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Analysis of pristinamycin‐resistant Staphylococcus epidermidis isolates in the Tunisian Bone Marrow Transplant Center
Author(s) -
Achour W.,
Bouchami O.,
Galopin S.,
Leclercq R.,
Ben Hassen A.
Publication year - 2008
Publication title -
letters in applied microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.698
H-Index - 110
eISSN - 1472-765X
pISSN - 0266-8254
DOI - 10.1111/j.1472-765x.2007.02318.x
Subject(s) - staphylococcus epidermidis , microbiology and biotechnology , bone marrow transplant , bone marrow transplantation , biology , staphylococcus , bone marrow , medicine , staphylococcus aureus , bacteria , genetics , immunology
Aims: We report the analysis of genetic determinants conferring resistance to pristinamycin in Staphylococcus epidermidis strains and epidemiology typing of these strains by pulsed‐field gel electrophoresis. Methods and Results: Staphylococcus epidermidis (346 isolates) were searched for strains with pristinamycin resistance. Pristinamycin‐resistant strains (seven isolates) were isolated in five patients with haematological cancer in the Bone Marrow Transplant Centre of Tunisia in 2002. Resistance to pristinamycin was observed in 2% of isolates. The seven pristinamycin‐resistant strains shared resistance to oxacillin (MIC = 8–512 μg ml −1 ), gentamicin (MIC = 16–512 μg ml −1 ), erythromycin (MIC > 1024 μg ml −1 ), lincomycin (MIC > 1024 μg ml −1 ), pristinamycin (MIC = 4–16 μg ml −1 ) and rifampin (MIC = 128–256 μg ml −1 ). erm genes were amplified: ermA from six strains and ermC from one. vga gene encoding streptogramins A resistance (pristinamycin résistance) was amplified from all strains and typed as vgaA by analysis after electrophoresis of restriction profiles of vga amplicons (two fragments with Sau3A of 164 and 378 bp; one fragment with Eco RI). Pulsed‐field gel electrophoresis (PFGE) of SmaI chromosomal DNA digests of the seven S. epidermidis isolates divided them into two distinct pattern types: pulsed‐field type A (classified from A1 to A6 subtypes) and type B. The six strains harbouring ermA genes belonged to the PFGE type A while the strain harbouring ermC genes belonged to the PFGE type B. We characterized an epidemic strain carrying the vga A and ermA genes responsible for the outbreak. Conclusions: Two clones of pristinamycin‐resistant S. epidermidis were isolated in our patients. One of them, isolated in all patients, had expanded over six months suggesting acquisition by cross‐contamination. Significance and Impact of the study: Increasing isolation of pristinamycin resistant S. epidermidis strains is an alarming indicator of nosocomial dissemination. The vector will be determined to establish a system of epidemiological surveillance.