Dr. E. Murakami Centre for Lyme

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Pathophysiology

 

B. burgdorferi is injected into the skin by the feeding infected Ixodes tick, usually after the tick has fed for more than 48 hours. (Dr. M has seen the infection of B. burgdorferi show itself in the form of the rash in as little time as 2 hours after a bite.) Initial infection is established at the tick bite site, and may or may not present itself as a rash. After skin penetration B burgdorferi moves throughout the extracellular matrix by binding to cellular components and interacting with various other cellular bodies. This leads to expansion of the rash. [10]

 

Borrelia disseminates from skin to other organs quickly. It replicates, kills host cells and emerges through the membrane of that cell. Within days to weeks after infection, Borrelia can be found in the blood, cerebrospinal fluid, myocardium, retina, muscle, bone, spleen, liver, meninges and brain cells. [5]

  

The host immune response to Borrelia integrates both cell-mediated and humoral mechanisms. Most patients have an IgM antibody response against OspC or the flagellar protein (41-kDa) of Borrelia within days after onset of disease. Humoral immune responses may be initially limited and a clinically detectable level of antibodies may be delayed. Early antibiotic treatment may delay the B-lymphocytic response. During the chronic phase, antibodies against a variety of Borrelia epitopes become detectable. Although the B-cell response in the chronic phase is highly active, it is not preventive of future infection(s). [3] [10]

  

Persistent clinical symptoms, such as those of chronic joint inflammation, have been attributed to autoimmunity. Activated T lymphocytes and lymphokines of the helper T-cell phenotype (CD4 cells) play a major role in the pathogenesis of Lyme arthritis. [10]

  

  

Reference1

Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2006;43:1089-1134.[Abstract] http://www.ncbi.nlm.nih.gov/pubmed/17029130[Full Text] http://www.journals.uchicago.edu/doi/full/10.1086/508667

  

Reference2

Hengge UR, Tannapfel A, Tyring SK, et al. Lyme borreliosis. Lancet Infect Dis. 2003;3:489-500. [Abstract] http://www.ncbi.nlm.nih.gov/pubmed/12901891

  

Reference5

Steere AC, Coburn J, Glickstein L. The emergence of Lyme disease. J Clin Invest. 2004;113:1093-1101.[Abstract] http://www.ncbi.nlm.nih.gov/pubmed/15085185[Full Text] http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15085185

  

Reference9

Aguero-Rosenfeld ME, Wang G, Schwartz I, et al. Diagnosis of Lyme borreliosis. Clin Microbiol Rev. 2005;18:484-509.[Abstract] http://www.ncbi.nlm.nih.gov/pubmed/16020686

  

Reference3

Steere AC. Lyme disease. N Engl J Med. 2001;345:115-125.[Abstract] http://www.ncbi.nlm.nih.gov/pubmed/11450660

  

Reference6

Stanek G, Strle F. Lyme borreliosis. Lancet. 2003;362:1639-1647.[Abstract] http://www.ncbi.nlm.nih.gov/pubmed/14630446

  

Reference10

Singh SK, Girschick HJ. Lyme borreliosis: from infection to autoimmunity. Clin Microbiol Infect. 2004;10:598-614.[Abstract] http://www.ncbi.nlm.nih.gov/pubmed/15214872