Osong Public Health and Research Perspectives

Original Articles

Analysis of Resistance to Macrolide–Lincosamide–Streptogramin B Among mecA-Positive Staphylococcus 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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Objectives

Genetic determinants conferring resistance to macrolide, lincosamide, and streptogramin B (MLS_B) via ribosomal modification such as, erm, msrA/B and ereA/B genes are distributed in bacteria. The main goals of this work were to evaluate the dissemination of MLS_B resistance phenotypes and genotypes in methicillin-resistant Staphylococcus 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 MLS_B-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 MLS_B, inducible resistance MLS_B and MS_B resistance were 56.2%, 22.9%, and 16.6%, respectively. Of 11 isolates with the inducible resistance MLS_B phenotype, ermC, ermB, ermA and ereA were positive in 81.8%, 63.6%, 54.5% and 18.2% of these isolates, respectively. In isolates with the constitutive resistance MLS_B phenotype, the prevalence of ermA, ermB, ermC, msrA, msrB, ereA and ereB 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.

Citations

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The Effect of Lactobacillus acidophilus PTCC 1643 on Cultured Intestinal Epithelial Cells Infected with Salmonella 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

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Abstract PDF

Objectives

Gastrointestinal disorders caused by Salmonella enterica serovar Enteritidis (SesE) 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 towards SesE. The purpose of this work was to assess the effect of L. acidophilus PTCC 1643 on cultured intestinal epithelial cells infected with SesE.

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 with SesE. At 2 and 4 hours post-infection, we measured changes in the expression levels of TLR2 and TLR4 via real-time polymerase chain reaction.

Results

Treatment with L. acidophilus inhibited SesE-induced increases in TLR2 and TLR4 expression in the infected HT29 cells. Moreover, the expression of TLR2 and TLR4 in cells that were pretreated with L. acidophilus and then infected with SesE was significantly higher than that in cells infected with SesE without pretreatment. Taken together, the results indicated that L. acidophilus had an anti-inflammatory effect and modulated the innate immune response to SesE by influencing TLR2 and TLR4 expression.

Conclusion

Our findings suggested that L. acidophilus PTCC 1643 was able to suppress inflammation caused by SesE infection in HT29 cells and reduce TLR2 and TLR4 expression. Additional in vivo and in vitro studies are required to further elucidate the mechanisms underlying this anti-inflammatory effect.

Citations

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