Colonisation with resistant Klebsiella pneumoniae in a Cambodian neonatal unit is driven by person-to-person transmission, transmissibility varies by sequence type, and antibiotic consumption generally increases the risk of acquisition.
SKAP2 is critical for hematopoietic cell protection against Klebsiella infection in mouse lungs, for full phosphorylation of Src Family Kinases, Syk, and Pyk2, and for Klebsiella-induced reactive oxygen species production.
High-level transposon insertional mutagenesis and a broader spectrum of resistance-conferring mutations for selected carbapenems facilitate the evolution of carbapenem resistance in Klebsiella pneumonia clinical isolates.
Patterns of antibiotic use and the connectivity between wards are independently associated with the incidence of antimicrobial-resistant infections in hospital networks.
A multidisciplinary platform featured by patient-derived RPEs is established to study the disease-causing mechanisms of BEST1 mutations, and demonstrates gene-supplemented rescue of the mutation-caused deficiency in Ca2+-dependent Cl- current in human RPE.
The high-resolution x-ray structure of an asymmetrical SeCitS dimer, present in the inward- and outward-facing state, provides a complete mechanism of substrate and ion translocation in a sodium-dependent symporter.
Moving patients between wards and prescribing high levels of antibiotics increases the spread of bacterial infections that are resistant to treatment in hospitals.
Building on previous work (Wilkinson et al, 2016), it is shown that inhibition of RecBCD-induced DNA break repair can be used as a co-antibacterial strategy with quinolones.
Interbacterial interactions can promote mutagenesis, and possibly adaptation, when intoxicated cells survive exposure to type VI secretion-delivered DNA deaminase toxins.
Morphological and fitness defects imposed on amoebae hosts by Burkholderia symbionts demonstrates symbiont species-specific effects and provides evidence of host adaptation to naturally acquired symbionts.
