According to the Health Protection Agency1, bacteraemias caused by gram negative rods are now the most common type seen in NHS hospitals. Gram negative rods (GNR) include commonly encountered bacteria such as Escherichia coli, Klebsiella pneumoniae and Pseudomonas aeruginosa. Bloodstream infections caused by such bacteria are associated with high mortality rates.
However, as these species look identical under the microscope when gram stained, specific treatment decisions must often wait a further 24-48 hours after gram staining until the specific pathogen is identified.
Accurate species identification is important as P. aeruginosa is relatively resistant to many antibiotics to which enterobacteria such as K.pneumoniae and E.coli are susceptible. This makes choosing the correct antibiotic to treat patients with GNR bacteraemia potentially difficult. As a result, patients with such bloodstream infections may be subjected to unnecessary broad spectrum antimicrobial therapy. This can lead to subsequent infections with multi-drug resistant pathogens and possible toxicity complications. Conversely under treatment can increase the risk of adverse patient outcomes2.
It is therefore critical that clinicians are able to rapidly decide when to initiate or discontinue anti-pseudomonal therapy for patients with GNR positive blood cultures. The new QuickFISH™ GNR kit fulfils this need by providing a positive species level identification (E.coli/K.pneumoniae/P.aeruginosa) directly from blood cultures in 20 minutes.
Based on the proven PNA-FISH technology from AdvanDx, it allows species identity to be reported at the same time as the gram stain result. In this way the clinician can ensure early, appropriate therapy for patients with P.aeruginosa infections while minimising the unnecessary use of agressive anti-Pseudomonal therapies and broad-spectrum antibiotics.
This article was published previously in Alpha Laboratories’ Leading Edge Newsletter – Summer 2013.
1. HPA – www.hpa.org.uk
2. Kumar, A et al Chest 136: 1237-1248 (2009)
3. Della-Latta et al J. Clin. Microbiol. 49, 2259–2261 (2011)