An ESBL-producing Klebsiella pneumoniae strain isolated from a nosocomial outbreak becomes resistant to all clinically available antibiotics by acquisition of a plasmid-mediated AmpC beta-lactamase
Abstract number: 1134_01_52
Burak S., Wiedemann B., Wiegand I.
Outbreaks caused by multiresistant Klebsiella pneumoniae strains, especially extended-spectrum beta-lactamase (ESBL)-producing strains, are an increasing serious problem. Carbapenems are valuable therapeutic options against those strains, as, even with a porin loss, ESBL-producing K. pneumoniae remain susceptible to carbapenems. But they may become carbapenem-resistant because of porin loss in combination with plasmid-mediated AmpC beta-lactamase production. In this work, we analysed the molecular background of a multiresistant clinical ESBL-producing K. pneumoniae isolate. We wanted to examine its ability to become carbapenem-resistant by acquisition of a plasmid-mediated AmpC enzyme.
K. pneumoniae 5111 was isolated during an outbreak of multiresistant ESBL-producing K. pneumoniae in the surgical ICU of a german university hospital in April 2002. MIC values were determined by broth microdilution according to NCCLS. Resistance genes were detected by PCR and sequencing. Conjugation experiments were performed by filtermating using two different clinical E. coli and one K. pneumoniae isolate harbouring the AmpC beta-lactamase CMY-2 on different plasmids as donor strains and K. pneumoniae 5111 as the recipient.
Strain 5111 was resistant to all tested beta-lactams except carbapenems and also resistant to aminoglycosides, quinolones, tetracyclines, cotrimoxazol and chloramphenicol. The beta-lactam resistance is caused by production of the ESBL SHV-12. Cefoxitin resistance indicates a porin loss. Two chromosomal mutations in gyrA and one in parC are responsible for the quinolone resistance. The strain carries at least six genes for aminoglycoside-modifying enzymes and four additional resistance genes. Conjugation experiments were successful with one E. coli donor strain with a conjugation frequency of 1.7 × 108. The transconjugant had acquired the AmpC CMY-2 and was resistant to carbapenems.
The examined strain becomes completely resistant to all clinically available antibiotics by acquisition of a plasmid-mediated AmpC beta-lactamase by conjugation. Conjugation events can also occur in vivo in the gastrointestinal tract of colonized patients. Appropriate surveillance is therefore necessary for early identification of such strains and prevention of their spread.
|Session name:||XXIst ISTH Congress|
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