CONTROL OF POSTHARVEST INFECTION OF
PHYTOPHTHORA FRUIT ROT IN DURIAN
WITH FOSETYL-A1 AND RESIDUE LEVELS IN FRUIT
SCIENTIFIC NAME: Durio zibethinus
FAMILY: Bombacaceae
INTRODUCTION
Phytophthora root and foot rot of durian is a serious and widespread disease in all durian-producing areas in Thailand. The causal organism, Phytophthora palmivora (Butler) attacked mainly the root and foot of the mature tree. It may infect the bark of the trunk, twigs, and the fruit. It also caused damping-off of young seedings (8). This lethal disease has wiped out many durian orchards in recent years. It also caused considerable losses of harvested fruit during marketing.
The pathogen is soil-borne and may spread by soil, water, and air. It survives in infected tissue and in soil in the form of chlamydospores, sporangia, and mycelia (6). Sporangia were produced profusely on agar medium. Under moist conditions, zoospores liberated from the sporangia were able to establish more than 50% infection on tissue after 7 hr and 100% infection after 17 hr (6). Optimum temperature for mycelial growth was reported at 23.0-29.0°C. Minimum temperature was at 11.5°C and maximum, 33.0°C (6).
Several fungicides such as fosetyl-A1 (or Aliette), metalaxyl (or Ridomyl), and propamocarb hydrochloride (or Previcur N) have demonstrated the effectiveness against genera of phycomycetous fungi including Phytophthora (1, 2, 5).
Fosetyl-A1 and propamocarb-HC1 have either systemic or short range systemic action and best results are obtained by soil drench and foliar spray. Control of Phytophthora root and foot rot in durian is thus based mainly on preventive measure as soil drench and foliar spray with fungicide or curative measure applied as fungicide paint on the infected trunk or twigs.
In spite of the preharvest treatment, a certain amount of harvested fruit showed Phytophthora fruit rot during handling and marketing. The present study was to investigate the use of fosetyl-A1 in durian against Phytophthora fruit rot and the residue levels of fosetyl-A1 and its metabolite in plant tissue, phosphonic acid, in the treated fruit.
MATERIALS AND METHODS
Experimental fruit and test design: Durian fruit cv. Mon Tong were harvested on June 16, 1987 from a commercial orchard in Bayong province, Thailand. Fruit were received in the Postharvest Technology Laboratory in the afternoon of the day of harvest and subsequent treatments carried out on the same day.
Fruit were harvested either from trees which had received a preharvest folial spray or did not. In treatments with preharvest spray, spraying was conducted 28 days before harvest with fosetyl A1 at 2 or 4 g a. i./l as specified. The spray volume was 25 l/tree. Fungicides evaluated for postharvest dipping included fosetyl-A1 (or Aliette 80% a.i. wettable powder manufactured by May and Baker Ltd.) and propamocarb-HC1 (or Previcur N 722 g a.i./l as a 66.5% aqueous solution manufactured by Schering AG Berlia/Berakamen).
All fruit were artificially inoculated to achieve 100% infection. There were eight treatments included in the experiment. Each treatment comprised 8-10 fruit. The test was a completely randomized block design.
Preparation and application of inoculum for artificial inoculation: The isolate of P. palmivora used for artificial inoculation was obtained from the Division of Plant Pathology and Microbiology, Department of Agriculture. The fungus was cultured on Difco PDA in Petri dish for 4 days at room temperature (22°C). Mycelial agar block cut with a sterile 4 mm cork borer was used as a source of inoculum. Inoculation was carried out by puncturing the fruit once on the rind to a depth of 5 mm with a sterile 1 mm thick inoculation pin. Site of wounding was marked for easy identification. Agar block was then placed with mycelial surface down on the site of the wound. In treatments requiring a postharvest fungicide dipping, wounded fruit were dipped in specified fungicide for 2 min and the fruit left to dry in air before inoculation.
Inoculated fruit were held at a room maintained at 22°C and 95-100% relative humidity. This high humidity was achieved by placing the fruit between a sheet of polyethylene film and sprayed on the film with a fine mist of water afterwards.
Determination of fungicide residue: This was carried out by May and Baker (Thailand) Ltd. Fruit were stored at room temperature (30°C) for 4 days before the samples were peeled and frozen. The frozen samples were packed in polystyrene boxes with dry ice and dispatched, by air freight, to the Analytical Chemistry Department, May and Baker Ltd., England, where determination of fungicide residue was carried out. Samples were subjected to extraction by water/propanol and methylation by diazomethane. A gas chromatograph with a flame thermionic (rubidium bead) detector and a glass column packed with 20% carbowax 20 M on chromosorb W HP with chromosorb 101 packed at the injector end, was used for the determination of the methyl derivatives of phosphonic acid and fosetyl A1 in mg per kg of edible pulp. Results were the average of two analyses.
Evaluation of fruit: Disease development was monitored daily by measuring the diameter of the lesion. Disease index (DI) for each fruit was scored on a 4-point scale on which 0 = no apparent symptom, 1 = very slight symptom with lesion size from 0.1 to 1.0 cm, edible aril was not affected, 2 = symptom slight with lesion size from 1.1 to 2.0 cm, 3 = moderate with lesion size from 2.1 to 4.0 cm, up to 4 = severe with lesion size larger than 4.1 cm. Data on lesion size and disease index were analyzed by an analysis of variance and LSD test for significance between means (P = 0.05). The percentage of disease-free fruit in a treatment were recorded. Disease score for a given treatment was expressed as:
| Disease score = sum of DI points x 100 |
| number of fruit in the treatment x 4 |
On the resultant 0 to 100 scale, 0 = disease free or no apparent symptom, 25 = market acceptable fruit, having only slight evidence of symptom, 50 = fruit with apparent symptom, barely acceptable by consumer, and 75 to 100 = fruit with large lesion, not marketable to totally unacceptable.
RESULTS AND CONCLUSION
Disease development in artificially-inoculated fruit which had received a preharvest folial spray of fosetyl-A1 at 2 or 4 g a.i./l did not significantly differ from the control. The most significant reduction in fruit rot was observed in fruit receiving a postharvest dipping of fosetyl A1 at 4 g a.i./l and in fruit with a preharvest fungicide spraying at 2 or 4 g a.i./l followed by a postharvest dipping of the fruit in the fungicide of the same strength.
Control fruit developed a moderate to severe degree of rotting within 4 days. Rotting was severe and extensive by day 6. Disease scores of the control were 90 and 100 on day 4 and 6 respectively. Disease scores of the three best treatments mentioned above ranged 0-25 on day 4 and 55 on day 6.
The three best treatments were (1) fosetyl-A1 applied as a postharvest dip at 4 g a.i./l and (2) preharvest fungicide spraying at 2 or (3) 4 g a.i./l followed by postharvet dip in the fungicide of the same strength.
Fosetyl-A1 was found to be metabolized rapidly by the plant into phosphonic acid (2, 4). Phosphonic acid was also used for residue determination in the fruit (3). Residue level of phosphonic acid in fruit found in these three treatments mentioned above were less than 0.5, 1.2, and 3.3 mg per kg of edible pulp respectively. Phosphonic acid, 3.8 mg per kg of pulp, was also found in the fruit receiving a preharvest spray at 4 g a.i./l.
Residue levels of fosetyl-A1 in durian, regardless of the treatment were negligible.
In conclusion, fosetyl-A1 was able to provide a certain degree of decay control. The poor eradicate activity in our present test was probably due to the inoculation method used. The use of mycelial agar block as a source of inoculum was much more drastic than the use of spore suspension or the contact infection under natural conditions. This study indicated the possibility and the need for further study on the use of fosetyl-A1 as a postharvest treatment against natural contact infection of Phytophthora fruit rot in durian. The residue levels of such treated fruit were well below the established tolerance on grapes and citrus allowed in many countries.
LITERATURE CITED
1. ANON. 1981. Previcur N Fungicide. AG Agrochemical Division, Schering, Berlin, Germany.
2. ANON. Aliette Fungicide. May and Baker Limited.
3. Cohen, E., Y. Shalom, Y Exelrod, I. Adota and I. Rosenberger. Control and prevention of contact infection of brown rot disease with phosethyl A1 and residue levels in postharvest treated citrus fruit. Paper submitted for publication in "Pesticide Science" approved on June 1986. (In press).
4. Eckert, J. W. , B. F. Bretschneider and M. Ratnayake. 1981. Investigation on new postharvest fungicide for citrus fruits in California. Proc. Int. Soc. Citriculture. International citrus congress held in Tokyo Nov. 9-12, 1981.
5. Eckert, J.W. 1983. Control of postharvest disease with antimicrobial agents. P. 278- 279. In: M. Lieberman (eds.) Postharvest physiology and crop preservation. Plenum press, New York and London.
6. Kobayashi, N., T. Kamhangridthirong and V. Kueprakone. 1978. Studies on the soil borne diseases of economic plants in Thailand, with special reference to Phytophthora diseases. DOA. Min. of Agric. and Coop, Thailand.
7. Maycey, R.A. and J.R. Outram. 1987. Residue studies on durian fruit. A Scientific report from the Analytical Chemistry Department of May and Baker Limited.
8. Suzui, T., U. Kueprakone and T. Kamhangridthirong. 1976. Phytophthora disease on some economic plants in Thailand. DOA. Min. of Agric and Coop, Thailand.
DATE: July 1989
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