Tuesday, August 14, 2007

Lyme Dease

Lyme disease (Borreliosis) is a bacterial infection with a spirochete from the species complex Borrelia burgdorferi, which is most often acquired from the bite of an infected Ixodes, or black-legged, tick, also known as a deer tick. The deer tick is not the only carrier of this disease. The deer tick is frequently mistaken for a dog tick which is more common and larger in size. Borrelia burgdorferi sensu stricto is the predominant cause of Lyme disease in the U.S.; Lyme disease in Europe is more often caused by Borrelia afzelii or Borrelia garinii.

The disease varies widely in its presentation, which may include a rash and flu-like symptoms in its initial stage, followed by the possibility of musculoskeletal, arthritic, neurologic, psychiatric and cardiac manifestations. In most cases of Lyme disease, symptoms can be eliminated with antibiotics, especially if treatment is begun early in the course of illness.

A percentage of patients with Lyme disease have symptoms that last months to years after treatment with antibiotics. These symptoms can include muscle and joint pains, arthritis, stiff neck, cognitive defects, neurological complaints or fatigue. The cause of these continuing symptoms is not yet known. There is some evidence that they may result from an autoimmune type of response, in which a person’s immune system continues to respond even after the infection has been cleared, as well as evidence of ongoing infection with the spirochete.

Delayed or inadequate treatment may often lead to "late stage" Lyme disease that is disabling and difficult to treat. Amid great controversy over diagnosis, testing and treatment, two different standards of care for Lyme disease have emerged.

History
The first record of a condition associated with Lyme disease dates back to 1883 in Breslau, former Germany, where a physician named Alfred Buchwald described a degenerative skin disorder now known as Acrodermatitis Chronica Atrophicans.

In a 1909 meeting of the Swedish Society of Dermatology, Arvid Afzelius presented research about an expanding, ring like lesion he had observed. Afzelius published his work 12 years later and speculated that the rash came from the bite of an Ixodes tick, meningitic symptoms and signs in a number of cases and that both sexes were affected. This rash is now known as erythema migrans (EM), the skin rash found in early stage Lyme disease.

In the 1920s, French physicians Garin and Bujadoux described a patient with meningoencephalitis, painful sensory radiculitis, and erythema migrans following a tick bite, and they postulated the symptoms were due to a spirochetal infection. In the 1940s, German neurologist Alfred Bannwarth described several cases of chronic lymphocytic meningitis and polyradiculoneuritis, some of which were accompanied by erythematous skin lesions.

In 1948 spirochete-like structures were observed in skin specimens by Swedish dermatologist Carl Lennhoff. In the 1950s relations between tick bite, lymphocytoma, EM and Bannwarth's syndrome are seen throughout Europe leading to the use of penicillin for treatment.

Interest in tick-borne infections in the U.S. began with the first report of tick-borne relapsing fever (Borrelia hermsii) in 1915, following the recognition of five human patients in Colorado. In 1970 a physician in Wisconsin named Rudolph Scrimenti reports the first case of EM in U.S. and treats it with penicillin based on European literature.

The full syndrome now known as Lyme disease was not recognized until a cluster of cases originally thought to be juvenile rheumatoid arthritis was identified in three towns in southeastern Connecticut in 1975, including the towns Lyme and Old Lyme, which gave the disease its popular name. This was investigated by Allen Steere, and others from Yale University. The recognition that the patients in the United States had EM led to the recognition that "Lyme arthritis" was one manifestation of the same tick-borne condition known in Europe.

Before 1976, elements of Borrelia burgdorferi sensu lato infection were called or known as Tickborne meningopolyneuritis, Garin-Bujadoux syndrome, Bannworth syndrome, Afzelius syndrome, Montauk Knee or sheep tick fever. Since 1976 the disease is most often referred to as Lyme disease, Lyme borreliosis or simply borreliosis.

In 1980 Steere, et al, began to test antibiotic regimens in adult patients with Lyme disease.

In 1982 a novel spirochete was cultured from the mid-gut of Ixodes ticks in Shelter Island, New York, and subsequently from patients with Lyme disease. The infecting agent was then identified by Jorge Benach at the State University of New York at Stony Brook, and soon after isolated by Willy Burgdorfer, a scientist at the National Institutes of Health, who specialized in the study of spirochete microorganisms. The spirochete was named Borrelia burgdorferi in his honor. Burgdorfer was the partner in the successful effort to culture the spirochete, along with Alan Barbour.

After identification of the Lyme disease agent, Borrelia burgdorferi, antibiotics were selected for testing, guided by in vitro antibiotic sensitivities, including tetracycline antibiotics, amoxicillin, cefuroxime axetil, intravenous and intramuscular penicillin and intravenous ceftriaxone.

After the isolation of the spirochete from the mid-gut of Ixodes ticks, how ticks actually transmitted this new pathogen was the subject of much discussion. The hypothesis that Lyme disease spirochetes were transmitted via the salivary gland route of Ixodes ticks was confirmed when spirochetes were actually identified in tick saliva in 1987.

Microbiology
Borrelia bacteria, the causative agent of lyme disease. Magnified 400 times.Lyme disease is caused by spirochetal bacteria from the genus Borrelia, which has at least 37 known species, 12 of which are Lyme related, and an unknown number of genomic strains. The Borrelia species known to cause Lyme disease are collectively known as Borrelia burgdorferi sensu lato, and have been found to have greater strain diversity than previously estimated.

Until recently it was thought that only three genospecies caused Lyme disease: B. burgdorferi sensu stricto (predominant in North America, but also in Europe), B. afzelii, and B. garinii (both predominant in Eurasia). However, newly discovered genospecies have also been found to cause disease in humans.

Borrelia is a gram negative bacterium.

Transmission

By ticks
Hard-bodied (Ixodes) ticks are the primary Lyme disease vectors. There have also been reports of lyme disease from cats and kittens. In Europe, Ixodes ricinus (known commonly as the sheep tick, castor bean tick, or European castor bean tick) is the transmitter. In North America, Ixodes scapularis (black-legged tick or deer tick) has been identified as the key to the disease's spread on the east coast, while on the west coast the primary vector is Ixodes pacificus (Western black-legged tick). It is important to note that the majority of infections are caused by ticks in the nymph stage, as adult ticks do not become infected through feeding.

Another possible vector is Amblyomma americanum (Lone Star tick), which is found throughout the southeastern U.S. as far west as Texas, and increasingly in northeastern states as well.

It is believed that the longer the duration of tick attachment, the greater the risk of disease transmission; typically, for the spirochete to be transferred, the tick must be attached for a minimum of 24 hours, although only the first part of this statement can be said to be strictly correct.

Unfortunately only about 20% of persons infected with Lyme disease by the deer tick are aware of having had any tick bite, making early detection difficult in the absence of a rash. Tick bites usually go unnoticed due to the small size of the tick in its nymphal stage, as well as tick secretions that prevent the host from feeling any itch or pain from the bite.

New research suggests that transmission can occur within a few hours of tick attachment, and that the rate of transmission by infected ticks may be much higher than previously assumed.

Congenital
Lyme disease can be transmitted from an infected mother to fetus through the placenta during pregnancy, possibly resulting in stillbirth. The risk of transmission is minimized if the mother receives prompt antibiotic treatment. Antibiotics that can be given to pregnant women with Lyme disease include amoxicillin, cefuroxime axetil, or penicillin (oral or intramuscular).

Other
There is at least one case report of transmission by a biting fly. Lyme spirochetes have been found in biting flies as well as mosquitos. Some researchers believe biting insects do not feed long enough to transmit the infection, while others including Borrelia burgdorferi discoverer Willy Burgdorfer believe more research is needed. Sexual transmission has been anecdotally reported; Lyme spirochetes have been found in semen[34] and breast milk,however sexual transmission of the spirochete by these routes is not known to occur.

Lyme Dease

Lyme Dease

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