Highlights d Cities possess a consistent ''core'' set of non-human microbes d Urban microbiomes echo important features of cities and city-life d Antimicrobial resistance genes are widespread in cities d Cities contain many novel bacterial and viral species

Thermal stress increases the incidence of coral disease, which is predicted to become more common with climate change, even on pristine reefs such as those surrounding Palmyra Atoll in the Northern Line Islands that experience minimal anthropogenic stress. Here we describe a strain of Vibrio coralliilyticus, OCN014, which was isolated from Acropora cytherea during an outbreak of Acropora white syndrome (AWS), a tissue loss disease that infected 25% of the A. cytherea population at Palmyra Atoll in 2009. OCN014 recreated signs of disease in experimentally infected corals in a temperature-dependent manner. Genes in OCN014 with expression levels positively correlated with temperature were identified using a transposon-mediated genetic screen. Mutant strains harbouring transposon insertions in two such genes, toxR (a toxin regulator) and mshA (the 11th gene of the 16-gene mannose-sensitive hemagglutinin (MSHA) type IV pilus operon), had reduced infectivity of A. cytherea. Deletion of toxR and the MSHA operon in a second strain of V. coralliilyticus, OCN008, that induces acute Montipora white syndrome in a temperature-independent manner had similarly reduced virulence. This work provides a link between temperature-dependent expression of virulence factors in a pathogen and infection of its coral host.

A high number of coral colonies, Montipora spp., with progressive tissue loss were reported from the north shore of Kaua‘i by a member of the Eyes of the Reef volunteer reporting network. The disease has a distinct lesion (semi-circular pattern of tissue loss with an adjacent dark band) that was first observed in Hanalei Bay, Kaua‘i in 2004. The disease, initially termed Montipora banded tissue loss, appeared grossly similar to black band disease (BBD), which affects corals worldwide. Following the initial report, a rapid response was initiated as outlined in Hawai‘i’s rapid response contingency plan to determine outbreak status and investigate the disease. Our study identified the three dominant bacterial constituents indicative of BBD (filamentous cyanobacteria, sulfate-reducing bacteria, sulfide-oxidizing bacteria) in coral disease lesions from Kaua‘i, which provided the first evidence of BBD in the Hawaiian archipelago. A rapid survey at the alleged outbreak site found disease to affect 6-7% of the montiporids, which is higher than a prior prevalence of less than 1% measured on Kaua‘i in 2004, indicative of an epizootic. Tagged colonies with BBD had an average rate of tissue loss of 5.7 cm2/day over a two-month period. Treatment of diseased colonies with a double band of marine epoxy, mixed with chlorine powder, effectively reduced colony mortality. Within two months, treated colonies lost an average of 30% less tissue compared to untreated controls.

Ghrelin is a gastric hormone that has been implicated in the neurobiology of alcohol drinking. We have recently developed a ghrelin receptor (growth hormone secretagogue receptor; GHSR) knockout (KO) rat model, which exhibits reduced food consumption and body weight. In addition, recent preliminary work suggests that the gut‐microbiome, which appears to interact with the ghrelin system, may modulate alcohol drinking. In the present study, we investigated the effects of GHSR deletion on alcohol consumption utilising GHSR KO and wild‐type (WT) rats in three separate alcohol consumption paradigms: (i) operant self‐administration (30‐minute sessions); (ii) drinking in the dark (DID) (4‐hour sessions); and (iii) intermittent access (24‐hour sessions). These paradigms model varying degrees of alcohol consumption. Furthermore, we aimed to investigate the gut‐microbiome composition of GHSR KO and WT rats before and after alcohol exposure. We found that the GHSR KO rats self‐administered significantly less alcohol compared to WT rats in the operant paradigm, and consumed less alcohol than WT in the initial stages of the DID paradigm. No genotype differences were found in the intermittent access test. In addition, we found a significant decrease in gut‐microbial diversity after alcohol exposure in both genotypes. Thus, the present results indicate that the ghrelin system may be involved in drinking patterns that result in presumably increased alcohol exposure levels. Furthermore, GHSR may constitute a potential pharmacological target for the reduction of binge‐alcohol consumption. The potential functional role of the gut‐microbiome in alcohol drinking, as well as interaction with the ghrelin system, is an interesting topic for further investigation.