House finches with high coccidia burdens experience more severe experimental Mycoplasma gallisepticum infections
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IMMUNOLOGY AND HOST-PARASITE INTERACTIONS - SHORT COMMUNICATION
House finches with high coccidia burdens experience more severe experimental Mycoplasma gallisepticum infections Chava L. Weitzman 1 Dana M. Hawley 1
&
Courtney Thomason 1,2
&
Edward J. A. Schuler 1,3
&
Ariel E. Leon 1
&
Sara R. Teemer 1 &
Received: 26 March 2020 / Accepted: 9 July 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Parasites co-infecting hosts can interact directly and indirectly to affect parasite growth and disease manifestation. We examined potential interactions between two common parasites of house finches: the bacterium Mycoplasma gallisepticum that causes conjunctivitis and the intestinal coccidian parasite Isospora sp. We quantified coccidia burdens prior to and following experimental infection with M. gallisepticum, exploiting the birds’ range of natural coccidia burdens. Birds with greater baseline coccidia burdens developed higher M. gallisepticum loads and longer lasting conjunctivitis following inoculation. However, experimental inoculation with M. gallisepticum did not appear to alter coccidia shedding. Our study suggests that differences in immunocompetence or condition may predispose some finches to more severe infections with both pathogens. Keywords Co-infection . Coccidia . Conjunctivitis . Mycoplasma gallisepticum
Introduction Free-living hosts typically house a complex suite of parasites and pathogens that interact with each other, and their host, through bottom-up (resource-mediated) and top-down (immune-mediated) processes (Pedersen and Fenton 2007). Indirect interactions such as immune-mediated processes, whereby parasites interact with each other through modulation of their host, are particularly relevant for co-infecting parasites Chava L. Weitzman, Courtney Thomason and Edward J. A. Schuler contributed equally to this work. Handling Editor: Una Ryan Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00436-020-06814-0) contains supplementary material, which is available to authorized users. * Chava L. Weitzman [email protected] 1
Department of Biological Sciences, Virginia Tech, Blacksburg, VA, USA
2
Tennessee Department of Environment and Conservation, Division of Remediation, Oak Ridge, TN, USA
3
Department of Microbiology and Immunology, Virginia Commonwealth Medical Center, Richmond, VA, USA
that do not occupy the same host tissues. For example, in humans, immune stimulation by the gastrointestinal pathogen Helicobacter pylori suppresses co-infection of the lung pathogen Mycobacterium tuberculosis (TB) as a consequence of both infections stimulating T-helper 1 (Th1) immunity (Perry et al. 2010). When two parasites stimulate different immune components, an immunological bias against one invader can facilitate a second parasite’s invasion or severity. In buffalo, individuals that produced a strong T-helper type 2 (Th2) response to combat nematode infections had lower Th1 immunity and were more likely to be invaded by bovine
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