CHAPTER
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Overview of Postharvest Pathology James E. Adaskaveg ■ Helga Förster ■
Department of Microbiology and Plant Pathology, University of California, Riverside, CA, USA ■
Dov B. Prusky Department of Postharvest Science, Agricultural Research Organization, the Volcani Center, Rishon LeZion, Israel
Consumption of fresh fruits and vegetables has become an indispensable part of a wholesome diet in many parts of the world as awareness for a healthy nutrition has increased over the past decades. In the United States, per capita consumption increased by approximately 25% between 1976 and 2009 (Cook 2011). Widespread availability of these horticultural crops is compromised by postharvest losses that have been estimated at 5 to 25% in developed countries and at 20 to 50% in developing countries, depending on the commodity, cultivar, as well as marketing and handling practices (Kader 2002). Agricultural commodities may be exposed to numerous conditions that can lead to post harvest losses in quality and quantity. These range from simple water loss to compositional changes, senescence, physiological breakdown, mechanical injury, enhanced ripening, and deterioration of the crop by decay organisms. Although there are markets that accept some level of reduced quality, consumers in most markets expect fresh fruits and vegetables to be of superior appearance and acceptability. The agricultural economy in many parts of the world has changed from a local to a global market with increased emphasis on international trade because of high demand for high-quality fruit in selected markets and the need to redistribute our food supply for a
growing human population. The costs of storage and long-distance transportation, as well as high consumer standards for a perfect fruit result in narrow profit margins that make any loss from decay unacceptable for the producer and packer. Oftentimes, adverse conditions are brought about by changes in growing and handling practices of crops in modern agriculture that have the goal to provide more efficient means of production and distribution, but also to attract new consumers. For example, the current trend for marketing ripened fruits instead of mature fruit offers additional challenges because these fruits are more susceptible to injury, pathogen infection, and decay development. Longer storage times and transportation to local, national, and international markets may increase the potential for fruit injury and decay. Diseases that were once secondary or minor may become major limiting factors, or new problems from previously unknown pathogens may develop. Therefore, as any plant disease, postharvest decays develop as interactions among the components of the disease triangle (Fig. 1.1): host (type of commodity and cultivar), pathogen (type of pathogen and amount of inoculum present), and environment (conditions during crop cultivation, harvest, storage, and transportation) (Adaskaveg et al. 2002). The current status and a change in any of these components will influence the
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F I G . 1 .1 . Multiple disease triangles associated with the pre- to postharvest continuum of crop production and distribution of a commodity. Interactions of multiple pathogens, environments, and different stages of the host during its development determine postharvest levels of decay. Monocyclic diseases only have one infection cycle per crop whereas polycyclic diseases have several. (Courtesy J. E. Adaskaveg and H. Förster—© APS)
occurrence and amount of disease development and will affect the control measures to be taken. Any modification in production, handling, or processing of commodities may result in an increased risk for decay and must be carefully evaluated. Thus, postharvest handling strategies have to be based on a sound knowledge of the host-pathogen-environment interrelationships for the periods before and after arrival of the commodity at the packinghouse and final marketplace.
POSTHARVEST PATHOGENS AND THE INFECTION PROCESS Fungi, including some yeasts, are the most common cause of postharvest diseases of fruits and vegetables. Bacteria frequently cause disease in some vegetables and tubers, but they are generally rare in tree fruits and berries where the acidic pH creates less favorable micro environments for bacterial growth. Taxonomy and genera ■
of bacteria causing postharvest decays or disorders are shown in Tables 1.1 and 1.2. Virus diseases may develop in the field and intensify postharvest disease expression in certain root or tuber crops, but they do not infect fruit after harvest. Furthermore, numerous postharvest disorders are known that have abiotic, noninfectious causes. These include nutritional disorders (e.g., bitter pit of pome fruits), disorders caused by environmental factors (e.g., damage from extreme temperatures in the field or during storage; pithy brown core of pear caused by suboptimal oxygen:carbon dioxide ratios during controlled atmosphere storage), or physio logical disorders (e.g., superficial scald of pome fruits). Damage to harvested fruit may also occur by inappropriate application of postharvest treatments including excessive rates of fruit coatings. These non-infectious disorders are not covered in this book. Fungi are single- or multicellular organisms. When multi-celled, they commonly grow as filaments or hyphae that form the somatic stage, the mycelium. The mycelial stage develops from germinating propagules
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T A B L E 1 .1 . Taxonomic groups with causal organisms of postharvest decays of fruits and vegetablesa,b Domain Prokaryota Kingdom Eubacteria Phylum Actinobacteria Elongated cells that branch into filaments, Gram-positive. e.g., Clavibacter, Streptomyces spp. Phylum Firmicutes Spherical or rod-shaped cells, mostly with a Gram-positive cell wall structure; many produce endospores, which are resistant to desiccation and can survive extreme conditions. e.g., Bacillus, Leuconostoc spp. Phylum Proteobacteria Variable shapes (Alphaproteobacteria have stalks or buds, Betaproteobacteria have variable shapes, Gammaproteobacteria are mostly rod-shaped); Gram-negative with an outer membrane mainly composed of lipopolysaccharides. Many have flagella, but some are nonmotile or rely on bacterial gliding. e.g., Alphaproteobacteria - Acetobacter, Gluconobacter; Betaproteobacteria - Acidovorax; Gammaproteobacteria - Dickeya, Enterobacter, Pantoea, Pectobacterium, Pseudomonas, Tatumella, Xanthomonas spp. Domain Eukaryota Kingdom Stramenopila Phylum Oomycota Asexual reproduction by biflagellate zoospores produced inside sporangia; sexual reproduction by oospores. e.g., Phytophthora, Pythium spp. Kingdom Fungi
Phylum Mucoromycota (previously Zygomycota) Asexual reproduction by non-motile sporangiospores produced inside sporangia; sexual reproduction by zygospores. e.g., Rhizopus, Mucor spp.
Phylum Ascomycota Asexual reproduction by conidia that are often produced on conidiophores; sexual reproduction by ascospores formed inside asci. Sub-phylum Taphrinomycotina (yeasts or yeast-like with fission or budding, sometimes filamentous) Sub-phylum Saccharomycotina (true yeasts with budding) e.g., Saccharomyces spp. Sub-phylum Pezizomycotina (filamentous Ascomycota) e.g., Alternaria, Aspergillus, Botryosphaeria, Ceratocystis, Colletotrichum, Diaporthe, Epicoccum, Fusarium, Galactomyces, Glomerella, Magnaporthe, Monilinia, Mycosphaerella, Neofabraea, Neofusiccocum, Neonectria, Penicillium, Phoma, Phomopsis, Pleospora, Septoria, Ulocladium spp. a Courtesy J. E. Adaskaveg, H. Förster, and D. B. Prusky—© APS.
(continued )
b Only taxa containing postharvest pathogens are listed. Some genera classified previously in the Deuteromycota
have been re-classified as taxa in the Ascomycota or Basidiomycota based on known genetic relatedness.
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T A B L E 1 .1 . Taxonomic groups with causal organisms of postharvest decays a,b of T Afruits B L E and 1 .1 .vegetables Continued Phylum Basidiomycota Asexual reproduction yeast-like, by conidia, or absent; sexual reproduction by basidiospores formed on basidia. Sub-phylum Agaricomycotina e.g., Copriniopsis, Cryptococcus, Rhizoctonia, Athelia (syn. Sclerotium) spp.
such as spores designed for dissemination (e.g., sporangiospores, conidia, ascospores, basidiospores) or spores for perennation (e.g., zygospores, chlamydospores); but in some cases, from penetrating structures (appressoria) that are responsible for host invasion and ultimately decay development. Most postharvest fungal pathogens belong to the Eumycota or true fungi that represent one of the eukaryotic kingdoms of life on earth in addition to the kingdoms of plants, animals, and Stramenopila (also known as Chromista) (Tables 1.1 and 1.2). Post harvest fungi in the Eumycota are commonly members of the phylum Ascomycota that form asexual conidia (i.e., mitospores) by a diverse range of mechanisms and sexual spores (i.e., meiospores) within an ascus or sac. Other true fungi that cause postharvest decays belong to the Mucoromycota that produce asexual sporangiospores inside sporangia and sexual zygospores. The Mucoromycota are represented mainly by the genera Rhizopus, Gilbertella, and Mucor. Species in the fungal phylum Basidiomycota, with few exceptions, are not postharvest pathogens. Several postharvest pathogens belong to the kingdom Stramenopila that morpho logically look similar to true fungi. They typically reproduce by asexual, motile zoospores that develop inside sporangia and sexually by oospores. Postharvest pathogens in the Stramenopila belong to the phylum Oomycota, and the most common genera are Phyto phthora and Pythium. Pathogens in the Ascomycota are usually present in decay lesions in the somatic, asexual state (anamorph) of mycelium and conidia. The sexual state (teleomorph) is rarely seen in culture or in diseased commodities; in some species, it has never been reported. Historically, Ascomycota fungi often had separate anamorph and teleomorph names. Until recently, the teleomorph name was given priority in the scientific naming of fungi, but changes in fungal nomenclature now only allow for one name, ending the dual naming of organisms (Zhang et al. 2013). In general, the earliest published name has priority. In many cases, this is the
anamorphic name because the asexual state is more commonly observed and was described before the sexual state. For Zygomycota or Stramenopila, only a holomorph name exists. The asexual spores are the main infective propagules of most postharvest pathogens because they are often continually produced in large numbers, but they are generally not designed for long-term survival. Fungal spores are mostly airborne or disseminated by splashing water. Insects and human activity can also have a role in spore dispersal. If a spore is deposited in a moist, fresh wound, it germinates rapidly if temperature and nutritional conditions are favorable (Fig. 1.2A and B). Germination of spores is preceded by water uptake that is often causing the spores to swell (Fig. 1.2C). Water and oxygen are essential for germination to occur. Frequently, fruit surfaces are too dry to allow germination, but spores in fresh wounds germinate due to the presence of moisture. Organic carbon compounds (e.g., sugars and/or organic acids) in readily available forms for assimilation often enhance germination and are required by some fungi. Spore germination is a vulnerable period in the life of a fungus. During swelling, spores are susceptible to the lethal effects of gamma and ultraviolet irradiation, low and high temperatures, absence of oxygen, and exposure to toxic chemicals. Once underway, germination generally cannot be disrupted for any long period of time without loss of the ability to resume normal growth. Decay is commonly initiated after direct infection of the fruit. In some cases, however, fungi may colonize senescent floral parts at flowering and only much later grow into the fruit and cause decay. For example, floral parts of pomegranates, grapes, and strawberries are infected by Botrytis cinerea near the end of the flowering period (Nair and Allen 1993; Tedford et al. 2005). In pomegranates, dead styles and stamens colonized by the fungus are retained within the crown of the fruit. Only as fruit ripen does the fungus successfully invade the arils and connective internal tissues of the pomegranate.
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Overview of Postharvest Pathology 7
T A B L E 1 . 2 . Examples of classification of prokaryotic and eukaryotic pathogens in selected kingdoms and phyla causing postharvest decays of fruits and vegetablesa Domain: Prokaryota Kingdom: Eubacteria Phylum: Proteobacteria Class: Gammaproteobacteria Order: Enterobacterales Domain: Eukaryota Family: Pectobacteriaceae Kingdom: Stramenopila Genus: Pectobacterium Phylum: Oomycota Species: P. carotovorum Class: Oomycetes Order: Peronosporales Domain: Eukaryota Family: Peronosporaceae Kingdom: Fungi Genus: Phytophthora Phylum: Mucoromycota Species: P. citrophthora Class: Mucoromycetes Order: Mucorales Domain: Eukaryota Family: Mucoraceae Kingdom: Fungi Genus: Rhizopus Phylum: Ascomycota Species: R. stolonifer Class: Leotiomycetes Order: Helotiales Domain: Eukaryota Family: Sclerotiniaceae Kingdom: Fungi Genus: Monilinia Phylum: Basidiomycota Species: M. fructicola Class: Tremellomycetes Order: Tremellales Family: Tremellaceae Genus: Cryptococcus Species: C. laurentii a Courtesy J. E. Adaskaveg, H. Förster, and D. B. Prusky—© APS.
F I G . 1 . 2 . A, Non-germinated, catenulate conidia and B, germinated conidia of Monilinia fructicola. C, Germinated and non-germinated spores of Rhizopus stolonifer. Note the swelling of germinating compared to non-germinated spores (arrows). Bars = 30 µm. (Courtesy J. E. Adaskaveg and H. Förster—© APS)
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Many post harvest pathogens only enter the host through wounds or natural openings such as growth cracks, stomata, or lenticels. For example, germinating conidia of Colletotrichum gloeosporioides have been observed to penetrate stomata of papaya fruit (Prusky 1996), and conidia of Alternaria alternata have been described to infect through lenticels of mango fruit (Prusky et al. 2006). Other pathogens such as Monilinia, Colletotrichum, or Phytophthora species (Fig. 1.3A and B) can also directly penetrate the host epidermis or epicarp. Wounds are often created at harvest, either involuntarily during handling, or by the harvest procedure itself when the fruit is separated from the plant. For example, some stem-end rots of avocado, mango, papaya, banana, pineapple, and watermelon result from infection when the stem is severed at harvest (Chau and Alvarez 1979; Hawajulige and Wijesundera 2014; Pathak and Srivastava 1967; Twizeyimana et al. 2014), whereas for others, the stem is already infected before harvest and the pathogen starts actively growing when tissues senesce (Johnson et al. 1992). Cut peduncles of apple and pear may be colonized by B. cinerea or Penicillium expansum and during storage, the pathogens progress from the peduncle into the fruit tissue. In some fruit species, stems may be the first part to become senescent. Senescence is likely a factor in Alternaria stem-end rots of citrus fruits (Bautista-Baños 2014).
F I G . 1 . 3 . Phloxine-stained germinating cysts of Phytophthora citrophthora forming appressoria and directly penetrating the epicarp of an orange fruit. A, Germinating cyst near a stoma; B, cytoplasm separating from cyst wall (arrow) and moving into the elongating germ tube. Appressorium (ap) and infection hypha (ih) penetrating into fruit. Note that the infection hyphae was not stained because it penetrated the epicarp. Bars = 10 µm. (Courtesy J. E. Adaskaveg and H. Förster—© APS)
The germinated spore of pathogens that is able to directly penetrate the host epidermis forms a thickwalled appressorium that adheres tightly to the host surface by mucilaginous material produced by the germ tube. On the underside, the appressorium forms an infection peg and then an infection hypha (Fig. 1.3B). Penetration of the host cuticle and epidermis is achieved by the secretion of cutin- and cell wall-degrading enzymes. The process is facilitated by considerable pressure that builds up inside the appressorium. After penetration, the infection peg increases in diameter, and the pathogen may start actively colonizing the host tissue. When environmental conditions or host physiology are conducive for penetration but not for active growth of the pathogen, however, it enters a dormant or quiescent state. Quiescent infections may be visible or non-visible. The parasitic relationship remains suspended until host resistance mechanisms are deactivated or certain nutrients become available during fruit ripening. Fungal growth may then resume, colonizing the fruit, and eventually causing decay. Quiescent infections are known for several postharvest pathogens. Examples are C. gloeo sporioides and other species of Colletotrichum that cause anthracnose of many fruits including apple, avocado, mango, and papaya. Fruit are generally infected while developing in the orchard. Before ripening, fruit are highly resistant, but then become susceptible when preformed antifungal compounds are degraded (Prusky et al. 1991; Prusky 1996). Thus, anthracnose typically is a decay of ripening fruit. In other cases, the invading fungus can modulate its environment inside the resistant fruit. For example, Colletotrichum species secrete ammonia that increases the pH immediately around the infection peg and sub-cuticular vesicle. This activates certain pathogenesis-related enzymes of the fungi and initiates host colonization. Quiescent infections are also known for species of Monilinia and Botrytis causing decays of stone fruits (Adaskaveg et al. 2000; Melga rejo et al. 2010). The incidence of quiescent brown rot infections in the orchard has been correlated with the occurrence of postharvest brown rot (Emery et al. 2000; Michailides et al. 2010). During colonization of the fruit tissue, the fungal mycelium grows by apical elongation and branching. The advancing hyphae excrete toxins that kill the host cells (i.e., necrotrophy) and extracellular enzymes that degrade complex host substances into low-molecularweight compounds that can enter the fungal cell. These compounds provide the nutrition and energy for the fungus to grow and continue its life cycle. The process of extracellular digestion and absorption of the breakdown products is known as assimilation, and it is dependent
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Overview of Postharvest Pathology 9
on the ripening and softening of the fruit, the presence of water to allow for diffusion of pathogen enzymes to the substrate and degraded substrates (i.e., metabolites) back into the pathogen. Enzymatic degradation of host tissue manifests itself as development of decay. Pathogens such as Rhizopus stolonifer or Geotrichum species that excrete high amounts of pectolytic enzymes cause host tissues to rapidly disintegrate, resulting in a very soft, watery rot. In the final step of the fruit rotting process, the production of spores completes the infection cycle. Sporulation is important because new inoculum is produced for dissemination of the pathogen. Another important aspect is that the sporulating individuals in a pathogen population are those that survived the selection pressures that occurred during production, harvest, and handling of the commodity. These selected individuals will carry on the species as the surviving population and with this, the characteristics that favored survival. This eventually will lead to pathogen populations that are more adapted to certain handling processes including the use of postharvest fungicide treatments (e.g., resistance development to the fungicide), as well as storage conditions (e.g., temperature, humidity).
IDENTIFICATION OF POSTHARVEST DECAYS Plant diseases can be identified visually based on the presence of characteristic symptoms or signs of the pathogen on the host, by isolation and identification of the causal agent, or by direct detection of the pathogen inside diseased tissue using molecular methods. Many postharvest decays can be properly identified based on the symptoms they cause, but still, different diseases may result in very similar symptoms. Therefore, in many cases, a combination of these methods is used to obtain an accurate diagnosis. Disease symptoms are visible interactions of the host with the pathogen. Common symptoms of postharvest decays are lesions of different shapes and color on the fruit surface and decayed fruit tissues (Fig. 1.4). The decay can range from very soft to firm, and a characteristic odor may be present. Signs of diseases are visible parts or products of the pathogen on the plant surface (Fig. 1.4). These may be somatic or reproductive structures that can be highly distinctive for a specific fungal pathogen. Thus, the mycelium may have characteristic features, asexual and much less commonly sexual ■
F I G . 1 . 4 . Symptoms and signs of postharvest decays of A, apple-pears (Asian pears) and B and C, lemons. A, Symptoms are a stem-end rot (left), and signs of the causal gray mold pathogen Botrytis cinerea are sporulating mycelia (right). B, Early symptoms of sour rot decay of lemon and C, signs of the causal pathogen Geotrichum citri-aurantii are white mycelium and arthrospores. (Courtesy J. E. Adaskaveg and H. Förster—© APS)
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spores may be produced in certain fruiting bodies, and spores may be unique in shape, size, and pigmentation. Signs of the pathogen, however, are often not present or are atypical, especially when the commodity was treated with certain fungicides before or after harvest or when stored at low relative humidity or in controlled atmospheres. For example, the postharvest fungicide imazalil is known to inhibit sporulation of the green mold pathogen of citrus, Penicillium digitatum (Fig. 1.5). Signs of the pathogen can sometimes be induced by incubating the diseased specimen in a moist chamber. This, however, may also induce growth of secondary organisms, obscuring the presence of the primary pathogen. An overnight freezing incubation technique (ONFIT) has been developed for the detection of quiescent brown rot infections in stone fruits (Michailides et al. 2010). In this method, plant material is surface-sterilized, frozen at –16°C for 15 h, and then observed for brown rot symptoms and sporulation of the pathogen after 5 to 7 days. Here again, other fungal organisms can be found colonizing the fruit, and some training is required. Signs of the presence of bacteria may be droplets of ooze on decayed tissues (Fig. 1.6) or streaming out of infected tissue when submerged in water. This may be all that is needed for identification if only a single bacterial disease has been reported for a host, and observed symptoms match the ones described. The identification of postharvest decays is often more accurately accomplished by isolating and identifying the
causal pathogen. For isolation of fungi, several small pieces of tissue from the margin of the decay are removed aseptically from underneath the fruit skin and plated onto an appropriate growth medium. Potato dextrose agar will support growth of many fungi. The medium
F I G . 1 . 6 . Bacterial ooze on the cut stem end of lettuce infected by Pectobacterium carotovorum. (Courtesy J. E. Adaskaveg and H. Förster—© APS)
F I G . 1 . 5 . Orange fruit internally inoculated with Penicillium digitatum: A, not treated or B, treated with the postharvest fungicide imazalil that inhibits sporulation of the pathogen. (Courtesy J. E. Adaskaveg and H. Förster—© APS)
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may be acidified with lactic acid or antibiotics added to inhibit growth of bacterial contaminants. Plates are incubated at 20 to 25°C, which is suitable for most fungi. Some pathogens, however, such as Phytophthora syringae or P. hibernalis, causal agents of brown rot of citrus fruits, are more adapted to cooler temperatures, and isolation plates need to be incubated between 15 and 20°C. Plates should be monitored daily, and fungal growth from the edge of developing colonies is transferred to fresh media plates. These transfers are then allowed to grow, and identification can be done based on characteristic fungal structures. If all of the plated colonies can be assigned to the same fungus, the identification of the decay agent will be strengthened. Oftentimes, however, cultures will remain in a mycelial state without sporulation, and proper identification is not possible. Other times, contaminants may overgrow a slower growing pathogen, leading to misdiagnosis. Common contaminants are species of Alternaria and Cladosporium that in some cases may also be pathogens. This will further complicate identification of the primary pathogen. Contamination and isolation of secondary saprophytes is more likely to occur when samples are in an advanced stage of decay. Therefore, the sample preferably should not be completely deteriorated. For isolation of bacteria, diseased tissue is incubated or macerated in water, and the suspension is streaked onto a growth medium. Single colonies are isolated and can be characterized by their shape and appearance including color and consistency, Gram-staining, by utilization of diagnostic carbohydrates by the bacterium, by serological techniques, or by fatty acid profiling (Schaad et al. 2001). To confirm that the isolated fungus or bacterium is the actual pathogen causing the disease, Koch’s postulates can be followed. For this, the host is inoculated with the isolated organism, the developing symptoms are observed, and the decay agent is re-isolated. If symptoms are the same for the original decay and the decay resulting from the inoculation, and if the same organism was re-isolated as in the original isolation, there is strong evidence that this organism is the causal agent of the disease. These Koch’s postulates (Agrios 2005) are rarely conducted for routine diagnoses but are important in the study of new diseases. Identification of isolated fungi and bacteria is increasingly being done molecularly. Identification based on detection of species-specific proteins by enzyme-linked immunosorbent assays (ELISA) has been more widely used in the past. Current approaches are mostly relying on detection of specific DNA sequences by DNA hybridization or PCR amplification and various derivations
Overview of Postharvest Pathology 11
of these techniques such as macro- and microarrays, loop-mediated isothermal amplification (LAMP), and rolling circle amplification. Specific detection of target organisms in these methods is based on the use of one or several of the many species-specific probes or primers that have been published. Alternatively, certain DNA regions can be amplified and sequenced. Sequences are then submitted to a search in the Basic Local Alignment Search Tool (BLAST) that matches the most closely related organism for which a sequence was deposited in GenBank, an open-access sequence database. Sequencing of several genomic regions may be required for organisms in some species complexes where species are closely related. Advanced molecular methods also enable the direct detection of the pathogen in plant tissue without its culturing and purification, and quantitative PCR (qPCR) can be used to determine the amount of pathogen present. These DNA-based methods have been reviewed previously, and more details can be found in Capote et al. (2012), Martinelli et al. (2015), Mirmajlessi et al. (2015), Raja et al. (2017), Schaad et al. (2001); Spring and Thines (2010), and Tsui et al. (2011).
SUSCEPTIBILITY OF FRUITS AND VEGETABLES TO INFECTION Differences in susceptibility to infection by pathogens among crop cultivars are most evident during production in the field, however, the cultivar used can also have an impact on the occurrence of postharvest decays. For example, among twelve apple cultivars evaluated, cv. Royal Gala was the most resistant to B. cinerea, P. expansum, and Mucor piriformis, whereas anatomical differences in cvs. Fuji and Oregon Spur II contributed to resistance to the bull’s eye rot pathogen Neofabraea malicorticis (Spotts et al. 1999). This was correlated with the presence of open sinuses between the calyx and the core cavity of more susceptible cultivars as well as the force needed to break the epidermis. Peach and nectarine cultivars that tend to develop suture cracks are more likely to develop decay (Ogawa and English 1991), and certain lines of white-flesh peaches and nectarines with higher sugar content, lower acidity, and thin skin have been found to be more susceptible to sour rot caused by Geotrichum candidum (Adaskaveg et al. 2007). Avocado cultivars ‘Hass’ and ‘Fuerte’ are both susceptible to infection by C. gloeosporioides, but only ‘Fuerte’ developed substantial symptoms, and this was correlated with a more rapid decline in the level of antifungal compound in the latter cultivar (Prusky et al. 1991). ■
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Rootstocks of tree crops can also have an impact on postharvest decay development. For example, susceptibility of avocado to anthracnose caused by C. gloeo sporioides was higher when ‘Hass’ scions were grafted to Duke 6 as compared to ‘Velvick’ rootstocks (Willingham et al. 2001). This was related to significantly different concentrations of antifungal dienes and of nutrients in leaves and fruit. Similarly, citrus rootstocks significantly affected the development of stem-end rind breakdown and postharvest decay of some varieties (Ritenour et al. 2004). Fruits are classified into climacteric and nonclimacteric types based on their pattern of ethylene production and respiration during maturation and ripening (Kader 2002; Paliyath and Murr 2008). Climacteric fruits such as apples, avocados, bananas, peaches, and tomatoes show a large increase in respiration and ethylene production during ripening (Fig. 1.7). Fruit soften, and yellow colors intensify through loss of chlorophyll and increase of carotenoid pigments. The peak of the respiratory curve approximates the time that fruit are considered ripe for consumption. After the climax, respiration gradually decreases as the fruit senesce. In climacteric fruits, harvesting before the start of the climacteric rise in respiration is the best way to attain maximum post harvest life. The climacteric rise can be initiated prematurely by exposing fruit to ethylene. If some of the fruit have started to ripen, the ethylene they produce may trigger the respiratory rise among the remaining fruit. Similarly, rotting or badly bruised fruit may release sufficient ethylene to trigger ripening. With climacteric fruits, it is essential not only to reduce the respiratory rate but, if possible, minimize and delay the
climacteric rise and associated ripening processes. This is best achieved by low temperature or by a combination of low temperature, modified atmospheres, and the ethylene inhibitor 1-methylcyclopropene (1-MCP) during storage. Non-climacteric fruits such as cherries, citrus fruits, strawberries, and pineapples do not exhibit the increase in respiration and ethylene production during ripening and also do not show an increase in sugar due to the absence of large reserves of starch at harvest. Instead, respiration decreases gradually, and increase in sugar content is limited. It is important to maintain fruit in a healthy condition after harvest by lowering the respiration rate to the minimum that still permits normal cellular function and prevents metabolism by anaerobic pathways that result in fruit off-flavors and reduced quality. Fruit are generally quite resistant to decay until they reach maturity. As commodities mature and then ripen, their chemical composition changes. For example, starches are converted to sugars and water, and fruit become sweeter and more juicy. At the same time, much of the fruit’s resistance to disease is lost. In climacteric fruits, the climacteric rise in respiration roughly coincides with a striking reduction in resistance to many pathogens. Inhibition of ripening by use of 1-MCP may reduce decay development, suggesting that modulating the physiological process of ripening can change susceptibility to decay in some fruit. Fruit become susceptible to their common pathogens as they ripen but also to the attack of pathogens they were resistant to when they were immature or mature. For example, as stone fruits approach maturity, they are increasingly susceptible to the main diseases of the crop, including brown rot caused by Monilinia fructicola and gray mold caused by B. cinerea. As these fruits completely ripen or become senescent, however, other fungi such as Rhizopus, Geotrichum, Penicillium, Alternaria, or Aspergillus species can cause postharvest decays.
MECHANISMS OF HOST RESISTANCE TO FUNGAL ATTACK To establish an infection, the pathogen must over come the natural defenses of the plant host. These include pre-infectional barriers that prevent or inhibit pathogen penetration and post-infectional responses to disease development (Adaskaveg 1992). These barriers or responses of host resistance can be structural or biochemical in nature. Pre-infectional structural barriers of ■
F I G . 1 . 7. Fruit respiration over time during ripening for climacteric and non-climacteric fruit types. (Courtesy J. E. Adaskaveg and H. Förster—© APS)