Abstract

Aim of the paper was to study antimicrobial activity of cinnamaldehyde and carvacrol at different concentrations on the panel of 12 selected and characteristic food pathogens and spoilage microorganisms. Cinnamaldehyde and carvacrol were diluted in a set of lipophilic and hydrophilic diluents down to concentrations of 0.5%, 1%, 2% and 3%, respectively. Suspensions of the test microorganisms were diluted down to 1 McFarland turbidometric unit and 0.1 mL of prepared inoculum was surface inoculated on tryptic soy agar. After absorption of inoculum, a nanofybrillic cellulose disc has been applied at the center of the each Petri dish and 32 μL of respective dilution of cinnamaldehyde and carvacrol was pipetted. After subsequent incubation, radius of inhibition zone for each tested microorganism had been measured. Results of the study indicated that the strongest inhibitory effect of cinnamaldehyde occurred in C. perfringens (5.29-20.60 mm), E. faecalis (8.28-19.40 mm) and L. sakei (4.80-11.10 mm) even at the lowest concentration (0.5%). S. cerevisiae proved to be absolutely resistant at all concentrations tested. Faecal Enterobacteriaceae contaminants (E. coli, E. coli O157:H7, P. mirabilis and S. Typhimurium) have also been quite inhibited, while the difference of E. coli inhibition zones (0,00-5.40 mm) compared to those of S. Typhimurium (0.86-6.93 mm) were not statistically significant (p = 0,910). Strain of enterohaemorrhagic E. coli (O157:H7) exhibited statistically significant wider zone of inhibition when being compared with nonpathogenic E. coli (p = 0.037) at all concentrations tested. When it comes to spoilage-related microbiota, B. thermosphacta and P. aeruginosa, there were no growth inhibition at 0.5% of cinnamaldehyde. However, at concentration range from 1% to 3%, B. thermosphacta has been more strongly inhibited (p = 0.0048) than P. aeruginosa (2.20-6,98 mm versus 0.32-1.48 mm, respectively). Regarding antimicrobial activity of cinnamaldehyde to L. monocytogenes and S. aureus, both microorganisms were inhibited, where as S. aureus was statistically significantly inhibited than L. monocytogenes (p = 0.0248). The most potent inhibition on growth carvacrol exhibited on S. aureus (7.24-15.10 mm) and L. sakei (5.23-9.32 mm). S. cerevisiae and P. aeruginosa were absolutely resistant to it. E. faecalis and L. monocytogenes were resistant at concentration range from 0.5%-2%, while the inhibition zone at 3% was minimal (2.09 mm and 1 mm, respectively). P. mirabilis and S. Typhimurium were inhibited at 2% and 3%, respectively and there was no statistically significant difference in radius of inhibition zones (p = 0.412), while absolute values of inhibition radius were as similar as those of E. faecalis and L. monocytogenes (1.21-2.80 mm and 1.56-3.38 mm, respectively). E. coli and E. coli O157:H7 were resistant at 0.5% and 1% carvacrol, respectively, whereas there was no statistically significant difference in radius of inhibition zones which occurred at 2% and 3% (p = 0.254). Food-spoilage microbiota, B. thermosphacta and C. perfringens were sensitive to carvacrol starting at 1%. B. thermosphacta had throught all concentrations tested, wider and statistically significant inhibition zones compared to C. perfringens (p = 0.0112). These results establish starting point for experimental application of the natural antimicrobial additives in active food packaging.

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