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Borrelia
burgdorferi are helical shaped bacteria about 10-25µm
long.
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Lymes Disease, lime disease, lymes
Introduction
Lyme disease was named in 1977 when arthritis was observed in a cluster of
children in and around Lyme, Connecticut. Other clinical symptoms and
environmental conditions suggested that this was an infectious disease
probably transmitted by an arthropod. Further investigation revealed that
Lyme disease is caused by the bacterium,
Borrelia burgdorferi. These bacteria are transmitted
to humans by the bite of infected deer ticks and cause more than 16,000
infections in the United States each year.
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From left to right: The deer tick (Ixodes
scapularis) adult female, adult male, nymph, and larva on a
centimeter scale.
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Black-legged ticks (
Ixodes scapularis) are 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 (Ixodes pacificus).
Ixodes ticks are much smaller than common dog and
cattle ticks. In their larval and nymphal stages, they are no bigger than
a pinhead. Ticks feed by inserting their mouths into the skin of a host
and slowly take in blood.
Ixodes ticks are most likely to transmit infection
after feeding for two or more days.
Individuals who live
or work in residential areas surrounded by tick-infested woods or
overgrown brush are at risk of getting Lyme disease. Persons who work or
play in their yard, participate in recreational activities away from home
such as hiking, camping, fishing and hunting, or 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.
Lyme Disease Symptoms
Clinical
Description:
Lyme disease most often presents with a characteristic "bull's-eye" rash,
erythema migrans, accompanied by nonspecific lyme disease symptoms such as fever,
malaise, fatigue, headache, muscle aches (myalgia), and joint aches
(arthralgia). 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.
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Image:
Western Blot (IgG) Serodiagnostic Testing.
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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.
Prevention and Control
Avoid tick
habitats: Whenever
possible, avoid entering areas that are likely to be infested with ticks,
particularly in spring and summer when nymphal ticks feed. Ticks favor a
moist, shaded environment, especially areas with leaf litter and low-lying
vegetation in wooded, brushy or overgrown grassy habitat. Both deer and
rodent hosts must be abundant to maintain the enzootic cycle of
B. burgdorferi. Sources for information on the
distribution of ticks in an area include state and local health
departments, park personnel, and agricultural extension
services.
Use personal
protection measures: If you are going to be in areas that are tick
infested, wear light-colored clothing so that ticks can be spotted more
easily and removed before becoming attached. Wearing long-sleeved shirts
and tucking pants into socks or boot tops may help keep ticks from
reaching your skin. Ticks are usually located close to the ground, so
wearing high rubber boots may provide additional protection.
The
risk of tick attachment can also be reduced by applying insect repellents
containing DEET (n,n-diethyl-m toluamide) to clothes and exposed skin, and
applying permethrin (which kills ticks on contact) to clothes. DEET can be
used safely on children and adults but should be applied according to
Environmental Protection Agency (EPA) guidelines to reduce the possibility
of toxicity.
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Use tweezers to remove
ticks. |
Perform a tick
check and remove attached ticks: The transmission of
B. burgdorferi (the bacteria that causes Lyme
disease) from an infected tick is unlikely to occur before 36 hours of
tick attachment. For this reason, daily checks for ticks and promptly
removing any attached tick that you find will help prevent infection.
Embedded ticks should be removed using fine-tipped tweezers. DO NOT use
petroleum jelly, a hot match, nail polish, or other products. Grasp the
tick firmly and as closely to the skin as possible. With a steady motion,
pull the tick's body away from the skin. The tick's mouthparts may remain
in the skin, but do not be alarmed. The bacteria that cause Lyme disease
are contained in the tick's midgut or salivary glands. Cleanse the area
with an antiseptic.
Taking preventive
antibiotics after a tick bite: The relative cost-effectiveness of
post-exposure treatment of tick bites to avoid Lyme disease in endemic
areas (areas where the disease is known to occur regularly) is dependent
on the probability of
B. burgdorferi infection after a tick bite. In most
circumstances, treating persons who only have a tick bite is not
recommended. Individuals who are bitten by a deer tick should remove the
tick promptly, and may wish to consult with their health care provider.
Persons should promptly seek medical attention if they develop any early
signs and early Lyme disease symptoms, ehrlichiosis, or babesiosis.
Strategies to
reduce tick abundance: The number of ticks in endemic residential
areas may be reduced by removing leaf litter, brush- and wood-piles around
houses and at the edges of yards, and by clearing trees and brush to admit
more sunlight and reduce the amount of suitable habitat for deer, rodents,
and ticks. Tick populations have also been effectively suppressed through
the application of pesticides to residential properties. Community-based
interventions to reduce deer populations or to kill ticks on deer and
rodents have not been extensively implemented, but may be effective in
reducing the community-wide risk of Lyme disease. New approaches such as
deer feeding stations equipped with pesticide applicators to kill ticks on
deer, and baited devices to kill ticks on rodents, are currently under
evaluation.
Lyme disease
vaccine: As of February 25, 2002 the manufacturer announced that
the LYMErix™ Lyme disease vaccine will no longer be commercially
available.
Treatment for Lyme Disease
If diagnosed early enough, proper antibiotic treatment of Lyme disease
can avoid the costs and complications of infection and late-stage illness.
According to treatment experts, antibiotic treatment for 3-4 weeks with doxycycline or amoxicillin is generally effective in early disease. Cefuroxime axetil or erythromycin can be used for persons allergic to penicillin or who cannot take tetracyclines. Later disease, particularly with objective neurologic manifestations, may require treatment with intravenous ceftriaxone or penicillin for 4 weeks or more, depending on disease severity. In later disease, treatment failures may occur and retreatment may be necessary. (The Medical Letter, Vol. 42(Issue 1077), May 1, 2000)
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