Lyme borreliosis

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  • A Correction to this article was published on 03 August 2017

Abstract

Lyme borreliosis is a tick-borne disease that predominantly occurs in temperate regions of the northern hemisphere and is primarily caused by the bacterium Borrelia burgdorferi in North America and Borrelia afzelii or Borrelia garinii in Europe and Asia. Infection usually begins with an expanding skin lesion, known as erythema migrans (referred to as stage 1), which, if untreated, can be followed by early disseminated infection, particularly neurological abnormalities (stage 2), and by late infection, especially arthritis in North America or acrodermatitis chronica atrophicans in Europe (stage 3). However, the disease can present with any of these manifestations. During infection, the bacteria migrate through the host tissues, adhere to certain cells and can evade immune clearance. Yet, these organisms are eventually killed by both innate and adaptive immune responses and most inflammatory manifestations of the infection resolve. Except for patients with erythema migrans, Lyme borreliosis is diagnosed based on a characteristic clinical constellation of signs and symptoms with serological confirmation of infection. All manifestations of the infection can usually be treated with appropriate antibiotic regimens, but the disease can be followed by post-infectious sequelae in some patients. Prevention of Lyme borreliosis primarily involves the avoidance of tick bites by personal protective measures.

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Figure 1: Age and sex distribution and seasonality of Lyme borreliosis.
Figure 2: Distribution of Ixodes ticks that transmit Borrelia burgdorferi s.l. to humans.
Figure 3: Morphology and cellular architecture of Borrelia burgdorferi.
Figure 4: Mechanisms of innate immune recognition of Borrelia burgdorferi.
Figure 5: Dermatological manifestations of Lyme borreliosis.
Figure 6: The stages and most common clinical features of Lyme borreliosis.

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Acknowledgements

A.C.S. has received funding from the US National Institutes of Health (NIH) (R01 AI-101175), the English–Bonter–Mitchell Foundation and the Eshe Fund. F.S. was supported by the Slovenian Research Agency (P3-0296). L.T.H. has received funding from the NIH (R21 AI-126757, R21 AI-103905, U01 AI-109656 and R21 AI-111317) and the Steven and Alexandra Cohen Foundation. J.A.B. has received funding from the NIH (R21 AI-119457). X.L. has received funding from the NIH (R01 AI-103173). J.W.R.H. is supported by the European Commission (grant agreement 602272). However, none of these funding sources had a role in the preparation or approval of this manuscript.

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Introduction (A.C.S.); Epidemiology (P.S.M.); Mechanisms/pathophysiology (L.T.H. and X.L.); Diagnosis, screening and prevention (A.C.S. and F.S.); Management (G.P.W. and F.S.); Quality of life (A.C.S. and F.S.); Outlook (J.A.B., A.C.S., P.S.M. and J.W.R.H.); Overview of Primer (A.C.S.).

Correspondence to Allen C. Steere.

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Competing interests

A.C.S. declares grant support from Immunetics, Inc. and Viramed. F.S. has served as a consultant to Baxter Biosciences regarding Lyme vaccine development and has been a member of the steering committee of the European Society of Clinical Microbiology and Infectious Diseases Study Group on Lyme Borreliosis (ESGBOR). G.P.W. has received research grants from Immunetics Inc., Institute for Systems Biology, Rarecyte, Inc. and Quidel Corporation. G.P.W. also owns equity in Abbott, has been an expert witness in malpractice cases involving Lyme borreliosis and is an unpaid board member of the American Lyme Disease Foundation. J.A.B. declares grant support from Immunetics, Inc. and Diasorin. J.W.R.H. is a member of the steering committee of ESGBOR. L.T.H., X.L. and P.S.M. declare no competing interests.

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Steere, A., Strle, F., Wormser, G. et al. Lyme borreliosis. Nat Rev Dis Primers 2, 16090 (2016) doi:10.1038/nrdp.2016.90

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