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- Analysis of Resistance to Macrolide–Lincosamide–Streptogramin B Among
mecA -PositiveStaphylococcus Aureus Isolates - Mahmoud Khodabandeh, Mohsen Mohammadi, Mohammad Reza Abdolsalehi, Azadeh Alvandimanesh, Mehrdad Gholami, Meysam Hasannejad Bibalan, Abazar Pournajaf, Ramin Kafshgari, Ramazan Rajabnia
- Osong Public Health Res Perspect. 2019;10(1):25-31. Published online February 28, 2019
- DOI: https://doi.org/10.24171/j.phrp.2019.10.1.06
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- 186 Download
- 27 Crossref
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Abstract
PDF Objectives Genetic determinants conferring resistance to macrolide, lincosamide, and streptogramin B (MLSB) via ribosomal modification such as,
erm ,msrA/B andereA/B genes are distributed in bacteria. The main goals of this work were to evaluate the dissemination of MLSB resistance phenotypes and genotypes in methicillin-resistantStaphylococcus aureus (MRSA) isolates collected from clinical samples.Methods A total of 106 MRSA isolates were studied. Isolates were recovered from 3 hospitals in Tehran between May 2016 to July 2017. The prevalence of MLSB-resistant strains were determined by D-test, and then M-PCR was performed to identify genes encoding resistance to macrolides, lincosamides, and streptogramins in the tested isolates.
Results The frequency of constitutive resistance MLSB, inducible resistance MLSB and MSB resistance were 56.2%, 22.9%, and 16.6%, respectively. Of 11 isolates with the inducible resistance MLSB phenotype,
ermC ,ermB ,ermA andereA were positive in 81.8%, 63.6%, 54.5% and 18.2% of these isolates, respectively. In isolates with the constitutive resistance MLSB phenotype, the prevalence ofermA ,ermB ,ermC ,msrA ,msrB ,ereA andereB were 25.9%, 18.5%, 44.4%, 0.0%, 0.0%, 11.1% and 0.0%, respectively.Conclusion Clindamycin is commonly administered in severe MRSA infections depending upon the antimicrobial susceptibility findings. This study showed that the D-test should be used as an obligatory method in routine disk diffusion assay to detect inducible clindamycin resistance in MRSA so that effective antibiotic treatment can be provided.
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- The Effect of
Lactobacillus acidophilus PTCC 1643 on Cultured Intestinal Epithelial Cells Infected withSalmonella enterica serovar Enteritidis - Mona Moshiri, Mohammad Mehdi Soltan Dallal, Farhad Rezaei, Masoumeh Douraghi, Laleh Sharifi, Zahra Noroozbabaei, Mehrdad Gholami, Abbas Mirshafiey
- Osong Public Health Res Perspect. 2017;8(1):54-60. Published online February 28, 2017
- DOI: https://doi.org/10.24171/j.phrp.2017.8.1.07
- 4,328 View
- 24 Download
- 10 Crossref
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Abstract
PDF
Objectives Gastrointestinal disorders caused by
Salmonella enterica serovar Enteritidis (Se sE) are a significant health problem around the globe. Probiotic bacteria have been shown to have positive effects on the immune responses.Lactobacillus acidophilus was examined for its capability to influence the innate immune response of HT29 intestinal epithelial cells towardsSe sE. The purpose of this work was to assess the effect ofL. acidophilus PTCC 1643 on cultured intestinal epithelial cells infected withSe sE.Methods HT29 cells were cultured in Roswell Park Memorial Institute medium supplemented with 10% fetal bovine serum and 1% penicillin/streptomycin. The cells were treated with
L. acidophilus PTCC 1643 after or before challenge withSe sE. At 2 and 4 hours post-infection, we measured changes in the expression levels ofTLR2 andTLR4 via real-time polymerase chain reaction.Results Treatment with
L. acidophilus inhibitedSe sE-induced increases inTLR2 andTLR4 expression in the infected HT29 cells. Moreover, the expression ofTLR2 andTLR4 in cells that were pretreated withL. acidophilus and then infected withSe sE was significantly higher than that in cells infected withSe sE without pretreatment. Taken together, the results indicated thatL. acidophilus had an anti-inflammatory effect and modulated the innate immune response toSe sE by influencingTLR2 andTLR4 expression.Conclusion Our findings suggested that
L. acidophilus PTCC 1643 was able to suppress inflammation caused bySe sE infection in HT29 cells and reduceTLR2 andTLR4 expression. Additional in vivo and in vitro studies are required to further elucidate the mechanisms underlying this anti-inflammatory effect.-
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