Antimicrobial resistance
Who gets carbapenem-resistant Klebsiella, and does it kill more?
Open access · cc by · source: Europe PMC
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.
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
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
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.
Methodology
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.
Limitations
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.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
A carbapenemase-only screen would have missed all of them.
The mechanism of resistance is not always the one surveillance looks for. In a Brazilian matched case-control study, none of 20 carbapenem-resistant K. pneumoniae isolates produced a carbapenemase such as KPC; most combined a CTX-M-2 ESBL with disrupted porin genes, spread across seven clones.
Evidence for the claim as stated.
Whether resistance itself raises mortality is design-dependent. The Tanzanian cohort found inadequate empiric cover independently predicted death, but the Brazilian case-control study (50% vs 27.5% mortality, p = 0.085, only 20 cases) and the oncology cohort (no factor significantly predicted death) could not show an independent effect, likely because of small samples and severely ill comparison groups.
Same question, contrary or null result.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Whether resistance itself raises mortality is design-dependent. The Tanzanian cohort found inadequate empiric cover independently predicted death, but the Brazilian case-control study (50% vs 27.5% mortality, p = 0.085, only 20 cases) and the oncology cohort (no factor significantly predicted death) could not show an independent effect, likely because of small samples and severely ill comparison groups.
History
When this study was placed
Dated entries from the concept change log — when this paper was added or removed as support, challenge, or qualifier on a claim.
Placed as supporting evidence on Antimicrobial Resistance
The mechanism of resistance is not always the one surveillance looks for. In a Brazilian matched case-control study, none of 20 carbapenem-resistant K. pneumoniae isolates produced a carbapenemase such as KPC; most combined a CTX-M-2 ESBL with disrupted porin genes, spread across seven clones.
Placed as a challenge on Antimicrobial Resistance
Whether resistance itself raises mortality is design-dependent. The Tanzanian cohort found inadequate empiric cover independently predicted death, but the Brazilian case-control study (50% vs 27.5% mortality, p = 0.085, only 20 cases) and the oncology cohort (no factor significantly predicted death) could not show an independent effect, likely because of small samples and severely ill comparison groups.
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