Abstract Forest fragmentation and connectivity define how mammalian hosts of the blacklegged tick (Ixodes scapularis Say, Acari: Ixodidae) utilize the landscape, ultimately guiding the spatial spread of associated pathogens. Mammalian hosts also exhibit pathogen-specific reservoir competencies, fueling continued debate as to their role as both drivers of tick density and moderators of pathogens maintained in the environment. This analysis examines the role of forest connectivity as a proxy for species richness and white-tailed deer (Odocoileus virginianus, Zimmermann) density in the spread of the human pathogenic Ap-ha and non-pathogenic Ap-v1 genotypes of Anaplasma phagocytophilum (Foggie, Rickettsiales: Anaplasmataceae). The prevalence of each genotype is used to examine the ecological mechanisms of amplification and dilution, as they each utilize specific mammalian hosts with varying reservoir competencies. We calculated patch- and landscape-level forest connectivity using the Sinuous Connection Reduction indices at 808 tick sampling sites located within 88 wildlife management units in New York State. The relationship between connectivity metric values, tick sampling, and genotyping results was then assessed using zero-inflated Poisson and Tweedie distribution generalized linear mixed models. Our analysis revealed that white-tailed deer density was positively related to I. scapularis density, Ap-v1 prevalence, and Ap-v1 entomological risk. Conversely, white-tailed deer density was negatively related to Ap-ha prevalence and exhibited no relation to Ap-ha entomological risk. These results provide evidence that white-tailed deer act as dilution hosts with respect to anaplasmosis risk in New York and support a broader Ap-ha amplification effect where increases in mammalian host biodiversity yield increased anaplasmosis risk and disease spread.
O’Connor et al. (Fri,) studied this question.