Analysis of thrombus risk factors for routine blood test indicators in outpatients during the large-scale SARS-CoV-2 outbreak period / 中国热带医学

@#Abstract: Objective To investigate the impact of SARS-CoV-2 virus infection on the risk of thrombosis in COVID-19 outpatient patients with mild and regular symptoms. Methods Outpatient patients during the SARS-CoV-2 large-scale infection period after the policy adjustment for COVID-19 in Beijing in 2022 were selected as the observation group, and the dynamic zero-clearing period before the policy adjustment and outpatient patients during the 2022/2021/2020 period were taken as the three control groups. The patients with physiological factors that may increase the risk of coagulation, such as thrombotic diseases, malignant tumors, female pregnancy and other physiological factors, were excluded. Pediatric patients under 14 years old were also excluded. Age was expressed as median (interquartile). The changes in blood routine, fibrin/fibrinogen degradation products, and D-Dimer in Beijing outpatient patients were studied with statistical method and data analysis techniques. Results Compared with the control groups, the observation group showed a statistically significant decrease in red blood cells (RBC), hemoglobin (Hb), and hematocrit (HCT) levels, and an increase in monocytes (MONO) and platelet (PLT) counts, all showed statistically significant differences (P<0.0001). The proportion of fibrinogen degradation product (FDP) and D-Dimer of observation group exceeding the range increased significantly. Compared with the three control groups, the number of outpatient fibrinogen degradation products (FDP) in the observation group of patients aged 50 years and verage number of patients under 50 years old in the observation group with D-Dimer exceeding the threshold increased by more than 48.98%, and the monthly average number of patients with D-Dimer exceeding the threshold in patients aged 50 or older increased by 346%-998%. Conclusions The results of this study suggest that outpatient patients with mild or regular SARS-CoV-2 infection are also at risk for thrombotic events, and monitoring blood coagulation indicators such as D-dimer is recommended to avoid the sudden onset of thrombosis-related fatal complications .

Characterization of a multidrug-resistant Klebsiella pneumoniae ST3330 clone responsible for a nosocomial outbreak in a neonatal intensive care unit.

BACKGROUND: The incidence of Klebsiella pneumonia (Kp), which has often been found to produce, extended spectrum beta-lactamase (ESBL), is rising rapidly and poses a serious risk to neonates. To date, the mechanisms related to the spread of ESBL-Kp have not been fully elucidated. This study aimed to investigate the phenotypes, genotypes, and genetic relatedness of ESBL-KP that caused an outbreak of sepsis among neonates in an intensive care unit of a Beijing hospital. METHODS: Between April 2016 and May 2018, 21 non-repetitive clinical ESBL-Kp isolates were collected from a neonatal intensive care unit (NICU) in Beijing, China and were retrospectively analyzed. Pulsed-field gel electrophoresis (PFGE) was used to analyze genetic relatedness, a VITEK 2 AST test kit was used to test antimicrobial susceptibility, sequence type (ST) was analyzed through multilocus sequence typing (MLST), and resistance genes were identified by PCR. Virulence gene profiles, biofilm formation assay, and serum killing assay were used for virulence-associated determinants. RESULTS: All strains expressed the same antibiotype, combining ESBL production, third generation cephalosporins resistance and carbapenems sensitive. Sixteen of them produced ß-lactamases (CTX-M-3 and TEM-1B), while others possessed CTX-M-15, CTX-M-24, CTX-M-66, TEM-1C, SHV-26, SHV172, and OXA-1. PFGE confirmed 5 types (A, B, C, D and E) and MLST identified a ST3330 clone (16 strains), a ST2791 clone (2 strains), a ST37 clone (1 strain), a ST34 clone (1 strain), and a ST2740 clone (1 strain). PFGE type A strains, which belong to ST3330, were identified as the main pathogens involved in the outbreak. All isolates contained virulence genes iutA and mrk. PFGE type A carried both mrk (type 3 fimbriae, biofilm formation) and fimH (type 1 fimbriae), and other STs possessed mrk. Isolates belonging to the endemic ST3330 lineage produced more biofilm than other ST isolates (median OD590 1.829 vs. 0.2280, respectively; P<0.0001). All five PFGE types isolates showed serum high sensitivity (grade 1). CONCLUSIONS: The dissemination and outbreak of ESBL-producing K. pneumoniae in this study seemed to be clonal, and the outbreak was mainly caused by ST3330 K. pneumoniae. The detection of genes (mrk and fimH) belonging to the biofilm formation may partly explain the epidemic strain has high colonization and diffusion potential.

Draft Genome Sequence of an Escherichia coli Sequence Type 410 Isolate Harboring bla NDM-5 Genes with gyrA and parE Mutations, Isolated from Urine Culture in China.

Escherichia coli sequence type 410 (ST410) is now an international high-risk clone and is responsible for a large number of clinical infections. Here, we report the draft genome sequence of an ST410 clinical isolate harboring multiple bla NDM-5 genes that was obtained from urine culture in China.

Whole genome sequence of an Escherichia coli ST410 isolate co-harbouring blaNDM-5, blaOXA-1, blaCTX-M-15, blaCMY-2, aac(3)-IIa and aac(6')-Ib-cr genes isolated from a patient with bloodstream infection in China.

OBJECTIVES: Mortality associated with carbapenemase-producing Enterobacteriaceae is high as there are few therapeutic options. Escherichia coli sequence type 410 (ST410) is currently an international high-risk clone and is responsible for a large number of clinical infections. Here we report the draft genome sequence of a ST410 clinical E. coli isolate (ECS9) co-harbouring blaNDM-5, blaOXA-1, blaCTX-M-15, blaCMY-2, aac(3)-IIa and aac(6')-Ib-cr genes, obtained from a patient with bloodstream infection in China. METHODS: The genome of E. coli ECS9 was sequenced using an Illumina HiSeqTM 4000 instrument with a 150-bp paired-end approach. Generated sequence reads were assembled using Velvet 1.2.10. Contigs were annotated using Rapid Annotation using Subsystem Technology (RAST), and further whole-genome sequence data analyses were performed. RESULTS: Escherichia coli ECS9 belongs to multilocus sequence typing (MLST) ST410. The total number of assembled bases was 4 935 145 bp, with 5077 protein-coding sequences. The presence of the blaNDM-5, blaOXA-1, blaCTX-M-15 and blaCMY-2 genes was detected in addition to other antimicrobial resistance genes conferring resistance to fluoroquinolones, aminoglycosides, trimethoprim, sulfonamides and tetracyclines. CONCLUSION: To our knowledge, this is the first report of anE. coli ST410 strain co-harbouring blaNDM-5, blaOXA-1, blaCTX-M-15, blaCMY-2, aac(3)-IIa and aac(6')-Ib-cr, obtained from a bloodstream infection in China. The presented genome sequence of carbapenemase-producing E. coli strain ST410 could provide further insight into the acquisition of multiple resistance genes by this successful lineage.

Induction of adhesion molecule expression in co-culture of human bronchial epithelial cells and neutrophils suppressed by puerarin via down-regulating p38 mitogen-activated protein kinase and nuclear factor κB pathways.

OBJECTIVE: In this study, we aimed to investigate the expressions of adhesion molecules on human bronchial epithelial cells and neutrophils in co-culture system, assess the effects of puerarin on suppressing these adhesion molecules expressions, and explore the roles of two crucial signal-transduction elements p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor kappa B (NF-κB) in modulating adhesion molecules expressions. METHODS: Neutrophils and BEAS-2B cells (one human bronchial epithelial cell line) were co-cultured, and adhesion molecules expressions on cell surface were detected using flow cytometry. The mRNA levels of adhesion molecules were assessed by real-time quantitative polymerase chain reaction (real-time qPCR). Phosphorylated p38 MAPK and inhibitor κB were analyzed by Western blot. RESULTS: In co-culture system, adhesion molecules expressions on BEAS-2B cells and neutrophils were enhanced significantly (P<0.05). Correspondingly, the mRNA levels of adhesion molecules were also increased greatly. Moreover, the pretreatment of peurarin obviously suppressed adhesion molecules expressions on cell surface. Furthermore, phosphorylated p38 MAPK and inhibitor κB in BEAS-2B cells and neutrophils were elevated in co-culture system, but decreased significantly after upon the treatment of peurarin (P<0.05). CONCLUSIONS: Coculture boosted the interactions between human bronchial epithelial cells and neutrophils mimicking airway inflflammation, whereas peurarin decreased the expression of adhesion molecules on cell surface by suppressing the activities of p38 MAPK and NF-κB pathways, and exhibiting its anti-inflflammation activity.

In vitro study of injury on human bronchial epithelial cells caused by gunpowder smog.

Smog inhalation is associated with acute respiratory symptoms in exposed victims. However, despite the evidence from cell injury caused by smog, a stable and practical apparatus used to treat cells with smog is necessary. The aim of this study is to develop a cell research platform of smoke inhalation injury. In the smog-generation device, a wireless electromagnetic heater was used to ignite gunpowder and generate smog. The quality of black powder was checked by the black powder burn rate, and experimental smog was indirectly checked by the amount of cell damage. The temperature and humidity were set at 37 °C ± 1 °C and ≥95% in the smog-cells reaction chamber, respectively. Factors including gunpowder dosages, smog-exposure time, the cell density, modes of exposure, volumes of smog, test durations, volumes of the cell culture medium and combustion velocity were measured. Coefficient variation of different batches of gunpowder and smog were less than 4% and 9%, respectively. With larger gunpowder dosage and longer exposure time, cell injury appeared to increase. When cells were cultured in 4 × 10(4)/well density in culture medium (1 mL/well), exposed to more than 10 L smog with filter screens above plates, detected after 24 h culture in cell incubator and gunpowder burned out within 5 s, smog had the best effect on cell injury. In conclusion, the experimental device can produce test smog stably and safely. The apparatus treating cells with smog can induce cell injury effectively, and the injury is positively correlated with smog concentration and exposure time.