阿摩線上測驗
3.腸內菌科細菌對下列何種藥物通常具有內生抗藥性（intrinsic resistance）？
(A)streptomycin
(B)vancomycin
(C)sulfonamides
(D)chloramphenicol
統計： A(202), B(2020), C(105), D(102), E(0) #2626638
詳解 (共 4 筆)
| 菌種 | 內生抗藥性抗生素 | 機轉 |
| G+菌 | 1. Aztreonam 2. Polymyxin (B/E) 3. Quinolone類(Nalidixic acid、Fluoroquinolone) | 1.對PBP-3 (G-菌常見)以外的PBP親和力不佳[1] 2.缺乏G-菌外膜成分(lipopolysaccharide)無法作用[2] 3.G+菌的plasmid普遍都有efflux pumps基因可以排出此類藥物[3] |
| G-菌 | 1. glycopeptides類(Vancomycin、Teicoplanin) 2. Daptomycin | 1.極性分子無法穿透G-菌的脂雙層外膜[4] 2. G-菌的細胞膜上帶負電的phospholipid比例較低，Daptomycin無法造成足夠膜電位干擾[5] |
| 厭氧菌 | 1. β-lactam類 2. Quinolone類 3. Aminoglycoside類 | 1.厭氧菌多數都會產生β-lactamase、單一菌種PBP種類多、藥物通透力不佳[6] 2.厭氧菌的DNA gyrase和topoisomerase IV突變機率高、有efflux pumps排出藥物[7] 3.需氧主動運輸才能進入細菌內[8] |
| Enterococcus faecalis、Enterococcus faecium | 1. β-lactam類 2. Trimethoprim / Sulfamethoxazole (SXT) 3. Aminoglycoside類 4. Macrolide類(Lincosamide、Streptogarmin) | 1. PBP種類多與β-lactam親和度不佳、產生β-lactamase[9] 2.利用環境中的葉酸代替(但in vitro常有false susceptibility)[9] 3.藥物通透力差、內源性酵素將藥物的hydroxyl group或amino group的氫鍵轉換成共價鍵改變構形[9] 4.efflux pumps排出藥物[9] |
| Listeria monocytogenes | Cephalosporins | 與PBP-2a以外的PBP親和力不佳、efflux pumps排出藥物[10] |
| Escherichia coli | Macrolide類(Lincosamide、Streptogarmin) | erm基因產物造成rRNA的構形改變(甲基化)、產生β-lactamase (ESBLs)、efflux pumps排出藥物[11] |
| Klebsiella屬、Enterobacter屬、Proteus屬 | β-lactam類 | 產生β-lactamase (ESBLs、KPC)[12] |
| Pseudomonas aeruginosa | 1. β-lactam類 2. Trimethoprim / Sulfamethoxazole (SXT) 3.Tetracycline | 藥物通透力不佳、efflux pumps排出藥物、產生β-lactamase[13] |
| Stenotrophomonas maltophilia | 1. β-lactam類 2. Quinolone類 3. Aminoglycoside類 | 1.產生β-lactamase (Metallo-β-lactamase (MBL)) 2. DNA gyrase和topoisomerase IV突變率上升 3.產生aminoglycoside N6'-acetyltransferase分解藥物[14][15][16] |
| Acinetobacter屬 | β-lactam類 | 產生β-lactamase、efflux pumps排出藥物[17] |
參考資料
[1]Rittenbury M. S. (1990). How and why aztreonam works. Surgery, gynecology & obstetrics, 171 Suppl, 19–23.
[2]Vestergaard, M., Nøhr-Meldgaard, K., Bojer, M. S., Krogsgård Nielsen, C., Meyer, R. L., Slavetinsky, C., Peschel, A., & Ingmer, H. (2017). Inhibition of the ATP Synthase Eliminates the Intrinsic Resistance of Staphylococcus aureus towards Polymyxins. mBio, 8(5), e01114-17. https://doi.org/10.1128/mBio.01114-17
[3]Reygaert W. C. (2018). An overview of the antimicrobial resistance mechanisms of bacteria. AIMS microbiology, 4(3), 482–501. https://doi.org/10.3934/microbiol.2018.3.482
[4]Yarlagadda, V., Manjunath, G. B., Sarkar, P., Akkapeddi, P., Paramanandham, K., Shome, B. R., Ravikumar, R., & Haldar, J. (2016). Glycopeptide Antibiotic To Overcome the Intrinsic Resistance of Gram-Negative Bacteria. ACS infectious diseases, 2(2), 132–139. https://doi.org/10.1021/acsinfecdis.5b00114
[5]Randall, C. P., Mariner, K. R., Chopra, I., & O'Neill, A. J. (2013). The target of daptomycin is absent from Escherichia coli and other gram-negative pathogens. Antimicrobial agents and chemotherapy, 57(1), 637–639. https://doi.org/10.1128/AAC.02005-12
[6]Rasmussen, B. A., Bush, K., & Tally, F. P. (1997). Antimicrobial resistance in anaerobes. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 24 Suppl 1, S110–S120. https://doi.org/10.1093/clinids/24.supplement_1.s110
[7]Hecht D. W. (2004). Prevalence of antibiotic resistance in anaerobic bacteria: worrisome developments. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 39(1), 92–97. https://doi.org/10.1086/421558
[8]Kong, J., Wu, Z. X., Wei, L., Chen, Z. S., & Yoganathan, S. (2020). Exploration of Antibiotic Activity of Aminoglycosides, in Particular Ribostamycin Alone and in Combination With Ethylenediaminetetraacetic Acid Against Pathogenic Bacteria. Frontiers in microbiology, 11, 1718. https://doi.org/10.3389/fmicb.2020.01718
[9]Miller, W. R., Munita, J. M., & Arias, C. A. (2014). Mechanisms of antibiotic resistance in enterococci. Expert review of anti-infective therapy, 12(10), 1221–1236. https://doi.org/10.1586/14787210.2014.956092
[10]Krawczyk-Balska, A. and Markiewicz, Z. (2016), The intrinsic cephalosporin resistome of Listeria monocytogenes in the context of stress response, gene regulation, pathogenesis and therapeutics. J Appl Microbiol, 120: 251-265. https://doi.org/10.1111/jam.12989
[11]Alekshun, M. N., & Levy, S. B. (2007). Molecular mechanisms of antibacterial multidrug resistance. Cell, 128(6), 1037–1050. https://doi.org/10.1016/j.cell.2007.03.004
[12]Okamoto, K., Gotoh, N., & Nishino, T. (2001). Pseudomonas aeruginosa reveals high intrinsic resistance to penem antibiotics: penem resistance mechanisms and their interplay. Antimicrobial agents and chemotherapy, 45(7), 1964–1971. https://doi.org/10.1128/AAC.45.7.1964-1971.2001
[13]Mohanty, S., Baliyarsingh, B., & Nayak, S. K. (2020). Antimicrobial Resistance in Pseudomonas aeruginosa: A Concise Review. In M. Mareș, S. H. E. Lim, K. Lai, & R. Cristina (Eds.), Antimicrobial Resistance - A One Health Perspective. IntechOpen. https://doi.org/10.5772/intechopen.88706
[14]Çıkman, A., Parlak, M., Bayram, Y., Güdücüoğlu, H., & Berktaş, M. (2016). Antibiotics resistance of Stenotrophomonas maltophilia strains isolated from various clinical specimens. African health sciences, 16(1), 149–152. https://doi.org/10.4314/ahs.v16i1.20
[15]Valdezate, S., Vindel, A., Loza, E., Baquero, F., & Cantón, R. (2001). Antimicrobial susceptibilities of unique Stenotrophomonas maltophilia clinical strains. Antimicrobial agents and chemotherapy, 45(5), 1581–1584. https://doi.org/10.1128/AAC.45.5.1581-1584.2001
[16]Jia, W., Wang, J., Xu, H., & Li, G. (2015). Resistance of Stenotrophomonas maltophilia to Fluoroquinolones: Prevalence in a University Hospital and Possible Mechanisms. International journal of environmental research and public health, 12(5), 5177–5195. https://doi.org/10.3390/ijerph120505177
[17]Lin, M. F., & Lan, C. Y. (2014). Antimicrobial resistance in Acinetobacter baumannii: From bench to bedside. World journal of clinical cases, 2(12), 787–814. https://doi.org/10.12998/wjcc.v2.i12.787
