Why Is Chronic Lyme Borreliosis Chronic?

Abstract

Chronic Lyme borreliosis (CLB) can present not only in different organs but also in different patterns. Although many theories exist about the mechanisms leading to CLB, it is known that viable Borrelia burgdorferi can persist for decades and cause late skin manifestations of acrodermatitis chronica atrophicans (ACA). Thus, the immunopathogenetic findings in ACA can serve as a model for studying the chronic course of Lyme borreliosis. Recent findings indicate that the most important cell for antigen presentation, the epidermal Langerhans cell (LC), is invaded by B. burgdorferi in early Lyme borreliosis. Therefore, LCs were stained immunohistochemically with different markers to investigate their functional activity. Numbers of CD1a+ LCs were reduced in erythema migrans but normal or slightly elevated in ACA. In both diseases there was also a marked downregulation of major histocompatibility complex class II molecules on LCs, as measured by staining of human leukocyte antigen DR. This phenomenon might be a mechanism that protects against the presentation of autoantigens and may be the cause of the impaired capacity of LCs to eliminate B. burgdorferi antigens, thus explaining why CLB is chronic.

Serum-starvation-induced changes in protein synthesis and morphology of Borrelia burgdorferi

“…Cysts have been observed in vitro in human CSF (Brorson & Brorson, 1998a) and in vivo in the tissues of Lyme-disease-infected humans (Aberer et al, 1997 ;Hulinska et al, 1994). It is not known whether the cysts observed in those studies are the same as the cysts described in this report.…”

“…Brorson & Brorson (1997) demonstrated that cells of B. burgdorferi undergo a morphological transformation from motile spirochaetes into non-motile, spherical cyst-forms when incubated for "4 weeks in BarbourStoenner-Kelly (BSKII) medium without the addition of rabbit serum, a routinely added media supplement thought to provide cells with a source of fatty acids (Barbour & Hayes, 1986). Cyst-forms have also been observed in Lyme disease patient tissues (Hulinska et al, 1994 ;Aberer et al, 1997). It has been reported that these forms of B. burgdorferi are viable and capable of transforming back into motile spirochaetes, although survival was not accurately quantified (Brorson & Brorson, 1997).…”

Lysine-Dependent Multipoint Binding of theBorrelia burgdorferiVirulence Factor Outer Surface Protein E to the C Terminus of Factor H

“…Borrelia spirochetes can persist in the human body for prolonged periods, even for decades, as shown in patients with acrodermatitis chronica atrophicans (ACA) 3 lesions (6). In some patients with chronic disease, immune or other less wellcharacterized mechanisms are the cause of the symptoms.…”

Lyme Disease: The Quest for Magic Bullets

“…Fact: B. burgdorferi assumes different forms in different hosts [41][42][43][44][45][46][47] . The most troublesome is the so-called cyst form that may lie dormant in the human host, thus evading antibiotic therapy that targets replicating bacteria [41][42][43][44][45] .…”

“…The most troublesome is the so-called cyst form that may lie dormant in the human host, thus evading antibiotic therapy that targets replicating bacteria [41][42][43][44][45] . The non-replicating cyst form is undoubtedly the key to persistence of infection with the Lyme disease spirochete, and any antibiotic approach to Lyme disease that fails to recognize this pathogenic entity may fail to eradicate the infection, leading to chronic disease [46,47] .…”