We initiated a worldwide collaborative study, including 455 episodes of bacteremia, to elucidate the clinical patterns of Klebsiella pneumoniae. Historically, community-acquired pneumonia has been consistently associated with K. pneumoniae. Only four cases of community-acquired bacteremic K. pneumoniae pneumonia were seen in the 2-year study period in the United States, Argentina, Europe, or Australia; none were in alcoholics. In contrast, 53 cases of bacteremic K. pneumoniae pneumonia were observed in South Africa and Taiwan, where an association with alcoholism persisted (p=0.007). Twenty-five cases of a distinctive syndrome consisting of K. pneumoniae bacteremia in conjunction with community-acquired liver abscess, meningitis, or endophthalmitis were observed. A distinctive form of K. pneumoniae infection, often causing liver abscess, was identified, almost exclusively in Taiwan.

Highly invasive, community-acquired Klebsiella pneumoniae infections have recently emerged, resulting in pyogenic liver abscesses. These infections are caused by hypervirulent K. pneumoniae (hvKP) isolates primarily of capsule serotype K1 or K2. Hypervirulent K1 isolates belong to clonal complex 23 (CC23), indicating that this clonal lineage has a specific genetic background conferring hypervirulence. Here, we apply whole-genome sequencing to a collection of K. pneumoniae isolates to characterize the phylogenetic background of hvKP isolates with an emphasis on CC23. Most of the hvKP isolates belonged to CC23 and grouped into a distinct monophyletic clade, revealing that CC23 is a unique clonal lineage, clearly distinct from nonhypervirulent strains. Separate phylogenetic analyses of the CC23 isolates indicated that the CC23 lineage evolved recently by clonal expansion from a single common ancestor. Limited grouping according to geographical origin was observed, suggesting that CC23 has spread globally through multiple international transmissions. Conversely, hypervirulent K2 strains clustered in genetically unrelated groups. Strikingly, homologues of a large virulence plasmid were detected in all hvKP clonal lineages, indicating a key role in K. pneumoniae hypervirulence. The plasmid encodes two siderophores, aerobactin and salmochelin, and RmpA (regulator of the mucoid phenotype); all these factors were found to be restricted to hvKP isolates. Genomic comparisons revealed additional factors specifically associated with CC23. These included a distinct variant of a genomic island encoding yersiniabactin, colibactin, and microcin E492. Furthermore, additional novel genomic regions unique to CC23 were revealed which may also be involved in the increased virulence of this important clonal lineage.

We derive an action whose equations of motion contain the Poisson equation of Newtonian gravity. The construction requires a new notion of Newton-Cartan geometry based on an underlying symmetry algebra that differs from the usual Bargmann algebra. This geometry naturally arises in a covariant 1/c expansion of general relativity with c being the speed of light. By truncating this expansion at subleading order we obtain the field content and transformation rules of the fields that appear in the action of Newtonian gravity. The equations of motion generalize Newtonian gravity by allowing for the effect of gravitational time dilation due to strong gravitational fields.

Differences in clinical manifestations are due to virulence factors expressed by the organism.

The plasmid-mediated colistin resistance gene, mcr-1, was detected in an Escherichia coli isolate from a Danish patient with bloodstream infection and in five E. coli isolates from imported chicken meat. One isolate from chicken meat belonged to the epidemic spreading sequence type ST131. In addition to IncI2, an incX4 replicon was found to be linked to mcr-1. This report follows a recent detection of mcr-1 in E. coli from animals, food and humans in China.

We study the non-relativistic expansion of general relativity coupled to matter. This is done by expanding the metric and matter fields analytically in powers of 1/c 2 where c is the speed of light. In order to perform this expansion it is shown to be very convenient to rewrite general relativity in terms of a timelike vielbein and a spatial metric. This expansion can be performed covariantly and off shell. We study the expansion of the Einstein-Hilbert action up to next-to-next-to-leading order. We couple this to different forms of matter: point particles, perfect fluids, scalar fields (including an off-shell derivation of the Schrödinger-Newton equation) and electrodynamics (both its electric and magnetic limits). We find that the role of matter is crucial in order to understand the properties of the Newton-Cartan geometry that emerges from the expansion of the metric. It turns out to be the matter that decides what type of clock form is allowed, i.e. whether we have absolute time or a global foliation of constant time hypersurfaces. We end by studying a variety of solutions of non-relativistic gravity coupled to perfect fluids. This includes the Schwarzschild geometry, the Tolman-Oppenheimer-Volkoff solution for a fluid star, the FLRW cosmological solutions and anti-de Sitter spacetimes.

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Extraintestinal pathogenic Escherichia coli (ExPEC) is the main cause of urinary tract infections and septicemia. Significant attention has been given to the ExPEC sequence type ST131, which has been categorized as a “high-risk” clone. High-risk clones are globally distributed clones associated with various antimicrobial resistance determinants, ease of transmission, persistence in hosts, and effective transmission between hosts. The high-risk clones have enhanced pathogenicity and cause severe and/or recurrent infections. We show that clones of the E. coli ST410 lineage persist and/or cause recurrent infections in humans, including bloodstream infections. We found evidence of ST410 being a highly resistant globally distributed lineage, capable of patient-to-patient transmission causing hospital outbreaks. Our analysis suggests that the ST410 lineage should be classified with the potential to cause new high-risk clones. Thus, with the clonal expansion over the past decades and increased antimicrobial resistance to last-resort treatment options, ST410 needs to be monitored prospectively.