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.
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. 
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).  
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. 
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.
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Hengge UR, Tannapfel A, Tyring SK, et al.
Lyme borreliosis. Lancet Infect Dis. 2003;3:489-500.
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
Aguero-Rosenfeld ME, Wang G, Schwartz I,
et al. Diagnosis of Lyme borreliosis. Clin Microbiol Rev.
Steere AC. Lyme disease. N Engl J Med.
Stanek G, Strle F. Lyme borreliosis.
Lancet. 2003;362:1639-1647.[Abstract] http://www.ncbi.nlm.nih.gov/pubmed/14630446
Singh SK, Girschick HJ. Lyme borreliosis:
from infection to autoimmunity. Clin Microbiol Infect.