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科学家为加强血管植入物感染的检测与治疗铺平了道路
翻译：周超群 审核：陈志锦 （SIFIC热点团队）
心血管疾病的上升和流行，导致了血管植入物等医疗植入物使用的显著增长。不幸的是，植入物装置使用的增加伴随着更多的装置相关感染，以及严重的并发症，甚至死亡！《美国病理学杂志》的一项研究报告了植入物感染的有害后遗症，包括可以保护细菌并作为复发性感染源的生物膜的形成。这项新研究有望使研究人员未来开发出更好的诊断和管理血管植入物感染策略成为可能。
德国耶拿大学医院医学微生物学研究所所长，兼首席研究员BettinaLöffler博士说道：“金黄色葡萄球菌是引起植入物感染的主要原因之一，因为它容易粘附到植入装置的表面并形成厚厚的生物膜，而生物膜可以保护细菌免受患者免疫应答或抗生素治疗的杀灭。但是这些生物膜难以检测，因为它们一般不伴随临床症状。目前，对这些感染没有有效的治疗策略。生物膜需要抗生素浓度高达正常值1000倍时方能起效，如此高浓度在临床上是不可行的。了解血管植入物上生物膜形成的潜在发病机理具有非常重要的，以便可以找到快速有效的治疗方法，而不必求助于如手术切除等侵入性操作。”
研究人员开发了一种新型小鼠模型，更真实地模拟出人体状况。将导管放置在右颈动脉内，在导管插入7天后将细菌引入尾静脉，细菌经由血流到达导管。Löffler解释说：“使用该模型，正如在人体中一样，细菌需要克服血流的应力、血流引起的剪应力和宿主的免疫系统，才能在导管上形成生物膜感染。”通过在小鼠中建立这种新型模型，研究人员看到了大量使用小鼠进行基因操作的可能性，这将容许对疾病的诸多不同方面加以研究，以鉴别出更好和更可靠的血管植入物感染治疗和检测的策略。
研究中一个有趣的发现是，尽管所有测试的金黄色葡萄球菌菌株不一定都能在细胞培养物中形成高生物膜水平，但它们在体内都形成了生物膜。这一发现证明，体内血管植入物的定植是所有金黄色葡萄球菌感染的一般特征，并且这些细菌高度适应于它们的环境。
使用PET成像，在血管植入物感染期间，研究者在导管部位发现高水平的炎症。MR成像显示，由于感染后生物膜形成，通过导管时血液流速会减少。
Löffler说：“我们的模型考虑了受感染植入物的发病机理的所有步骤，并且最大限度代表了临床情况。它为微生物学和免疫学实验提供了一个坚实的平台，可以为这些毁灭性感染发病机制以及诊断与治疗提供重要的洞悉。”
资料来源：Elsevier Health Sciences
原文：Scientists Pave the Way for Enhanced Detection and Treatment of Vascular Graft Infections
A rising prevalence of cardiovascular disease has generated substantial growth in the use of medical implants, such as vascular grafts. Unfortunately, the increased use of implanted devices has been accompanied by more device-associated infections, serious complications, and death. A study in The American Journal of Pathology reports the detrimental aftereffects of infected grafts, including the formation of biofilms that can shelter bacteria and function as a source of recurrent infection. This new research should enable researchers to develop better strategies to diagnose and manage vascular graft infections.
"Staphylococcus aureus (S. aureus) is one of the leading causes of infected grafts because it readily adheres to the surface of the implanted device and forms thick biofilm layers. Biofilms can shelter bacteria from the patient's immune responses or antibiotic treatment. These biofilm layers are difficult to detect because they are often unaccompanied by clinical symptoms," noted lead investigator Bettina Löffler, MD, director of the Institute of Medical Microbiology, Jena University Hospital in Germany. "Currently, there are no effective treatment strategies against these infections. Biofilms require antibiotic concentrations up to 1000 times higher than normal and these concentrations are not clinically feasible. It is of great importance to understand the underlying pathogenesis of biofilm formation on vascular grafts in order to find quick and effective treatment possibilities without having to resort to invasive procedures such as surgical removal."
The researchers developed a new mouse model that more closely mimics the human condition. The catheter is placed within a blood vessel (the right carotid artery) and bacteria reach the catheter via the blood stream (bacteria are introduced into tail veins seven days after the catheter is inserted). "Just as in humans, with this model the bacteria need to overcome the stress of the blood flow, the shear stress induced by the blood flow, and the host's immune system to form a biofilm infection on the catheter," explained Löffler. By establishing this novel model in mice investigators opened up the possibility to use the vast array of genetically manipulated mice available, which will allow the study of many different aspects of the disease and identification of better and more reliable treatment and detection strategies for vascular graft infections.
An interesting finding of the study was that all S. aureus strains tested formed biofilms in vivo, regardless of whether they formed high biofilm levels in cell culture. This finding demonstrates that colonization of vascular grafts in vivo is a general characteristic of all S. aureus infections and that these bacteria are highly adaptive to their environment.
Using PET imaging, the investigators discovered a high level of inflammation at the site of the catheter during vascular graft infections. MR imaging revealed that blood flow velocity was decreased through the catheter due to infection and biofilm formation.
"Our model takes all steps of the pathogenesis of infected implants into account and closely represents the clinical situation," said Löffler. "It provides a solid platform for microbiological and immunological experiments that could provide crucial insights into the pathogenesis as well as the diagnosis and treatment of these devastating infections."
Source: Elsevier Health Sciences
图文编辑：宋小船 审稿：卢先雷 陈文森
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