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Abstract:

Borreliae are divided into relapsing fever (RF) and Lyme borreliosis groups. All species are vectored by blood-feeding arthropods and, with few exceptions, cause zoonotic infections, with humans being rare and dead-end hosts. Human infection is most commonly self-limited, may be asymptomatic, or may cause disease ranging from acute and relapsing fevers to staged illness that may involve the skin and musculoskeletal, neurological, and cardiovascular systems. RF borreliae are vectored by lice or ticks. Louse-transmitted RF has been known to humans for thousands of years and has been the cause of massive epidemics. In contrast, tick-transmitted RF was first described only in the late 1800s, and human disease, which presents in smaller clusters, is now known to occur throughout most of the world. In parts of northwest Africa, it is one of the most common bacterial infections, and in Tanzania, it is a leading cause of prenatal and child mortality. Lyme borreliosis was reported in 19th-century literature from Europe. The disease garnered little notoriety and was largely unknown until 1975, when a group of parents in Lyme, CT, expressed concerns of a seeming epidemic of inflammatory arthritis among local children. Ensuing investigations linked antecedent tick bites with rashes and arthritis among children and adults. The causative agent, , and transmission by ticks were described shortly thereafter. Cases reported to the CDC have increased steadily, and it has become and remains the most prevalent vector-borne disease in North America. Lyme borreliosis is thought to be significantly underreported in the United States, Canada, and much of Europe.

Citation: Schriefer M. 2015. , p 1037-1054. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch59
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FIGURE 1

Two genera of ticks are vectors for relapsing fever and Lyme borreliosis: (a) and (b). doi:10.1128/9781555817381.ch59.f1

Citation: Schriefer M. 2015. , p 1037-1054. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch59
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FIGURE 2

Scanning electron micrograph of (provided by Gerhard Wanner, Munich, Germany). doi:10.1128/9781555817381.ch59.f2

Citation: Schriefer M. 2015. , p 1037-1054. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch59
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FIGURE 3

Borrelia spirochetes. in a thin smear of patient blood (bright-field microscopy, Giemsa stain) (a) and culture (dark-field microscopy) (b). doi:10.1128/9781555817381.ch59.f3

Citation: Schriefer M. 2015. , p 1037-1054. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch59
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FIGURE 4

Two-step approach for serodiagnosis. doi:10.1128/9781555817381.ch59.f4

Citation: Schriefer M. 2015. , p 1037-1054. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch59
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FIGURE 5

Whole-cell immunoblot for identification of diagnostic bands with MAbs. The antigen used is strain PKo. Lane G, IgG blot from a patient with late disease; lane M, IgM blot from a patient with early disease; lanes 1 to 11, different MAbs against the respective reactive proteins. (Modified from .) doi:10.1128/9781555817381.ch59.f5

Citation: Schriefer M. 2015. , p 1037-1054. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch59
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Tables

Generic image for table
TABLE 1

Characteristics of arthropod-borne borreliae

Citation: Schriefer M. 2015. , p 1037-1054. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch59
Generic image for table
TABLE 2

Distribution of species of in European isolates from CSF, skin, and synovial fluid specimens

Citation: Schriefer M. 2015. , p 1037-1054. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch59
Generic image for table
TABLE 3

Specimen types used for the diagnosis of Lyme borreliosis

Citation: Schriefer M. 2015. , p 1037-1054. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch59
Generic image for table
TABLE 4

Sensitivity of methods for pathogen detection (PCR and culture) in Lyme borreliosis

Citation: Schriefer M. 2015. , p 1037-1054. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch59
Generic image for table
TABLE 5

Sensitivity of antibody detection methods in the diagnosis of Lyme disease

Citation: Schriefer M. 2015. , p 1037-1054. In Jorgensen J, Pfaller M, Carroll K, Funke G, Landry M, Richter S, Warnock D (ed), Manual of Clinical Microbiology, Eleventh Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817381.ch59

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