RESUMO
Background: Acinetobacter baumannii is an increasingly important cause of nosocomial infections worldwide. In addition to the intrinsic resistance of Acinetobacter baumannii to many antibiotics, available treatment approaches with older antibiotics are significantly associated with an increase in multiresistant strains. The aim of this study was to evaluate the synergistic effect of tazobactam with meropenem and ciprofloxacin against carbapenems and drug resistant Acinetobacter baumannii isolated from burn patients in a tertiary burn center in Tehran. Materials and methods: In this study, a total of 47 clinical isolates of A. baumannii were included from burn patients admitted to the Shahid Motahari Burns Hospital, Tehran, from June 2018 to August 2018. The disk diffusion method was used to determine resistance patterns. The synergistic effect of tazobactam with meropenem and ciprofloxacin was evaluated by determining the MIC. A PCR assay was performed to determine bla OXA-40-like , bla OXA-58-like and bla OXA-24-like . Results: Antibiotic susceptibility testing revealed that all of the isolates were resistant to meropenem and ciprofloxacin. The MIC values decreased in the cases of combined use of ciprofloxacin and meropenem with tazobactam. The blaOXA-24-like gene was the predominant carbapenemase gene (93.6%), followed by bla OXA-40-like , which was detected in 48.9% of isolates. None of the A. baumannii isolates harbored the bla OXA-58-like gene. Conclusions: Based on in-vitro antimicrobial susceptibility in the current study, the MIC of tazobactam combined with meropenem or ciprofloxacin have been shown to be variable. Furthermore, the data acquired from such in vitro conditions should be confirmed by reliable results from sufficiently controlled clinical trials.
RESUMO
AIM: This study was aimed to investigate the presence of H. pylori and its virulence genotypes in dental plaques of Iranian patients with chronic periodontitis. BACKGROUND: Helicobacter pylori is a Gram-negative bacterium that is associated with atrophic gastritis, peptic ulcer, and gastric cancer. Several studies have detected this bacterium in the oral cavity, suggesting it as a potential reservoir. METHODS: A hundred individuals were divided in 2 groups: 50 patients with chronic periodontitis (case group), and 50 subjects in non-periodontitis (control group). Supragingival and subgingival plaque samples were collected from the individuals using wood wedges and sterile paper points respectively, and prepared for PCR analysis. RESULTS: Totally, H. pylori DNA was detected in 5 out of 100 (5%) dental plaques. Of 5 dental plaques positive for H. pylori, cagA gene was detected in 4 specimen, 3 in periodontitis group and one in non-periodontitis group. The H. pylori vacA s1m1 genotype was predominantly detected in 2/5 samples. The babA2 gene was detected in all (5/5) H. pylori-positive dental plaques. There was no significant correlation between the presence of H. pylori genotypes from dental plaques and chronic periodontitis (P > 0.05). CONCLUSION: Our results revealed that the rate of H. pylori is very low in the dental plaques of Iranian patients with chronic periodontitis. Majority of H. pylori strains from oral cavity were highly virulent based on the main clinically virulence factors they carried.
