Abstract:
Klebsiella pneumoniae is a multiresistant and persistent bacterium, responsible for multiple
nosocomial infections, a panoply of transferable genetic elements such as integration and
conjugation elements, conjugative plasmids, transposons, integrals, which offer this germ new
virulence and antibiotic resistance traits, such as “BLSE” and “Carbapenemas” enzymes
encoded by acquired chromosomal and plasmid genes responsible for the degradation of β-
lactams and carbapenems. Antibiotic resistance is also ensured by point mutations or by
acquired genes coding for changing the affinity of the antibiotic for its target or for efflux
pumps that reject it, new resistance genes have recently been acquired in this bacterium
(blaOXA-48, blaNDM-1) and the emergence of a new carbapenem-resistant strain in Europe called
‘ST23’. The persistence is ensured in Klebsiella pneumoniae by a mechanism called
“metabolic dormancy” which is summarized in a reversible metabolic slowdown which itself
is done by various mechanisms : Toxin-antitoxin type II, ppGpp, the SOS system, Stopping
multiplication and all cellular activity and inhibiting the effect of antibiotics that target
different cellular processes such as translation, replication, transcription. Klebsiella
pneumoniae also opts for a filamentous form which allows it to grow horizontally while
preventing the scissiparity in order to conserve the energy provided during the division and be
able to perpetuate. These three adaptive phenomena: resistance, persistence and
morphological plasticity have made antibiotic therapy ineffective against this germ ; as a
result new treatment techniques have recently been innovated in order to cure Klebsiella
pneumoniae infections
