Background:The mouth provides an environment that allows the colonization and growth of a wide variety of microorganisms, especially bacteria. One of the most effective ways to reduce oral microorganisms is using mouthwashes.Objectives:The aim of this study was to investigate the antibacterial effects of chlorhexidine mouthwashes (manufacture by Livar, Behsa, Boht) on common oral microorganisms.Materials and Methods:In this in vitro study, isolated colonies of four bacteria, including Streptococcus mutans, S. sanguinis, S. salivarius and Lactobacillus casei, were prepared for an antimicrobial mouth rinse test. The tube dilution method was used for determining the minimum inhibitory concentrations (MIC) and minimum bactericidal concentrations (MBC).Results:The MICs for Kin gingival, Behsa and Boht mouthwashes were 0.14, 0.48 and 1000 micrograms/mL using the tube method for S. mutans, respectively. The MBCs for the mentioned mouthwashes were 0.23, 1.9 and 2000 micrograms/mL for S. mutans, respectively. The MICs for Kin gingival, Behsa and Boht mouthwashes were 0.073, 0.48 and 250 micrograms/mL using the tube method for S. sanguinis, respectively. The MBCs for the mentioned mouthwashes were 0.14, 1.9 and 1000 micrograms/mL for S. sanguinis, respectively.Conclusions:The Kin Gingival chlorhexidine mouthwash has a greater effect than Behsa and Boht mouthwashes on oral microorganisms and is recommended to be used for plaque chemical inhibition.
Background: Metallo-β-Lactamases (MBL) are usually encoded on the gene cassettes harboring integrons and disseminated easily among Acinetobacter baumannii isolates. This study was aimed to investigate the association of the genes encoding MBL with the presence of class 1 and 2 integrons among multidrug-resistant (MDR) A.baumannii isolates. Methodology: A total of 85 non-duplicated A.baumannii isolates were collected and evaluated for the amplification of bla OXA-51. The presence of genes encoding MBLs, including bla IMP , bla VIM , bla SIM , bla SPM , bla GIM , bla DIM and bla NDM , as well as intI 1 and intI 2 was evaluated by PCR. Also, the production of MBLs was screened phenotypically by the combination of EDTA and meropenem. Results: In this study, 77 out of 85 isolates were MDR. Also, 34 isolates had only intI 1 , 10 had only intI 2 and 15 had both intI 1 and intI 2 . The phenotypic detection of MBLs was found in 30 isolates, among which bla VIM was as the most common the gene encoding MBL followed by bla IMP , bla SPM and bla SIM . The gene cassettes analysis revealed that class 1 integron is often responsible for transferring the genes harboring MBLs. Conclusion: The production of MBLs among A. baumannii strains is one of the main mechanisms of resistance to carbapenems. Therefore, the development of inexpensive screening methods for the phenotypic detection of MBLs in clinical laboratories settings is essential. Also, our data revealed that the class 1 integron is often responsible for the dissemination of the MBL genes among A. baumannii isolates.
Background The aim of this study was to evaluate the antimicrobial resistance and genetic basis for metronidazole (Mtz) and clarithromycin (Cla) resistance in strains of Helicobacter pylori , isolated from patients with gastroduodenal disorders. Patients and methods A total of 157 H . pylori isolates (from 22 gastric cancer, 38 peptic ulcer disease, and 97 non-ulcer dyspepsia patients) were analyzed for drug susceptibility to Mtz and Cla, by gradient diffusion test (E-test, MAST). The PCR and sequence analysis of the rdxA and frxA for Mtz-resistant strains and the 23S rRNA for Cla-resistant strains were used to determine the genetic basis of drug resistance in H. pylori strains. Increased expression of TolC homologous genes ( hefA ) that upregulates efflux pump activity was determined in multidrug-resistant (MDR) strain of H. pylori by real-time PCR technique. Results Among 157 H . pylori isolates, 32 (20.4%) strains were resistant to at least one of the antimicrobial agents. The highest resistance rate was attributed to Mtz (n=69, 43.94%). Among the resistant strains of H. pylori , 15 cases (9.55%) were detected as MDR. Mutations in the rdxA (85.5%) and A2143G point mutations (63.1%) in the 23S rRNA were the most common cause of resistance to Mtz and Cla in strains of H. pylori , respectively. In MDR strains, the rdxA mutation and A2143G-point mutation in the 23S rRNA were the most abundant mutations responsible for drug resistance. The relative expression of hefA in MDR strains (mean 3.706) was higher than the susceptible strains (mean 1.07). Conclusion Mutational inactivation and efflux pump overexpression are two mechanisms that increase the resistance to H. pylori antimicrobial agents and the rate of MDR strains. In Iran, the mutations of rdxA and frxA in Mtz-resistant strains and A2143G and A2142G of the 23S rRNA in Cla-resistant strains were significant. The screening for these mutations could help to prevent antibiotic resistance, and to determine the most effective anti- H. pylori drugs.
Pyogenic spinal infection continues to represent a worldwide problem. In approximately one-third of patients with pyogenic spondylodiscitis, the infectious agent is never identified. Of the cases that lead to organismal identification, bacteria are more commonly isolated from the spine rather than fungi and parasites. This study applied universal prokaryotic 16S rRNA PCR as a rapid diagnostic tool for the detection of bacterial agents in specimens from patients suspected of pyogenic spondylodiscitis. Gram and Ziehl-Neelsen staining were used as a preliminary screening measure for microbiologic evaluation of patient samples. PCR amplification targeting 16S rRNA gene was performed on DNA extracted from 57 cases including specimens from epidural abscesses, vertebral, and disc biopsies. Positive samples were directly sequenced. MRI findings demonstrated that disc destruction and inflammation were the major imaging features of suspected pyogenic spondylodiscitis cases, as 44 cases showed such features. The most common site of infection was the lumbar spine (66.7%), followed by thoracic spine (19%), the sacroiliac joint (9.5%), and lumbar-thoracic spine (4.8%) regions. A total of 21 samples amplified the 16S rRNA-PCR product. Sanger sequencing of the PCR products identified the following bacteriological agents: Mycobacterium tuberculosis (n = 9; 42.9%), Staphylococcus aureus (n = 6; 28.5%), Mycobacterium abscessus (n = 5; 23.8%), and Mycobacterium chelonae (n = 1; 4.8%). 36 samples displayed no visible 16S rRNA PCR signal, which suggested that non-bacterial infectious agents (e.g., fungi) or non-infectious processes (e.g., inflammatory, or neoplastic) may be responsible for some of these cases. The L3–L4 site (23.8%) was the most frequent site of infection. Single disc/vertebral infection were observed in 9 patients (42.85%), while 12 patients (57.15%) had 2 infected adjacent vertebrae. Elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) inflammatory markers were noted in majority of the patients. In conclusion, microbiological methods and MRI findings are vital components for the proper diagnosis of pyogenic spondylodiscitis. Our findings suggest that molecular methods such as clinical application of 16S rRNA PCR and sequencing may be useful as adjunctive diagnostic tools for pyogenic spondylodiscitis. The rapid turnaround time of 16S rRNA PCR and sequencing submission and results can potentially decrease the time to diagnosis and improve the therapeutic management and outcome of these infections. Although S. aureus and M. tuberculosis were the most common causes of pyogenic spinal infections in this study, other infectious agents and non-infectious etiologies should be considered. Based on study results, we advise that antibiotic therapy should be initiated after a definitive etiological diagnosis.
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