総説 Clostridium Difficile 感染症

Clostridium difficile infection.
Leffler DA, Lamont JT.
N Engl J Med. 2015 Apr 16;372(16):1539-48. doi: 10.1056/NEJMra1403772.


Clostridium difficile is an anaerobic gram-positive, spore-forming, toxin-producing bacillus that is transmitted among humans through the fecal–oral route. The relationship between the bacillus and humans was once thought to be commensal,1 but C. difficile has emerged as a major enteric pathogen with worldwide distribution. In the United States, C. difficile is the most frequently reported nosocomial pathogen. A surveillance study in 2011 identified 453,000 cases of C. difficile infection and 29,000 deaths associated with C. difficile infection; approximately a quarter of those infections were community-acquired.2 Nosocomial C. difficile infection more than quadruples the cost of hospitalizations,3 increasing annual expenditures by approximately $1.5 billion in the United States.4 In this article, we review the changing epidemiology of this infection, discuss risk factors and preventive strategies, outline current recommendations for treatment, and highlight developing strategies for disease control.







Figure 3. Rates of Cure and Changes to the Microbiota after Fecal Microbial Transplantation for Recurrent Clostridium difficile Infection.
Among patients with recurrent C. difficile infection, the rate of cure without relapse was higher among those who received an infusion of donor feces than among those who received vancomycin with or without bowel lavage (Panel A). Fecal microbial diversity in recipients before and after the infusion of donor feces is compared with the diversity in healthy donors (Panel B). Microbial diversity is expressed by Simpson’s Reciprocal Index. The index ranges from 1 to 250, with higher values indicating more diversity. The box- and-whisker plots indicate interquartile ranges (boxes), medians (dark hori- zontal lines in the boxes), and highest and lowest values (whiskers above and below the boxes).
van Nood E, Vrieze A, Nieuwdorp M, et al. Duodenal infusion of donor feces for recurrent Clostridium difficile. N Engl J Med 2013;368:407-15.

文献 腹腔内膿瘍 外科的ドレナージ vs 経皮的ドレナージ

Am Surg 2011 Jul;77(7):862-7.

Differences in morbidity and mortality with percutaneous versus open surgical drainage of postoperative intra-abdominal infections: a review of 686 cases.
Politano AD, Hranjec T, Rosenberger LH, Sawyer RG, Tache Leon CA.

Abstract
Intra-abdominal infections following surgical procedures result from organ-space surgical site infections, visceral perforations, or anastomotic leaks. We hypothesized that open surgical drainage is associated with increased patient morbidity and mortality compared with percutaneous drainage. A single-institution, prospectively collected database over a 13-year period revealed 2776 intra-abdominal infections, 686 of which required an intervention after the index operation. Percutaneous procedures (simple aspiration or catheter placement) were compared with all other open procedures by univariate and multivariate analyses. Analysis revealed 327 infections in 240 patients undergoing open surgical drainage and 359 infections in 260 patients receiving percutaneous drainage. Those undergoing open drainage had significantly higher Acute Physiology Score (APS) and Acute Physiology and Chronic Health Evaluation (APACHE) II scores and were more likely to be immunosuppressed, require intensive care unit treatment, and have longer hospital stays. Mortality was higher in the open group: 14.6 versus 4.2 per cent (P = 0.0001). Variables independently associated with death by multivariate analysis were APACHE II, dialysis, intensive care unit (ICU) care, age, immunosuppression, and drainage method. Open intervention for postsurgical intra-abdominal infections is associated with increased mortality compared with percutaneous drainage even after controlling for severity of illness by multivariate analysis. Although some patients are not candidates for percutaneous drainage, it should be considered the preferential treatment in eligible patients.

松田講演付記 LRSA：リネゾリド耐性MRSA JAMA 2010;303:2260-2264

Linezolid resistance is extremely uncommon in Staphylococcus aureus.

Objective: To report an outbreak with linezolid and methicillin-resistant S aureus (LRSA) in an intensive care department and the effective control measures taken.

Design, Setting, and Patients: Outbreak study of consecutive critically ill patients colonized and/or infected with LRSA at an intensive care department of a 1000-bed tertiary care university teaching hospital in Madrid, Spain. Patients were placed under strict contact isolation. Daily updates of outbreak data and recommendations for the use of linezolid were issued. Extensive environmental sampling and screening of the hands of health care workers were performed.

Main Outcome Measures: Linezolid use and clinical and epidemiological characteristics and outcomes using minimal inhibitory concentrations, pulsed-field gel electrophoresis, and polymerase chain reaction of LRSA isolates.

Results: Between April 13 and June 26, 2008, 12 patients with LRSA were identified. In 6 patients, LRSA caused ventilator-associated pneumonia and in 3 patients it caused bacteremia. Isolates were susceptible to trimethoprim-sulfamethoxazole, glycopeptides, tigecycline, and daptomycin. Genotyping identified 1 predominant clone and 3 other types. Cfr-mediated linezolid resistance was demonstrated in all isolates. Potential hospital staff carriers and environmental samples were negative except for one. Six patients died, 5 of them in the intensive care unit, with 1 death attributed to LRSA infection. Linezolid use decreased from 202 defined daily doses in April 2008 to 25 defined daily doses in July 2008. Between July 2008 and April 2010, no new cases have been identified in the weekly surveillance cultures or diagnostic samples.

Conclusions: The first clinical outbreak, to our knowledge, with LRSA mediated by the cfr gene developed at our center, was associated with nosocomial transmission and extensive usage of linezolid. Reduction of linezolid use and infection-control measures were associated with the termination of the outbreak.

現在知られているMRSAがリネゾリドに耐性を獲得する機序は以下の２つです。
1. cfr遺伝子の獲得
2. 23S rRNAのpoint mutation: G2576Tなど
通常，リネゾリドのMRSAに対するMICは1 μg/dLあるいは2 μg/dLです。

キーボードから院内感染を拡大の可能性

米シカゴのノースウェスタン・メモリアル病院は10日,人体に有害な多くの細菌がコンピューターのキーボードの上で24時間以上生存するとの研究結果をまとめた。病院でのハイテク投資が加速するなかで，感染症増悪の脅威となる可能性が増すとしている。研究報告は，素手であればキーボード上の細菌に汚染された医師や看護士の手を通じて，患者が細菌に感染する可能性があると説明する。この病院で疫学を担当するゲリー・ノースキン医師は，「病院で電子カルテを導入する傾向がみられるようになっており，全病室にコンピューターを設置する病院も出てきている」と述べた。ノースキン医師は、感染を予防する最良の方法は，まめに手洗いを行うこととしている。
（ロイター） - 4月11日15時10分

（コメント）病院には実に汚いkeyboardがたくさんころがっている。あまりに汚いので僕は良く酒精綿で拭いてあげている。まず，僕の当直はtebleをアルコール綿で拭くところから始まる。しかし，以前行ったkeyboard面の環境培養検査ではMRSAや緑膿菌が検出されたことはない。