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Background <p>Colistin-resistant <i>Acinetobacter baumannii</i> (CR <i>A. baumannii</i>) is recognized as one of the most antibiotic-resistant bacterial pathogens, highlighting the urgent need for alternative treatment options. This study investigated the inhibitory potential of eugenol, cinnamaldehyde, and carvacrol against CR <i>A. baumannii</i> and its associated biofilm community.</p> Methods <p>The minimum inhibitory concentrations (MICs) and antibiofilm activities were assessed via broth microdilution and microtiter plate assays against three CR <i>A. baumannii</i> isolates. Time-kill assays were conducted to measure bactericidal activity against isolates. Additionally, membrane integrity was assessed by evaluating protein and nucleic acid leakage. The expression of biofilm-related genes (<i>ompA</i>, <i>csuE</i>, and <i>bap</i>) was analyzed using qRT-PCR.</p> Results <p>Disk diffusion showed inhibition zones of 18 ± 2&#xa0;mm for eugenol, 30 ± 1&#xa0;mm for cinnamaldehyde, and 31 ± 1&#xa0;mm for carvacrol. MICs were 416&#xa0;µg/mL for eugenol, 205&#xa0;µg/mL for cinnamaldehyde, and 190&#xa0;µg/mL for carvacrol. At a concentration of 2× MIC, bacterial eradication was achieved within 10&#xa0;h for three natural compounds. At MIC, bacterial eradication occurred within 12&#xa0;h for both carvacrol and cinnamaldehyde and 24&#xa0;h for eugenol. Carvacrol and cinnamaldehyde also caused significant protein and nucleic acid leakage. All three compounds effectively inhibited biofilm formation and disrupted established biofilms. Notably, expression levels of biofilm-associated genes, including <i>ompA</i>, <i>csuE</i>, and <i>bap</i>, were significantly downregulated following treatment with eugenol and carvacrol.</p> Conclusion <p>Eugenol, cinnamaldehyde, and carvacrol exhibited potent antibacterial and antibiofilm effects against CR <i>A. baumannii</i>, highlighting their potential as natural therapeutic candidates for managing infections caused by resistant strains.</p>

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Natural compounds for colistin-resistant Acinetobacter baumannii biofilm control: eugenol, cinnamaldehyde, and carvacrol

  • 期刊论文

  • 发表日期：

    2025年7月18日

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  • Milad Kashi,
  • Zahra Chegini,
  • Amin Khoshbayan,
  • Aref Shariati,
  • Abbas Farahani

摘要

Background

Colistin-resistant Acinetobacter baumannii (CR A. baumannii) is recognized as one of the most antibiotic-resistant bacterial pathogens, highlighting the urgent need for alternative treatment options. This study investigated the inhibitory potential of eugenol, cinnamaldehyde, and carvacrol against CR A. baumannii and its associated biofilm community.

Methods

The minimum inhibitory concentrations (MICs) and antibiofilm activities were assessed via broth microdilution and microtiter plate assays against three CR A. baumannii isolates. Time-kill assays were conducted to measure bactericidal activity against isolates. Additionally, membrane integrity was assessed by evaluating protein and nucleic acid leakage. The expression of biofilm-related genes (ompA, csuE, and bap) was analyzed using qRT-PCR.

Results

Disk diffusion showed inhibition zones of 18 ± 2 mm for eugenol, 30 ± 1 mm for cinnamaldehyde, and 31 ± 1 mm for carvacrol. MICs were 416 µg/mL for eugenol, 205 µg/mL for cinnamaldehyde, and 190 µg/mL for carvacrol. At a concentration of 2× MIC, bacterial eradication was achieved within 10 h for three natural compounds. At MIC, bacterial eradication occurred within 12 h for both carvacrol and cinnamaldehyde and 24 h for eugenol. Carvacrol and cinnamaldehyde also caused significant protein and nucleic acid leakage. All three compounds effectively inhibited biofilm formation and disrupted established biofilms. Notably, expression levels of biofilm-associated genes, including ompA, csuE, and bap, were significantly downregulated following treatment with eugenol and carvacrol.

Conclusion

Eugenol, cinnamaldehyde, and carvacrol exhibited potent antibacterial and antibiofilm effects against CR A. baumannii, highlighting their potential as natural therapeutic candidates for managing infections caused by resistant strains.