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Cultivation Methods of Spirochetes from Borrelia burgdorferi Sensu Lato Complex and Relapsing Fever Borrelia
Published on: November 25, 2022
[Pathogenetic-clinical problems of Lyme borreliosis]
Teresa Hermanowska-Szpakowicz1, Joanna M Zajkowska, Sławomir A Pancewicz
1Kliniki Chorób Zakaźnych i Neuroinfekcji, AM w Białymstoku.
Abstract:
In this article a short review of pathogenesis and clinical manifestations of Lyme disease is presented. As regards pathogenesis, attention was paid to the mosaic protein structure of the B. burgdorfieri spirochete, particularly of outer surface proteins (Osp) that influence the clinical course and diagnosis of the disease. The presence of various atypical spirochete forms: spheroplastic L (without cell walls), cystic, and granular "blebs" may lead to a chronic form of the disease and to a low efficacy of antibiotic therapy. An important part of the pathogenesis is epithelial damage, stimulating the production of inflammatory cytokines (mainly IL-1, TNF-alpha, IFN-gamma), adhesive molecules and acute-phase proteins. Moreover, in the course of the disease not only an impairment of phagocytosis and chemotaxis was found, but also B. burgdorfieri spirochete binding by antibodies into immunological complexes that may maintain chronic inflammation. In terms of the Asbrink classification, complaints predominating in the clinical picture of an early and late stage of the disease were presented, with an emphasis on neuroborreliosis.
Insights
Lyme disease pathogenesis involves Borrelia burgdorferi spirochete structure and atypical forms, impacting treatment efficacy and chronic inflammation. Understanding these factors is crucial for diagnosing and managing Lyme disease, including neuroborreliosis.
Area of Science:
- Microbiology
- Immunology
- Infectious Diseases
Context:
- Lyme disease is a tick-borne illness caused by Borrelia burgdorferi.
- Understanding its pathogenesis is key to effective treatment and diagnosis.
- The study reviews current knowledge on disease mechanisms and clinical presentations.
Purpose:
- To provide a concise review of Lyme disease pathogenesis and clinical manifestations.
- To highlight the role of Borrelia burgdorferi spirochete structure and atypical forms in disease progression.
- To emphasize the importance of understanding inflammatory pathways and immune responses in Lyme disease.
Summary:
- Borrelia burgdorferi's outer surface proteins (Osp) and atypical forms (spheroplastic, cystic, granular) influence Lyme disease's clinical course and treatment outcomes.
- Epithelial damage triggers inflammatory cytokines (IL-1, TNF-alpha, IFN-gamma), adhesive molecules, and acute-phase proteins.
- Impaired phagocytosis, chemotaxis, and antibody-bound immune complexes contribute to chronic inflammation and disease persistence, particularly in neuroborreliosis.
Impact:
- Informs clinical diagnosis and treatment strategies for Lyme disease.
- Highlights potential reasons for antibiotic therapy failure in chronic Lyme disease.
- Provides insights into the immunological mechanisms underlying persistent inflammation in Lyme disease.
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