Lyme Diagnostic and Therapeutic Center

What is Lyme disease?

Lyme disease was first identified in 1976 in the Connecticut area of the United States, in children who were initially believed to be suffering from juvenile rheumatoid arthritis (1). Five years later, Burgdorfer and his colleagues discovered a spirochetal bacterium, which was named Borrelia burgdorferi, in a nymphal tick known as Ixodes scapularis. It was soon determined that this bacterium was the cause of early Lyme disease, thereby confirming the spirochetal etiology of the infection (2).
Therefore, Lyme borreliosis (Lyme disease) is caused by spirochetes of the Borelia burgdorferi sensu lato complex, which are spread via ticks.

The one most frequently associated with spreading the illness in North America is Borelia burgdorferi sensu stricto. In Europe, at least five Lyme Borrelia species (Borelia afzelii, Borelia garinii, Borrelia burgdorferi, Borrelia spielmanii, and Borrelia bavariensis) can cause the disease, resulting in a broader spectrum of possible clinical manifestations than in North America. Other species have been discovered, however they are not as dangerous as the preceding ones.

Borrelia aphthousis is the only known pathogen that causes the chronic skin condition acrodermatitis chronica atrophicans (3). Borelia garinii is more commonly detected in cases of neuroboreliosis (4) and central nervous system diseases (5). Borelia spielmanii has so far only been described as a cause of erythema migrans. The other species can apparently give rise to all clinical manifestations of boreliosis.

1.     Steere, Allen C., Jenifer Coburn, and Lisa Glickstein. "The emergence of Lyme disease." The Journal of clinical investigation 113.8 (2004): 1093-1101.
2. Zhang, Jing-Ren, and Steven J. Norris. "Genetic variation of the Borrelia burgdorferi gene vlsE involves cassette-specific, segmental gene conversion." Infection and immunity 66.8 (1998): 3698-3704.
3. Ohlenbusch, Andreas, et al. "Etiology of the acrodermatitis chronica atrophicans lesion in Lyme disease." Journal of Infectious Diseases 174.2 (1996): 421-423.
4. Wilske, Bettina, et al. "Diversity of OspA and OspC among cerebrospinal fluid isolates of Borrelia burgdorferi sensu lato from patients with neuroborreliosis in Germany." Medical microbiology and immunology 184.4 (1996): 195-201.
5. Eiffert, Helmut, et al. "Nondifferentiation between Lyme disease spirochetes from vector ticks and human cerebrospinal fluid." Journal of Infectious Diseases 171.2 (1995): 476-479.