Pathogenesis of Relapsing Fever

Abstract

Relapsing fever (RF) is caused by several species of Borrelia; all, except two species, are transmitted to humans by soft (argasid) ticks. The species B. recurrentis is transmitted from one human to another by the body louse, while B. miyamotoi is vectored by hard-bodied ixodid tick species. RF Borrelia have several pathogenic features that facilitate invasion and dissemination in the infected host. In this article we discuss the dynamics of vector acquisition and subsequent transmission of RF Borrelia to their vertebrate hosts. We also review taxonomic challenges for RF Borrelia as new species have been isolated throughout the globe. Moreover, aspects of pathogenesis including symptomology, neurotropism, erythrocyte and platelet adhesion are discussed. We expound on RF Borrelia evasion strategies for innate and adaptive immunity, focusing on the most fundamental pathogenetic attributes, multiphasic antigenic variation. Lastly, we review new and emerging species of RF Borrelia and discuss future directions for this global disease.The definite cause of RF was not established until 1868 when the German scientist Otto Obermeier caister.com/cimb 519 Curr.

Borrelia miyamotoi FbpA and FbpB Are Immunomodulatory Outer Surface Lipoproteins With Distinct Structures and Functions

“…In the United States, tick-borne relapsing fever (TBRF) is caused by the spirochetes Borrelia hermsii and Borrelia turicatae. Whereas these spirochetes are vectored by the soft tick of the Ornithodoros genus, a related TBRF pathogen, Borrelia miyamotoi, is transmitted by ixodid ticks that also vector the agent of Lyme disease (LD), Borreliella burgdorferi (1)(2)(3)(4)(5)(6). A recent study suggests that B. miyamotoi is more widespread in some areas of the U.S. than previously recognized (7).…”

“…Although BMD-, TBRF-, and LD-causing spirochetes are ticktransmitted, their lifestyles within vertebrate hosts differ (10,11). In the context of vertebrate infection, LD Borreliella are thought to survive within the skin and briefly in the bloodstream as a means to disseminate to deeper distal tissues (12)(13)(14), while TBRF and BMD Borrelia predominantly exist in host blood, indicating a heightened need to evade both soluble and cellular blood-borne immune components (1,15).…”

CD55 Facilitates Immune Evasion by Borrelia crocidurae, an Agent of Relapsing Fever

“…To delineate the role of CD55 in B. crocidurae pathogenesis, studies can focus on identifying interacting ligand(s) on the B. crocidurae or B. persica surface. Our results also suggest that relapsing fever species can be further divided into CD55 binding and nonbinding species, and studies can explore whether CD55 binding is related to multiphasic antigenic variation ( 20 ).…”

Identifying platelet-derived factors as amplifiers ofB. burgdorferi-induced cytokine production

“…So far, only few studies have studied the role of platelets in B. burgdorferi infection, and there are some reports concerning platelets in the pathogenesis of relapsing fever by Borrelia recurrentis [ 64 , 65 ]. It has been hypothesized that B. burgdorferi -induced vascular damage [ 66 , 67 ] is followed by platelet activation and aggregation, leading to binding of B. burgdorferi to platelets, mediated by integrin α IIb β 3 , yet only if these platelets have been previously activated [ 68–70 ].…”