Edwardsiella tarda is pathogen of fish and other animals. The aim of this study was to investigate the viable but nonculturable (VBNC) state and virulence retention of this bacterium. Edwardsiella tarda CW7 was cultured in sterilized aged seawater at 4°C. Total cell counts remained constant throughout the 28-day period by acridine orange direct counting, while plate counts declined to undetectable levels (<0.1 CFU/ml) within 28 days by plate counting. The direct viable counts, on the other hand, declined to ca. 10 9 CFU/ml active cells and remained fairly constant at this level by direct viable counting. These results indicated that a large population of cells existed in a viable but nonculturable state. VBNC E. tarda CW7 could resuscitate in experimental chick embryos and in the presence of nutrition with a temperature upshift. The resuscitative times were 6 days and 8 days, respectively. The morphological changes of VBNC, normal, and resuscitative E. tarda CW7 cells were studied with a scanning electron microscope. The results showed that when the cells entered into the VBNC state, they gradually changed in shape from short rods to coccoid and decreased in size, but the resuscitative cells did not show any obvious differences from the normal cells. The VBNC and the resuscitative E. tarda CW7 cells were intraperitoneally inoculated into turbot separately, and the fish inoculated with the resuscitative cells died within 7 days, which suggested that VBNC E. tarda CW7 might retain pathogenicity.Edwardsiella tarda, an enteric gram-negative bacterium of the Enterobacteriaceae, is the causative agent of the systemic disease edwardsiellosis in freshwater and marine fish worldwide. The bacterium causes septicemia with extensive skin lesions and affects internal organs, such as the liver, kidney, spleen, and muscle (33, 52). It has been isolated from a variety of animals, including fish, birds, mammals, and reptiles (12,27,31,46,47), and environmental water (32, 50). Several potential virulence properties have been suggested to contribute to the pathogenesis of E. tarda, namely, the production of dermatotoxin (45) and hemolysin (14) and the ability to resist phagocyte-mediated destruction and to invade epithelial cells (19,22,43). However, little is known about the pathogenic mechanism of E. tarda, and the causes of disease occurrence are still elusive.Many bacteria have developed strategies for metamorphosis into more or less sophisticated survival forms in response to harsh environmental conditions, such as a temperature change, high salinity, or nutrient deprivation (4, 5). The formation of viable but nonculturable (VBNC) cells of bacteria has been proposed as a strategy to survive adverse conditions (10). The first clear evidence of the existence of the VBNC state in pathogens was provided by Xu et al. It has been demonstrated that VBNC cells are active in metabolism (16,20,53) and are able to recover from their dormant state, becoming metabolically active and fully culturable (26,40,48). Some pathogens in the VBNC ...

The aim of this study was to investigate the viable but nonculturable (VBNC) state of the bacterium. Vibrio alginolyticus VIB283 was cultured in sterilized seawater microcosm at 4 degrees C. Culturability of the cells in the microcosm was monitored by spread plate count (PC) on 2216E agar, PCs declined to undetectable levels (<0.1 CFU/ml) within 90 days. Total cell counts remained constant throughout the period as determined by acridine orange direct count (AODC). The direct viable counts, on the other hand, declined from 10(10) to 10(9) CFU/ml active cells and remained fairly constant at this level by direct viable count (DVC), which indicated that a large population of cells entered into the VBNC state. The VBNC cells could be resuscitated by temperature upshift with and without the presence of nutrition. The resuscitated time were 16 h and 8 days respectively. The resuscitation was not achieved in chick embryos. The morphology of the VBNC, normal and resuscitated cells was studied with scanning electron microscope and flow cytometry. The cells changed from rod or arc to coccoid and decreased in size when entered into the VBNC state. The resuscitated and the normal cells had almost no morphological differences.

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Background: The incidence of central venous catheter-related bloodstream infection (CRBSI) for continuous renal replacement therapy (CRRT) in kidney intensive care unit (ICU) patients is worthy of particular attention and recently, we analyzed clinical characteristics and risk factors of CRBSI for CRRT in our kidney ICU patients. Methods: To be part of this retrospective study, 1,523 patients who had a central venous catheter (CVC) for CRRT during the period April 2010 to May 2015 in our centre were enrolled. The clinical features and pathogens of CRBSI patients were investigated. Patients who also had CRRT of kidney ICU hospitalization without CRBSI were enrolled in a 1: 2 ratio as control. Risk factors of the CRBSI were analyzed. Results: A total of 57 patients had central venous CRBSI. The incidence of the infection was 3.7%. The mean rate of CRBSI was 3.9 per 1,000 catheter days, and the catheter median indwelling time was 14 (7–30) days. The most common pathogens were Gram-positive bacteria, which were noted in 29 cases (50.9%), followed by Gram-negative bacteria (36.8%). The most common pathogens causing CRBSI were Staphylococcus aureus (10 cases) and sewer enterobacteriaceae (10 cases) followed by Staphylococcus epidermidis (9 cases). CVC insertion sites included internal jugular vein (33 cases) and femoral vein (24 cases), accounting for 2.9% of internal jugular vein catheterization (1,140 cases) and 6.3% of femoral vein catheterization (383 cases) respectively. In total, 16, 20, 7 and 14 cases of CRBSI were noted in Spring, Summer, Autumn and Winter, accounting for 28.1, 35.1, 12.3 and 24.6% respectively. The most common infectious manifestations were chills (68.4%), fever (100%), and septic shock (49.1%). Multivariate analysis showed that catheterization of the femoral vein, long catheter indwelling time, low CD4+ lymphocytes and high acute physiology and chronic health evaluation (APACHE) II scores were independent factors associated with CRBSI. Conclusions: The incidence of CRBSI in our kidney ICU was 3.7%. Central venous CRBSI for CRRT was associated with catheterization of the femoral vein, long catheter indwelling time, compromised immune function and high APACHE II scores. Understanding pathogens and risk factors for central venous CRBSI in kidney ICU can help doctors prevent and treat CRBSI earlier.

Spinal cord injury (SCI) is one of the most severe traumatic injuries that results in dysfunction of limbs and trunk below the damaged section. Recent studies have shown that gastrodin (GAS) could improve the recovery of SCI. In the current study, we aimed to examine the possible mechanism underlying the effect of GAS on recovery of SCI in rats. In rats with SCI, GAS improved locomotor functions and decreased permeability of blood-spinal cord barrier, as illustrated by increase of Basso-Beattie-Bresnahan scores and decrease of Evans blue leakage. In addition, GAS inhibited inflammation, as evidenced by decrease of proinflammatory cytokines, including tumor necrosis factor α (TNFα) and interleukin-1β (IL-1β) in rats following SCI. Moreover, increase of TBARS content and decrease of glutathione (GSH) content and superoxide dismutase (SOD) activities in SCI rats were inhibited by GAS. Furthermore, GAS enhanced mRNA expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), catalytic subunit of γ-glutamylcysteine ligase (GCLc) and modified subunit of γ-glutamylcysteine ligase (GCLm). The data suggested that GAS may promote the recovery of SCI through the enhancement of Nrf2-GCLc/GCLm signaling pathway, and subsequent improvement of oxidative stress and inflammation, resulting in decrease of permeability of BSCB and improved recovery of locomotor function in rats with SCI. The results have provided novel insights into GAS-related therapy of SCI and associated neurodegenerative diseases.

Rheumatoid arthritis (RA) is an autoimmune disease that progresses from inflammation to cartilage destruction. Inspired by the similar characteristics of inflammatory granulation tissue to those of tumors, the newly emerged tumor therapy called thermochemotherapy is proposed to treat RA. Meanwhile, the repair of cartilage injury via tissue engineering is paid attention simultaneously. A first‐line antirheumatic drug (MTX; methotrexate) and transforming growth factor β1 (TGF‐β1) are loaded in nano‐Fe3O4 composite chitosan‐polyolefin to construct a multifunctional hydrogel (DN‐Fe‐MTX‐TGFβ1). The mechanical properties of the hydrogel are equivalent to that of articular cartilage to guarantee its role as a scaffold. A long‐term release ability and the magnetocaloric properties of the hydrogel assure its effect to provide sustained local thermochemotherapy. The effective ability of the hydrogel for both anti‐inflammation and cartilage repair is demonstrated. This work indicates a promising way to combine thermochemotherapy and tissue engineering for the effective treatment of RA for the first time.

By employing a mixed metal synthesis strategy, a heterometallic MOF, [In3Tb3(TATAB)4(OH)6(H2O)3]∙12DMF∙9H2O (1), has been constructed based on a nitrogen-rich ligand 4,4′,4″-s-triazine-1,3,5-triyltri-p-aminobenzoic (H3TATAB). Compound 1 shows a 3D doubly interpenetrated framework...

Carbapenems and tigecycline are two important classes of antimicrobial agents to treat the infections caused by Enterobacterales. Here, we reported a plasmid carrying both bla IMP−26 and tet(A) variant in clinical Klebsiella pneumoniae KP-1572. MIC results showed that K. pneumonia KP-1572 was resistant to a wide range of antimicrobials. The bla IMP−26 and tet(A) variant were located on an identical plasmid, which was indicated by S1-PFGE and southern blotting hybridization and can be successfully transferred by electroporation. Whole-plasmid sequencing and analysis revealed that a 142,993-bp-sized plasmid, designated pIMP1572, contains an IncFII k backbone and a variable region harboring bla IMP−26 and tet(A) variant. The plasmid pIMP1572 was apparently originated from a tet(A)-carrying IncFII k plasmid but with a deletion length of 6,216-bp and a multiple drug resistance region (MDRR) insertion of 25,259 bp. The plasmid pIMP1572 in the present study represents the first report of the IncFII k plasmid co-carrying bla IMP and tet(A) variant, which should be monitored.