The aim was to evaluate the susceptibility of bla producing Enterobacteriaceae to Slovakian Thymus vulgaris essential oil (TVEO) alone and in combination with cefotaxime (CTX). TVEO composition was determined by gas chromatograph-mass spectrometer (GC/MS). Susceptibility to 21 antibiotics was determined by disc diffusion assay. Genes characterization for resistance to β-lactams was accomplished by polymerase chain reaction (PCR). The antibacterial activity was investigated by standard methods. The synergistic interaction was determined by checkerboard test. Thymol (34.5%), p-cymene (22.27%) and linalool (5.35%) were the major components present in the TVEO. The identified strains were multi-drug resistant (MDR). TVEO showed high activity against all MDR strains, including bla producing isolates, with inhibition zones and MIC values in the range of 24-40 mm/10μL and 2.87-11.5 μg/mL, respectively. TVEO in combination with CTX showed a synergistic action against bla producing Escherichia coli (FICI 0.28) and an additive effect vs ESBL producing Enterobacter cloacae (FICI 0.987).

The objectives of this study were to undertake the microbiological and molecular characterization of Corynebacterium diphtheriae isolates collected in Algeria during epidemic and post-epidemic periods between 1992 and 2015. Microbiological characterization includes the determination of biotype and toxigenicity status using phenotypic and genotypic methods. Antimicrobial susceptibility was determined by the E-test method. Molecular characterization was performed by multi-locus sequence typing. In total, there were 157 cases of C. diphtheriae isolates, 127 in patients with respiratory diphtheria and 30 with ozena. Isolates with a mitis biotype were predominant (122 out of 157; 77.7%) followed by belfanti (28 out of 157; 17.8%) and gravis biotype (seven out of 157; 4.5%). Toxigenic isolates were predominant in the period 1992-2006 (74 out of 134) whereas in the period 2007-2015, only non-toxigenic isolates circulated (23 out of 23). All 157 isolates were susceptible to erythromycin, gentamicin, vancomycin and cotrimoxazole. Reduced susceptibility to penicillin G, cefotaxime, tetracycline and chloramphenicol was detected in 90 (57.3%), 88 (56.1%), 112 (71.3%) and 90 (57.3%) isolates, respectively. Multi-locus sequence typing analysis indicates that sequence type 116 (ST-116) was the most frequent, with 65 out of 100 isolates analysed, in particular during the epidemic period 1992-1999 (57 out of 65 isolates). In the post-epidemic period, 2000-2015, 13 different sequence types were isolated. All belfanti isolates (ten out of 100 isolates) belonged to closely related sequence types grouped in a phylogenetically distinct eBurst group and were collected exclusively in ozena cases. In conclusion, the epidemic period was associated with ST-116 while the post-epidemic period was characterized by more diversity. Belfanti isolates are grouped in a phylogenetically distinct clonal complex.

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One hundred and two Escherichia coli strains isolated from healthy broiler chickens collected from April 2012 to November 2014 in seven geographic areas of western Algeria were studied. Susceptibility pattern to 11 antimicrobial agents was determined by disk diffusion method as recommended by the Clinical Laboratory Standard Institute (CLSI). Antibiograms revealed high levels of resistance to quinolones and fluoroquinolones including nalidixic acid (100%), flumequin (86, 27%) and enrofloxacin (84, 31%), and to other antibiotics, notably: tetracycline (92, 15%), trimethoprim-sulfamethoxazol (80, 39%) and amoxicillin (68, 62%). However, a moderate percentage of strains were resistant to neomycin (31, 37%), chloramphenicol (27, 45%) and nitrofurantoin (21, 56%). Only 7, 84% of the isolates were resistant to gentamicin and all the isolates were susceptible to colistin. All isolated E. coli were resistant to at least three antibiotics. 96, 08% and 91, 12% of the isolates were resistant to at least four and five antimicrobials, respectively. Twenty eight antibiotic resistance patterns of E. coli strains were detected, of which 11 were present significantly. The results of this survey indicate very high levels of resistance to quinolones and to other antibiotics in E. coli from healthy broiler chickens in Algeria, and suggested that this reservoir of resistance may affect the therapeutic potential of fluoroquinolones in human and veterinary medicine.

AimMultidrug-resistant (MDR) Enterobacteriaceae have frequently been reported, in both human and veterinary medicine, from different parts of the world as a consequence of antibiotic usage. However, there is a lack of published data regarding antimicrobial resistance in non-Escherichia coli (E. coli) Enterobacteriaceae from animals in Algeria. This study aimed to evaluate the frequency of resistance to antibiotics with a focus on quinolones and to investigate the presence of qnr genes inEnterobacteriaceaeof poultry origin.Materials and MethodsA total of 310 samples of poultry origin were collected from 2010 to 2014 from broiler and layer farms and hatcheries located in different geographic areas of Western Algeria (including Mostaganem, Oran, Mascara, Relizane, Chlef, Tiaret, and Tissemsilt). Antimicrobial susceptibility testing was performed using disc diffusion assay. Polymerase chain reaction and sequencing accomplished the characterization of qnr genes (qnrA, qnrB, and qnrS).ResultsA total of 253 Enterobacteriaceaestrains were isolated in this study. These isolates exhibited high levels of resistance to quinolones and other families of antibiotics. All the strains isolated in this study were resistant to at least one antibiotic. Among them, 233 (92.09%) were considered MDR. Among the 18 randomly selected nalidixic acid (NA)-resistant Enterobacteriaceaeisolates, one E. coli and one Enterobacter cloacae were carrying qnrS1. By contrast, qnrA and qnrB were not detected in this study.ConclusionThis is the first report on the identification of the qnrS gene in E. cloacae isolated from animal source in Algeria. Further studies have to be conducted to determine the real prevalence of qnr genes.