Corynebacterium striatum is an emerging, multidrug-resistant pathogen that frequently causes nosocomial infections worldwide. This study aimed to investigate phylogenetic relationship and presence of genes responsible for antimicrobial resistance among C. striatum strains associated with an outbreak at the Shanxi Bethune Hospital, China, in 2021. Fecal samples were collected from 65 patients with C. striatum infection at Shanxi Bethune Hospital between February 12, 2021 and April 12, 2021. C. striatum isolates were identified by 16S rRNA and rpoB gene sequencing. E-test strips were used to examine the antimicrobial susceptibility of the isolates. Whole-genome sequencing and bioinformatics analysis were employed to assess the genomic features and identify antimicrobial resistance genes of the isolates. Crystal violet staining was conducted to determine the ability of biofilm formation of each isolate. A total of 64 C. striatum isolates were identified and categorized into 4 clades based on single nucleotide polymorphisms. All isolates were resistant to penicillin, meropenem, ceftriaxone, and ciprofloxacin but susceptible to vancomycin and linezolid. Most isolates were also resistant to tetracycline, clindamycin, and erythromycin, with susceptibility rates of 10.77, 4.62, and 7.69%, respectively. Genomic analysis revealed 14 antimicrobial resistance genes in the isolates, including tetW, ermX, and sul1. Crystal violet staining showed that all isolates formed biofilms on the abiotic surface. Four clades of multidrug-resistant C. striatum spread in our hospitals possibly due to the acquisition of antimicrobial resistance genes.

Background: Lipids take part in many pathophysiological processes of sepsis, thus, the variation of lipid composition may have clue on the severity and pathogen to sepsis. The objective of our study is to expand the profile of lipid compositions and screen potential biomarkers in intensive care unit (ICU) patients with sepsis. Methods: Patients admitted to the ICU clearly diagnosed with celiac sepsis were included in this prospective study. Age-matched healthy participants from the Physical Examination Center were used as the control group. Blood samples were obtained from patients within the first 12 h of admission. We analysed different components of the lipid metabolism between the sepsis patients and controls and described characteristic features during sepsis. Results: Thirty patients with celiac sepsis and 30 sex- and age-matched healthy controls were enrolled in this study. The lipid metabolic signature was obviously different between the sepsis patients and healthy controls and was mostly downregulated in sepsis patients. We identified 65 lipid species. Sixty-four lipid molecules were found to be significantly downregulated in sepsis patients, and only the level of one phosphatidylethanolamine (PE) molecule, PE (34:2) was higher in the sepsis patients with sepsis group comparing with the control group. The analysis of metabolic pathway illustrated the different lipid molecules were closely related to Phosphatidylcholine (PC), Lysophosphatidylcholine (LPC), and PE. Conclusion: Sepsis contributes to impaired expression of most lipids, which mainly result in the disorder of glycerolipid metabolic pathway, including Phosphatidylcholine (PC), Lysophosphatidylcholine (LPC), and PE.

Aims To perform a prospective diagnostic study exploring the clinical utility of metagenomic next-generation sequencing (mNGS) in diagnosing community-acquired pneumonia (CAP), and revealing resistome differences in bronchoalveolar lavage fluid (BALF) from CAP patients with varying severity of admission base on Pneumonia Patient Outcomes Research Team (PORT) risk classes. Methods and results We compared the diagnostic performances of mNGS and conventional testing for the detection of pathogens in BALF from 59 CAP patients, and performed resistome differences analysis of metagenomic data from 59 BALF samples, namely, 25 from CAP patients with PORT score I (I group), 14 from CAP patients with PORT score II (II group), 12 from CAP patients with PORT score III (III group), and 8 from CAP patients with PORT score IV (IV group). The diagnostic sensitivities of mNGS and conventional testing for the detection of pathogens in BALF in patients with CAP were 96.6% (57/59) and 30.5% (18/59), respectively. There was a significant difference in the overall relative abundance of resistance genes between the four groups (P = 0.014). The results of principal coordinate analysis based on Bray-Curtis dissimilarities showed that there were significant differences in the composition of resistance genes among the I, II, III, and IV groups (P = 0.007). A large number of antibiotic resistance genes, such as those affiliated with multidrug, tetracycline, aminoglycoside, and fosfomycin resistance, were enriched in the IV group. Conclusions In conclusion, mNGS has a high diagnostic value in CAP. There were significant differences present in microbiota resistance to antibiotics in BALF from CAP patients in different PORT risk classes, which should attract enough attention.

BACKGROUND:In patients with community-acquired pneumonia (CAP), the risk and protective factors influencing discharge outcomes have not been fully elucidated. Therefore, we aimed to investigate the factors affecting discharge outcomes and provide a theoretical basis for improving the cure rate of patients with CAP. METHODS:We describe a retrospective epidemiological study of patients with CAP conducted from 2014 to 2021. We used age, sex, co-morbidities, multilobar involvement, severe pneumonia, the main abnormal symptoms present on admission, and pathogen-targeted therapy as variables that may affect discharge outcomes. These variables were included in subsequent logistic regression analyses. Discharge outcomes were divided into remission and cure. RESULTS:Of a total of 1008 patients with CAP, 247 patients were discharged as remission. The results of multivariate logistic regression analyses showed that age >65 years, smoking history, co-morbidity of chronic obstructive pulmonary disease, co-morbidity of chronic heart disease, co-morbidity of diabetes, co-morbidity of malignancy, co-morbidity of cerebrovascular disease, pleural effusion, hypoxemia, respiratory failure, electrolyte disturbances, and severe pneumonia were independently associated with poor discharge outcomes (all P < 0.05), while pathogen-targeted therapy (odds ratio: 0.32, 95% confidence interval: 0.16-0.62) was found as a protective factor. CONCLUSIONS:Age > 65 years, the presence of co-morbidities, the presence of admission symptoms such as electrolyte disturbances, and severe pneumonia are associated with a poor discharge outcome, while pathogen-targeted therapy is associated with a good discharge outcome. Patients with CAP with a defined pathogen are more likely to be cured. Our results suggest that accurate and efficient pathogen testing is essential for CAP inpatients.

Objective:This work aims to investigate the phenotype-characteristics of drug resistance and the possible mechanisms of extensively drug-resistance Klebsiella pneumoniae(XDRKP). Methods:Screened by the previous drug susceptibility results, 116 clinical Klebsiella pneumoniae isolates were collected from Shanxi Bethune Hospital from January 2018 to December 2020. Matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF MS) rapid microbial identification system and VITEK-compact 2 were used. The modified carbapenem inactivation method (mCIM) combining with EDTA carbapenem inactivation method (eCIM) was used to identify the strains′ carbapenemase phenotypes, which were compared with subsequent qPCR results. The qPCR amplification combining with agarose gel electrophoresis were carried out to detect various drug-resistant related genes, including: carbapenemase genes: blaKPC, blaNDM, blaVIM, blaIMP, blaOXA; aminoglycosides resistance genes: ① 16S rRNA methylase genes: rmtA, rmtC, rmtD, rmtG, rmtH, armA, npmA, rmtB, rmtE, rmtF, ② variant of aminoglycosides acetyltransferase gene: aac(6′)-Ib-cr; quinolone resistance genes: DNA gyrase protection protein qnr family: qnrA, qnrB, qnrC, qnrD, qnrS, efflux pump protein gene: oqxAB, qepA, variant of aminoglycoside acetyltransferase gene: aac(6′)-Ib-cr; and tigecycline-resistant Tet protein genes: efflux pump protein gene: tet (A), tet (L), ribosome protection protein gene: tet (M), tigecycline modified enzyme gene: tet (X). Each isolate′s phenotype and resistance gene result were compared and analyzed correspondingly. Results:A total number of 116 XDRKP isolates were collected in 3 years, 115 of which are identified as carbapenem resistant. Both cephalosporins and quinolones resistant rate were 100%, while the resistant rate of aminoglycosides antibiotic gentamicin, tobramycin and amikacin was 95.69% (111/116), 94.83% (110/116), or 88.79% (103/116) respectively. Sulfonamide antibiotics and tigecycline showed a relatively lower resistant rate. Compared with PCR amplification results, mCIM combining with eCIM phenotype testing had a high conformity, up to 95.65% (110/115). Positive rate of each resistance related gene was: blaKPC 90.52% (105/116), blaNDM 10.34% (12/116), rmtB 81.90% (95/116), armA 2.59% (3/116), oqxAB 65.52% (76/116), qnrB 6.03% (7/116), qnrS 12.93% (15/116), aac(6′)-Ib-cr 7.76% (9/116), or tet(A) 21.55% (25/116), respectively. Other resistance related genes were not detected. Corresponding analysis between the resistant phenotypes and resistance related genes indicated that a total of 65 XDRKP didn′t have a matched pairs, i.e. bacteria′s resistance to specific antibiotic could not be interpreted by carrying some associated resistant genes.Conclusions:The wide distribution of resistant genes and multiple-antibiotic-inactivated trait of some genes(such as aac(6′)-Ib-cr and oqxAB) in XDRKP are potential causes of the generation of extensively drug resistant phenotype. Different XDRKP isolates may carry one or more resistant genes in responding to specific antibiotic. In addition, there are some bacteria with an unmatched phenotype-gene feature indicating that both resistance genes′ regulation and some other mechanisms also play a role in development of XDR.

目的 通过研究本院近3年耐碳青霉烯阴沟肠杆菌,探讨其临床分布及相关耐药基因分布情况.方法 收集2017年1月至2020年9月山西白求恩医院分离的33株耐碳青霉烯阴沟肠杆菌为研究对象,利用全自动快速生物质谱检测系统(美国Bruker,MicroflexLT/SH)进行细菌鉴定,VITEK2-Compact全自动微生物分析系统进行细菌药敏试验.采用改良碳青霉烯灭活试验进行耐药表型筛选.采用PCR方法检测碳青霉烯酶基因(blaIMP、blanC、 blaNDM、blaVM和blaOXA-48).对所有菌株进行MLST分型和同源性分析.质粒接合转移实验研究耐药质粒的传播.结果 22株阴沟肠杆菌对厄他培南、亚胺培南、美罗培南均耐药,11株仅对厄他培南耐药.其中16株阴沟肠杆菌产NDM-1,4株产NDM-5,2株产IPM-1,1株菌同时产NDM-1和KPC-2.11株仅对厄他培南耐药阴沟肠杆菌中有两株检出blaNDM-1、两株检出blaKPC-2基因.MLST分型主要流行株为ST418型.质粒接合转移实验有14株转移成功.结论 本院耐碳青霉烯类阴沟肠杆菌从2017年逐年增加,2020年出现暴发流行.携带的碳青霉烯酶基因以blaNDM为主,ST418型菌株占多数.耐药基因可通过质粒水平传播,所以加强临床耐药菌株筛检及控制对临床抗感染治疗作用关键.

Background: In stent restenosis (ISR) is one of the major complications after stent implantation. Thus, there is a growing interest in identifying a biomarker for the onset of ISR. High levels of serum homocysteine (Hcy) have been associated with the progression of cardiovascular disease. Therefore, the study was carried out to quantify the correlation between serum Hcy and ISR severity. Compared with coronary angiography (CAG), Hcy levels provided a significantly better clinical detection of ISR severity after PCI. Methods: A total of 155 patients were recruited from Shanxi Bethune hospital, from 6 months to 2 years post PCI. Serum Hcy levels and postoperative angiography results were used to differentiate the patients into two experimental groups: ISR (>50% diametrical stenosis), and non-ISR. The non-ISR included two subgroups: intimal hyperplasia (10–50% diametrical stenosis), and recovery (<10% diametrical stenosis). In addition, a group of 80 healthy individuals was used as a negative control. The correlation between homocysteine level and ISR severity t was analyzed for all groups. In addition, the correlation between serum Hcy level and the severity of ISR in the experimental group was analyzed by the Pearson correlation test. Results: The serum Hcy level in the experimental group and control group was determined to be (20.21 ± 11.42) μmol/L and (15.11 ± 10.25) μmol/L respectively. The level of serum Hcy in the experimental group was significantly higher than in the control group (t-value of 2.385; p-value of 0.019). The serum Hcy level in the restenosis and the intimal hyperplasia group was (25.72 ± 13.71) μmol/L and (17.35 ± 7.70) μmol/L respectively. The serum Hcy level in the restenosis group was significantly higher than in the intimal hyperplasia group (t-value of 2.215; p-value of 0.033). The level of serum Hcy in the group without a plaque in the stent was (16.30 ± 6.08) μmol/L, whereas in the control group was (15.11 ± 10.25) μmol/L. The no plaque group had a slightly higher serum Hcy level than the control group (t-value of 0.634; p-value of 0.528). All included patients were divided into four quartiles based on the serum Hcy concentration: quartile 1 (8.90–13.20 μmol/L), quartile 2 (13.30–16.45 μmol/L), quartile 3 (16.60–24.25 μmol/L) and quartile 4 (24.30-65.30 μ mol/L). The incidence of ISR was 5, 6.25, 7.5 and 15%, in the 1,2,3 and four quartiles respectively. The serum Hcy level in the experimental group was (20.21 ± 11.42) μmol/L, the severity of in-stent restenosis was (0.25 ± 0.31), (R-value was 0.234; p-value was 0.037), indicating a correlation between serum Hcy and the severity of restenosis (p < 0.05). Taking coronary angiography as the gold standard, a ROC curve analysis was performed on the serum Hcy levels for the experimental group. The area under the curve (AUC) was 0.718 (95% CI 0.585-0.854, p < 0.001), indicating that the serum Hcy concentration could predict ISR. On the ROC curve, the best critical value of serum Hcy concentration for predicting ISR was 20.05 μmol/L, with a sensitivity of 45% and specificity of 88.1%. Conclusion: A positive correlation was observed between homocysteine and the severity of restenosis after PCI, The level of Hcy could serve as a predictive biomarker for the severity of ISR.

耐酪氨酸冢村菌是一种革兰阳性棒状杆菌，临床微生物实验室鉴定常与奴卡菌、马红球菌和戈登菌等难区分。耐酪氨酸冢村菌引起的人类感染病例报道较少，且临床表现易被误诊为结核分枝杆菌感染。然而，随着糖尿病、肾病、肿瘤等慢性疾病患者增多，这种微生物对于免疫力低下患者被认为是一种条件致病菌，甚至可以导致严重感染，正确的病原学诊断非常重要。本文报道1例最初诊断结核性腹膜炎，进一步培养确诊由耐酪氨酸冢村菌引起腹壁脓肿，最终抗感染治疗成功的患者。

Objective. This study is aimed at teasing out the correlation of plasma D-dimer (D-D) levels to age, metastasis, TNM stage (tumor-node-metastasis classification), and treatment in non-small-cell lung cancer (NSCLC) patients of different ages, to facilitate early diagnosis of hypercoagulable state, choose appropriate treatment, and use appropriate anticoagulants. Hence, thrombosis and complications caused by excessive anticoagulants can be prevented; thrombus or disseminated intravascular coagulation (DIC) and other complications in elderly patients with NSCLC can be reduced or avoided. By monitoring the level of plasma D-D in patients with NSCLC, recurrence and metastasis can be predicted in the early stage and the TNM stage can be evaluated. Methods. A total of 670 patients with NSCLC were selected in Shanxi Bethune Hospital from March 2014 to October 2020 as the experimental group, and 950 healthy people were selected from the physical examination center of the same hospital as the control group. The data of patients with NSCLC diagnosed for the first time without any treatment were collected and grouped based on metastasis, TNM stage, treatment, and pathological type, and the correlation with plasma D-D level was analyzed. Plasma D-D levels were measured by immunoturbidimetry on an ACL TOP 700 Automatic Coagulation Analyzer. The patients were further divided into two groups according to different treatment methods, and the differences in plasma D-D levels between patients receiving chemotherapy and those receiving targeted therapy in different treatment cycles were analyzed. The correlation between D-D levels and age in healthy controls was analyzed. The difference in D-D levels between NSCLC patients and healthy controls of the same age was analyzed. Results. All data of both the experimental group and the control group were normally distributed. The average age of the experimental group was 61.31±6.23 (range: 36-92) years. The average age of the control group was 61.14±11.12 (range: 35-85) years. There was no significant difference in gender between the experimental group and the control group (p>0.05). The plasma D-D level of NSCLC patients was significantly higher than that of the healthy controls (p<0.05). No significant difference in plasma D-D level was found between NSCLC patients of different genders, and the finding was similar between healthy controls of different genders (p>0.05). Significant difference in the D-D level was found between the groups of 30-59 years and 60-69 years (p<0.05), between groups of 60-69 years and 70-79 years (p<0.05), and between 70-79 years and ≥80 years (p<0.05). The plasma D-D level of patients≤79 years old increased with age, but it decreased in those over 80 years old. According to Pearson correlation analysis, there was a positive correlation between the D-D level and the age of NSCLC patients under 79 years old (p<0.05). The differences in D-D levels between the four age groups were statistically significant (p<0.05), showing an upward trend of the D-D level in healthy controls with the increase of age. There were statistically significant differences in D-D levels between NSCLC patients and healthy controls of the matching age group (p<0.05), suggesting that NSCLC patients had significantly higher D-D levels than healthy people of the same age group. The differences in D-D levels between NSCLC patients without metastasis, NSCLC patients with metastasis, and healthy people were statistically significant (p<0.05). The patients with metastasis had the highest D-D level, and healthy people had the lowest D-D level. The difference in plasma D-D levels between patients of different TNM stages was statistically significant (p<0.05). Patients with an advanced TNM stage tended to have higher D-D levels. The TNM stage and D-D level of NSCLC patients changed significantly before and after treatment. An earlier stage was related to a more obvious change in D-D levels after treatment with a statistically significant difference (p<0.05). A more advanced stage was associated with a smaller change in the D-D level after treatment, with no statistically significant difference (p>0.05). The plasma D-D levels before and after four cycles of chemotherapy or targeted therapy were higher than those of the healthy control group, and the differences were statistically significant (p<0.05). The D-D level of patients after chemotherapy was significantly lower than that before chemotherapy (p<0.05), but there was no significant difference before and after targeted therapy (p>0.05). The D-D level after the first cycle of chemotherapy was higher than that before chemotherapy. The level of D-D after the third and fourth cycles was significantly lower than that before chemotherapy (p<0.05). No significant difference was found between the D-D level before treatment and that after four cycles of chemotherapy (p>0.05). Conclusion. It is suggested that coagulation test indexes should be included to evaluate the treatment regimen for NSCLC patients. Most patients with NSCLC are in a hypercoagulable state, which is related to age, tumor invasion and metastasis, recurrence, and treatment. Regular monitoring of plasma D-D levels can facilitate early diagnosis of a hypercoagulable state and timely and appropriate use of anticoagulants, to avoid or reduce complications such as venous thromboembolism in NSCLC patients and to prevent the risk of bleeding caused by excessive anticoagulants. Clinicians can choose the treatment with less harm and maximum benefit for NSCLC patients based on the plasma D-D level. When in a hypercoagulable state, the body’s blood viscosity increases, making it more conducive to the growth and infiltration of tumor cells. Our study shows that the recurrence and metastasis of NSCLC are related to coagulation indexes, which provides a theoretical basis for the early diagnosis and treatment of recurrent and metastatic NSCLC.

目的 研究山西大医院碳青霉烯类耐药肺炎克雷伯菌(CRKP)分离株的临床分布,主要耐药表型和耐药基因,评估CRKP菌株在改良碳青霉烯类灭活实验(mCIM)中的诊断能力.方法 以41株CRKP菌株为研究对象,采用VITEK-2全自动微生物分析仪进行鉴定和药敏试验.使用mCIM进行产酶菌株筛选.使用PCR方法检测KPC、NDM等基因.结果 41株临床分离株主要来自重症医学科,占24.39％.标本类型主要为痰标本,占31.71％.41株对90％以上的常用药物具有耐药性,其中40株携带KPC基因,1株携带KPC和NDM基因,1株携带NDM基因.mCIM可以准确的检测出碳青霉烯酶.结论 KPC型碳青霉烯酶是临床分离的CRKP株中的主要酶,通过使用mCIM可以有效地发现产生耐碳青霉烯酶的菌株.

Balantidium coli human infection predominantly occurs in tropical and subtropical regions in the world. Human case is extremely rare in China. This report details a case of B. coli infection in a 68-year-old man in China, who presented with history of abdominal pain, tenesmus, diarrhea with blood and was diagnosed as B. coli-caused dysentery. Our case indicates possible occurrence of Balantidium coli-related disease in cooler climates. This case is presented not only because of its rarity but also for future references.

目的 通过检测分析耐碳青霉烯肺炎克雷伯菌(CRKP)的流行病学资料,研究耐药趋势及耐药机制.方法 收集山西白求恩医院2018年1月至2019年1月临床分离的耐碳青霉烯肺炎克雷伯菌,对其进行鉴定、药敏及表型筛选.通过PCR方法检测主要碳青霉烯耐药基因[A类丝氨酸酶(KPC),B类金属β-内酰胺酶(NDM型、IMP型、VIM型)以及D类丝氨酸酶(OXA)-48等]和外膜孔道蛋白基因(OmpK35、OmpK36),并对孔道蛋白基因检测的阳性菌株采用实时荧光定量PCR进行基因表达的相对定量分析.结果 经分析,CRKP的分离率为4.91％.CRKP时间分布以2019年1月分离率最高,为29.27％;CRKP年龄主要集中在21～ 80岁,其中以41 ～ 50岁分离率最高,为24.39％;科室分布以重症医学科为主,分离率为24.39％,其次为普通外科21.95％、康复医学科14.63％及神经外科12.20％;标本分布以痰标本为主,分离率为31.71％,其次为尿19.51％、血19.51％及分泌物12.20％.CRKP对亚胺培南、厄他培南的耐药率分别为90.24％、100.00％;对环丙沙星及阿米卡星的耐药率分别为95.12％和56.10％,对β-内酰胺类、氨基糖苷类耐药率均较高.改良碳青霉烯灭活实验(mCIM)和EDTA-改良碳青霉烯灭活实验(eCIM)显示有31株(75.61％)菌株表型表现为丝氨酸酶,有3株(7.32％)为金属酶;检出的碳青霉烯酶基因,有39株(95.12％)为KPC型,1株(2.44％) NDM型,1株(2.44％)同时具有以上KPC型和NDM型;只有1株(2.44％)菌株缺失OmpK36基因,余均存在OmpK35及OmpK36.进一步分析OmpK35中41株只有9株(21.95％)表达下调,而OmpK36中40株有38株(95.00％)表达下调.结论 CRKP耐药现象严峻,感染年龄以中青年为主,且主要集中在重症医学科,以痰液标本为主;其CRKP的耐药机制主要为产KPC型丝氨酸酶和外膜孔道蛋白OmpK36缺失及表达下降.

目的 研究该院临床分离的耐碳青霉烯肺炎克雷伯菌的耐药分子学机制.方法 分析该院临床微生物实验室分离的耐碳青霉烯肺炎克雷伯菌株(CRKP),采用基质辅助激光解析电离飞行时间质谱(MAL-DI-TOF MS)和全自动微生物分析仪(VITEK-2 compact)鉴定细菌并进行药物敏感试验分析,采用改良Hodge试验(MHT)和碳青霉烯酶灭活试验(CIM)进行表型确证;聚合酶链式反应(PCR)法检测碳青霉烯酶基因型,并进行基因测序BLAST比对和多位点序列分析(MLST).结果 46株耐碳青霉烯肺炎克雷伯菌对常用抗菌药物均表现出高耐药性;耐碳青霉烯表型确证均呈阳性,PCR检测结果显示其中包括A类碳青霉烯酶(KPC-2型)和B类金属酶(NDM-1和IMP-4),MLST分型以ST11型为主.结论 该院分离的耐碳青霉烯肺炎克雷伯菌的耐药分子学机制主要以产KPC-2型碳青霉烯酶的ST11型为主,同时有少量其他型别的检出,加强院内感染监测强度和力度,以及进一步规范抗菌药的合理使用显得尤为重要.

目的 系统评价改良碳青霉类灭活试验对耐碳青霉烯类耐杆菌科细菌的准确性.方法 检索PubMed、EMBASE、中国知网、万方、中国生物医学文献数(CBM)数据库及Cochrane图书馆,并辅以文献追溯、手工检索,检索时间为2015年1月1日-2019年6月16日.严格按照纳入和排除标准进行文献筛选,参照诊断准确性研究质量评价工具对纳入文献进行质量评价后,进行meta分析.结果 共纳入8篇文献,合计1154份非重复标本.结论 mCIM试验对于产碳青霉烯酶肠杆菌科细菌的表型检测具有很高的敏感度、特异度和准确性.

Objective To investigate the Imipenem resistant Acinetobacter baumannii and the re-lationship between drug resistance and genes of OXA-23. Methods A total of 70 isolates of imipenem re-sistant Acinetobacter bauman(IRAB)and 30 of imipenem sensitive Acinetobacter bauman(ISAB)were col-lected. The sensitivity of antimicrobial agents was detected by broth microdilution method. The polymerase chain reaction(PCR)technique and sequence analysis were used to detect the genes. Results For in addi-tion to add ring element(4. 3% ),low percentages,penicillium acinetobacter baumannii on carbon alkene antimicrobial drug resistant rate are higher,and penicillium carbon alkene antimicrobial sensitive bacteria were more sensitive to most antibiotics,PCR according to the results of this study in IRAB OXA-23 detected 64 strains,detection rate of 91. 4% ,the ISAB OXA-23 check out 8 strains,the detection rate was 26. 7% , and the difference was statistically significant( P<0. 01). Conclusion Carbapene-resistant acinetobacter baumannii has a serious drug resistance,which is closely related to OXA-23.

目的 探讨耐亚胺培南的鲍曼不动杆菌的耐药性与外排泵基因adeB的关系,为临床合理使用抗生素提供依据,防止和抑制鲍曼不动杆菌耐药菌株的增加.方法 收集本院2017年1月-12月临床分离的非重复鲍曼不动杆菌122株,其中亚胺培南耐药鲍曼不动杆菌(IRAB) 96株,亚胺培南敏感鲍曼不动杆菌(ISAB) 26株.采用微量肉汤稀释法进行药物敏感性分析试验;应用PCR及序列分析的方法分析外排泵基因adeB.结果 IRAB对大多数抗生素最小抑制浓度(MIC)值均较高,但对替加环素仍保持较高的敏感性,而ISAB对多数抗生素均较敏感.PCR扩增结果显示IRAB的adeB检出率为96.8％.adeB基因与GenBank注册号CP026943.1基因相似性为99％.结论 本院分离到的鲍曼不动杆菌对亚胺培南有较高的耐药性,与adeB基因关系密切.

鲍曼不动杆菌(AB)为革兰阴性条件致病菌.为了解我院AB的分布和耐药情况,探索其可能的耐药机制,本研究回顾性分析2016—2017年本院临床分离的AB其标本来源、科室分布及耐药情况,现报告如下.

孔兹创伤球菌是一种兼性厌氧菌,最初被认为是人类皮肤、特别是下肢的正常菌.孔兹创伤球菌引起的人类感染较少见,只有少数病例报道.然而,随着糖尿病、肿瘤等慢性疾病及处于免疫力低下的患者增多,这种微生物已被认为是一种条件致病菌,甚至可以导致严重感染.本文报道1例由孔兹创伤球菌引起的严重糖尿病足感染,最终抗感染治疗成功的患者.

目的 血管紧张素-Ⅱ(Ang-Ⅱ)联合β-氨基丙腈(BAPN)腹腔注射建立小鼠主动脉夹层模型.方法 80只C57BL/6J小鼠(3周龄,雄性)分为对照组和7个实验组,分别为:Ang-Ⅱ组、BAPN 0.1 g/kg组、BAPN 0.33 g/kg组、BAPN 0.67 g/kg组、Ang-Ⅱ+BAPN 0.1 g/kg组、Ang-Ⅱ+BAPN 0.33 g/kg组、Ang-Ⅱ+BAPN 0.67 g/kg组.对照组每8 h给予腹腔注射0.9％氯化钠注射液0.1 ml,Ang-Ⅱ组每8 h腹腔注射4.0 mg/kg Ang-Ⅱ,3种不同剂量的BAPN组每日分别给予腹腔注射0.1、0.33、0.67 g/kg BAPN,3个联合用药组分别在每8 h腹腔注射4.0 mg/kg Ang-Ⅱ的基础上,分别给予腹腔注射0.1、0.33、0.67 g/kg BAPN.每组均于相同时间点应用鼠尾测压器检测并记录小鼠血压,持续14 d,中途死亡小鼠直接解剖,取出主动脉.14 d后处死小鼠,取出主动脉行病理观察.结果 未注射Ang-Ⅱ的3个BAPN组小鼠血压与对照组比较差异无统计学意义(P＞0.05);注射Ang-Ⅱ的4个组血压与对照组比较差异有统计学意义(P＜0.05).对照组无主动脉夹层形成,HE染色显示血管壁结构完整;7个实验组HE染色显示部分小鼠血管壁弹力纤维破坏,假腔形成,炎性细胞浸润,提示主动脉夹层形成.BAPN 0.1 g/kg组、BAPN 0.33 g/kg组、BAPN 0.67 g/kg组,随着BAPN注入剂量的增加,主动脉夹层的发生率逐渐上升,分别为10％、30％、50％,部分小鼠因主动脉破裂死亡,3组分别为0、1、4只;Ang-Ⅱ组和Ang-Ⅱ+BAPN 0.1 g/kg组主动脉夹层发生率较低(均为30％),死亡分别为1、0只;Ang-Ⅱ+BAPN 0.33 g/kg组和Ang-Ⅱ+BAPN 0.67 g/kg组主动脉夹层发生率分别为70％和80％,Ang-Ⅱ+BAPN 0.33 g/kg组死亡2只,而Ang-Ⅱ+BAPN 0.67 g/kg组8只形成主动脉夹层的小鼠均死亡.Ang-Ⅱ+BAPN 0.33 g/kg组主动脉夹层发生率高,死亡率不高,符合小鼠主动脉夹层模型的要求.结论 Ang-Ⅱ联合BAPN腹腔注射能成功诱导小鼠主动脉夹层模型.