The expanding Lyme Borrelia complex—clinical significance of
G. Stanek and M. Reiter
Institute for Hygiene and Applied Immunology, Medical University of Vienna, Vienna, Austria
Ten years after the discovery of spirochaetes as agents of Lyme disease in 1982 in the USA, three genomic species had diverged from
the phenotypically heterogeneous strains of Borrelia burgdorferi isolated in North America and Europe: Borrelia afzelii, B. burgdorferi sen-
su stricto (further B. burgdorferi), and Borrelia garinii. Whereas B. burgdorferi remained the only human pathogen in North America, all
three species are aetiological agents of Lyme borreliosis in Europe. Another seven genospecies were described in the 1990s, including
species from Asia (Borrelia japonica, Borrelia turdi, and B. tanukii), North America (Borrelia andersonii), Europe (Borrelia lusitaniae and Bor-
relia valaisiana), and from Europe and Asia (Borrelia bissettii). Another eight species were delineated in the years up to 2010: Borrelia sinica
(Asia), Borrelia spielmanii (Europe), Borrelia yangtze (Asia), Borrelia californiensis, Borrelia americana, Borrelia carolinensis (North America),
Borrelia bavariensis (Europe), and Borrelia kurtenbachii (North America). Of these 18 genomic species B. afzelii, B. burgdorferi and B. garinii
are the confirmed agents of localized, disseminated and chronic manifestations of Lyme borreliosis, whereas B. spielmanii has been
detected in early skin disease, and B. bissettii and B. valaisiana have been detected in specimens from single cases of Lyme borreliosis.
The clinical role of B. lusitaniae remains to be substantiated.
Keywords: Borrelia afzelii, Borrelia burgdorferi, Borrelia garinii, clinical relevance, genomic species
Article published online: 15 February 2011
Clin Microbiol Infect 2011; 17: 487–493
Corresponding author: G. Stanek, Institute for Hygiene and
Applied Immunology, Medical University of Vienna, Kinderspitalgasse
15, 1095 Vienna, Vienna, Austria
Lyme borreliae may be considered postmodern pathogens,
because the illness they cause varies, does not have a pre-
dictable incubation period or course, and is likely to have a
variable response. Protean manifestations and the absence of
techniques to identify the organism in cases of Lyme borre-
liosis lead to bizarre ideas, and fantasies [1–3].
From Lyme Spirochaete to Borrelia
burgdorferi Sensu Lato
In 1982, after the discovery of Lyme spirochaetes in hard ticks
from Long Island, NY, USA , the aetiology of Lyme disease
was confirmed by the cultivation of these spirochaetes from
skin, blood and cerebrospinal fluid (CSF) of patients [5,6]. The
Lyme spirochaete was identified as a new species of the genus
Borrelia . It very quickly became evident that not only did
the clinical presentation of a Borrelia burgdorferi infection in
Europe differ somewhat from that in North America, but so
did the isolates from Lyme borreliosis patients and from ticks
[8–10]. It was observed that an increasing number of Euro-
pean isolates of Lyme borreliae from patients and ticks were
phenotypically heterogeneous and differed from the American
type strain of B. burgdorferi. Thus, it was concluded that
B. burgdorferi may comprise different genomic species, which,
however, share common epitopes that are recognized by cer-
tain monoclonal antibodies. A serotyping system based on
monoclonal antibody reactivity against the outer surface pro-
tein OspA was introduced. At the subspecies level, heteroge-
neity was demonstrated by restriction endonuclease analysis,
hybridization with whole B. burgdorferi DNA or specific
probes, and plasmid analysis. Genetic analysis of the broad
variety of phenotypically defined strains was required in order
to identify genotypic clusters . The first result of an
approach to classify Lyme borreliae on the basis of genomic
ª2011 The Authors
Clinical Microbiology and Infection ª2011 European Society of Clinical Microbiology and Infectious Diseases
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Stanek and Reiter
The expanding Lyme Borrelia complex
ª2011 The Authors
Clinical Microbiology and Infection ª2011 European Society of Clinical Microbiology and Infectious Diseases, CMI, 17, 487–493