Food losses, defined as a reduction in the quantity and quality of food during production and storage, impact food safety and security. Losses caused by plant pathogens are among the most significant. Chemical pesticides have been extensively used to prevent microbial diseases. Their toxicity and reduced efficacy, however, have encouraged investigators to develop alternatives. Alternatives based on microbial biopesticides tend to be safer and more environmentally benign than conventional pesticides. In recent years, formulations based on biopesticides have progressively increased in number and diversity and have attracted commercial interest. Understanding the mechanisms by which biopesticides control the disease is fundamental to achieving optimal disease control. Biocontrol mechanisms can be divided into two main categories: those related to the ability to inhibit pathogens or their virulence factors, and those that enhance host plant fitness and induce disease resistance. Here, the first type of strategy is reviewed, which is directly mediated by physical contact between biocontrol agents and pathogens or indirectly by exposure of a pathogen to antimicrobial or microbial-inhibiting compounds produced by the microbial antagonist. Mechanisms involving physical contact include mycophagy, destruction of pathogenic bacteria by bacteriophages or predation, and disease inhibition by topical applications of specific dsRNA. Indirect mechanisms that do not involve direct contact with a pathogen include the production of antimicrobial compounds, competition, and virulence factor suppression by quorum quenching. These topics are reviewed and discussed.

Lotmaria passim currently appears to be the predominant trypanosome in honey bees worldwide. Although, the specific effects of L. passim by single or mixed with other gut parasites such as Nosema ceranae on honey bees’ health is still unclear. We consequently measured bees’ survival, parasite loads, the expression of antimicrobial peptides (AMPs) and vitellogenin gene. Thus, (1) bees naturally infected with L. passim, (2) healthy bees inoculated with Nosema ceranae, (3) bees naturally infected with L. passim and inoculated with N. ceranae and (4) healthy bees (control) were maintained under controlled conditions. Honey bees infected with N. ceranae or with mixed infections of L. passim and N. ceranae had significantly lower survival rates than the control group at 20 days post-inoculation (dpi). A competitive suppression was also detected, provided that the L. passim load was significantly affected by the presence of N. ceranae at 15 dpi. Expressions of the AMPs defensin and hymenoptaecin rapidly (two hours post-inoculation) increased in bees infected with N. ceranae and mixed infections. However, this effect was not continuous. In fact, expressions of abaecin, defensin, hymenoptaecin and vitellogenin decreased drastically at 15 dpi in bees with both single and mixed infections. The decrease in the expression of AMPs and vitellogenin throughout this period was consistent with the reduced survivals observed in this study, indicating that mixed infections of L. passim and N. ceranae, and even into a scenario of competition between them, may have a synergic effect on the survival and immune-related gene expressions (biomarkers) of worker bees.