Nature Microbiology最新文献

The current panzootic spread of high pathogenicity avian influenza virus (HPAIV) subtype H5N1 clade 2.3.4.4b has caused unprecedented mortality in wild animals worldwide¹. In 2022, the virus caused mass mortality of seabirds and marine mammals in South America, which raised concerns about HPAIV spreading to Antarctica. The wildlife in Antarctica is seasonally dense due to high populations found in breading colonies of birds and mammals, and many Antarctic sites are remote and difficult to access, meaning that HPAIV could have dramatic effects on its fauna without immediately being noticed. As a result, surveillance efforts in this area are crucial.

The detection of HPAIV in the sub-Antarctic islands of South Georgia was first reported in October 2023. It caused considerable mortalities of seabirds (for example, skuas, gulls and albatrosses) and marine mammals (for example, elephant seals and sea lions) during the subsequent months². Recent phylogenetic analyses of the viral sequences from South Georgia demonstrated a single introduction from South America². Wildlife mortality suspected to be related to HPAIV was reported in Antarctica as early as November 2023 (ref. ³). The first case of HPAIV in Antarctica was confirmed in skuas (Stercorarius sp.) found dead in January 2024 near the Argentinian Primavera Base (Danco Coast, Antarctic Peninsula) and tested in February 2024 in a molecular diagnostic laboratory set up at the Spanish Gabriel de Castilla Station (Deception Island, South Shetland Islands)⁴. Having this on-site laboratory showed it was possible to perform the diagnoses in Antarctica itself, which gives results much faster and avoids the risk of losing sample quality during transport to laboratories outside Antarctica. HPAIV was later reported in dead skuas near the Czech Johann Gregor Mendel base⁵. The finding of sporadic or potential cases of HPAIV-infected skuas indicated that the virus had reached Antarctica. In response, we launched the Australis expedition to investigate the spread and impact of HPAIV at several remote sites, following a direct field diagnostic approach with a mobile laboratory on board.

Although diet is a substantial determinant of the human gut microbiome, the interplay between specific foods and microbial community structure remains poorly understood. Coffee is a habitually consumed beverage with established metabolic and health benefits. We previously found that coffee is, among >150 items, the food showing the highest correlation with microbiome components. Here we conducted a multi-cohort, multi-omic analysis of US and UK populations with detailed dietary information from a total of 22,867 participants, which we then integrated with public data from 211 cohorts (N = 54,198). The link between coffee consumption and microbiome was highly reproducible across different populations (area under the curve of 0.89), largely driven by the presence and abundance of the species Lawsonibacter asaccharolyticus. Using in vitro experiments, we show that coffee can stimulate growth of L. asaccharolyticus. Plasma metabolomics on 438 samples identified several metabolites enriched among coffee consumers, with quinic acid and its potential derivatives associated with coffee and L. asaccharolyticus. This study reveals a metabolic link between a specific gut microorganism and a specific food item, providing a framework for the understanding of microbial dietary responses at the biochemical level.

Dietary zinc deficiency is a major risk factor for pneumonia. Acinetobacter baumannii is a leading cause of ventilator-associated pneumonia and a critical public health threat due to increasing rates of multidrug resistance. Patient populations at increased risk for A. baumannii pneumonia are also at increased risk of zinc deficiency. Here we established a mouse model of dietary zinc deficiency and acute A. baumannii pneumonia to test the hypothesis that host zinc deficiency contributes to A. baumannii pathogenesis. We showed that zinc-deficient mice have significantly increased A. baumannii burdens in the lungs, dissemination to the spleen and higher mortality. During infection, zinc-deficient mice produce more pro-inflammatory cytokines, including IL-13. Administration of IL-13 promotes A. baumannii dissemination in zinc-sufficient mice, while antibody neutralization of IL-13 protects zinc-deficient mice from A. baumannii dissemination and mortality during infection. These data highlight the therapeutic potential of anti-IL-13 antibody treatments, which are well tolerated in humans, for the treatment of pneumonia.

Chemical cues mediate interactions between marine phytoplankton and bacteria, underpinning ecosystem-scale processes including nutrient cycling and carbon fixation. Phage infection alters host metabolism, stimulating the release of chemical cues from intact plankton, but how these dynamics impact ecology and biogeochemistry is poorly understood. Here we determine the impact of phage infection on dissolved metabolite pools from marine cyanobacteria and the subsequent chemotactic response of heterotrophic bacteria using time-resolved metabolomics and microfluidics. Metabolites released from intact, phage-infected Synechococcus elicited strong chemoattraction from Vibrio alginolyticus and Pseudoalteromonas haloplanktis, especially during early infection stages. Sustained bacterial chemotaxis occurred towards live-infected Synechococcus, contrasted by no discernible chemotaxis towards uninfected cyanobacteria. High-throughput microfluidics identified 5′-deoxyadenosine and 5′-methylthioadenosine as key attractants. Our findings establish that, before lysis, phage-infected picophytoplankton release compounds that attract motile heterotrophic bacteria, suggesting a mechanism for resource transfer that might impact carbon and nutrient fluxes across trophic levels.

Difficulties in antibiotic treatment of Mycobacterium tuberculosis (Mtb) are partly thought to be due to heterogeneity in growth. Although the ability of bacterial pathogens to regulate growth is crucial to control homeostasis, virulence and drug responses, single-cell growth and cell cycle behaviours of Mtb are poorly characterized. Here we use time-lapse, single-cell imaging of Mtb coupled with mathematical modelling to observe asymmetric growth and heterogeneity in cell size, interdivision time and elongation speed. We find that, contrary to Mycobacterium smegmatis, Mtb initiates cell growth not only from the old pole but also from new poles or both poles. Whereas most organisms grow exponentially at the single-cell level, Mtb has a linear growth mode. Our data show that the growth behaviour of Mtb diverges from that of model bacteria, provide details into how Mtb grows and creates heterogeneity and suggest that growth regulation may also diverge from that in other bacteria.

Microbiomes contribute to variation in many plant and animal traits, suggesting that microbiome-mediated traits could evolve through selection on the host. However, for such evolution to occur, microbiomes must exhibit sufficient heritability to contribute to host adaptation. Previous work has attempted to estimate the heritability of a variety of microbiome attributes. Here we show that most published estimates are limited to vertebrate and plant hosts, but significant heritability of microbiome attributes has been frequently reported. This indicates that microbiomes could evolve in response to host-level selection, but studies across a wider range of hosts are necessary before general conclusions can be made. We suggest future studies focus on standardizing heritability measurements for the purpose of meta-analyses and investigate the role of the environment in contributing to heritable microbiome variation. This could have important implications for the use of microbiomes in conservation, agriculture and medicine.

Conjugative plasmids are important drivers of bacterial evolution. Most plasmids lack genes for conjugation and characterized origins of transfer (oriT), which has hampered our understanding of plasmid mobility. Here we used bioinformatic analyses to characterize occurrences of known oriT families across 38,057 plasmids, confirming that most conjugative and mobilizable plasmids lack identifiable oriTs. Recognizable oriT sequences tend to be intergenic, upstream of relaxase genes and specifically associated with relaxase types. We used these criteria to develop a computational method to search for and identify 21 additional families of oriT-containing sequences in plasmids from the pathogens Escherichia coli, Klebsiella pneumoniae and Acinetobacter baumannii. Sequence analyses found 3,072 occurrences of these oriT-containing sequences across 2,976 plasmids, many of which encoded antimicrobial resistance genes. Six candidate oriT-containing sequences were validated experimentally and were shown to facilitate conjugation in E. coli. These findings expand our understanding of plasmid mobility.