Abstract
Habitat fragmentation and wildlife disease are two widespread drivers of biodiversity loss, yet few empirical studies have explored their interactions. In this study, we utilized a naturally fragmented island system to examine the impacts of fragmentation on genetic diversity and amphibian infection dynamics. We determined the impacts of fragmentation on genetic diversity at the immunity locus MHC IIB, a hypothesized predictor of disease susceptibility. Contrary to expectations, island populations lost genetic diversity at this locus while simultaneously experiencing positive selection at MHC IIB. We then used Next-Generation Sequencing to identify a variety of potential eukaryotic parasites from amphibian skin swabs. Island populations exhibited higher potential parasite richness (proportion of eukaryotic microbe operational taxonomic units or OTUs from parasitic taxa) relative to mainland populations. MHC homozygotes hosted a lower diversity of potential parasites, and population-level MHC diversity was negatively associated with parasite richness. Our results show that genetic erosion can occur at the MHC IIB locus following fragmentation, which may contribute to increased susceptibility to parasites.
Highlights
Habitat loss and fragmentation are arguably the most widespread drivers of biodiversity loss (Perfecto and Vandermeer, 2010)
We examined the effects of fragmentation on amphibian immunogenetic diversity at the major histocompatibility complex (MHC) IIB locus and potential susceptibility to a diversity of parasites
In a previous study examining immunogenetic diversity in island vertebrates, MHC diversity remained high while overall diversity dropped (Aguilar et al, 2004)
Summary
Habitat loss and fragmentation are arguably the most widespread drivers of biodiversity loss (Perfecto and Vandermeer, 2010). Habitat fragmentation can significantly impact population resilience against stressors including emerging infectious diseases (Dobson and Foufopoulos, 2001) These effects include the loss of genetic diversity over time due to genetic drift compounded by inbreeding (Newmark, 1995; Zuidema et al, 2017), which in turn may increase disease susceptibility (Altizer et al, 2003). Low genetic diversity has been associated with increased levels of parasitism, which suggests that there is a relationship between immune function and genetic diversity (Macdougall-Shackleton et al, 2005) and that genetically eroded individuals may be more susceptible to opportunistic infections (Anaissie, 1992) These associations between inbreeding and disease may be related to loss of resistance alleles at immunogenetic loci—genetic regions that are important in pathogen recognition and immune response
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