By Simon Houston Ph.D, Caroline E. Cameron Ph.D. (auth.), Monica E. Embers (eds.)
This booklet explores the various mechanisms during which the main customary Spirochetal pathogens persist in a fit immune-competent host. between them are the direct and oblique suppression of host immune indications, section and antigenic edition, escaping popularity by means of host supplement proteins, and seclusion into immune privileged websites. We additionally discover antibiotic remedy for regulate of an infection, a baffling subject that lends itself to exalted interpretation.
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Additional resources for The Pathogenic Spirochetes: strategies for evasion of host immunity and persistence
Sample text
FEMS Immunol Med Microbiol 6:273–279 Bansal RC, Cohn H, Fani K, Lynfield YL (1978) Nephrotic syndrome and granulomatous hepatitis in secondary syphilis. Arch Dermatol 114:1228–1229 Baseman JB, Hayes EC (1980) Molecular characterization of receptor binding proteins and immunogens of virulent Treponema pallidum. J Exp Med 151:573–586 Baughn RE, Musher DM (2005) Secondary syphilitic lesions. Clin Microbiol Rev 18:205–216 Belisle JT, Brandt ME, Radolf JD, Norgard MV (1994) Fatty acids of Treponema pallidum and Borrelia burgdorferi lipoproteins.
The spirochete has developed an intricate system of genetically based survival mechanisms that allow it to adapt to each of its environments, whether mammalian or tick, in order to maintain its life cycle. B. burgdorferi lives within the confines of each host without causing harm, however, when transmitted to humans the scenario changes and the organism becomes pathogenic when infecting this host. Because the tick that transmits B. burgdorferi is very small, humans quite often are unaware that they have been bitten and subsequently become infected, even though the tick feeds for 4–5 days and borreliae do not venture out of the tick until around 48 h post-attachment (Piesman 1993; Ohnishi et al.
Burgdorferi migrate to and infect heart, spleen, bladder, joint, and ear tissues, but not the central nervous system (CNS) as in humans. Murine species also do not display EM or other signs of pathology commonly associated with human Lyme disease (an exception is some inbred strains of mice will develop arthritis and carditis) despite the rodents remaining chronically infected throughout their lifespan. Therefore, mouse models are useful to study chronic infection mechanisms, but may reflect the biology of borrelial persistence in reservoir hosts as seen in nature rather than as a disease model.