Affiliation:
1. Department of Molecular Biology and Microbiology, Tufts University, Boston, Massachusetts, USA
2. Tufts University, Tufts Lyme Disease Initiative, Boston, Massachusetts, USA
3. Department of Infectious Disease and Global Health, Tufts University, North Grafton, Massachusetts, USA
Abstract
ABSTRACT
Borrelia burgdorferi
, a Lyme disease spirochete, causes a range of acute and chronic maladies in humans. However, a primary vertebrate reservoir in the United States, the white-footed deermouse
Peromyscus leucopus
, is reported not to have reduced fitness following infection. Although laboratory strains of
Mus musculus
mice have successfully been leveraged to model acute human Lyme disease, the ability of these rodents to model
B. burgdorferi-P. leucopus
interactions remains understudied. Here, we compared infection of
P. leucopus
with
B. burgdorferi
B31 with infection of the traditional
B. burgdorferi
murine models—C57BL/6J and C3H/HeN
Mus musculus
, which develop signs of inflammation akin to human disease. We find that
B. burgdorferi
was able to reach much higher burdens (10- to 30-times higher) in multiple
M. musculus
skin sites and that the overall dynamics of infection differed between the two rodent species. We also found that
P. leucopus
remained transmissive to larval
Ixodes scapularis
for a far shorter period than either
M. musculus
strain. In line with these observations, we found that
P. leucopus
does launch a modest but sustained inflammatory response against
B. burgdorferi
in the skin, which we hypothesize leads to reduced bacterial viability and rodent-to-tick transmission in these hosts. Similarly, we also observe evidence of inflammation in infected
P. leucopus
hearts. These observations provide new insight into reservoir species and the
B. burgdorferi
enzootic cycle.
IMPORTANCE
A Lyme disease-causing bacteria,
Borrelia burgdorferi
, must alternate between infecting a vertebrate host—usually rodents or birds—and ticks. In order to be successful in that endeavor, the bacteria must avoid being killed by the vertebrate host before it can infect a new larval tick. In this work, we examine how
B. burgdorferi
and one of its primary vertebrate reservoirs,
Peromyscus leucopus
, interact during an experimental infection. We find that
B. burgdorferi
appears to colonize its natural host less successfully than conventional laboratory mouse models, which aligns with a sustained seemingly anti-bacterial response by
P. leucopus
against the microbe. These data enhance our understanding of
P. leucopus
host-pathogen interactions and could potentially serve as a foundation to uncover ways to disrupt the spread of
B. burgdorferi
in nature.
Funder
HHS | NIH | National Institute of Allergy and Infectious Diseases
Global Lyme Alliance
Publisher
American Society for Microbiology
Cited by
1 articles.
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