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Abstract
Borrelia burgdorferi is the etiological agent of Lyme disease, a multisystemic, multistage, inflammatory infection resulting in patients experiencing cardiac, neurological, and arthritic complications when not treated with antibiotics shortly after exposure. The spirochetal bacterium transmits through the Ixodes vector colonizing the dermis of a mammalian host prior to hematogenous dissemination and invasion of distal tissues all the while combating the immune response as it traverses through its pathogenic lifecycle. The innate immune response controls the borrelial burden in the dermis, but is unable to clear the infection and thereby prevent progression of disease. Dissemination in the mammalian host requires temporal regulation of virulence determinants to allow for vascular interactions, invasion, and colonization of distal tissues. Virulence determinants and/or adhesins are highly heterogenetic among environmental B. burgdorferi strains with particular genotypes being associated with the ability to disseminate to specific tissues and the severity of disease, but fail to generate cross-protective immunity between borrelial strains. The unique motility of B. burgdorferi rendered by the endoflagella serves a vital function for dissemination and protection from immune recognition. Progress has been made toward understanding the chemotactic regulation coordinating the activity of the two polar localized flagellar motors and their role in borrelial virulence, but this regulation is not yet fully understood. Distinct states of motility allow for dynamic interactions between several B. burgdorferi adhesins and host targets that play roles in transendothelial migration. Transmigration across endothelial and blood–brain barriers allows for the invasion of tissues and elicits localized immune responses. The invasive nature of B. burgdorferi is lacking in proactive mechanisms to modulate disease, such as secretion systems and toxins, but recent work has shown degradation of host extracellular matrices by B. burgdorferi contributes to the invasive capabilities of the pathogen. Additionally, B. burgdorferi may use invasion of eukaryotic cells for immune evasion and protection against environmental stresses. This review provides an overview of B. burgdorferi mechanisms for dissemination and invasion in the mammalian host, which are essential for pathogenesis and the development of persistent infection.
Highlights
Lyme disease, the leading tick-borne infection in the United States, occurs in multiple stages and is a multisystemic disease due to the etiologic agent Borrelia burgdorferi [1,2,3,4]
B. burgdorferi engages numerous adhesins that are important for mammalian infection, but the specific contributions of these adhesins for dissemination or invasion are not fully elucidated
The specific mechanisms known to contribute to borrelial dissemination in the form of vascular interaction and invasion by transmigration under in vitro conditions or during mammalian infection has been the focus of this review
Summary
The leading tick-borne infection in the United States, occurs in multiple stages and is a multisystemic disease due to the etiologic agent Borrelia burgdorferi [1,2,3,4]. The spirochetal bacterium is transmitted when an Ixodes tick vector colonized with B. burgdorferi takes a blood meal on reservoir mammals, such as small rodents and birds, or accidental human hosts, resulting in the colonization of dermal tissue and develops into a localized infection [7]. This earliest stage of Lyme disease is characterized by a painless bulls-eye rash, called an erythema migrans, experienced by approximately 70–80% of patients at the site of the tick bite [1,2,3]. A subset of patients continues to present with arthritic symptoms that has been designated postinfectious, antibiotic-refractory Lyme arthritis [8]
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