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Generalized Niches: A Tentative Definition
Niches protect Borrelia burgdorferi from the immune system or the antibiotic (Preac-Mursic et al., 1989) or render toxin released by Bb "invisible" to the immune system (more). The protection may wane with time and so will the size of the spirochete or toxin population within the niche.
Niches are provided by the host in the form of
physical compartments (immune privileged sites),
but they can also be produced by Bb itself in the form of
chemical or microbiological defense mechanisms.
Hiding from the Immune System, in: Tobias A Rupprecht, Uwe Koedel, Volker Fingerle and Hans-Walter Pfister "The Pathogenesis of Lyme Neuroborreliosis: From Infection to Inflammation", Mol Med. 2008 Mar-Apr; 14(3-4): 205-212, and
the overview in Chapter Background Information of J.J. Burrascano's essay "Managing Lyme Disease")
- physical compartments:
Host provided niches are sites poorly accessible to antibiotics and normal
- modulation of the host's immune and hormone system:
- chemical or microbiological defense mechanisms:
Bb might provide its own chemical and microbiological niches
In the model simulating the flare
cycles in the presence of antibiotics, the term "niche" is used in this
by shedding glycoprotein
that forms strong complexes with antibodies (Schutzer
et al., 1994), thereby enabling the organism itself to escape immune surveillance (Lawrence et al.,
by producing beta-lactamases, reducing the permeablity of the outer cell
membrane or modifying the target of the antibiotic, the "penicillin binding
proteins", so that the attachment of the antibiotic is reduced (Chambers
et al., 1998),
by changing its outer surface (Zhang et al., 1997), e.g. developing cell wall deficient (CWD) forms (Preac-Mursic et al. 1996). Mattman 1993 interprets
the ubiquitous CWD forms of bacteria and fungi as states of a variable
equilibrium between cell wall (ZW)
and outer membrane (AM)
dissolving and rebuilding processes, the former being driven by lysozymes of the organism itself and external stressors, e.g. antibiotics. According to Phillips et al. 1998 immune system and antibiotics shift this equilibrium in blood of Lyme patients to CWD forms. Together with the blood the CWD forms of Bb may spread throughout the host. Because the penetration of both the immune system and antibiotic into an organ (or compartment) varies from organ to organ, so will the equilibrium form of Bb. In some locations even the parent (spirochetal) form may be able to exist. Thus, the blood compartment may be thought of as a niche releasing Bb into other host compartments.
by producing biofilms or settling in biofilms already present.
The basic concept underlying the model is that the niche has the following properties:
The literature gives examples
of such locations (i.e. intracellular locations) in which Bb were found.
See also literature on mechanisms of cell invasion.
The immune system or antibiotic needs long periods, possibly several months, to empty a niche.
Since the toxins (antigen, pathogen) within a niche are only "poorly visible" to the immune system, they do not stimulate an inflammatory immune response while in the niche.
- Depending on the concentration in the niche (and other parameters), a niche releases its content into the compartments under immune system or antibiotic surveillance, the "visible" compartments responsible for the symptoms.
- Stricker RB, Counterpoint: Long-Term Antibiotic Therapy Improves Persistent Symptoms Associated with Lyme Disease, Clin Infect Dis. (2007) 45 (2): 149-157
- Bergström S, Reactivation and immune evasion of Borrelia infection, Project description, Umea, Sweden, April 2005
Liang FT, Brown EL, Wang T, Iozzo RV and Fikrig E, Protective Niche for Borrelia burgdorferi to Evade Humoral Immunity. American Journal of Pathology. 2004;165:977-985>
Zajkowska J, Hermanowska-Szpakowicz T, Rubel J. [Atypical forms of Borrelia burgdorferi-clinical consequences], Pol Merkuriusz Lek. 2005 Jan;18(103):115-9. Polish.
defense mechanisms include
- plasmid encoded genes,
- morphologic variants,
- cysts formation,
- colonies formation,
- antigenic variation, and
- resistance to iron deprivation
version: December 27, 2012
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