S. Ben Redjeb
Tunis University
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Featured researches published by S. Ben Redjeb.
Diagnostic Pathology | 2011
Samia Hammami; I. Boutiba-Ben Boubaker; Rafiaa Ghozzi; Mabrouka Saidani; S Amine; S. Ben Redjeb
BackgroundTwenty four non replicate imipenem resistant P. aeruginosa were isolated between January and November 2008, in the kidney transplantation unit of Charles Nicolle Hospital of Tunis (Tunisia). This study was conducted in order to establish epidemiological relationship among them and to identify the enzymatic mechanism involved in imipenem resistance.MethodsAnalysis included antimicrobial susceptibility profile, phenotypic (imipenem-EDTA synergy test) and genotypic detection of metallo-β-lactamase (MBL) (PCR), O-serotyping and pulsed-field gel electrophoresis.ResultsAll strains showed a high level of resistance to all antimicrobials tested except to colistin. The presence of MBL showed concordance between phenotypic and genotypic methods. Sixteen isolates were identified as VIM-2 MBL-producers and 13 of them were serotype O4 and belonged to a single pulsotype (A).ConclusionsThis study describes an outbreak of VIM-2-producing P. aeruginosa in a kidney transplantation unit. Clinical spread of blaVIM-2 gene is a matter of great concern for carbapenem resistance in Tunisia.
Journal of Medical Microbiology | 2012
M. Hraoui; I. Boutiba-Ben Boubaker; M. Rachdi; A. Slim; S. Ben Redjeb
Between 2007 and 2009, 226 clinical strains of Streptococcus agalactiae, recovered from female genital specimens and from gastric fluid or ear specimens from infected newborns, were isolated at the Laboratory of Microbiology of Charles Nicolle Hospital of Tunis. They were investigated to determine the prevalence of antibiotic resistance and to characterize the mechanisms of resistance to macrolide and tetracycline. All strains were susceptible to penicillin, ampicillin and quinupristin-dalfopristin. They were resistant to chloramphenicol (3.1%), rifampicin (19.1%), erythromycin (40%) and tetracycline (97.3%); 3.1% were highly resistant to streptomycin and 1.3% to gentamicin. Among the erythromycin-resistant isolates, 78.7% showed a constitutive macrolide-lincosamide-streptogramin B (MLS(B)) phenotype with high-level resistance to macrolides and clindamycin (MIC(50) >256 µg ml(-1)), 10% showed an inducible MLS(B) phenotype with high MICs of macrolides (MIC(50) >256 µg ml(-1)) and low MICs of clindamycin (MIC(50)=8 µg ml(-1)) and 2.2% showed an M phenotype with a low erythromycin-resistance level (MIC range=12-32 µg ml(-1)) and low MICs of clindamycin (MIC range: 0.75-1 µg ml(-1)). All strains were susceptible to quinupristin-dalfopristin and linezolid (MIC(90): 0.75 µg ml(-1) for each). MLS(B) phenotypes were genotypically confirmed by the presence of the erm(B) gene and the M phenotype by the mef(A) gene. Resistance to tetracycline was mainly due to the tet(M) gene (93.1%) encoding a ribosome protection mechanism. This determinant is commonly associated with the conjugative transposon Tn916 (P≤0.0002). tet(O) and tet(T) existed in a minority (2.2% and 0.4%, respectively). The efflux mechanism presented by tet(L) was less frequently present (4.5%). No significant association was found between erm(B) and tet(M) genes.
Pathologie Biologie | 2003
I. Boutiba-Ben Boubaker; Jalel Boukadida; O Triki; Naila Hannachi; S. Ben Redjeb
Resume Un episode epidemique dinfections urinaires a Pseudomonas aeruginosa multiresistant aux antibiotiques notamment a limipeneme sest declaree a l’unite de reanimation chirurgicale du service d’urologie de lhopital Charles Nicolle de Tunis, posant de serieux problemes therapeutiques. Une enquete epidemiologique a revele la presence de la souche epidemique dans plusieurs endroits de cette unite. Le genotypage effectue par macrorestriction enzymatique par Xba1 et separation electrophoretique par la technique CHEF (CHEF DRII Biorad, 180V/24xa0h) a revele l’existence de 2 clones differents, chacun ayant ete retrouve au moins une fois dans l’environnement. Ainsi, le milieu hospitalier constitue une source majeure de contamination par P. aeruginosa dou la necessite dune surveillance reguliere pour la mise en place des mesures de prevention necessaires.
Clinical Microbiology and Infection | 2011
M. Hraoui; I. Boutiba-Ben Boubaker; Alexandra Doloy; E. Samir; S. Ben Redjeb; Anne Bouvet
To further understand the epidemiology of Streptococcus pyogenes or group A streptococcus (GAS) infections in Tunisia, phenotypic and genomic markers of GAS isolates, including antibiotic susceptibility, biotypes, T and emm types and toxin gene profiles, have been characterized. A total of 103 isolates, collected between 2000 and 2006, were investigated; 47 were recovered from invasive infections, and 56 from non-invasive infections. Rates of resistance to tetracycline, erythromycin, clindamycin and rifampin were 70.8%, 4.8%, 4.8% and 0.9%, respectively. High levels of resistance to streptomycin and kanamycin were observed in 1.9% and 4.8% of isolates, respectively. Biotype 3 was most common. Twenty different T patterns were observed, with a predominance of T3/13/B3264, and 38 different emm types. In both invasive and non-invasive isolates, emm118 (9.7%), emm42 (8.7%), emm1 (7.8%), st432 (6.8%), emm28 (5.8%) and emm76 (5.8%) were the most prevalent types; emm1, emm76 and emm18 were mainly observed among invasive infections, whereas emm118 (12.5%), emm42 (10.7%) and emm28 (8.9%) were predominant among non-invasive infections. The speB gene was detected in all isolates, but there were variable frequencies of speA, speC and ssa (20.3%, 32% and 25.2% respectively). Significant associations of emm1, emm18 and emm3 with speA and of emm4 and st432 with ssa were found. This first report from Tunisia revealed a unique emm distribution of GAS that differs from those of other regions. This information on the distribution of such emm types will be useful for the development of an appropriate vaccine in a country where the incidence of rheumatic fever remains high.
Pathologie Biologie | 2012
S. Ferjani; Mabrouka Saidani; S. Ennigrou; M. Hsairi; S. Ben Redjeb
AIM OF THE STUDYnThe aim of this study is to assess the relation between virulence genotype, phylogenetic group and susceptibility to fluoroquinolones and the urinary tract infection type including pyelonephritis and cystitis due to Escherichia coli.nnnMATERIALS AND METHODSnBetween 2006 and 2007, 129 non-duplicate E.xa0coli isolates from pyelonephritis (n=56) and cystitis (n=73) were prospectively collected. The antibiotic susceptibility was done by disk diffusion method. The phylogenetic groups, A, B1, B2 and D and 18 virulence genes were determined by multiplex PCR. Statistical analysis was done with the Pearson χ2 test, Mann-Whitney U-test, Kruskal-Wallis test and stepwise multivariable logistic regression analysis, P values below 0.05 were considered statistically significant.nnnRESULTSnFor the pyelonephritis group, sex ratio was 0.3, the median age for women was 30 years and for men it was 54 years. For the cystitis group, sex ratio was 0.4, the median age for women was 41.5 years and for men it was 67.8 years. Significant statistical correlations were found between pyelonephritis isolates and susceptibility to ciprofloxacin (P=4 10(-5)), papG allele II (P=2 10(-6)), hlyA (P=10(-03)), iroN (P=0.04), iha (P=0.03) and ompT (P=0.03) virulence genes, high virulence score (P=0.008) and B2 phylogenetic group (P=0.03). In multivariate logistic regression analysis, papG II as predictor of pyelonephritis, no correlation could be established for the cystitis group.nnnCONCLUSIONnOur findings argue for a direct link between pyelonephritis, virulence factors, susceptibility to fluroquinolones and B2 phylogenetic group among uropthogenic E.xa0coli.
Clinical Microbiology and Infection | 2004
I. Boutiba-Ben Boubaker; R. Ben Abbes; H. Ben Abdallah; K. Mamlouk; Faouzia Mahjoubi; A. Kammoun; Adnene Hammami; S. Ben Redjeb
Pathologie Biologie | 2006
S. Ben Ayed; I. Boutiba-Ben Boubaker; E. Samir; S. Ben Redjeb
Clinical Microbiology and Infection | 2004
I. Boutiba-Ben Boubaker; Rafiaa Ghozzi; H. Ben Abdallah; K. Mamlouk; A. Kamoun; S. Ben Redjeb
Pathologie Biologie | 2008
M. Rachdi; I. Boutiba-Ben Boubaker; S. Moalla; Hanène Smaoui; Adnene Hammami; A. Kechrid; S. Ben Redjeb
Pathologie Biologie | 2006
Sonia Ktari; Faouzia Mahjoubi; S. Jaoua; A. Karray; N. Marty; S. Ben Redjeb; Adnene Hammami