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SDSS-V will be an all-sky, multi-epoch spectroscopic survey of over six million objects. It is designed to decode the history of the Milky Way Galaxy (MW), trace the emergence of the chemical elements, reveal the inner workings of stars, and investigate the origin of planets. It will also create an integral-field spectroscopic map of the interstellar gas in the Galaxy and the Local Group that is 1,000 times larger than the current state of the art and at high enough spatial resolution to reveal the self-regulation mechanisms of galactic ecosystems. SDSS-V will pioneer systematic, spectroscopic monitoring across the whole sky, revealing changes on timescales from 20 minutes to 20 years. The survey will thus track the flickers, flares, and radical transformations of the most luminous persistent objects in the universe: massive black holes growing at the centers of galaxies.The scope and flexibility of SDSS-V will be unique among both extant and anticipated spectroscopic surveys: it is all-sky, with matched survey infrastructures in both hemispheres; it provides near-infrared and optical multi-object fiber spectroscopy that is rapidly reconfigurable to serve high target densities, targets of opportunity, and time-domain monitoring; and it provides optical, ultrawide-field integral field spectroscopy. SDSS-V, with its programs anticipated to start in 2020, will be perfectly timed to multiply the scientific output from major space missions (e.g., TESS, Gaia, Spektr-RG-eROSITA) and ground-based projects. SDSS-V builds on the 25-year heritage of SDSS's advances in data analysis, collaboration spirit and infrastructure, and product deliverables in astronomy. The project is now refining its science scope, optimizing the survey strategies, and developing new hardware that builds on the SDSS-IV infrastructure. We present here an overview of the current state of these developments. SDSS-V is actively seeking to build its consortium of institutional and individual members for a worldwide, partner-driven collaboration.

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Carbapenem-resistant Enterobacteriaceae (CRE) are among the most severe threats to the antibiotic era. Multiple different species can exhibit resistance due to many different mechanisms, and many different mobile elements are capable of transferring resistance between lineages. We prospectively sampled CRE from hospitalized patients from three Boston-area hospitals, together with a collection of CRE from a single California hospital, to define the frequency and characteristics of outbreaks and determine whether there is evidence for transfer of strains within and between hospitals and the frequency with which resistance is transferred between lineages or species. We found eight species exhibiting resistance, with the majority of our sample being the sequence type 258 (ST258) lineage of Klebsiella pneumoniae. There was very little evidence of extensive hospital outbreaks, but a great deal of variation in resistance mechanisms and the genomic backgrounds carrying these mechanisms. Local transmission was evident in clear phylogeographic structure between the samples from the two coasts. The most common resistance mechanisms were KPC (K. pneumoniae carbapenemases) beta-lactamases encoded by bla KPC2 , bla KPC3 , and bla KPC4 , which were transferred between strains and species by seven distinct subgroups of the Tn4401 element. We also found evidence for previously unrecognized resistance mechanisms that produced resistance when transformed into a susceptible genomic background. The extensive variation, together with evidence of transmission beyond limited clonal outbreaks, points to multiple unsampled transmission chains throughout the continuum of care, including asymptomatic carriage and transmission of CRE. This finding suggests that to control this threat, we need an aggressive approach to surveillance and isolation.carbapenem resistance | Enterobacteriaceae | comparative genomics | whole-genome sequencing | molecular evolution

Use of an antimicrobial agent selects for overgrowth of a bacterial strain that has a gene expressing resistance to the agent. It also selects for the assembly and evolution of complex genetic vectors encoding, expressing, linking, and spreading that and other resistance genes. Once evolved, a competitive construct of such genetic elements may spread widely through the world's bacterial populations. A bacterial isolate at any place may thus be resistant-not only because nearby use of antimicrobials had amplified such a genetic construct locally, but also because distant use had caused the construct or its components to evolve in the first place and spread there. The levels of resistance at any time and place may therefore reflect in part the total number of bacteria in the world exposed to antimicrobials up until then. Tracing the evolution and spread of such genetic elements through bacterial populations far from one another, such as those of animals and humans, can be facilitated by newer genetic methods.

SUMMARY Many studies report the high prevalence of multiply drug-resistant (MDR) strains. Because MDR infections are often significantly harder and more expensive to treat, they represent a growing public health threat. However, for different pathogens, different underlying mechanisms are traditionally used to explain these observations, and it is unclear whether each bacterial taxon has its own mechanism(s) for multidrug resistance or whether there are common mechanisms between distantly related pathogens. In this review, we provide a systematic overview of the causes of the excess of MDR infections and define testable predictions made by each hypothetical mechanism, including experimental, epidemiological, population genomic, and other tests of these hypotheses. Better understanding the cause(s) of the excess of MDR is the first step to rational design of more effective interventions to prevent the origin and/or proliferation of MDR.