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Transferable antibiotic resistance in nosocomial Stenotrophomonas maltophilia strain

J Blahová1, K Králiková, V Krcméry

  • 1Institute of Preventive and Clinical medicine, Limbová, Bratislava, Slovak Republic.

Insights

Stenotrophomonas maltophilia caused neonatal conjunctivitis and showed antibiotic resistance. Resistance genes transferred to other bacteria, highlighting potential public health concerns.

Area of Science:

  • Medical Microbiology
  • Infectious Diseases

Background:

  • Stenotrophomonas maltophilia is an opportunistic pathogen.
  • Neonatal conjunctivitis can be caused by various bacteria.
  • Antibiotic resistance in bacteria poses a significant public health threat.

Purpose of the Study:

  • To investigate the antibiotic resistance profile of Stenotrophomonas maltophilia isolated from a neonate.
  • To determine the genetic basis of antibiotic resistance transfer in S. maltophilia.

Main Methods:

  • Bacterial isolation and identification.
  • Antibiotic susceptibility testing.
  • Bacterial conjugation experiments.
  • Enzyme inhibition assays (using EDTA and clavulanate).

Main Results:

  • Stenotrophomonas maltophilia strain 298/85 isolated from neonatal conjunctivitis was resistant to most antibiotics, except cefepime and trimethoprim.
  • Resistance determinants for carbenicillin and cephaloridine were transferred to Escherichia coli and Proteus mirabilis.
  • Transconjugants exhibited co-resistance to kanamycin, cefotaxime, and aztreonam.
  • Hydrolysis of imipenem, cefotaxime, and aztreonam was observed and inhibited by EDTA and clavulanate, respectively.
  • Ceftazidime hydrolysis was not inhibited by clavulanate, suggesting distinct resistance mechanisms.

Conclusions:

  • The study identified a multidrug-resistant Stenotrophomonas maltophilia strain causing neonatal conjunctivitis.
  • The findings demonstrate the transferability of antibiotic resistance genes, posing a risk of further spread.
  • Distinct mechanisms of beta-lactamase activity were suggested based on differential inhibition by clavulanate.

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