Vol 6 No 1-2 (2017)

Published: 2017-07-13

Original Articles

  • XML | PDF | downloads: 278 | views: 386 | pages: 1-7
    Background:    The main cause of toxic shock is TSST-1 toxin which is produced by S. aureus.  Finding of TSST-1 toxin in burnt children is very important to prevent TSS and its consequences. Methods:     The aim of this study was to investigate the presence of gene encoding TSST-1 toxin in wound specimens by PCR. In this case-control study, 90 children who were admitted to the burn unit, were divided in two groups of 45 patients, namely febrile (cases group) and non-febrile (control group). Samplings were done from the burn wounds and were tested by PCR with specific primers of tstH gene. Finally, all data including demographic characteristics, percentage of burnt surface severity and the PCR results were analyzed, statistically.Results:    The positive PCR results indicated the expression of tstH gene in 37.7% of the febrile children and 11.1% of the non-febrile children with a statistically significant difference (p <0.003). The means and the standard deviations for the percentage of burnt surfaces (i.e. severity) in the samples with the positive and negative PCR results were 30.9±16.93 and 20.09±11.02, respectively with a statistically significant difference (p <0.01). No difference with respect to age and sex could be detected between positive and negative PCR results.Conclusion:    A direct association between the expression of tstH and the occurrence of fever in the burnt children was observed. Furthermore, increased surface area of the wounds was also positively related to the expression of tstH.
  • XML | PDF | downloads: 322 | views: 369 | pages: 8-14
    Background:    Dental caries is a biofilm-dependent disease mainly causes by cariogenic bacteria that colonize dental surfaces, especially Streptococcus mutans. Nickel is a safe metal element which routinely used in dental compounds. The antibacterial and anti-biofilm effects of nickel nanoparticles (Ni-NPs) have been determined in limited studies, but the anti-biofilm effects of Ni-Nps on S. mutans have not been investigated before, so this study was aimed to investigate the anti-biofilm effects of Ni-NPs on S. mutans ATCC 35668.Methods:    Biofilm formation by S. mutans ATCC 35668 was assayed by Microtiter Dish Biofilm Formation Assay and absorbance was measured by ELISA reader at 550 nm. The amounts of biofilm formation were also measured in the presence of 1, 01 and 0.01mg/mL concentrations of Ni- NPs by the same protocol and the mean amounts were compared between groups. Eight replicates were considered for each experiment. Data was statistically analyzed by SPSS16 software.Results:    According to the statistical analysis, the amounts of biofilm formation were significantly reduced in the presence of all the tested concentrations of Ni-NPs.Conclusion:    The current findings showed the potent anti-biofilm effects of Ni-NPs even in a concentration as low as 0.01 mg/ mL, so it is proposed for different applications in dentistry, considering its anti-biofilm effects. However, further studies
  • XML | PDF | downloads: 347 | views: 392 | pages: 15-20
    Background:   The aim of the present study was to determine the prevalence of phylogenetic groups/subgroups, fimbrial genes, and antibiotic susceptibility of E. coli isolated from urinary tract infections in Karaj city, Iran.Methods:  A total of 107 E. coli isolates were confirmed by standard bacteriological tests. The phylogenetic group, fimbrial genes and antibiotic resistance genes was determined by PCR method. Antibiotic resistance of all the isolated E.coli against nine antimicrobial agents was determined by disk diffusion method.Results:   PCR assays showed the prevalence of fimbrial genes among the studied isolates were 31.7% and 9.3% for papEF and afaBC, respectively. Most of papEF genes were placed in D phylogroup (18.6%) and D1 subgroup (14.01%) and the percentage of afaBC (2.8%) were similar in B1, B2 and D phylogroups. The frequency of tetA and tetB genes were 22.4% and 17.7%. Isolates which contained tetA were distributed mainly in D group (14.01%) and those which contained tetB were divided in D group (7.48%). Antimicrobial susceptibility testing showed the maximum resistance rate to cephalexin (CN: 100%) and the minimum resistance level to ciprofloxacin (CP: 36.5%).Conclusion:   The present study showed that phylogenetic groups A and D were predominant. Virulence factors such as papEF and afaBC belonged to D phylogenetic group. Multidrug resistance E. coli isolates tends to be in the non-B2 phylogenetic groups. Due to high antibiotic resistance, appropriate control should be considered in medicine to control the development of novel resistant isolates.
  • XML | PDF | downloads: 320 | views: 347 | pages: 21-27
    Background:   Excessive use of broad-spectrum antibiotics in hospitals has led to the emergence of highly resistant strains of Pseudomonas aeruginosa. The main mechanism of resistance of this bacterium to fluoroquinolones and carbapenems are the modification of type II topoisomerases (DNA gyrase and topoisomerase IV) and alterations in the OprD porin, respectively. The aim of this study was to examine for the occurrence of mutations related to fluoroquinolone resistance of gyrA and parC genes and mutational inactivation of oprD gene of clinical isolates using DNA sequencing technique.Methods:  A total of 60 P. aeruginosa isolates were collected from the hospitalized patients in the Intensive Care Units (ICUs) of Al-Zahra hospital located in Isfahan, Iran. The pattern of sensitivity to antibiotics was determined using CLSI disk diffusion and MIC methods. The assay was based on a DNA sequencing method using polymerase chain reaction (PCR) for amplification and sequencing of the selected genes.Results:   The results show that replacement of Ile for Thr-83 in gyrA was the only replacement, while other substitutions not observed. No mutations were found in parC. The most frequent amino acid alterations were E185Q, P186G, and V189T, found in five resistance isolates, However, nucleotide insertions and deletions mutations not observed.Conclusion:  Our study suggested that mutation of gyrA and oprD genes may play a minor role in fluoroquinolone and carbapenem resistance and other mechanisms may contribute to the fluoroquinolone and carbapenem resistance of P. aeruginosa.
  • XML | PDF | downloads: 267 | views: 352 | pages: 28-35
    Background:   S. epidermidis is one of predominant members of human normal microflora, however it may be the main cause of nosocomial infections related to medical devices put into the body and thus the biofilm formation is a main route for pathogenesis which is affected by icaADBC operon.  In this study, the prevalence of IS256 sequence among ica-positive and biofilm non-producer clinical isolates of S. epidermidis was investigated. Methods:   In this study, 100 clinical isolates of S. epidermidis were collected from different infections. The IS256 sequence, icaADBC operon and biofilm formation by microtiter plate assay were evaluated among them. The antibiotic susceptibility of these isolates was done with disc diffusion by using cefoxitin, ciprofloxacin, erythromycin, gentamycin, oxacillin and tetracycline discs. Results:    Of 100 isolates, 18 (18%) were ica operon-positive from which 18%, 14%, 16% and 17% contained icaA, icaD, icaB and icaC genes, respectively. Moreover, 14 of 18 (77.77%) ica-positive isolates amplified the IS256 gene. The biofilm formation by microtiter plate assay showed that 18 (18%) isolates were strong biofilm producers, 21 (21%) produced intermediate level biofilm and 14 (14%) and 47 (47%) isolates were weak and non-biofilm producers, respectively. in the antibiotic susceptibility test, the majority of isolates were resistant to oxacillin and lowest resistance was against ciprofloxacin.Conclusion:   The statistical analysis with p<0.05 exhibited that there was a reverse relation between biofilm production and the insertion of IS256, and in fact the higher prevalence of IS256 among isolates, the biofilm formation declined. Data showed that amongst most of ica-positive isolates, the IS256 was detected and therefore other genetic factors affect the expression of this operon.
  • XML | PDF | downloads: 286 | views: 378 | pages: 36-44
    Background:  This study was conducted to detect the prevalence of EHEC virulence genes and antimicrobial resistance profile of Escherichia coli strains belonging to B2 phylogroup implicated in Urinary tract infections in Semnan, Iran.Methods:   From 240 urine samples 160 E. coli strains were isolated, biochemically. Then, E. coli isolates were examined by Multiplex-PCR for phylogenetic typing and detection of virulence genes (hly, stx1, stx2, eae) associated with Enterohemorrhagic E. coli. Finally, Antimicrobial resistance of E. coli isolates were characterized using Disk Diffusion method.  Results:  From 160 E. coli isolates, 75 strains (47%) were assigned to B2 phylogenetic group and prevalence of virulence genes were as follow: hly (21.3%), stx1 (16%), stx2 (10.6%) and eae (6.7%), subsequently.  Phenotypic antimicrobial resistance of B2 isolates showed that all isolates were sensitive to Meropenem and Furazolidone and then highest frequency of resistance was observed to Streptomycin, Oxytetracycline, Neomycin, Nalidixic acid and Ampicillin (98.7% to 49.3%). Also low resistance prevalence was observed in case of Ceftizoxime, Lincospectin, Imipenem, Chloramphenicol and flurefenicole (16% to 1.3%).Conclusion:   The data suggest a high prevalence of antibiotic resistance in UPEC strains belonging to B2 phylogroup even for the antimicrobials using in pet and farm animals and their potential to cause EHEC specific clinical symptoms which may represent a serious health risk since these strains can be transmitted to GI tract and act as a reservoir for other uropathogenic E. coli and commensal strains.
  • XML | PDF | downloads: 366 | views: 516 | pages: 45-55
    Background:    Bacterial secondary infection of pressure ulcers (bedsores), so called as decubitus ulcers, leads to ulcer development and it interferes with the healing process. Thus, such infections can be lethal due to the sepsis if no constructive medicinal measures regarded. Drug resistance of bacteria in pressure ulcers leads to healing inhibition. Molecular identification of bacteria involved in such infections seem necessary as culture and phenotypic approaches may result in misidentification. . The purpose of this study was to isolate and identify aerobic bacteria detected in bedsores in three Hospitals: Rasool-e-Akram, Imam Hossein and Tajrish Shohada Hospitals, Tehran, Iran.Methods:    To this end, decubitus ulcer samples of 49 patients were obtained using sterile swabs. After direct microscopic examination, the swabs were used to streak BHI agar plates supplemented with %5 defibrinated sheep blood for enrichment of probable aerobic cultures. Bacterial isolates diagnosed by biochemical tests. Antibiotic susceptibility of the isolates determined based on CLSI guideline. For molecular identification, PCR amplification of the 16S rRNA gene performed using Eubacterial universal primers. Then, the PCR products were sequenced and the nucleotide sequences of the PCR products were analyzed by BLASTN similarity search program available at NCBI. Results:   Among the isolates, Pseudomonas aeruginosa (36%) had the highest frequency, followed by Staphylococcus aureus (32%) and Escherichia coli (30%). The frequencies of Klebsiella pneumonia and Proteus spp. were 10% and 8%, respectively. Most of the isolated bacteria showed a widespread antibiotic resistance. Molecular identification of the bacterial isolates resulted in 6 isolates of Escherichia coli, two isolates of each of Proteus mirabilis and Shigella spp., 4 isolates of Enterobacter cloacae, and 1 isolate of each of Cronobacter sakazakii and Morganella morganii.Conclusion:   Results showed that Pseudomonas aeruginosa and Staphylococcus aureus as the most frequent bacterial species detected in pressure ulcers; however, bacterial prevalence may be different in different hospital wards.