Lyme disease historical perspective

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Anmol Pitliya, M.B.B.S. M.D.[2], Ilan Dock, B.S.

Overview

In 1883, Alfred Buchwald was the first to describe a condition associated with Lyme disease which is now known as acrodermatitis chronica atrophicans. Arvid Afzelius first observed ring-like lesions, now known as Erythema migrans, and associated the rash with tick bites. In the United States, Lyme disease was not recognized until 1975, when a cluster of cases was identified in three towns in Southeastern Connecticut (including towns Lyme and Old Lyme), which gave Lyme disease its popular name. In 1981, the infectious agent (a spirochete) was isolated by Willy Burgdorfer, a researcher at the National Institutes of Health, from the midgut of Ixodes ticks. The spirochete was named Borrelia burgdorferi in honor of Willy Burgdorfer.

Historical Perspective

Dr. Willy Burgdorfer, an American-Swiss scientist, discovered the bacterial pathogen responsible for causing Lyme disease Source - Rocky Mountain Laboratories, National Institutes of Health

In 1883 in Breslau (formerly in Germany, now known as Wrocław, Portland), Alfred Buchwald, a German physician, was the first to describe a condition associated with Lyme disease. He described the condition as diffuse idiopathic skin atrophy. The condition is a degenerative skin disorder now known as acrodermatitis chronica atrophicans. In 1909, Arvid Afzelius, a Swedish physician, presented research about an expanding, ring-like lesion he had observed. In 1921, Arvid Afzelius published his work and stated that the rash was due to the bite of an Ixodes tick. He also concluded that meningitis signs and symptoms occur in a number of cases; this rash is now known as erythema migrans (EM), the skin rash found in early stage Lyme disease. In 1911, Andrew Balfour, a Scottish parasitologist of the Wellcome Research Laboratory in Khartoum, identified "infective granules" or spore-type "cysts" as the cause of persistence of spirochetal infection in Sudanese Fowl. In 1913, B. Lipschütz, an Austrian dermatologist, described similar rash as erythema chronicum migrans (ECM). In 1915, tick-borne relapsing fever (Borrelia hermsii) was first reported in the U.S following recognition of five human patients in Colorodo. This led to an increased interest in tick-borne infections in the U.S. In the 1920s, Garin and Bujadoux, French physicians, described a patient with meningoencephalitis, painful sensory radiculitis, and erythema migrans following a tick bite, and postulated that the symptoms were due to a spirochetal infection. In the 1940s, Alfred Bannwarth, a German neurologist, described several cases of chronic lymphocytic meningitis and polyradiculoneuritis, some of which were accompanied by erythematous skin lesions.

• In 1948, Carl Lennhoff, a Swedish dermatologist, observed spirochete-like structures in skin specimens.
• In the 1950s, relations between tick bites, lymphocytoma, EM, and Bannwarth's syndrome were seen throughout Europe, leading to the use of penicillin for treatment.
• In 1970, Rudolph Scrimenti, a U.S. physician from Wisconsin, reported the first case of erythema migrans in U.S. and treated it with penicillin based on European literature.
• In the United States, Lyme disease was not recognized until a cluster of cases was identified in three towns in Southeastern Connecticut in 1975. These towns included Lyme and Old Lyme, which gave Lyme disease its popular name. The cases were originally thought to be juvenile rheumatoid arthritis. This was further investigated by Dr. David Snydman and Dr. Allen C. Steere of the Epidemic Intelligence Service, and by others from Yale University. They recognized that the patients in the United States had erythema migrans and "Lyme arthritis" was one manifestation of the same tick-borne condition known in Europe.
• Before 1976, elements of B. burgdorferi sensu lato complex infection were known as "tickborne meningopolyneuritis," "Garin-Bujadoux syndrome," "Bannworth syndrome," "Lymphocytic meningoradiculitis," "Afzelius syndrome," "Montauk Knee" or "sheep tick fever." Since 1976, the disease has been most often referred to as Lyme disease, Lyme borreliosis, or simply borreliosis.
• In 1976, Jay Sanford, a former physician at the Walter Reed Army Institute of Research, published a chapter in the book The Biology of Parasitic Spirochetes. In it, Dr. Sanford stated: "The ability of borrelia, especially tick-borne strains, to persist in the brain and in the eye during remission after treatment with arsenic or with penicillin or even after apparent cure, is well known.”
• In 1980, Allen C. Steere, a rheumatologist at Yale University, and his colleagues began to test antibiotic regimens in adult patients with Lyme disease.
• In 1981, Jorge L. Benach, a pathologist at the State University of New York at Stony Brook identified a novel spirochete which was cultured from the midgut of Ixodes ticks in Shelter Island, New York, and subsequently from patients with Lyme disease. Soon after, the infectious agent was isolated by Willy Burgdorfer, a researcher at the National Institutes of Health, who specialized in the study of microorganisms such as Borrelia and Rickettsia. The spirochete was named Borrelia burgdorferi in his honor. Willy Burgdorfer and Alan Barbour were partners in the successful effort to culture the spirochete.
• After identification of B. burgdorferi as the causative agent of Lyme disease, antibiotics were selected for testing, guided by in vitro antibiotic sensitivities, including tetracycline antibiotics, amoxicillin, cefuroxime axetil, intravenous and intramuscular penicillin, and intravenous ceftriaxone.
• In 1987, B. burgdorferi spirochetes were identified in tick saliva, confirming the hypothesis that transmission occurred via tick salivary glands.

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