Chapter 14 : Lyme Borreliosis

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Lyme borreliosis (Lyme disease) is unequivocally a persistent infectious disease. , the agent of Lyme disease, persists in both humans and animals, despite a vigorous and effective immune response by the infected host. The agent of Lyme disease also owes its survival to its propensity to infect a wide variety of mammalian and avian hosts, thereby allowing geographic spread and adaptation to new niches. The majority (60 to 80%) of patients with Lyme disease develop an expanding annular skin lesion (erythema migrans) at the site of the tick bite. Borrelia plasmids are fundamentally different from plasmids of other bacteria in that they contain essential, rather than nonessential, extrachromosomal elements of the genome. The phenomenon of lateral gene transfer and recombination may have selective advantages in mixed populations of spirochetes but does not provide an explanation for the immune evasion of clonal populations of spirochetes during persistent infection. The proof of the pudding for antigenic variation is whether antigenic changes in spirochetes provide selective advantages for the variant subpopulation in evading immune clearance. No evidence for this phenomenon has been observed with . Analysis of the outer and inner membranes of spirochetes indicates that the majority of protein is associated with the inner membrane and that proteins associated with the outer membrane, including OspC, may have only limited surface exposure.

Citation: Barthold S. 2000. Lyme Borreliosis, p 281-304. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch14

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Enzyme-Linked Immunosorbent Assay
Outer Membrane Proteins
Human Lyme Disease
Immune Systems
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Image of FIGURE 1

Indirect immunohistochemistry of joint tissue from an infected SCID mouse probed with immune serum from a i-infected immunocompetent mouse. Immune serum contains antibodies that are reactive to spirochetes in joint tissue, but the target antigen(s) has not been implicated.

Citation: Barthold S. 2000. Lyme Borreliosis, p 281-304. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch14
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Image of FIGURE 2

Indirect immunofluorescence of the midgut of a flat (resting) tick labeled with antiserum to OspA. Spirochetes within the midgut of the tick are strongly reactive with OspA antibody. (Reprinted from reference .)

Citation: Barthold S. 2000. Lyme Borreliosis, p 281-304. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch14
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Image of FIGURE 3

Indirect immunofluorescence of the midgut of a tick that has fed upon a mouse immunized with OspA. Ingestion of OspA antibody has killed organisms, with no viable spirochetes remaining in the midgut. (Reprinted from reference .)

Citation: Barthold S. 2000. Lyme Borreliosis, p 281-304. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch14
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Image of FIGURE 4

Indirect immunofluorescence and confocal microscopy of a tick salivary gland following onset of feeding, demonstrating loss of OspA following migration to salivary glands during feeding. Spirochetes are labeled with antiserum to (A) but are not labeled with antiserum to OspA (B). (With permission from E. Fikrig.)

Citation: Barthold S. 2000. Lyme Borreliosis, p 281-304. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch14
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