The Connecticut town, Old Lyme, played a major role in Lyme disease history as it was here, in 1975, that a group of concerned parents questioned the alarming incidence of rheumatoid arthritis in their children. Researchers, including Allen C. Steere, moved in to investigate the cluster of around fifty cases and the children were diagnosed, incorrectly, with juvenile rheumatoid arthritis. In 1976 however a cluster of cases at a naval medical hospital in Connecticut forced clinicians to revise their opinions on the disease and Steere changed the diagnosis to Lyme Arthritis in 1977.
Following extensive investigation as to the cause of the condition the researcher Willy Burgdorferi identified, in 1981, the bacterium Borrelia burgdorferi sensu stricto as responsible for the development of Lyme disease in the cases in Connecticut.
These cases were not the first instance of Lyme disease however, with Alfred Buchwald documenting the disease back in 1883 albeit as a chronic skin condition now thought to be acrodermatitis chronica atrophicans. Subsequently, other variations of the Borrelia bacteria have been found to cause Lyme disease and these infectious bacteria are now known as Borrelia burgdorferi sensu lato which encompasses several individual bacterial species.
Lyme Disease History Around the World
Lyme disease has been observed in almost all of the US, along with many European countries, China, Japan, Australia, and Russia. The bacteria responsible for North American cases remains B. burgdorferi s.s., whilst Europe has B.afzelii and B.garinii as the major causative agents. The symptoms of infection by these bacteria vary, with arthritis more likely to occur following infection in North America, and neurological symptoms the more prevalent feature in European patients. The discrepancy between symptomology meant that, for many years, patients remained undiagnosed with the disease and failed to receive appropriate antibiotic treatment before the infection caused long-term damage. Several skin conditions, such as erythema migrans, and acrodermatitis chronica atrophicans observed in Europe were known to be caused by ticks but remained unconnected as part of a single illness; Lyme disease.
Borrelia afzelii is named after the researcher Arvid Afzelius who detailed cases of erythema migrans back in 1909 before speculating in 1921 on the origin of the disease as the Ixodes Scapularis tick. He also published work connecting the characteristic bull’s eye rash to the joint problems experienced by many sufferers of Lyme disease and paved the way for later work on the condition. Also in 1922 the same condition thought to cause erythema migrans, acrodermatitis chronica atrophicans, and joint pains was also associated with neurological problems, with psychiatric disorders linked to the disease in 1930. It is not until the cases in Old Lyme in 1975 that much else of note happens in Lyme disease history, although a dermatology professor, Rudolph Scrimenti, published a report on erythema migrans in 1970 and then detailed results of his success in treating the rash with antibiotics five years later.
Standard treatment of Lyme disease with oral and intravenous antibiotics began in 1983 with clinicians also defining the three stages of the condition, the early acute stage, the early disseminated stage, and later-stage Lyme disease. A few years later, in 1986, the backlash against Lyme disease began, with sceptics claiming that the disease did not exist. In response, the Lyme Disease Foundation was founded to support patients and clinicians, now just one of many such organizations purporting to do the same.
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