DOI: 10.5061/dryad.x95x69pgc
title: Pathogenic Leptospira isolated from rodents in New Orleans, Louisiana USA, and associated site information

description: Land use change can elevate disease risk by creating conditions beneficial
 to species that carry zoonotic pathogens. Observations of
 concordant global trends in pathogen prevalence and disease incidence have
 engendered concerns that urbanization could increase transmission
 risk of some pathogens. Yet host-pathogen relationships underlying
 transmission risk have not been well characterized within cities,
 even where contact between humans and species capable of
 transmitting pathogens of concern occur. We addressed this deficit
 by testing the hypothesis that areas in cities experiencing
 greater population loss and infrastructure decline (i.e.,
 counter-urbanization) can support a greater diversity of host species and
 a larger and more diverse pool of pathogens. We did so by characterizing
 pathogenic Leptospira infection relative to rodent host richness and
 abundance across a mosaic of abandonment in post-Katrina New Orleans
 (Louisiana, USA). We found that Leptospira infection loads were highest in
 areas that harbored higher rodent species richness. Areas with greater
 host co-occurrence also harbored a greater number of hosts, including the
 most competent hosts, indicating that Leptospira infection is
 amplified by increases in overall and relative host abundance.
 Evidence of shared infection among rodent hosts indicates that
 cross-species transmission of Leptospira likely increases
 infection at sites with greater host syntopy. Additionally, evidence that
 rodent co-occurrence and abundance and Leptospira infection load parallel
 abandonment suggests that counter-urbanization can elevate zoonotic
 disease risk within cities, particularly in underserved
 communities that are burdened with disproportionate concentrations of
 derelict properties.
description: All animals were collected in the field using live trapping as
 also outlined in https://doi.org/10.1016/j.landurbplan.2019.103710. Tissue samples were collected immediately at necropsy and frozen at -80C. To identify pathogenic <i>Leptospira </i>to species, we sequenced a partial region of the <i>glmU</i> gene using genomic kidney DNA from all individuals that tested positive for <i>Leptospira</i> infection in the qPCR screen. After PCR amplification following a standard protocol, we cleaned all PCR products with ExoSAP-IT (Affymetrix, Santa Clara, CA, USA) and completed final paired sequencing reactions consisting of 3.75 µL PCR grade H<sub>2</sub>0, 3.75 µL 5uM MgCl<sub>2</sub>, 1.0 µL each of 10 mM forward and reverse <i>glmU</i> primers (respectively) and 0.5 µL BigDye terminator (Applied Biosystems, Foster, CA, USA). We cleaned reactions using Sephadex columns prior to electrophoresis on an ABI 3730xl (Applied Biosystems). We aligned trimmed sequences with GenBank archived sequences of the <i>glmU</i> gene for all pathogenic <i>Leptospira</i>. We then constructed phylogenetic trees with all new and representative archived sequences using Bayesian Inference in MrBayes 3.2.6. Trees were built using the GTR+G model, and a Markov chain Monte Carlo analysis with four chains running for 8x10<sup>6</sup> generations. Trees were sampled every 1000 generations with the first 1000 trees discarded as burn-in. Convergence was determined when the final deviation of split frequencies fell below 0.02. We assigned sequences to<i> Leptospira</i> species based on relationships recovered in the final tree, with confirmation from BLAST comparisons.  
description: Information explaining each column is included in the metadata
 tab. Environmental data is only included for the subset of sites at which
 we targeted rats and mice (as explained in the manuscript). Data for every
 animal tested for <em>Leptospira </em>is included in the
 <em>Leptospira</em> tab. Not all animals tested were included
 in the final analysis.