Affiliation:
1. Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840
Abstract
ABSTRACT
Borrelia burgdorferi
, the causative agent of Lyme disease, exists in a complex enzootic cycle, transiting between its vector,
Ixodes
ticks, and a diverse range of vertebrate hosts.
B. burgdorferi
linear plasmid 38 (lp38) contains several genes that are differentially regulated in response to conditions mimicking the tick or mouse environments, suggesting that these plasmid-borne genes may encode proteins important for the
B. burgdorferi
infectious cycle. Some of these genes encode potential virulence factors, including hypothetical lipoproteins as well as a putative membrane transport system. To characterize the role of lp38 in the
B. burgdorferi
infectious cycle, we constructed a shuttle vector to selectively displace lp38 from the
B. burgdorferi
genome and analyzed the resulting clones to confirm the loss of lp38. We found that,
in vitro
, clones lacking lp38 were similar to isogenic wild-type bacteria, both in growth rate and in antigenic protein production. We analyzed these strains in an experimental mouse-tick infectious cycle, and our results demonstrate that clones lacking lp38 are fully infectious in a mouse, can efficiently colonize the tick vector, and are readily transmitted to a naive host.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
20 articles.
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