Mold spoilage of dairy products such as yogurt is a concern in dairy industry. Not only does it lead to substantial food waste, economic losses, and even brand image damage, but it may also cause public health concern due to the potential production of mycotoxin. Good hygiene practices are necessary to prevent contamination, but contamination may nevertheless occur at the production site and, not least, at the site of the consumer. In recent years, there has been a growing interest from consumers for “clean label” food products, which are natural, less-processed, and free of added, chemical preservatives, and a wish for shelf lives of considerable length in order to minimize food waste. This has sparked an interest in using lactic acid bacteria (LAB) or their metabolites as biopreservatives as a way to limit the growth of spoilage organisms in dairy products. A range of compounds produced by LAB with potential antifungal activity have been described as contributing factors to the inhibitory effect of LAB. More recently, growth inhibition effects caused by specific competitive exclusion have been elucidated. It has also become clear that the sensitivity toward both individual antifungal compounds and competition mechanisms differ among molds. In this review, the main spoilage molds encountered in dairy products are introduced, and an overview of the antifungal activity of LAB against different spoilage molds is presented including the main antifungal compounds derived from LAB cultures and the sensitivity of the spoilage molds observed toward these compounds. The recent findings of the role of competitive exclusion with emphasis on manganese depletion and the possible implications of this for biopreservation are described. Finally, some of the knowledge gaps, future challenges, and trends in the application of LAB biopreservation in dairy products are discussed.

Salmon is prone to be contaminated by Vibrio parahaemolyticus (V. parahaemolyticus), leading to the deterioration of salmon quality and the occurrence of food-borne diseases. In this study, we aimed to develop a novel xanthan-gum-based edible coating embedded with nano-encapsulated Litsea cubeba essential oil (LC-EO) for salmon preservation at 4 °C. First, the results of the growth curves and scanning electron microscopy (SEM) showed that LC-EO displayed potent antibacterial activity against V. parahaemolyticus; the optimal concentration of LC-EO in the liposomes was 5 mg/mL, and the maximal encapsulation efficiency (EE) was 37.8%. The particle size, polydispersity coefficient (PDI), and zeta potential of the liposomes were 168.10 nm, 0.250, and −32.14 mV, respectively. The rheological test results of xanthan-gum-based edible coatings incorporating liposomes showed that the prepared coating was suitable for applying on food surfaces. The results in the challenge test at 4 °C demonstrated that the treatment of 1:3 (liposome: xanthan gum, v/v) coating performed the best preservative properties, the coating treatment delayed the oxidation of salmon, and controlled the growth of V. parahaemolyticus. These findings suggest that the coatings formulated in this study could be used as a promising approach to control V. parahaemolyticus contamination and maintain salmon quality.

This study aimed to establish the influence of biofilm from clinical isolates of Candida albicans on fluconazole resistance, focusing on efflux pumps and azole-targeted enzymes. Twenty-three C. albicans clinical isolates were collected from two hospitals in Shanghai, China. Antifungal susceptibility tests were performed on biofilm and planktonic cells. A crystal violet assay was used to monitor biofilm growth. Real-time RT-PCR was performed to quantify the expression of the transporter-related genes MDR1, CDR1, and CDR2 as well as ERG11, a gene encoding an enzyme targeted by antifungal drugs. Fluconazole resistance was shown to increase in biofilm in a time-dependent manner. No significant differences were observed between different strains of C. albicans. Genes encoding efflux pumps were overexpressed in early stages of biofilm formation and could also be induced by fluconazole. While ERG11 was not upregulated in biofilm, it was overexpressed upon the addition of fluconazole to biofilm and planktonic cells. Gene expression also appeared to be related to the original genotype of the strain. The upregulation of genes encoding efflux pumps demonstrates their role in the development of fluconazole resistance during the early stages of C. albicans biofilm formation.