Lyme’s Disease
Introduction
Lyme disease was named in 1977 when
arthritis was observed in a cluster of
children in and around Lyme, CN
 Conditions suggested that this was an
infectious disease probably transmitted
by an arthropod
 Further investigation revealed that Lyme
disease is caused by the bacterium
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Causative Organism
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Borrelia burgdorferi
Loosely coiled
spirochete
8-20 micrometers
Vector
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Ixodes scapularis ticks are much smaller than common dog
and cattle ticks
Below adult female, adult male, nymph, and larva on a
centimeter scale.
Humans acquire disease from bite of nymphal or adult tick.
Three Stages of Disease
Localized rash – erythema chronicum
migrans
 Dissemination to multiple organ systems
 Chronic disseminated stage often with
arthritic symptoms
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Localized Rash
Dissemination
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Signs of early disseminated infection usually
occur days to weeks after the appearance of a
solitary erythema migrans lesion
Neurologic – Bell’s Palsy
Musculoskeletal manifestations may include
migratory joint and muscle pains
Late disseminated Lyme disease is intermittent
swelling and pain of one or a few joints.
Chronic Disseminated
Chronic arthritis
 Chronic axonal polyneuropathy
 Lyme disease morbidity may be severe,
chronic, and disabling.
 Rarely, if ever, fatal
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Diagnosis
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Diagnosed clinically, confirmed serologically.
Often appropriate to treat patients with early
disease solely on the basis of objective signs and a
known exposure.
CDC recommends testing initially with a sensitive
first test, ELISA or an IFA test, followed by
testing with the more specific Western
immunoblot (WB) test to corroborate equivocal or
positive results obtained with the first test.
Serology
Patients with early disseminated or latestage disease usually have strong
serological reactivity
 Antibodies often persist for months or years
following successfully treated or untreated
infection.
 seroreactivity alone cannot be used as a
marker of active disease
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Problems with Serology
IFA false positive may occur if patient has
syphilis, relapsing fever or RA.
 IFA interpretation highly subjective
 EIA lacks sensitivity in early disease.
 EIA false positives with syphilis, other
treponemes, IM and autoimmune disease.
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Western Blot
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Must be used if the Lyme IgG/IgM antibody
serology is equivocal or positive
"Osp" refers to outer surface protein of the
bacteria.
"kDa" is the abbreviation for "kilodalton," which
is used for molecular weight designations.
Lyme antibodies of importance are against the
following molecular weights of the B. burgdorferi
antigens: 23-25 kDa (Osp C); 31 kDa (Osp A); 34
kDa (Osp B); 39 kDa; 41 kDa; and 83-93 kDa7.
Lane 1, monoclonal antibodies defining selected antigens to B. burgdorferi Lane 2, human
serum (IgG) reactive with the 10 antigens scored in the currently recommended criteria for
blot scoring; lines indicate other calibrating antibodies. Molecular masses are in kilodaltons.
Treatment
Single dose doxycycline shortly after tick
bite.
 Lyme disease give doxycycline followed by
amoxacillin
 Neuroborreliosis requires IV antibiotic
therapy.
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