Who gets carbapenem-resistant Klebsiella, and does it kill more?
In one Brazilian hospital, longer use of a central venous catheter was the only independent risk factor for carbapenem-resistant Klebsiella infection, and resistance came from porin loss plus ESBL enzymes rather than a carbapenemase.
Source
A hospital-based matched case-control study to identify clinical outcome and risk factors associated with carbapenem-resistant Klebsiella pneumoniae infection
Study at a glance
- Design
- Case-control — Matched 1:2 case-control study for risk factors, plus a cohort comparison of in-hospital mortality, with molecular testing of isolates
- N
- N=60 · 20 patients with carbapenem-resistant K. pneumoniae infection (cases) and 40 matched patients with carbapenem-susceptible infection (controls); 17 isolates underwent molecular analysis
- Population
- Patients with healthcare-associated K. pneumoniae infections at a 620-bed private tertiary hospital in Sao Paulo, Brazil, January 2006 to August 2008
- Outcome
- Risk factors for carbapenem resistance, in-hospital mortality, and the genetic mechanism of resistance
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What they did
Using the hospital's infection-control database, the researchers identified every K. pneumoniae healthcare-associated infection over 32 months. Each patient with a carbapenem-resistant infection was matched to two patients with a susceptible infection by infection date, site and hospital unit, and medical records were reviewed for prior exposures. They also compared in-hospital death across all cases and controls and ran PCR, sequencing, enzyme assays and PFGE typing on the stored resistant isolates.
What they found
Carbapenem resistance was found in 20 of 236 K. pneumoniae infection episodes (8.5%). Half of the resistant-infection patients died in hospital versus 27.5% of controls, a difference that did not reach significance (p = 0.085). Several exposures (prior ICU stay, central line use, antibiotics) looked linked in simple analyses, but only duration of central venous catheter use remained independently associated (OR 1.08 per day). No isolate made a carbapenemase such as KPC; instead most carried the CTX-M-2 ESBL gene together with disrupted outer-membrane porin genes, and the isolates fell into seven clones with no clear outbreak.
The limits
What it doesn't show
With only 20 cases the study is underpowered, so the non-significant mortality difference and the failure of carbapenem exposure to predict resistance may reflect small numbers rather than true absence of effect. Colonisation status before infection was unknown, and the authors note that using susceptible-infection patients as controls can bias estimates of antibiotic exposure. It is a single private hospital, and resistance was judged with pre-2010 breakpoints, so results may not generalise to hospitals where KPC-producing strains dominate.
Key terms
- Carbapenem
- A last-line class of beta-lactam antibiotics (e.g. imipenem, meropenem) used for multidrug-resistant gram-negative infections.
- Matched case-control study
- A design that compares people with an outcome (cases) to similar people without it (controls), matched on key factors, to look back at exposures.
- ESBL (extended-spectrum beta-lactamase)
- A bacterial enzyme that breaks down many penicillins and cephalosporins; CTX-M-2 is one type.
- Porin
- An outer-membrane channel (here OmpK35/OmpK36) through which antibiotics enter the bacterium; losing porins lowers drug entry.
- Carbapenemase (e.g. KPC)
- An enzyme that directly destroys carbapenems; the most common resistance mechanism, which was absent in this hospital's isolates.
- PFGE
- Pulsed-field gel electrophoresis, a DNA fingerprinting method used to see whether isolates are the same clone and could be an outbreak.
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Quiz yourself
Which factor remained independently associated with carbapenem resistance in multivariable analysis?
Common questions
If mortality was 50% vs 27.5%, why isn't that a clear finding?
With 60 patients the difference was not statistically significant (p = 0.085), so chance cannot be ruled out; a larger study would be needed to confirm the harm.
How can bacteria resist carbapenems without a carbapenemase?
By combining an ESBL or other beta-lactamase that slowly degrades the drug with loss or disruption of porins, so less drug gets in to be neutralised.
Why does the choice of control group matter?
Controls infected with susceptible K. pneumoniae have also often had antibiotics, which can distort how strongly antibiotic exposure appears to predict resistance.
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