征集弹药和作战方案：8月8日兰州辩论赛，胡必杰 vs 陈佰义

icchina

由中华医学会、中华医学会微生物学与免疫学分会主办,中华医学会微生物与免疫学分会临床微生物学组协办的“中华医学会第十二次全国临床微生物学术年会”,定于2015年8月日在甘肃省兰州市召开。
大会组委会给俺安排了一场辩论：
2015年8月8日10：00-11：00，在会场的二号楼一层多功能厅，
主题是：重症感染起始经验性抗感染治疗
正方：需要广覆盖
反方：不需要广覆盖

俺很喜欢这个辩题。所以参加辩论不是问题，问题是对手是大名鼎鼎的陈佰义教授！
需要认真准备了，比如辩论策略、我方的各种论点、支持证据、对方的可能论点和反驳我方的证据等等。
闪念间，想到了SIFIC大本营。特发帖紧急请求大家援助
请为我方提供各种弹药，并为作战方案制定提出意见和建议。谢谢啦！

icchina

几年前，全国感控年会，举办过几场辩论赛。效果不错...

2012年济南年会将再次推出“感控辩论专场”，议题正在酝酿中...
https://bbs.sific.com.cn/forum.ph ... hlight=%B1%E7%C2%DB

鬼才

刚看到这一贴子，因时间紧，来不急翻译文献了，现将《哈里森内科学》2015年第19版，有关细菌感染治疗的原文片段复制在这里，今后有时间再翻译，请理解。
Antimicrobial agents have had a major impact on human health. Together with vaccines, they have contributed to reduced mortality, extended lifespan, and enhanced quality of life. Among drugs used in human medicine, however, they are distinctive in that their use promotes the occurrence of drug resistance in the pathogens they are designed to treat as well as in other “bystander” organisms. Indeed, the history of antimicrobial development has been driven in large part by the medical need engendered by the emergence of resistance to each generation of agents. Thus, the careful and appropriate use of antimicrobial drugs is particularly important not only for optimizing efficacy and minimizing adverse effects but also for minimizing the risk of resistance and preserving the value of existing agents. Although this chapter focuses on antibacterial agents, the optimal use of all antimicrobials depends on an understanding of each drug’s mechanism of action, spectrum of activity, mechanisms of resistance, pharmacology, and adverse effect profile. This information is then applied in the context of the patient’s clinical presentation, underlying conditions, and epidemiology to define the site and likely nature of the infection or other condition and thus to choose the best therapy. Gathering of microbiologic information is important for refining therapeutic choices on the basis of documented pathogen and susceptibility data whenever possible; this information also makes it possible to choose more targeted therapy, thereby reducing the risk of selection of resistant bacteria. Durations of therapy are chosen according to the nature of the infection and the patient’s response to treatment and are informed by clinical studies when they are available, with the understanding that shorter courses are less likely than longer ones to promote the emergence of resistance. This chapter provides specific information that is necessary for making informed choices among antibacterial agents.

鬼才

MECHANISMS OF ACTION AND RESISTANCE
MECHANISMS OF ACTION
Multiple essential components of bacterial cell structures and metabolism have been the targets of antibacterial agents used in clinical medicine, and the interaction of an agent with its target results in either inhibition of bacterial growth and replication (bacteriostatic effect) or bacterial killing (bactericidal effect). In general, targets have been chosen because they either do not exist in mammalian cells and physiology or are sufficiently different from their bacterial counterparts to allow selective bacterial targeting. Treatment with bacteriostatic agents is effective when the patient’s host defenses are sufficient to contribute to eradication of the infecting pathogen. In patients with impaired host defenses (e.g., neutropenia) or infections at body sites with impaired or limited host defenses (e.g., meningitis and endocarditis), bactericidal agents are generally preferred.

鬼才

Inhibition of Cell Wall Synthesis   The bacterial cell wall, which is external to the cytoplasmic membrane and has no counterpart in mammalian cells, protects bacterial cells from lysis under low osmotic conditions. The cell wall is a cross-linked peptidoglycan composed of a polymer of
alternating units of N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM), four-amino-acid stem peptides linked to each NAM, and a peptide cross-bridge that links adjacent stem peptides to form a netlike structure. Several steps in peptidoglycan synthesis are targets of antibacterial agents. Inhibition of cell wall synthesis generally results in a bactericidal effect that is linked to cell lysis. This effect results not only from the blocking of new cell-wall formation but from the uninhibited action of cell wall–remodeling enzymes called autolysins,
which cleave peptidoglycan as part of normal cell-wall growth.
In gram-positive bacteria the peptidoglycan is the most external cell structure, but in gram-negative bacteria an asymmetric lipid outer membrane is external to the peptidoglycan and contains diffusion channels called porins. The space between the cytoplasmic membrane peptidoglycan and the outer membrane is referred to as the periplasmic space. Most antibacterial drugs enter the gram-negative bacterial cell through a porin channel, since the outer membrane is a major diffusion barrier. Although the peptidoglycan layer is thicker in gram-positive (20–80 nm) than in gram-negative (1 nm) bacteria, peptidoglycan itself constitutes only a limited diffusion barrier for antibacterial agents.

鬼才

β-LACTAMS The β-lactam drugs, including penicillins, cephalosporins, monobactams, and carbapenems, target transpeptidase enzymes (also called penicillin-binding proteins, or PBPs) involved in the stempeptide cross-linking step.
GLYCOPEPTIDES The glycopeptides, including vancomycin, teicoplanin, telavancin, dalbavancin, and oritavancin, bind the two terminal d-alanine residues of the stem peptide, hindering the glycosyltransferase involved in polymerizing NAG–NAM units. Telavancin also binds to the lipid II intermediate that delivers cell-wall precursor subunits. Likewise, dalbavancin and oritavancin interact with the cell membrane, and oritavancin may also inhibit transpeptidases. Both β-lactams and glycopeptides interact with their targets external to the cytoplasmic membrane.
BACITRACIN (TOPICAL) AND FOSFOMYCIN These agents interrupt enzymatic steps in the production of peptidoglycan precursors in the cytoplasm.
未完，明天继续，先休息了。

xiesq999

这是一场真正的精英辩论赛,一定非常精彩!!!

王淑颖_Pz11C

前提是重症感染，起始，经验性。要是没有这个前提是比较困难的。在重症感染的起始进行经验性广覆盖，是基于目标人群，基于对病原学可能的判断来进行广覆盖。我们所掌握的专家共识、指南、系统性感染的病原谱、病原菌的流行病学、药物的PK/PD等知识都提供给了我们对于目标患者经验性治疗的科学依据，在重症感染患者的抢救治疗、起始治疗，进行经验性的广覆盖，尽最大可能挽救患者生命，是科学的。（最好有些重症感染广覆盖后预后改善的数据）

王淑颖_Pz11C

在患者病情改善后可以科学降阶梯治疗；在目标病原菌明确后可以科学的目标性治疗。这个广覆盖和精准治疗是统一的，一致的。
强强辩论一定很精彩！期待。

鬼才

Inhibition of Protein Synthesis  Most inhibitors of bacterial protein synthesis target bacterial ribosomes, whose difference from eukaryotic ribosomes allows selective antibacterial action. Some inhibitors bind to the 30S ribosomal subunit and others to the 50S subunit. Most protein synthesis–inhibiting agents are bacteriostatic; aminoglycosides are an exception and are bactericidal.

lzxfbylly

没能到现场的，有视频可看吗？

四叶草

作为正反，胡教授这边还是占优势的。因为无论是教科书、指南等都建议重症患者首选经验性广覆盖治疗，等病原菌出来后或病情稳定后再降阶梯治疗。教科书或共识是基于循证医学基础的，因此，只需在辩论中牢牢抓住这些既定的公认的观点，以不变应万变！  班门弄斧了！这是一场真正的巅峰对决，很遗憾不能亲临现场!预祝辩论赛圆满成功！

芳草心

巅峰对决,
强强辩赛。
千里挑一，
万分精彩。
胡大教授，
凯旋归来！
现场视频，
能否公开？
论坛回放，
官微暴晒。
家里家外，
开开眼界！

二进制

在细菌室原始标本涂片镜检配合下，甄别革兰氏阴性、或者阳性菌为该标本采集当时、为病灶来源感染致病菌，分别应对阴性、或者阳性菌首选经验性广覆盖治疗，似战士冲锋前火力全面猛攻。谢谢！

明玥

有否视频播出共大家一览“大家”风范？

缭绕

这个辩题是抽签还是自己选的？胡教授占绝对优势啊！
我们倒要为陈教授捏把汗，明显压倒一切的优势啊！
可能王辉教授的用意是想要唤起大家对目标治疗的重视。
我们可以想象下陈教授可能会抛出什么样的武器，毕竟是顶尖大牌！
重症=重症感染吗？
重症=合并有阳性菌、阴性菌、真菌吗？
重症，没有严重的基础疾病吗？
不采用全面覆盖，使用目标治疗，卫生经济学的证据？

福娃宝贝

现场视频能否公开？非常喜欢胡教授和陈教授的课，期待......