Lyme disease historical perspective
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
History
The first record of a condition associated with Lyme disease dates to 1883 in Breslau (formerly in Germany) where physician Alfred Buchwald described a degenerative skin disorder now known as acrodermatitis chronica atrophicans. In 1909, 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, and that meningitic symptoms and signs occur in a number of cases; this rash is now known as erythema migrans (EM), the skin rash found in early stage Lyme disease.[1] In 1911, parasitologist Andrew Balfour of the Wellcome Research Laboratory in Khartoum identified "infective granules" or spore-type "cysts" as the cause of persistence of spirochetal infection in the Sudanese Fowl.[2]
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.[3] 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.[4][5][6]
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.[7]
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.[8]
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.[9] This was investigated by Dr. David Snydman and Dr.Allen Steere of the Epidemic Intelligence Service, and by 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.[10]
Before 1976, elements of B. 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,[11][12] 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.” [13] Although the notion of persistent neurological infection was identified early on by military researchers such as Dr. Sanford, later Lyme researchers curiously denied the possibility of persistent Borrelia infection in the brain, with many researchers ignoring evidence of persistent infection.
In 1980 Steere, et al, began to test antibiotic regimens in adult patients with Lyme disease[14] 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 researcher at the National Institutes of Health, who specialized in the study of spirochete microorganisms such as Borrelia and Rickettsia. 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 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.[15][16] The mechanism of tick transmission was also the subject of much discussion. B. burgdorferi spirochetes were identified in tick saliva in 1987, confirming the hypothesis that transmission occurred via tick salivary glands.[17]
References
- ↑ Lipschütz B (1931). "Zur Kenntnis der "Erythema chronicum migrans"". Acta dermato-venereologica (in German). 12: 100–2.
- ↑ Balfour A (1911). "The Infective Granule in Certain Protozoa Infections, as Illustrated by the Spirochaetosis of Sudanese Fowls". THe British Medical Journal: 1296.
- ↑ Lenhoff C (1948). "Spirochetes in aetiologically obscure diseases". Acta Dermato-Venreol. 28: 295–324.
- ↑ Bianchi GE (1950). "Penicillin therapy of lymphocytoma". Dermatologica. 100 (4–6): 270–3. PMID 15421023.
- ↑ Hollstrom E (1951). "Successful treatment of erythema migrans Afzelius". Acta Derm. Venereol. 31 (2): 235–43. PMID 14829185.
- ↑ Paschoud JM (1954). "Lymphocytoma after tick bite". Dermatologica (in German). 108 (4–6): 435–7. PMID 13190934.
- ↑ Meador CN (1915). "Five cases of relapsing fever originating in Colorado, with positive blood findings in two". Colorado Medicine. 12: 365–9.
- ↑ Scrimenti RJ (1970). "Erythema chronicum migrans". Archives of dermatology. 102 (1): 104–5. PMID 5497158.
- ↑ Steere AC (2006). "Lyme borreliosis in 2005, 30 years after initial observations in Lyme Connecticut". Wien. Klin. Wochenschr. 118 (21–22): 625–33. doi:10.1007/s00508-006-0687-x. PMID 17160599.
- ↑ Sternbach G, Dibble C (1996). "Willy Burgdorfer: Lyme disease". J Emerg Med. 14 (5): 631–4. PMID 8933327.
- ↑ Mast WE, Burrows WM (1976). "Erythema chronicum migrans and "Lyme arthritis"". JAMA. 236 (21): 2392. PMID 989847.
- ↑ Steere AC, Malawista SE, Snydman DR; et al. (1977). "Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three connecticut communities". Arthritis Rheum. 20 (1): 7–17. PMID 836338.
- ↑ Sanford JP (1976). "Relapsing Fever—Treatment and Control". In Johnson RC (ed). Biology of Parasitic Spirochetes. Academic Press. ISBN 9780123870506.
- ↑ Steere AC, Hutchinson GJ, Rahn DW; et al. (1983). "Treatment of the early manifestations of Lyme disease". Ann. Intern. Med. 99 (1): 22–6. PMID 6407378.
- ↑ Luft BJ, Volkman DJ, Halperin JJ, Dattwyler RJ (1988). "New chemotherapeutic approaches in the treatment of Lyme borreliosis". Ann. N. Y. Acad. Sci. 539: 352–61. PMID 3056203.
- ↑ Dattwyler RJ, Volkman DJ, Conaty SM, Platkin SP, Luft BJ (1990). "Amoxycillin plus probenecid versus doxycycline for treatment of erythema migrans borreliosis". Lancet. 336 (8728): 1404–6. PMID 1978873.
- ↑ Ribeiro JM, Mather TN, Piesman J, Spielman A (1987). "Dissemination and salivary delivery of Lyme disease spirochetes in vector ticks (Acari: Ixodidae)". J. Med. Entomol. 24 (2): 201–5. PMID 3585913.