4.6 Article

Beta-lactam induced morphological changes in serum of extended- spectrum beta-lactamase-producing Klebsiella pneumoniae blood isolates

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MICROBES AND INFECTION
卷 25, 期 1-2, 页码 -

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ELSEVIER
DOI: 10.1016/j.micinf.2022.105036

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Antimicrobial resistance; Bacterial structures; Membrane attack complex; Serum resistance

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Klebsiella pneumoniae is an opportunistic pathogen that causes bacteremia. Ceftazidime and meropenem induce morphological changes in bacteria. The study analyzed the resistance and susceptibility of Klebsiella spp. Bacteremia isolates to these antibiotics in different serum conditions. The findings revealed that serum and beta-lactam antibiotics can induce morphological changes in bacteria, with some strains showing increased sensitivity to beta-lactam antibiotics.
Klebsiella pneumoniae is an opportunistic pathogen, which frequently causes bacteremia. Ceftazidime and meropenem, two important beta-lactam antibiotics for treatment of K. pneumoniae infections, induce morphological changes in bacteria when examined in vitro. Thirty clinical Klebsiella spp. Bacteremia isolates were analyzed for antimicrobial resistance and serum resistance. To determine whether com-plement influenced the resistance to ceftazidime of extended-spectrum beta-lactamase producing -isolates and sensitivity to meropenem, one serum resistant and one partly serum sensitive isolate were analyzed in normal human serum, heat-inactivated human serum, and growth medium with addition of beta-lactam antibiotics.HA391 was resistant to ceftazidime and had identical minimum inhibitory concentrations for mer-openem in normal human serum, heat-inactivated serum and RPMI. In normal human serum, HA233 was inhibited by ceftazidime and had lower inhibitory concentrations of meropenem. Morphological changes induced by serum and beta-lactam antibiotics were analyzed by light-and electron microscopy. Light microscopy showed elongation of bacteria treated with ceftazidime. By electron microscopy membrane attack complexes were observed for HA233 in normal human serum, thereby facilitating beta-lactam antibiotics access to the periplasmic space and the peptidoglycan layer, explaining the increased killing of HA233 by beta-lactam antibiotics. Complement did not enhance beta-lactam killing of HA391, underlining the importance of serum susceptibility.(c) 2022 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.

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