial resistance genes, and virulence factors were determined using available databases and bioinformatics tools. Conjugation experiments were performed using rifampicin-resistant Escherichia coli C600 as the recipient. RESULTS: The Kp0179 strain with hypermucoviscous phenotype was resistant to almost all ß-lactams, including ertapenem and imipenem. Whole genome sequencing revealed that Kp0179 belonged to K2-ST375 and contained blaNDM-IncX3 and a virulence plasmid ca. 121 kb. Kp0179 contained 5146 coding genes, 88 tRNAs, 25 rRNAs and 38 non-coding RNA genes. Among the six acquired antibiotic resistance genes, blaSHV-99, fosA, oqxAB were located on the chromosome, whereas blaNDM-1, qnrS1 and blaSHV-12 were located on the conjugative plasmid pNDM-Kp0179 (IncX3 type). Virulence gene analysis indicated that pLVPK-Kp0179 carried multiple virulence-encoding genes, such as iroBCDN, iucABCDiutA, rmpA and rmpA2. In addition to carrying a virulence plasmid, capsule formation (kvgA) and the type 3 fimbriae operon (mrkABCDFHIJ) were located on the chromosome of Kp0179. CONCLUSION: To our knowledge, this is the first report of a CR-HMKP K2-ST375 strain with a blaNDM-harboured conjugative IncX3 plasmid and a pLVPK-like virulence plasmid from a patient in China. Therefore, the spread of CR-HMKP K2-ST375 isolates in China should be closely monitored.

Improvement of Mechanical Property for PLA/TPU Blend by Adding PLA-TPU Copolymers Prepared via In Situ Ring-Opening Polymerization.

Polylactic acid (PLA)-thermoplastic polyurethane (TPU) copolymer (PTC) was prepared by melting TPU pellets in molten lactide, followed by in situ ring-opening coordination polymerization. The results from FTIR and 1H-NMR confirmed the formation of the copolymer. PLA/TPU blends with different TPU contents were prepared by melt blending method. SEM and mechanical properties showed a conspicuous phase separation between PLA and TPU. In order to further improve the mechanical properties of the blend, PTC was used as the compatibilizer and the effects of the PTC content on the properties of the blend were investigated. The addition of PTC made TPU particles smaller in PLA matrix and improved the compatibility. With the loading of 5 wt.% PTC, the impact strength of the PLA/TPU blend reached 27.8 kJ/m2, which was 31.1% and 68.5% higher than that of the blend without PTC and pure PLA, respectively. As the content of PTC was more than 5 wt.%, the mechanical properties declined since the compatibilizer tended to form separate clusters, which could reduce the part distributed between the dispersed phase and the matrix, leading to a reduction in the compatibility of the blend. Moreover, the DMA results confirmed PTC could improve the compatibility between PLA and TPU.

16S ribosomal assay for early diagnosis of gonococcal meningitis with negative CSF culture: A case report.

Gonococcal meningitis is an exceedingly rare infectious disease, and if not diagnosed and treated in time, it can be severe. We present a case of gonococcal meningitis occurring in a 31-year old healthy woman. She was admitted with fever and persistent headache without urogenital symptoms. Blood cultures were positive and identified as N.gonorrhoeae, but CSF and cervical secretions cultures were both negative. Further testing confirmed the presence of N.gonorrhoeae by 16S ribosomal gene amplification and sequencing in all samples. These results suggest that the case may be a disseminated infection caused by untreated gonorrhea. Our case also shows that nucleic acid detection plays an important role in the rapid and precise diagnosis of gonococcal meningitis and in finding the origin of the pathogen.

Fibrous form-stable phase change materials with high thermal conductivity fabricated by interfacial polyelectrolyte complex spinning.

Polyethylene glycol (PEG)-based composite phase change materials (PCMs) containing hydroxylated boron nitride (BN-OH), cellulose nanofiber (CNF), and chitosan (CS) were prepared by the method of interfacial polyelectrolyte complex spinning, based on in-situ ionic cross-linking between CNF and CS. The wrapping effect of cross-linked CNF/CS networks and the strong interfacial interactions contributed to superior shape-stability throughout the phase change process. Furthermore, the homogeneously dispersed BN-OHs was beneficial to the construction of the continuous thermal conductive paths, and the excellent interfacial interactions between BN-OH and the matrix would lower the heat loss caused by phonon scattering in the interface. As a result, the thermal conductivity of the PCMs containing 47.5 wt% BN-OH reached 4.005 W/mK, which was 22.56 times higher than that of the pure PEG. Combined with the excellent thermal reliability and thermal stability, the form-stable PCMs showed a promising application potential in the fields of electronic cooling or temperature-adaptable textiles.

Two cases of septic shock with different outcomes caused by non-O1/non-O139 Vibrio cholerae isolates.

In recent decades, increasing numbers of human infections have been linked to non-O1/non-O139 Vibrio cholerae. Septicemia resulting from non-O1/non-O139 V. cholerae infection is rare but has high mortality. The pathogenesis of non-O1/non-O139 V. cholerae septicemia is poorly understood. Here, we report two sporadic cases of septicemia following non-O1/non-O139 V. cholerae infection from an inland area of China. Patient 1 died rapidly within 24 hours, while patient 2 gradually recovered from septic shock. To explore the reasons for these divergent outcomes, we compared the two cases, tested the antibiotic sensitivity of the two isolates, and investigated their virulence genes and sequence types.

Preliminary study on the effect of brazilin on biofilms of Staphylococcus aureus.

Biofilms significantly enhance antibiotic resistance by inhibiting penetration of antibiotics and are shielded from the immune system via the formation of an extracellular polymeric matrix. Innovative and novel approaches are required for the inhibition of biofilm formation and treatment of biofilm-associated infectious diseases. In the current study, a biofilm model of Staphylococcus aureus was established in vitro to explore inhibitory effects of brazilin (BN) on biofilm formation and to evaluate damaging effects of BN in the presence and absence of vancomycin (VCM) on the biofilm. Antibiofilm-infection mechanisms of BN were observed. In these experiments, the clinical strain of S. aureus C-4-4 was isolated for biofilm formation. Crystal violet staining and fluorescence microscopy revealed that BN inhibited biofilm formation in vitro and the best effect was observed with two times the minimum inhibitory concentration of BN following 48 h incubation. Additionally, the results demonstrated that BN in combination with VCM enhanced the damage to biofilms, whereas VCM alone did not. The results of the reverse transcription-quantitative polymerase chain reaction analyses demonstrated that BN downregulated gene expression of intercellular adhesion (ica)A and upregulated icaR and the quorum-sensing (QS) system regulator accessory gene regulator A. In summary, BN inhibited S. aureus biofilm formation and destroyed biofilms, while simultaneously increasing permeability to VCM. BN was able to reduce production of the extracellular polymeric matrix and inhibited the QS system. These results support the use of BN as a novel drug and treatment strategy for S. aureus biofilm-associated infections.