Borrelia burgdorferi
B. burgdorferi, a newly identified Borrelia species, is the causativeagent
of Lyme disease. Lyme disease was first demonstrated in children in 1975,
during an outbreak of arthritis in Lyme, Connecticut, in the United States. The
causative agent of the fever was isolated by Burgdorfer in 1982 after whom the
spe-cies burgdorferi is named. B. burgdorferi is a fastidious
bacterium, which measures 4–30 mm in length and 0.2 mm in breadth. It is helical and Gram negative.
It is a microaerophilic spiro-chete, which can be grown on BSK
(Barbour–Stoenner–Kelly) medium at 33°C after incubation for 2 weeks or longer.
Lyme disease is a tick-borne disease
transmitted to humansby ixodid ticks. The incubation period varies from 7 to 14
days. After bite of the tick, B.
burgdorferi is inoculated through the skin and then spreads locally. The
local spread of the bacteria causes erythema migrans, a rash seen in
approximately two thirds of the cases. This skin rash may be a confluent patch
of erythema or may have central clearing. The lesion begins as a small macular
papule and becomes larger over the next many weeks and forms a large area of
lesion of 5–50 cm in diameter.
The patient may also complain
of fever, chills, myalgias, and headache during early stage of the disease,
with or without rash. Subsequently, during a period of time ranging from days
to months, the bacteria spread through blood circulation and cause a
disseminated disease. This disease is characterized by the presence of multiple
erythema migrans, systemic complica-tions (fever, myalgias, arthralgia,
malaise, and headache) and even septic meningitis; this disease usually
develops 3–10 weeks after the tick bite. The pathogenesis of these late manifesta-tions
is poorly understood. It is not known whether the live organisms cause these
manifestations or these manifestations occur due to an antigenic
cross-reactivity to Borrelia
antigens.
Lyme disease has been
reported from USA, Germany, Austria, Switzerland, and Scandinavian countries.
Lyme disease is a
zoonotic disease. Rodents, bear, and other mammals are the natural reservoir
hosts. Hard ticks (ixodid ticks) are
the vectors of the disease. The infection is transmitted by the hard tick from
mice to humans and occur by regurgita-tion during tick bite. Individuals
exposed to hard ticks are at increased risk for Lyme disease.
Clinical diagnosis of
the condition may be made by the presence of erythema migrans in the early
stage of the disease. Laboratory diagnosis of the condition is primarily
serological. Serodiagnosis depends on demonstration of specific antibod-ies in
the serum, which persist for many years even after eradi-cation of the
infection. ELISA and IIF are the most common serological tests employed for the
diagnosis of the disease. Western blot is used to confirm the specificity of
serum pos-itive by ELISA or IIF. Serology is positive in one-third of the
patients with the early disease, in 90% of patients with early disseminated
disease, and in all the patients with late disease. Microscopy is not
recommended because B. burgdorferi is
rarely seen in clinical specimens. Culture is also not used, because the
bacteria are difficult to culture.
Amoxicillin, tetracycline, cefuroxime, or ceftriaxone are effective for the treatment of Lyme disease. Avoidance of exposure to ticks and use of insecticides are the useful methods for prevention of the disease.
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