Lyme borreliosis is the most common tick-transmitted illness in the Northern Hemisphere [
1,
2]. It is caused by
Borrelia burgdorferi sensu lato [
3].
Human disease is associated with at least 3 Borrelia species: B. burgdorferi sensu stricto (B. burgdorferi), Borrelia afzelii, and Borrelia garinii. All isolates from North American patients have been members of the genomic group
B. burgdorferi, whereas European isolates have included at least 2 additional genospecies:
B. afzelii and
B. garinii [
4]. Although probably all 3 genospecies can cause all major manifestations, there are indications that infection with different
B. burgdorferi sensu lato genospecies results in distinct clinical manifestations of Lyme borreliosis, most probably as a consequence of their distinct organotropism. For example, in Europe,
B. afzelii is mostly associated with skin manifestations, such as erythema migrans (EM) and acrodermatitis chronica atrophicans, whereas
B. garinii is the main cause of Lyme neuroborreliosis [
1,
5–
8]. Differences in geographical distribution of genospecies may explain the distinctions between the clinical picture of Lyme borreliosis in Europe and in North America [
1,
2,
9]. Although data indicating the association of different
B. burgdorferi sensu lato genospecies with distinct clinical manifestations of Lyme borreliosis are relatively abundant and obvious [
1,
2,
7–
9], comparisons of the characteristics of individual clinical manifestations caused by different
Borrelia genospecies are quite scarce. In fact, information is limited to the reports concerning patients with EM [
10–
12]. Comparison of culture-confirmed EM caused by
B. afzelii with EM caused by
B. burgdorferi showed differences in epidemiological, clinical, and laboratory findings, suggesting 2 distinct syndromes that are caused by different agents [
10]. Two other studies have demonstrated several differences between EM due to
B. afzelii and
B. garinii [
11,
12].
.
.
