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Incidence and mechanisms of aminoglycoside resistance inPseudomonas aeruginosa serotype O11 isolates

Inzidenz und Mechanismus der Aminoglykosid-Resistenz beiPseudomonas aeruginosa O11-Isolaten

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Summary

Mechanisms of resistance to five aminoglycoside antibiotics: gentamicin (G), tobramycin (T), netilmicin (N), amikacin (A) and isepamicin (I), were assessed in 16 clinical isolates ofPseudomonas aeruginosa serotype O11, originating from five hospitals in Bratislava. All isolates werein vitro highly resistant to all mentioned aminoglycoside antibiotics (MIC>32 mg/l). Thirteen isolates produced three aminoglycoside-modifying enzymes (AGME), responsible for resistance to the respective aminoglycosides: AAC(6′)-I (T, N, A); APH (2″) (G, T); APH (3′)-VI (I). In addition to this, in four isolates a production of AAC(3)-II (G, T, N) was observed. In three isolates no production of AGME was observed. The strains studied were isolated mainly from urine. Several isolates were able to transfer aminoglycoside resistance by bacterial conjugation toP. aeruginosa 1008 rifr recipient. The transconjugants from these transfers expressed the same resistance pattern and nearly the same mechanisms of resistance as the donor strains.

Zusammenfassung

Bei 16 klinischen Isolaten vonPseudomonas aeruginosa Serotyp O11 aus fünf Krankenhäusern in Bratislava wurde der Mechanismus der Resistenz gegen fünf Aminoglykosid-Antibiotika untersucht; Gentamicin (G), Tobramycin (T), Netilmicin (N), Amikacin (A) und Isepamicin (I). Alle Isolate warenin vitro hochresistent gegen alle genannten Aminoglykosid-Antibiotika (MHK-Werte >32 mg/l). 13 der Isolate bildeten drei Aminoglykosid-modifizierende Enzyme (AGME), die für die Resistenz gegenüber den entsprechenden Aminoglykosiden verantwortlich waren: AAC(6′)-I (TNA): APH (2″) (G, T): APH (3′)-VI (I). Zusätzlich wurde bei drei Isolaten die Produktion von AAC(3)-II (G, T. N) beobachtet. In drei Isolaten fand sich keine Produktion von AGME. Die untersuchten Stämme waren überwiegend aus Urin isoliert worden. Mehrere der Isolate waren fähig, die Aminoglykosid-Resistenz durch bakterielle Konjugation auf denP. aeruginosa 1008 rifr Rezipienten zu übertragen. Die Transkonjugate von diesen Übertragungen exprimierten dasselbe Resistenzmuster und wiesen nahezu denselben Resistenzmechanismus auf wie die Spenderstämme.

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Authors and Affiliations

  1. Dept. of Microbiology and Virology, Comenius University, Mlynská dolina B-2, 842 15, Bratislava

    M. Kettner Ph. D., Sc. D., J. Kallová Ph. D. & M. Hletková

  2. National Institute for Hygiene and Epidemiology, 826 45, Bratislava, Slovakia

    P. Milošovič M. D.

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  1. M. Kettner Ph. D., Sc. D.
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  2. J. Kallová Ph. D.
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  3. M. Hletková
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  4. P. Milošovič M. D.
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Kettner, M., Kallová, J., Hletková, M. et al. Incidence and mechanisms of aminoglycoside resistance inPseudomonas aeruginosa serotype O11 isolates. Infection 23, 380–383 (1995). https://doi.org/10.1007/BF01713571

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  • DOI: https://doi.org/10.1007/BF01713571

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