disease resistance and associated decays ( Janick et al., 1996 ). In a survey of the New York market from 1972 to 1984, blue mold caused by Penicillium expansum was the most damaging parasitic postharvest disease of apple ( Cappellini et al., 1987
Abstract
Concentrations of patulin in blue mold lesions caused by Penicillium expansum Lk. ex Thom in pears and stone fruits were similar to those reported for apples. Of fruits tested, only the plum was a poor substrate for accumulation of the mycotoxin. The total patulin within disease lesions increased as the lesions enlarged. However, the concentration of patulin varied considerably, with the largest lesions usually yielding the lowest concentrations. Little or no patulin permeated healthy tissue surrounding the disease lesions unless fruits were overripe or had senescent breakdown.
Hexanal vapor is a natural, metabolizable fungicide that inhibits fungal activity and enhances the aroma biosynthesis in sliced apple fruit. Whole apple fruit were inoculated at two points per fruit with Penicillium expansum at a concentration of 0.5 × 105 spore/ml and treated with hexanal vapors. Inoculated fruit were exposed to hexanal for 48 hr and kept for another 72 hr in hexanal-free air at 22°C. Treatments included 8.2–12.3 μmol·L–1 (200–300 ppm), 14.5-18.6 μmol·L–1 (350–450 ppm), and 24.8-28.9 μmol·L–1 (600–700 ppm), each with an air control. At a concentration of 200–300 ppm hexanal, there was no fungal growth during treatment, but lesion development was evident on 100% of the treated fruit following cessation of treatment. After 72 hr holding in air, lesion diameter was significantly smaller for treated fruit. When inoculated apple fruit were exposed to 350–450 ppm and 600–700 ppm hexanal vapors, the decay rate was 44.7% and 23.9%, respectively, while the decay rate of inoculated control apple fruit was 100% and 98%, respectively, after 72 hr holding in air. The development of aroma volatiles was investigated for both treated and untreated whole apple fruit. Hexanal was actively converted to aroma volatiles by `Golden Delicious' fruit and there was no detectable hexanal emanations. The amount of hexylacetate, hexylbutanoate, hexylhexanoate, hexylpropionate, butylhexanoate, and hexyl-2-methybutanoate were about 2- to 4-fold higher in treated apple fruit than in untreated apple fruit. `Mutsu' apple fruit were treated with 350–450 ppm hexanal for 48 hr and processed into apple sauce within 4 hr. An informal sensory evaluation for processed `Mutsu' apple revealed no apparent flavor difference between treated and control fruit sauce.
Wooden fruit bins are a source of diapausing codling moth and postharvest pathogenic fungi. The redistribution of codling moths within bins is a problem where codling moth populations are being controlled by areawide codling moth sterile release programs, mating disruption programs, or both. Laboratory and fumigation chamber trials were carried out to determine the impact of relatively low levels of carbon dioxide on late-instar codling moth (Cydia pomonella L.) and two postharvest fruit pathogens, Penicillium expansum Link ex Thom and Botrytis cinerea Pers. ex Fr. Fumigation of diapausing codling moth with 40% CO2 in laboratory trials resulted in over 60% mortality after only 6 days of exposure and mortality increased with time of exposure. Significant mortality (68%) of diapausing codling moth larvae occurred after 14 days of exposure in the laboratory to 13% CO2 and a mean of 88% mortality was recorded after fumigation for 20 days. A significant number of P. expansum (46%) spores failed to germinate after laboratory exposure to 13% CO2 for 12 and 18 days respectively. Close to 100% of the P. expansum spores failed to germinate by day 20. When diapausing codling moth larvae and spores from both plant pathogens were placed in wooden fruit bins and fumigated for 21 days at 13% CO2, 75% of the diapausing codling moths died and 80% of the P. expansum spores failed to germinate. No effect on B. cinerea was observed.
Three polyamine biosynthesis inhibitors, α-difluoromethylornithine (DFMO), α-difluoromethylarginine (DFMA), and α-methylornithine (MeOrn), alone and in combination with CaCl2, were tested for their ability to reduce in vitro growth and soft rot development in apple (Malus domestica Borkh.) fruit caused by Botrytis cinerea Pers.:Fr. and Penicillium expansum Link. All three inhibitors reduced the in vitro growth of the pathogens. Calcium had no effect on fungal growth in vitro. Pressure infiltration of millimolar concentrations of DFMO or DFMA or 25 g·L-1 CaCl2 solutions into apples reduced subsequent soft rot development by B. cinerea and P. expansum >40%. A combination treatment of Ca and DFMO or DFMA reduced decay >67%. Treatment of apples with MeOrn was less effective at inhibiting decay development. None of the inhibitors affected polyamine levels in apple cortical tissues. Some injury to the fruit surface was observed with Ca treatments. Fruit treated with Ca and any of the inhibitors were less firm than those treated with Ca alone. Specific polyamine biosynthesis inhibitors in combination with Ca may prove useful in reducing postharvest decay in apples.
Postharvest heat treatments were applied to three apple (Malus domestica Borkh.) cultivars: `Anna', `Golden Delicious', and `Jonathan'. The temperatures ranged from 38 to 50 °C and from 5 to 96 hours. The temperatures of 50 °C for 5 or 10 hours and 46 °C for 10 hours controlled all developmental stages of San Jose scale on `Golden Delicious' and `Jonathan' fruit. Blue mold germination was prevented by 46, 42, and 38 °C after 28, 34, and 42 hours, respectively. The time needed to control the fungus was longer than that required to kill the insect. Apples were damaged by a 50 °C treatment but could withstand at least 12 hours at 46 °C and at least 24 hours at 42 °C. At 38 °C no damage was found on preclimacteric apples even after 96 hours, but if postclimacteric fruit were heated at 38 °C heat damage occurred. The treatments that did not cause damage maintained the fruit firmness during post storage ripening. The results are discussed in the context of developing integrated postharvest heat treatments.
Heating `Golden Delicious' apples (Malus domestica Borkh.) for 4 days at 38C or pressure-infiltrating them with a 4% CaCl2 solution reduced decay and maintained fruit firmness during 6 months of storage at 0C. Heating reduced decay caused by Penicillium expansum Link ex Thorn by ≈30%, while pressure infiltration with CaCl2 reduced decay by >60%. Pressure infiltration with CaCl2 after heating reduced decay by ≈40%. Pressure infiltration maintained firmness best (>84 N), as measured with a manually driven electronic fruit-firmness probe, followed by heat and CaCl2 (76 N), heat alone (71 N), and no treatment (control) (60 N). Force vs. deformation (FD) curves from a puncture test with a fruit-firmness probe mounted in a universal testing machine showed that fruit heated before storage were firmer than all nonheated fruit, except those pressure-infiltrated with 4% CaCl2. However, FD curves also showed that apples pressure-infiltrated with 4% CaCl2 differed quantitatively from apples in all other treatments, including those heated.
The viability of Penicillium expansum Link conidia in sporulating culture declined rapidly when exposed to 38 °C, and when conidia were exposed to 38 °C prior to inoculation of apple fruits (Malus ×domestica Borkh.), the resulting lesions were smaller than those on fruit inoculated with nonheated conidia. `Gala' apples were heated after harvest (38 °C for 4 days), pressure infiltrated with a 2% solution of CaCl2, or treated with the antagonist Pseudomonas syringae van Hall, alone or in combinations to reduce postharvest decay caused by Penicillium expansum. After up to 6 months in storage at 1 °C, no decay lesions developed on fruit that were heated after inoculation with P. expansum, or any combination of P. expansum, antagonist, or Ca. Parallel lots of heat-treated and nonheated fruit that were either infiltrated or not infiltrated with Ca were stored up to 6 months. They were then inoculated with P. expansum alone, or with the antagonist followed by P. expansum. Prior heat treatment did not influence lesion size. Calcium alone, the antagonist alone, and heat plus Ca all reduced the incidence of decay by ≈25%, whereas heat plus the antagonist reduced it by 70%. Calcium plus the antagonist or Ca plus the antagonist and heat reduced decay incidence by 89% and 91%, respectively. The integrated strategy of heat-treating fruit, followed by Ca infiltration and then treatment with an antagonist, may be a useful alternative to controlling postharvest decay with fungicides.
Acetic acid (AA) as a vapor at low concentrations was effective in preventing fruit decay by postharvest fungi. Fumigation with 2.7 or 5.4 mg AA/liter in air at 2 and 20C reduced germination of Botrytis cinerea Pers. and Penicillium expansum Link conidia to zero after they had been dried on 0.5-cm square pieces of dialysis tubing. Decay of `Golden Delicious', `Red Delicious', and `Spartan' apples (Malus domestica Borkh.) inoculated with 20 μl drops of conidia of B. cinerea (1.0 × 105 conidia/ml) or P. expansum (1.0 × 106 conidia/ml) was prevented by fumigating with 2.0 and 2.7 mg AA/liter, respectively. Tomatoes (Lycopersicon esculentum Mill.), grapes (Vitis vinifera L.), and kiwifruit [Actinidia deliciosa (A. Chev.) C.F. Liang et R. Ferguson var. deliciosa] inoculated with B. cinerea or navel oranges (Citrus sinensis L.) inoculated with P. italicum Wehmer did not decay when fumigated with 2.0 mg AA/liter at 5C. AA fumigation at low temperatures (1 and 5C) with 2.0 or 4.0 mg AA/liter prevented decay of `Spartan' and `Red Delicious' apples and `Anjou' pears (Pyrus communis L.) inoculated with B. cinerea and P. expansum, respectively. `Spartan' apples immersed in a suspension of P. expansum conidia (1.4 × 105 conidia/ml) and fumigated with 2.7 mg AA/liter at 5C had an average of 0.7 lesions per fruit compared to 6.1 for nontreated fruit. Increasing the relative humidity from 17% to 98% increased the effectiveness of AA fumigation at 5 and 20C. At the concentrations used in our trials, AA had no apparent phytotoxic effects on the fruit. The potential for commercial fumigation with AA to control postharvest decay of fruit and vegetables appears promising.
Vapors of several common vinegars containing 4.2% to 6.0% (= 2.5 to 3.6 mol·L-1) acetic acid effectively prevented conidia of brown rot [Monilinia fructicola (G. Wint.) Honey], gray mold (Botrytis cinerea Pers.:Fr.), and blue mold (Penicillium expansum Link) from germinating and causing decay of stone fruit (Prunus sp.), strawberries (Fragaria ×ananassa Duchesne), and apples (Malus ×domestica Borkh.), respectively. Fruit were fumigated in 12.7-L sealed containers in which vinegar was dripped on to filter paper wicks or vaporized by heating from an aluminum receptacle. Vapor from 1.0 mL of red wine vinegar (6.0% acetic acid) reduced decay by M. fructicola on `Sundrop' apricots (Prunus armeniaca L.) from 100% to 0%. Similarly, vapor from 1.0 mL of white vinegar (5.0% acetic acid) reduced decay in strawberries by B. cinerea from 50% to 1.4%. Eight different vinegars, ranging from 4.2% to 6.0% acetic acid, of which 0.5 mL of each vinegar was heat-vaporized, reduced decay by P. expansum to 1% or less in `Jonagold' apples. The volume of heat-vaporized white vinegar (5.0% acetic acid) necessary to reduce decay by P. expansum on `Jonagold' apples to zero was 36.6 μL·L-1 of air. Increasing the number of conidia on the apple surface reduced the effectiveness of vinegar vapor. The number of lesions caused by P. expansum on `McIntosh' apple decreased exponentially with increasing time of fumigation, approaching zero after about 6 hours. These results suggest that vinegar vapor could be an effective alternative to liquid biocides such as sodium hypochlorite for sterilization of surfaces contaminated by conidia of fungal pathogens.