Growth Kinetics of the Lyme Disease Spirochete (Borrelia Burgdorferi) in Vector Ticks (Ixodes Dammini)

Piesman, Joseph; Oliver, James R.; Sinsky, Richard J.

doi:10.4269/ajtmh.1990.42.352

Cited by 156 publications

(148 citation statements)

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“…It is interesting to speculate as to why the motility states that we observe in the dermis and in gelatin may be important during the enzootic cycle. The tick midgut seems to be a hospitable environment for Bb, as the spirochetes are found in high abundance at this site (21,36,37). However, during the blood meal, some spirochetes must leave the tick and transition to the mammalian host for the species to survive (38).…”

Section: Discussionmentioning

confidence: 99%

The heterogeneous motility of the Lyme disease spirochete in gelatin mimics dissemination through tissue

Harman

Dunham-Ems

Caimano

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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The Lyme disease spirochete Borrelia burgdorferi exists in nature in an enzootic cycle that involves the arthropod vector Ixodes scapularis and mammalian reservoirs. To disseminate within and between these hosts, spirochetes must migrate through complex, polymeric environments such as the basement membrane of the tick midgut and the dermis of the mammal. To date, most research on the motility of B. burgdorferi has been done in media that do not resemble the tissue milieus that B. burgdorferi encounter in vivo. Here we show that the motility of Borrelia in gelatin matrices in vitro resembles the pathogen's movements in the chronically infected mouse dermis imaged by intravital microscopy. More specifically, B. burgdorferi motility in mouse dermis and gelatin is heterogeneous, with the bacteria transitioning between at least three different motility states that depend on transient adhesions to the matrix. We also show that B. burgdorferi is able to penetrate matrices with pore sizes much smaller than the diameter of the bacterium. We find a complex relationship between the swimming behavior of B. burgdorferi and the rheological properties of the gelatin, which cannot be accounted for by recent theoretical predictions for microorganism swimming in gels. Our results also emphasize the importance of considering borrelial adhesion as a dynamic rather than a static process.

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Section: Discussionmentioning

confidence: 99%

The heterogeneous motility of the Lyme disease spirochete in gelatin mimics dissemination through tissue

Harman

Dunham-Ems

Caimano

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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“…The nymphal stage is the most clinically relevant because it is usually responsible for the transmission of spirochetes to humans, an accidental host outside of the enzootic cycle (11,12). Nymphal feeding induces the exponential expansion of spirochetes and migration of organisms out of the midgut into the hemocoel (13,14), a process facilitated by the acquisition of plasminogen (15,16). Once in the hemocoel, Lyme disease spirochetes must contend with the primary mediators of tick innate immunity, hemocytes and defensins, as they navigate toward the salivary glands (15,17).…”

Section: Introductionmentioning

confidence: 99%

Live imaging reveals a biphasic mode of dissemination of Borrelia burgdorferi within ticks

et al. 2009

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Lyme disease is caused by transmission of the spirochete Borrelia burgdorferi from ticks to humans. Although much is known about B. burgdorferi replication, the routes and mechanisms by which it disseminates within the tick remain unclear. To better understand this process, we imaged live, infectious B. burgdorferi expressing a stably integrated, constitutively expressed GFP reporter. Using isolated tick midguts and salivary glands, we observed B. burgdorferi progress through the feeding tick via what we believe to be a novel, biphasic mode of dissemination. In the first phase, replicating spirochetes, positioned at varying depths throughout the midgut at the onset of feeding, formed networks of nonmotile organisms that advanced toward the basolateral surface of the epithelium while adhering to differentiating, hypertrophying, and detaching epithelial cells. In the second phase of dissemination, the nonmotile spirochetes transitioned into motile organisms that penetrated the basement membrane and entered the hemocoel, then migrated to and entered the salivary glands. We designated the first phase of dissemination "adherence-mediated migration" and provided evidence that it involves the inhibition of spirochete motility by one or more diffusible factors elaborated by the feeding tick midgut. Our studies, which we believe are the first to relate the transmission dynamics of spirochetes to the complex morphological and developmental changes that the midgut and salivary glands undergo during engorgement, challenge the conventional viewpoint that dissemination of Lyme disease-causing spirochetes within ticks is exclusively motility driven.

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“…The population of spirochetes expands [156][157][158] and their protein synthesis alters [49,99,122,159,160]. Then, spirochetes migrate from the midgut to the salivary glands, allowing transmission into a new host.…”

Section: B Burgdorferi Infection Of Ticksmentioning

confidence: 99%

Biology of Infection with Borrelia burgdorferi

Tilly

Rosa

Stewart

2008

Infectious Disease Clinics of North America

183

177

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The spirochete Borrelia burgdorferi is a tick-borne obligate parasite whose normal reservoir is a variety of small mammals [1]. Whereas infection of these natural hosts does not lead to disease, infection of humans can result in Lyme disease, as a consequence of the human immunopathological response to B. burgdorferi [2,3]. Consistent with the pathogenesis of Lyme disease, bacterial products that allow B. burgdorferi to replicate and survive, rather than true "virulence factors," appear to be primarily what is required for the bacterium to cause disease in a susceptible host. In support of this idea, the genome sequence of B31, the type strain of B. burgdorferi sensu stricto [4,5], revealed that the bacterium lacks factors common to many bacterial pathogens, such as lipopolysaccharide, toxins, and specialized secretion systems. In this chapter, we will describe the basic biology of B. burgdorferi, and some of the bacterial components required to infect and survive in the mammalian and tick hosts.

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Growth Kinetics of the Lyme Disease Spirochete (Borrelia Burgdorferi) in Vector Ticks (Ixodes Dammini)

Cited by 156 publications

References 0 publications

The heterogeneous motility of the Lyme disease spirochete in gelatin mimics dissemination through tissue

The heterogeneous motility of the Lyme disease spirochete in gelatin mimics dissemination through tissue

Live imaging reveals a biphasic mode of dissemination of Borrelia burgdorferi within ticks

Biology of Infection with Borrelia burgdorferi

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