Lyme disease is a multi-systemic inflammatory disease caused by the bacterium Borrelia burgdorfer. It is a tick borne disease and the bacterium is harboured by the deer tick known by its biological name as Ixodes scapularis. Infection occurs when humans come in contact with the ticks (tick bites) and so disease prevalence is restricted within the population zone of the deer ticks. In 2004 alone, there were 19,804 reported cases of Lyme disease in the United States.[CDC] The most commonly observed symptom is appearance of skin lesions, while cardiac complications, neurological abnormalities, and rheumatologic problems also manifest in patients with the progression of the disease. In 1940, Bannwarth, a German neurologist, documented the appearance of erythematous skin lesions in cases of lymphocytic meningopolyneuritis. In the US, however, first instance of Lyme disease was reported only in 1975 when the abnormal condition of rheumatoid arthritis was observed among the juvenile population in the Old Lyme region of Connecticut. The bacterium Borrelia burgdorferi, belonging to the spirochete family (with appearance resembling a coiled spring) is the pathogen associated with Lyme disease. Typically ticks get infected during the larva stage when they feed on rodents (main source of blood) that carry the bacterium. These ticks then transmit the infection to animals and humans by attaching themselves to the body surface. Studies conducted on animals have shown that at least 24 hours of skin contact is necessary for the successful transmission of the bacterium to the host animal. The structural features of the spirochete facilitate rapid dissemination once inside the host. The presence of internal flagella assists in rapid motility while the special binding mechanisms enable the bacterium to attach itself to the host cells quickly and activate the protease mechanisms. The disease is categorized into three different levels based on the degree of dissemination in the host. In humans, infection by Borrelia burgdorferi produces both direct as well as indirect effects. While the appearance of skin lesions on the area of infection (erythema migrans)is a most commonly observed symptom of the microbial intrusion, secondary inflammatory responses are also noticed in many clinical cases. The different stages of infection with their respective symptoms are as follows. The â€Early localized infection’ represents the initial stage that falls within 30 days of receiving the bite. During this stage, skin rashes (erythema migrans ) at the bite site are clearly visible and the patient frequently displays other mild symptoms such as intermittent fever, headache, arthralgia, chills, etc. â€Early disseminated Lyme disease’ is the next stage which extends to months after the initial bite. By this stage, the infection is already spread to multiple organs through haematological or lymphatic circulation. Musculoskeletal and neurological complications are frequently observed conditions during this stage of the disease. Typically, around 10 to 15% of untreated patients show various degrees of disabling effects due to the effect of the disease on their peripheral nervous system. Some patients may also manifest cardiac symptoms such as palpitations, syncope, chest pain, etc. The third stage known as â€Chronic Lyme disease’ is a more acute period of disease where the central nervous system is also involved leading to more complex neurological dysfunctions (Subacute encephalopathy) and decreased cognitive ability. This stage may prolong years after the initial infection and often a period of latency followed by flaring up of the symptoms is observed among patients. [Julie L Puotinen]. Research has related the increased levels of Matrix Metalloproteinase (a class of metallopeptidases) in chronic Lyme disease patients. Increased levels of MMPs are commonly observed in patients suffering from Alzheimer’s disease, brain tumours multiple sclerosis etc. However, the research conducted by Dr. Perides and his co-workers has shown that an unusually high level (78%) of patients with Lyme disease reported to have matrix mettalloproteinase with electrophoretic mobility of 130 kDa in their cerebrospinal fluid. Further research in determining the roles of B burgdorferi in inducing MMP expression directly or as an inflammatory response is awaited. Let us explore the main treatment methods along with the recent research in this direction.
Please Rate this Article 5 out of 54 out of 53 out of 52 out of 51 out of 5
Not yet Rated
