The BCPD of fruits can be approached from the perspective of the host plant (different fruits), habitat for the microorganisms (wound, intact surface), and the pathogen's strategy used to infect fruit. The pathogen's strategy has been emphasized most frequently because many economically important postharvest diseases of fruits are caused by necrotrophic pathogens (Dennis 1983). These pathogens invade mainly through wounds, and require nutrients for spore germination and initiation of the pathogenic process, which makes them vulnerable to competition for nutrients from surrounding microorganisms. Other mechanisms of biocontrol described later in this chapter may also be involved, but the prevailing evidence suggests that their role is secondary (Janisiewicz and Korsten 2002). Incipient or latent infections that generally occur in the field are less prone to biological control because the pathogen has already established a parasitic relation with the host. However, these pathogens can be controlled by antagonists that prevent infection in the field, perpetuate latency by removal of nutrients from areas surrounding the appressoria, or perhaps those that can inhibit pathogen development by the production of antifungal substances or by direct parasitism (Koomen and Jeffries 1993; Korsten and Jeffries 2000; Leibinger et al. 1997).
The greatest progress in BCPD of fruits has been made against typical wound-invading necrotrophic postharvest pathogens such as Penicillium expansum which causes blue mold of apple, pear, and cherries, Botrytis cinerea which causes gray mold of pome fruits (Janisiewicz and Jeffers 1997), P. italicum and P. digitatum which causes blue and green-mold of citrus fruits, respectively (Droby et al. 1998), and against the wound invading phase of brown rot decay of stone fruits caused by Moniliniafructicola (Pusey et al. 1988). Although the likelihood of infection is dependent on the concentration of fungal spores, the biocontrol strategy has always focused on the preemptive colonization of the wounds by the antagonist to prevent infection, and not on reduction of the pathogen inoculum. Thus, the control of these decays was achieved by the application of antagonists to wounds, simultaneously with the pathogen or shortly after the infection took place. Other potential candidates for this type of biological control are pathogens invading through cut stem of bananas, mangos, and papayas (Eckert 1991). Since the development of the pathogen depends on fruit maturity and the environment, these factors have been critical in the pathogen-antagonist interaction and resulting biological control.
Significant successes were achieved with biocontrol of latent infections caused by Colletotrichum spp. on mango and avocado (Korsten and Jeffries 2000), and to a lesser extent by B. cinerea on strawberries (Helbig 2002; Ippolito et al. 1998; Peng and Sutton 1990; Takeda and Janisiewicz, unpublished results). Biological control of these diseases must start in the field, relies on multiple application of the antagonist, and is generally more difficult to achieve.
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