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.