10.5061/DRYAD.J6Q573N8R
Becker, Daniel
0000-0003-4315-8628
Indiana University Bloomington
Speer, Kelly
American Museum of Natural History
Brown, Alexis
Stony Brook University
Washburne, Alex
Montana State University
Fenton, Brock
Western University
Altizer, Sonia
University of Georgia
Streicker, Daniel
University of Glasgow
Plowright, Raina
Montana State University
Chizhikov, Vladimir
China Food and Drug Administration
Simmons, Nancy
American Museum of Natural History
Volokhov, Dmitriy
China Food and Drug Administration
Ecological and evolutionary drivers of hemoplasma infection and genotype
sharing in a Neotropical bat community
Dryad
dataset
2019
host shifts
parasite sharing
bacterial zoonosis
cophylogeny
Host specificity
2020-04-02T00:00:00Z
2020-04-02T00:00:00Z
en
74514 bytes
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CC0 1.0 Universal (CC0 1.0) Public Domain Dedication
Most emerging pathogens can infect multiple species, underscoring the
importance of understanding the ecological and evolutionary factors that
allow some hosts to harbor greater infection prevalence and share
pathogens with other species. However, our understanding of pathogen jumps
is primarily based around viruses, despite bacteria accounting for the
greatest proportion of zoonoses. Because bacterial pathogens in bats
(Order: Chiroptera) can have conservation and human health consequences,
studies that examine the ecological and evolutionary drivers of bacterial
prevalence and barriers to pathogen sharing are crucially needed. We here
studied hemotropic Mycoplasma spp. (i.e., hemoplasmas) across a
species-rich bat community in Belize over two years. Across 469 bats
spanning 33 species, half of individuals and two-thirds of species were
hemoplasma positive. Infection prevalence was higher for males and for
species with larger body mass and colony sizes. Hemoplasmas displayed high
genetic diversity (21 novel genotypes) and strong host specificity.
Evolutionary patterns supported co-divergence of bats and bacterial
genotypes alongside phylogenetically constrained host shifts. Bat species
centrality to the network of shared hemoplasma genotypes was
phylogenetically clustered and unrelated to prevalence, further suggesting
rare—but detectable—bacterial sharing between species. Our study
highlights the importance of using fine phylogenetic scales when assessing
host specificity and suggests phylogenetic similarity may play a key role
in host shifts for not only viruses but also bacteria. Such work more
broadly contributes to increasing efforts to understand cross-species
transmission and epidemiological consequences of bacterial pathogens.