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Microbiology and Epidemiology
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Borrelia burgdorferi, the causative agent of Lyme disease, is a fastidious microaerophilic spirochete. The human infection Lyme borreliosis is caused primarily by three pathogenic genospecies: B. burgdorferi sensu stricto (hereafter referred to as B. burgdorferi), Borrelia garinii, and Borrelia afzelii.
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B. burgdorferi is the sole cause of Lyme borreliosis in the United States; all three genospecies are found in Europe, and the latter two species occur in Asia.
Lyme disease is the most common vector-borne illness in the United States, with ~300,000 cases each year.
– Ixodes ticks transmit the disease.
– I. scapularis, which also transmits babesiosis and anaplasmosis, is found in northeastern and midwestern states; I. pacificus is found in western states.
The white-footed mouse is the preferred host for larval and nymphal I. scapularis. Adult ticks prefer the white-tailed deer as host.
Nymphal ticks transmit the disease to humans during the early summer months after feeding for ≥24 h.
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Clinical Manifestations
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Lyme disease usually begins with erythema migrans (EM; stage 1, localized infection) before disseminating (stage 2) or causing persistent infection (stage 3).
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Stage 1 (localized infection): After an incubation period of 3–32 days, EM develops at the site of the tick bite (commonly the thigh, groin, or axilla) in 80% of pts.
– The classic presentation is a red macule that expands slowly to form an annular lesion with a bright red outer border and central clearing. Central erythema, induration, necrosis, vesicular changes, or many red rings within an outer ring are also possible.
– Most pts do not remember the preceding tick bite.
Stage 2 (disseminated infection): Given that some pts do not notice EM, many pts present within days or weeks after infection with secondary annular skin lesions, nonspecific systemic signs and symptoms, neurologic deficits, or cardiac manifestations due to hematogenous spread.
– Nonspecific signs and symptoms include severe headache, mild neck stiffness, fever, chills, migratory musculoskeletal pain, arthralgias, malaise, and fatigue. These manifestations subside within a few weeks, even in untreated pts.
– Neurologic deficits occur in ~15% of pts and may include meningitis; encephalitis; cranial neuritis, including bilateral facial palsy; motor or sensory radiculoneuropathy; mononeuritis multiplex; ataxia; or myelitis. Lymphocytic pleocytosis (~100 cells/μL) is found in CSF, often along with elevated protein levels and normal or slightly low glucose concentrations.
– Cardiac involvement occurs in ~8% of pts. Atrioventricular (AV) block of fluctuating degree is most common, but acute myopericarditis is possible. Cardiac involvement usually lasts for only a few weeks but may recur in untreated pts.
Stage 3 (persistent infection): Of untreated pts in the United States, ~60% develop frank arthritis, usually consisting of intermittent attacks of oligoarticular arthritis in large joints (especially the knees) that last for weeks or months.