Interactions between Borrelia burgdorferi and its hosts across the enzootic cycle

2020 ◽  
Author(s):  
Jennifer D. Helble ◽  
Julie E. McCarthy ◽  
Linden T. Hu
Keyword(s):  
Borrelia Burgdorferi ◽  
Enzootic Cycle

scholarly journals Borrelia burgdorferi Requires Glycerol for Maximum Fitness During The Tick Phase of the Enzootic Cycle

2011 ◽  
Vol 7 (7) ◽  
pp. e1002102 ◽  
Author(s):  
Christopher J. Pappas ◽  
Radha Iyer ◽  
Mary M. Petzke ◽  
Melissa J. Caimano ◽  
Justin D. Radolf ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Enzootic Cycle

scholarly journals Borrelia burgdorferi Needs Chemotaxis To Establish Infection in Mammals and To Accomplish Its Enzootic Cycle

2012 ◽  
Vol 80 (7) ◽  
pp. 2485-2492 ◽  
Author(s):  
Ching Wooen Sze ◽  
Kai Zhang ◽  
Toru Kariu ◽  
Utpal Pal ◽  
Chunhao Li
Keyword(s):  
Borrelia Burgdorferi ◽  
Capillary Tube ◽  
Virulent Strain ◽  
Gene Encoding ◽  
Content Type ◽  
Immunodeficient Mice ◽  
Passage Number ◽  
Low Passage ◽  
Enzootic Cycle

ABSTRACTBorrelia burgdorferi, the causative agent of Lyme disease, can be recovered from different organs of infected animals and patients, indicating that the spirochete is very invasive. Motility and chemotaxis contribute to the invasiveness ofB. burgdorferiand play important roles in the process of the disease. Recent reports have shown that motility is required for establishing infection in mammals. However, the role of chemotaxis in virulence remains elusive. Our previous studies showed thatcheA2, a gene encoding a histidine kinase, is essential for the chemotaxis ofB. burgdorferi. In this report, thecheA2gene was inactivated in a low-passage-number virulent strain ofB. burgdorferi. In vitroanalyses (microscopic observations, computer-based bacterial tracking analysis, swarm plate assays, and capillary tube assays) showed that thecheA2mutant failed to reverse and constantly ran in one direction; the mutant was nonchemotactic to attractants. Mouse needle infection studies showed that thecheA2mutant failed to infect either immunocompetent or immunodeficient mice and was quickly eliminated from the initial inoculation sites. Tick-mouse infection studies revealed that although the mutant was able to survive in ticks, it failed to establish a new infection in mice via tick bites. The altered phenotypes were completely restored when the mutant was complemented. Collectively, these data demonstrate thatB. burgdorferineeds chemotaxis to establish mammalian infection and to accomplish its natural enzootic cycle.

scholarly journals The coenzyme A disulphide reductase of Borrelia burgdorferi is important for rapid growth throughout the enzootic cycle and essential for infection of the mammalian host

2011 ◽  
Vol 82 (3) ◽  
pp. 679-697 ◽  
Author(s):  
Christian H. Eggers ◽  
Melissa J. Caimano ◽  
Robert A. Malizia ◽  
Toru Kariu ◽  
Brian Cusack ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Rapid Growth ◽  
Coenzyme A ◽  
Mammalian Host ◽  
Enzootic Cycle

scholarly journals The infectivity gene bbk13 is important for multiple phases of the Borrelia burgdorferi enzootic cycle

2021 ◽  
Author(s):  
George F. Aranjuez ◽  
Amanda G. Lasseter ◽  
Mollie W. Jewett
Keyword(s):  
Borrelia Burgdorferi ◽  
Ixodes Scapularis ◽  
Feeding Activity ◽  
Molecular Genetic ◽  
Population Expansion ◽  
Tick Feeding ◽  
Disseminated Infection ◽  
Multi Stage ◽  
Pathogen Vector ◽  
Enzootic Cycle

Lyme disease is a multi-stage inflammatory disease caused by the spirochete Borrelia burgdorferi transmitted through the bite of an infected Ixodes scapularis tick. We previously discovered a B. burgdorferi infectivity gene, bbk13 , that facilitates mammalian infection by promoting spirochete population expansion in the skin inoculation site. Initial characterization of bbk13 was carried out using an intradermal needle inoculation model of mouse infection, which does not capture the complex interplay of the pathogen-vector-host triad of natural transmission. Herein, we aimed to understand the role of bbk13 in the enzootic cycle of B. burgdorferi . B. burgdorferi lacking bbk13 were unable to be acquired by naive larvae fed on needle inoculated mice. Using a capsule-feeding approach to restrict tick feeding activity to a defined skin site, we determined that delivery by tick bite alleviated the population expansion defect in the skin observed after needle inoculation of Δ bbk13 B. burgdorferi . Despite overcoming the early barrier in the skin, Δ bbk13 B. burgdorferi remained attenuated for distal tissue colonization after tick transmission. Disseminated infection of Δ bbk13 B. burgdorferi was improved in needle inoculated immunocompromised mice. Together, we established that bbk13 is crucial to the maintenance of B. burgdorferi in the enzootic cycle and that bbk13 is necessary beyond early infection in the skin, likely contributing to host immune evasion. Moreover, our data highlight the critical interplay between the pathogen, vector, and host as well as the distinct molecular genetic requirements for B. burgdorferi to survive at the pathogen-vector-host interface and to achieve productive disseminated infection.

scholarly journals Analysis of the RpoS regulon in Borrelia burgdorferi in response to mammalian host signals provides insight into RpoS function during the enzootic cycle

2007 ◽  
Vol 65 (5) ◽  
pp. 1193-1217 ◽  
Author(s):  
Melissa J. Caimano ◽  
Radha Iyer ◽  
Christian H. Eggers ◽  
Cynthia Gonzalez ◽  
Elizabeth A. Morton ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Mammalian Host ◽  
Host Signals ◽  
Insight Into ◽  
Enzootic Cycle
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