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Infection

, Volume 23, Issue 6, pp 380–383 | Cite as

Incidence and mechanisms of aminoglycoside resistance inPseudomonas aeruginosa serotype O11 isolates

  • M. Kettner
  • J. Kallová
  • M. Hletková
  • P. Milošovič
Originalia

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.

Keywords

Enzyme Infectious Disease General Practice Gentamicin Family Medicine 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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

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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Copyright information

© MMV Medizin Verlag GmbH München 1995

Authors and Affiliations

  • M. Kettner
    • 1
  • J. Kallová
    • 1
  • M. Hletková
    • 1
  • P. Milošovič
    • 2
  1. 1.Dept. of Microbiology and VirologyComenius UniversityBratislava
  2. 2.National Institute for Hygiene and EpidemiologyBratislavaSlovakia

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