Although it wouldn’t have a name or known causative agent for nearly one hundred years, Lyme disease research dates back to 1883 when a German physician, Alfred Buchwald, recorded serious deterioration of skin tissue called acrodermatitis chronica atrophicans (ACA). We now recognize ACA as a classic symptom of late-stage European Lyme disease.
In 1908, when Swedish dermatologist Arvid Afzelius first described the classic Lyme-related bullseye rash, erythema migrans (EM), he suspected it may have resulted from a tick bite but couldn’t prove it. Just over a decade later, the first case of neurologic Lyme (Lyme neuroborreliosis) was reported by Garin and Bujadoux. Then, in 1940, similar cases of nerve pain radiating from the spine after tick bites were reported in Germany by Bannwarth, and the condition was recognized as Garin–Bujadoux–Bannwarth syndrome.
The name “Lyme disease” comes from the town of Lyme, Connecticut, where it was first described as a separate illness in 1975 when a group of 51 children and adults reported arthritis-like symptoms, including pain and swelling in large joints, headaches, fever, weakness, skin rash, and fatigue. They coined the condition Lyme but didn’t know the cause.
Several years later in 1981, scientist Willy Burgdorfer discovered a new corkscrew-shaped bacterium, a spirochete, in the gut of deer ticks while studying rocky mountain spotted fever. This new spirochete, which was called Borrelia burgdorferi after Burgdorfer, was determined to be the causative agent in Lyme disease.