Humanization of wildlife gut microbiota in urban environments.

Urbanization is rapidly altering Earth's environments, demanding investigation of the impacts on resident wildlife. Here, we show that urban populations of coyotes (Canis latrans), crested anole lizards (Anolis cristatellus), and white-crowned sparrows (Zonotrichia leucophrys) acquire gut microbiota constituents found in humans, including gut bacterial lineages associated with urbanization in humans. Comparisons of urban and rural wildlife and human populations revealed significant convergence of gut microbiota among urban populations relative to rural populations. All bacterial lineages overrepresented in urban wildlife relative to rural wildlife and differentially abundant between urban and rural humans were also overrepresented in urban humans relative to rural humans. Remarkably, the bacterial lineage most overrepresented in urban anoles was a Bacteroides sequence variant that was also the most significantly overrepresented in urban human populations. These results indicate parallel effects of urbanization on human and wildlife gut microbiota and suggest spillover of bacteria from humans into wildlife in cities.

Vertebrate species, such as reptiles, birds or mammals, harbour distinct communities of microbes in their digestive systems. These miniature ecosystems ­ also known as microbiomes ­ are unique to each owner and species, reflecting their diverse lifestyles and evolutionary history. Urbanisation can disrupt these delicate intestinal communities. Humans and other animals living in cities have different gut microbes to their counterparts living in rural areas. And captive species in homes and zoos often acquire human gut bacteria in their digestive systems, which can lead to health problems in these animals. So far, it has been unclear whether such a humanization of gut bacteria also affects wild animals living in and around cities. To investigate this further, Dillard et al. compared the gut microbes of wild reptiles, birds, and mammals living in close contact with humans in North America, such as coyotes, crested anole lizards and white-crowned sparrows. DNA sequencing showed that in urban environments, the composition of gut bacteria living in all three wildlife species resembled the ones in humans. The types of bacteria overrepresented in the guts of urban humans were also overrepresented in urban wildlife. This suggests that urbanization can affect the composition of gut bacteria in wildlife species by disrupting or replacing portions of their microbiome. The reason for this pattern is unclear. It is possible that humans might be sharing their gut microbes directly with city animals, or that a human-like diet is causing the change. Given the role that gut microbes play in health and disease, it is important to find out whether these changes cause the animals any harm.

Epimicrobiota Associated with the Decay and Recovery of Orbicella Corals Exhibiting Dark Spot Syndrome.

Dark Spot Syndrome (DSS) is one of the most common diseases of boulder corals in the Caribbean. It presents as sunken brown lesions in coral tissue, which can spread quickly over coral colonies. With this study, we tested the hypothesis that similar to other coral diseases, DSS is a dysbiosis characterized by global shifts in the coral microbiome. Because Black Band Disease (BBD) was sometimes found following DSS lesions, we also tested the hypothesis that DSS is a precursor of BBD. To track disease initiation and progression 24 coral colonies were tagged. Of them five Orbicella annularis corals and three O. faveolata corals exhibited DSS lesions at tagging. Microbiota of lesions and apparently healthy tissues from DSS-affected corals over the course of 18 months were collected. Final visual assessment showed that five of eight corals incurred substantial tissue loss while two corals remained stable and one appeared to recover from DSS lesions. Illumina sequencing of the V6 region of bacterial 16S rRNA genes demonstrated no significant differences in bacterial community composition associated with healthy tissue or DSS lesions. The epimicrobiomes of both healthy tissue and DSS lesions contained high relative abundances of Operational Taxonomic Units assigned to Halomonas, an unclassified gammaproteobacterial genus, Moritella, an unclassified Rhodobacteraceae genus, Renibacterium, Pseudomonas, and Acinetobacter. The relative abundance of bacterial taxa was not significantly different between samples when grouped by tissue type (healthy tissue vs. DSS lesion), coral species, collection month, or the overall outcome of DSS-affected corals (substantial tissue loss vs. stable/recovered). Two of the tagged corals with substantial tissue loss also developed BBD during the 18-month sampling period. The bacterial community of the BBD layer was distinct from both healthy tissue and DSS lesions, with high relative abundances of the presumed BBD pathogen Roseofilum reptotaenium and an unclassified Bacteroidales genus, similar to previous results. Roseofilum was detected in all samples from this study, with the highest relative abundance in healthy tissue from DSS-affected corals sampled in August, suggesting that while DSS is not a precursor to BBD, DSS-affected corals are in a weakened state and therefore more susceptible to additional infections.

Draft genome sequence of Halomonas meridiana R1t3 isolated from the surface microbiota of the Caribbean Elkhorn coral Acropora palmata.

Members of the gammaproteobacterial genus Halomonas are common in marine environments. Halomonas and other members of the Oceanospirillales have recently been identified as prominent members of the surface microbiota of reef-building corals. Halomonas meridiana strain R1t3 was isolated from the surface mucus layer of the scleractinian coral Acropora palmata in 2005 from the Florida Keys. This strain was chosen for genome sequencing to provide insight into the role of commensal heterotrophic bacteria in the coral holobiont. The draft genome consists of 290 scaffolds, totaling 3.5 Mbp in length and contains 3397 protein-coding genes.