Gums John G, Boatwright D Wesston, Camblin Mark, Halstead Diane C, Jones Mark E, Sanderson Roger
Department of Pharmacy Practice, University of Florida, Gainesville, FL 32601, USA.
Ann Pharmacother. 2008 Jan;42(1):71-9. doi: 10.1345/aph.1H620. Epub 2007 Dec 19.
To review data to determine why pneumococcal isolates appear to be increasingly resistant to cefotaxime, historically regarded as having the same in vitro susceptibility to ceftriaxone, and what this observation might imply clinically.
Literature was accessed through MEDLINE (1966-October 2007) using the MeSH terms cefotaxime, ceftriaxone, susceptibility, microbial sensitivity tests, antibiotics, pneumococcal infections, Streptococcus pneumoniae, resistance, and cephalosporin resistance. Abstracts and surveillance databases were reviewed and unpublished data were provided by state departments of health and institutions.
All articles published in the English language that were identified from the data sources were evaluated.
An experimental model of pneumococcal infection in mice conducted 2 decades ago predicted that the delta T minimum inhibitory concentration (MIC) varied less for ceftriaxone than for cefotaxime. Studies of plasma and serum concentrations show that ceftriaxone remains at a concentration above the S. pneumoniae MIC for 100% of the dosing interval at 12 hours. Types of MIC susceptibility test methods for ceftriaxone and cefotaxime used against S. pneumoniae respiratory isolates were found to be similar. Data from state and county health departments found microbiological discrepancies between ceftriaxone and cefotaxime. In areas with high rates of penicillin-resistant S. pneumoniae (PRSP), isolates were twice as susceptible to ceftriaxone versus cefotaxime. Surveillance databases consistently show differences between susceptibility of S. pneumoniae to cefotaxime versus ceftriaxone over time. MIC and pulsed-field gel electrophoresis studies suggest that phenotypic discrepancies may account for penicillin resistance. Ongoing studies are examining S. pneumoniae isolates at the molecular level to determine the basis of difference in resistance to cefotaxime and ceftriaxone.
An increase in rates of PRSP and differences in S. pneumoniae isolate susceptibility between ceftriaxone and cefotaxime emphasize the necessity for hospital laboratories to detect these changes as they occur. Clinicians should select the most appropriate agent for patients with S. pneumoniae.
回顾相关数据，以确定肺炎球菌分离株为何似乎对头孢噻肟的耐药性日益增加（头孢噻肟在历史上被认为与头孢曲松具有相同的体外敏感性），以及这一观察结果在临床上可能意味着什么。
通过MEDLINE（1966年 - 2007年10月）检索文献，使用的医学主题词有头孢噻肟、头孢曲松、敏感性、微生物敏感性试验、抗生素、肺炎球菌感染、肺炎链球菌、耐药性和头孢菌素耐药性。对摘要和监测数据库进行了审查，并由各州卫生部门和机构提供了未发表的数据。
对从数据来源中识别出的所有英文发表文章进行评估。
20年前进行的小鼠肺炎球菌感染实验模型预测，头孢曲松的ΔT最低抑菌浓度（MIC）变化比头孢噻肟小。血浆和血清浓度研究表明，头孢曲松在12小时的给药间隔内100%的时间保持在高于肺炎链球菌MIC的浓度。针对肺炎链球菌呼吸道分离株使用的头孢曲松和头孢噻肟的MIC敏感性试验方法类型相似。来自州和县级卫生部门的数据发现头孢曲松和头孢噻肟之间存在微生物学差异。在青霉素耐药肺炎链球菌（PRSP）发生率高的地区，分离株对头孢曲松的敏感性是头孢噻肟的两倍。监测数据库始终显示肺炎链球菌对头孢噻肟和头孢曲松的敏感性随时间存在差异。MIC和脉冲场凝胶电泳研究表明，表型差异可能是青霉素耐药的原因。正在进行的研究正在分子水平上检查肺炎链球菌分离株，以确定对头孢噻肟和头孢曲松耐药性差异的基础。
PRSP发生率的增加以及肺炎链球菌分离株对头孢曲松和头孢噻肟敏感性的差异强调了医院实验室在这些变化发生时进行检测的必要性。临床医生应为肺炎链球菌感染患者选择最合适的药物。
