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分析肠炎沙门氏菌的抗生素诱导耐药性及其生物膜形成机制。

Analysis of antibiotic-induced drug resistance of enteritidis and its biofilm formation mechanism.

机构信息

Institute for Disease Control and Prevention, Heilongjiang Provincial Center for Disease Control and Prevention, Harbin, Heilongjiang Province, China.

Department of Infectious Diseases, Infectious Disease Hospital of Heilongjiang Province, Harbin, Heilongjiang Province, China.

出版信息

Bioengineered. 2021 Dec;12(2):10254-10263. doi: 10.1080/21655979.2021.1988251.

DOI:10.1080/21655979.2021.1988251
PMID:34637696
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8809914/
Abstract

This research was to explore antibiotic-induced drug resistance of and its biofilm formation mechanism. Kirby-Bauer (K-B) disk method recommended by Clinical and Laboratory Standards Institute (CLSI) was used to test drug sensitivity of Salmonella enteritidis to 16 kinds of antibiotics including ß-lactams, aminoglycosides, quinolones, sulfonamides, chloramphenicols, and tetracyclines. Polymerase chain reaction (PCR) was performed to detect carrying of drug resistance genes of 29 kinds of antibiotics including ß-lactams, aminoglycosides, quinolones, sulfonamides, chloramphenicols, and tetracyclines of . The expressions of esp, ebpA, ge1E, and fsrB genes in biofilm group and plankton group were detected when Salmonella was induced, and difference of gene expression was detected by FQ-PCR. The drug resistance rates of to nalidixic acid, ampicillin, streptomyces, and cefoperazone were high, which were 94.5%, 75%, 67%, and 52%, respectively. 94 strains of formed 22 kinds of drug resistance spectrum, the strains were generally resistant to 4-5 antibiotics, and some strains formed fixed drug resistance spectrum as follows: AMP-CFP-STR-NA-TE (22.6,21.7%), AMP-STR-NA-TE (17,16%), and AMP-CFP-STR-NA (11.1,10.6%). During biofilm formation, fsr can increase expression of ge1E and decrease expression of esp and ebpA. Consequently, was generally resistant to nalidixic acid, ampicillin, and streptomycin, and the multidrug resistance was severe. The drug resistance genes sul2, sul3, blaTEM-1-like, tet(A), and tet(G) were highly carried in . Esp, ebpA, ge1E, and fsrB genes were closely related to biofilm formation of .

摘要

本研究旨在探索肠炎沙门氏菌的抗生素诱导耐药性及其生物膜形成机制。采用临床和实验室标准协会(CLSI)推荐的 Kirby-Bauer(K-B)圆盘法检测肠炎沙门氏菌对包括β-内酰胺类、氨基糖苷类、喹诺酮类、磺胺类、氯霉素类和四环素类在内的 16 种抗生素的药敏性。聚合酶链反应(PCR)检测肠炎沙门氏菌携带的包括β-内酰胺类、氨基糖苷类、喹诺酮类、磺胺类、氯霉素类和四环素类在内的 29 种抗生素的耐药基因。当肠炎沙门氏菌被诱导形成生物膜时,检测生物膜组和浮游组中 esp、ebpA、ge1E 和 fsrB 基因的表达情况,并通过 FQ-PCR 检测基因表达差异。结果显示,肠炎沙门氏菌对萘啶酸、氨苄西林、链霉素和头孢哌酮的耐药率较高,分别为 94.5%、75%、67%和 52%。94 株肠炎沙门氏菌形成了 22 种耐药谱,这些菌株通常对 4-5 种抗生素耐药,有些菌株形成了固定的耐药谱,如 AMP-CFP-STR-NA-TE(22.6%,21.7%)、AMP-STR-NA-TE(17%,16%)和 AMP-CFP-STR-NA(11.1%,10.6%)。在生物膜形成过程中,fsr 可以增加 ge1E 的表达,降低 esp 和 ebpA 的表达。因此,肠炎沙门氏菌通常对萘啶酸、氨苄西林和链霉素耐药,且具有严重的多药耐药性。sul2、sul3、blaTEM-1-like、tet(A) 和 tet(G) 等耐药基因在肠炎沙门氏菌中携带率较高。Esp、ebpA、ge1E 和 fsrB 基因与肠炎沙门氏菌的生物膜形成密切相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/02efa908a98b/KBIE_A_1988251_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/86bfe505be0c/KBIE_A_1988251_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/c4523c669271/KBIE_A_1988251_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/7958262e55ee/KBIE_A_1988251_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/297ceb8d097d/KBIE_A_1988251_F0003a_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/a00afa25728f/KBIE_A_1988251_F0003b_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/279433280673/KBIE_A_1988251_F0003c_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/9df6eb9872fb/KBIE_A_1988251_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/46994b445863/KBIE_A_1988251_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/02efa908a98b/KBIE_A_1988251_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/86bfe505be0c/KBIE_A_1988251_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/c4523c669271/KBIE_A_1988251_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/7958262e55ee/KBIE_A_1988251_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/297ceb8d097d/KBIE_A_1988251_F0003a_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/a00afa25728f/KBIE_A_1988251_F0003b_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/279433280673/KBIE_A_1988251_F0003c_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/9df6eb9872fb/KBIE_A_1988251_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/46994b445863/KBIE_A_1988251_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d27/8809914/02efa908a98b/KBIE_A_1988251_F0006_OC.jpg

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