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
Wojciech J. Janisiewicz, Robert A. Saftner, William S. Conway and Philip L. Forsline
Lihua Fan, Jun Song and Randolph Beaudry
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.
J.E. Cossentine, P.L. Sholberg, L.B.J. Jensen, K.E. Bedford and T.C. Shephard
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.
Robert A. Saftner, William S. Conway and Carl E. Sams
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.
Ibrahim I. Tahir, Eva Johansson and Marie E. Olsson
distribution organizations. Infections by Pezicula malicorticis (bull's eye rot), Penicillium expansum (blue mould), and Colletotrichum gloeosporioides (bitter rot) are the main causes of decay during apple storage in Sweden ( Tahir, 2006 ). Because pre
Susan Lurie, Elazar Fallik, Joshua D. Klein, Frerenc Kozar and Kornel Kovacs
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.
Peter L. Sholberg and Paul Randall
control of B. cinerea . Subsequent studies showed that when ‘Crimson Seedless’ table grapes were fumigated with (E) -2-hexenal, gray mold was suppressed but not completely controlled ( Archbold et al., 1999 ). Penicillium expansum Link causes the
William S. Conway, Wojciech J. Janisiewicz, Joshua D. Klein and Carl E. Sams
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.
Harold E. Moline and James C. Locke
The antifungal properties of a hydrophobic neem (Azadirachta indica A. Juss.) seed extract (clarified neem oil) were tested against three postharvest apple (Malus domestica Borkh.) pathogens—Botrytis cinerea (pers.) ex Fr. (gray mold), Penicillium expansum Thom. (blue mold rot), and Glomerella cingulata (Ston.) Spauld. & Schrenk. (bitter rot). The antifungal activity of neem seed oil also was compared to that of CaCl2. A 2% aqueous emulsion of the clarified neem seed oil was moderately fungicidal to B. cinerea and G. cingulata in inoculated fruit, but bad little activity against P. expansum. Ethylene production was reduced 80% in fruit dipped in 2% neem seed oil compared to wounded, inoculated controls. Neem seed oil was as effective an antifungal agent as CaCl2, but the effects of the two combined were not additive.
S.-S.T. Hua, J.L. Baker and M. Flores-Espiritu
California is the major state for producing almonds, pistachios, and walnuts, with a total market value of $1.6 billion. Both domestic and export markets of these nuts presently allow a maximum level of aflatoxin B1 contamination in the edible nuts to be 20 ppb. Even very low degrees of infection of the nuts by A. flavus can result in aflatoxin levels above the mandatory standards. Biological control to reduce the population of and to inhibit the biosynthesis of A. flavus in orchards may be useful to decrease infection and thus aflatoxin content in the edible nuts. Certain saprophytic yeasts were shown to effectively compete with postharvest fungal pathogens such as Penicillium expansum and Botrytis cinerea. The potential of saprophytic yeasts to reduce aflatoxin contamination in tree nuts has not been hitherto extensively explored. A safe visual bioassay for screening yeasts antagonistic to A. flavus has been developed. The nor mutant of A. flavus has a defective norsolorinic acid reductase and blocks the aflatoxin biosynthetic pathway, resulting in the accumulation of norsolorinic acid, a bright red-orange pigment. We used the nor mutant in the assay to screen yeasts strains for their ability to inhibit aflatoxin production by visually scoring the accumulation of this pigment as well as the growth and sporulation of the fungus. Yeast strains that reduced the red-orange pigment accumulation in the nor mutant were identified and shown to inhibit aflatoxin biosynthesis of several toxigenic strains of A. flavus.