The ability of natural compounds to inactivate foodborne organisms adhered to surfaces was investigated with the ultimate aim of replacing synthetic biocides by more environmentally friendly, natural alternatives. The antimicrobial efficacy of 0.5, 1.0, and 2.0% chitosan and Spor-Klenz RTU (a commercial biocide based on hydrogen peroxide and peroxyacetic acid) and 0.5, 1.25, and 2.0 mM carvacrol was determined at 20 degrees C against Listeria monocytogenes, Salmonella enterica serovar Typhimurium, Staphylococcus aureus, and Saccharomyces cerevisiae adhered to stainless steel disks. Treatment with up to 2.0% chitosan reduced the viable cell count in the microbial films of the four test organisms by 2.4, 1.8, 2.3, and 0.9 log CFU/test surface (t.s.), respectively. By contrast, planktonic counts of the same organisms were reduced by 0.8 to 1.7 log CFU/ml at 2.0% chitosan. Treatment with 2 mM carvacrol reduced the viable counts of adhered listeriae, salmonellae, and yeasts by 2 to 3 log CFU/t.s. but S. aureus counts were reduced by only 0.9 log CFU/t.s. The efficacy of any single compound was species specific. In the case of microbial films prepared using listeriae and salmonellae, Spor-Klenz RTU was most biocidal, followed by carvacrol and then chitosan. However, dried films of S. aureus were most sensitive to chitosan and relatively resistant to carvacrol and Spor-Klenz RTU. By contrast, yeast films were most sensitive to carvacrol and least sensitive to chitosan. It was concluded that carvacrol and chitosan may have potential for use as natural biocides although optimization of conditions would be necessary.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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