Lyme disease Borrelia are obligately parasitic, tick- transmitted, invasive, persistent bacterial pathogens that cause disease in humans and non-reservoir vertebrates primarily through the induction of inflammation. During transmission from the infected tick, the bacteria undergo significant changes in gene expression, resulting in adaptation to the mammalian environment. The organisms multiply and spread locally and induce inflammatory responses that, in humans, result in clinical signs and symptoms. Borrelia virulence involves a multiplicity of mechanisms for dissemination and colonization of multiple tissues and evasion of host immune responses. Most of the tissue damage, which is seen in non-reservoir hosts, appears to result from host inflammatory reactions, despite the low numbers of bacteria in affected sites. This host response to the Lyme disease Borrelia can cause neurologic, cardiovascular, arthritic, and dermatologic manifestations during the disseminated and persistent stages of infection. The mechanisms by which a paucity of organisms (in comparison to many other infectious diseases) can cause varied and in some cases profound inflammation and symptoms remains mysterious but are the subjects of diverse ongoing investigations. In this review, we provide an overview of virulence mechanisms and determinants for which roles have been demonstrated in vivo, primarily in mouse models of infection.

中文翻译：

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莱姆病发病机制。

莱姆病疏螺旋体是专性寄生的、蜱传播的、侵入性的、持续存在的细菌病原体，主要通过诱导炎症在人类和非储层脊椎动物中引起疾病​​。在从受感染的蜱传播过程中，细菌的基因表达发生显着变化，从而适应哺乳动物环境。这些生物体在局部繁殖和传播，并诱导炎症反应，在人类中导致临床症状和体征。疏螺旋体毒力涉及多个组织的传播和定植以及逃避宿主免疫反应的多种机制。尽管受影响部位的细菌数量很少，但在非储库宿主中看到的大多数组织损伤似乎是由宿主炎症反应引起的。这种宿主对莱姆病疏螺旋体的反应在感染的传播和持续阶段，可引起神经系统、心血管系统、关节炎和皮肤病学表现。缺乏生物体（与许多其他传染病相比）可能导致各种甚至在某些情况下严重的炎症和症状的机制仍然是神秘的，但却是各种正在进行的研究的主题。在这篇综述中，我们概述了毒力机制和决定因素，其作用已在体内得到证实，主要是在小鼠感染模型中。