Introduction
Lyme disease is an infection caused by the
corkscrew-shaped bacteria Borrelia burgdorferi that is
transmitted by the bite of deer (Ixodes scapularis) and western black-legged (Ixodes
pacificus) ticks. The deer tick, which normally feeds on the white-footed mouse, the
white-tailed deer, other mammals, and birds, is responsible for transmitting Lyme disease
bacteria to humans in the northeastern and north-central United States. On the Pacific
Coast, the bacteria are transmitted to humans by the western black-legged tick.
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From left to right: The
deer tick (Ixodes scapularis) adult female, adult male, nymph, and larva on a
centimeter scale. |
Ixodes ticks are much smaller than common dog and cattle ticks. In their
larval and nymphal stages, they are no bigger than a pinhead. Adult ticks are slightly
larger. Ticks feed on blood by inserting their mouth parts (not their whole bodies) into
the skin of a host animal. They are slow feeders: a complete blood meal can take several
days. As they feed, their bodies slowly enlarge.
Risk: The number of annually reported cases of Lyme disease in the United States
has increased about 25-fold since national surveillance began in 1982, and a mean of
approximately 12,500 cases annually were reported by states to the Centers for Disease
Control and Prevention (CDC) from 1993-1997. In the United States, the disease is mostly
localized to states in the northeastern, mid-Atlantic, and upper north-central regions,
and to several counties in northwestern California. 
Most B. burgdorferi infections are thought to result from periresidential
exposure to infected ticks during property maintenance, recreation, and leisure
activities. Thus, individuals who live or work in residential areas surrounded by woods or
overgrown brush infested by vector ticks are at risk of getting Lyme disease. In addition,
persons who participate in recreational activities away from home such as hiking, camping,
fishing and hunting in tick habitat, and persons who engage in outdoor occupations, such
as landscaping, brush clearing, forestry, and wildlife and parks management in endemic
areas may also be at risk of getting Lyme disease.
Clinical Characteristics
Lyme disease most often presents with a
characteristic "bull's-eye" rash, erythema migrans, accompanied by nonspecific
symptoms such as fever, malaise, fatigue, headache, muscle aches (myalgia), and joint
aches (arthlagia).
The incubation period from infection to
onset of erythema migrans is typically 7 to 14 days but may be as short as 3 days and as
long as 30 days. Some infected individuals have no recognized illness (asymptomatic
infection determined by serological testing), or manifest only non-specific symptoms such
as fever, headache, fatigue, and myalgia.
Lyme disease spirochetes disseminate from the
site of the tick bite by cutaneous, lymphatic and blood-borne routes. The signs of early
disseminated infection usually occur days to weeks after the appearance of a solitary
erythema migrans lesion. In addition to multiple (secondary) erythema migrans lesions,
early disseminated infection may be manifest as disease of the nervous system, the
musculoskeletal system, or the heart.
Early neurologic manifestations include lymphocytic
meningitis, cranial neuropathy (especially facial nerve palsy), and radiculoneuritis.
Musculoskeletal manifestations may include migratory joint and muscle pains with or
without objective signs of joint swelling. Cardiac manifestations are rare but may include
myocarditis and transient atrioventricular blocks of varying degree.
B. burgdorferi
infection in the untreated or inadequately treated patient may progress to late
disseminated disease weeks to months after infection. The most common objective
manifestation of late disseminated Lyme disease is intermittent swelling and pain of one
or a few joints, usually large, weight-bearing joints such as the knee. Some patients
develop chronic axonal polyneuropathy, or encephalopathy, the latter usually manifested by
cognitive disorders, sleep disturbance, fatigue, and personality changes. Infrequently,
Lyme disease morbidity may be severe, chronic, and disabling. An ill-defined post-Lyme
disease syndrome occurs in some persons following treatment for Lyme disease. Lyme disease
is rarely, if ever, fatal.
Diagnosis: The diagnosis of Lyme disease is based primarily on
clinical findings, and it is often appropriate to treat patients with early disease solely
on the basis of objective signs and a known exposure. Serologic testing may, however,
provide valuable supportive diagnostic information in patients with endemic exposure and
objective clinical findings that suggest later stage disseminated Lyme disease. When
serologic
testing is indicated, CDC recommends
testing initially with a sensitive first test, either an enzyme-linked immunosorbent assay
(ELISA) or an indirect fluorescent antibody (IFA) test, followed by testing with the more
specific Western immunoblot (WB) test to corroborate equivocal or positive results
obtained with the first test.
Although antibiotic treatment in early localized disease
may blunt or abrogate the antibody response, patients with early disseminated or
late-stage disease usually have strong serological reactivity and demonstrate expanded WB immunoglobulin G (IgG) banding patterns to diagnostic B.
burgdorferi antigens. Antibodies often persist for months or years following
successfully treated or untreated infection. Thus, seroreactivity alone cannot be used as
a marker of active disease. Neither positive serologic test results nor a history of
previous Lyme disease assures that an individual has protective immunity. Repeated
infection with B. burgdorferi has been documented. B. burgdorferi can be
cultured from 80% or more of biopsy specimens taken from early erythema migrans lesions.
However, the diagnostic usefulness of this procedure is limited because of the need for a
special bacteriologic medium (modified Barbour-Stoenner-Kelly medium) and protracted
observation of cultures.
Polymerase chain reaction (PCR) has been used to amplify genomic
DNA of B. burgdorferi in skin, blood, cerobro-spinal fluid, and synovial fluid, but
PCR has not been standardized for routine diagnosis of Lyme disease.