An unusual and interesting outbreak of CPE was published recently in Clinical Infectious Diseases. Several key points: don’t rely solely on a PCR detecting the “Big 5” carbapenemases (NDM, KPC, OXA-48, IMP, VIM) – at some point you need to test for phenotypic carbapenemase activity; WGS can really help us in unravelling complex transmission routes; and covert plasmid propagation within and between species is a reality.
sequencing
Looking back on a CPE plasmid attack in the Northwest of England
A genomic study of 44 isolates of CPE from various species identified between 2008 and 2010, mainly from the Northwest of England, has concluded that plasmids played a key role in the early dissemination of CPE.
The carbapenemase is out there
A PNAS paper on the genomic diversity of carbapenemase producing bacteria in the US reports strong evidence of carbapenamase (an enzyme produced by bacteria that breaks down carabapenem antibiotics) activity but no sign of a carbapenemase gene. This provides a timely reminder that we are only really scratching the surface in our understanding of carbapenemases and how they work.
Biofilms make the hospital environment far from ‘inanimate’
Anybody doubting that biofilms really do exist on dry hospital surfaces needs to read this study: biofilms are there, they are complex, and they are common. A landmark study by the same Australian Vickery group published in 2012 first identified biofilms on a handful of dry hospital surfaces in an ICU. But this study is far more comprehensive and convincing.
Reflections on Infection Prevention and Control 