Rot of Sweet Potato

Huang, C. W.

, Yang, H. R.

, Lin, C. Y.

, Hsu, S. L.

, and Ni, H. F.

1 Chiayi Agricultural Experiment Branch, Taiwan Agricultural Research Institute

*Corresponding Author: [email protected]

ABSTRACT

Foot rot disease is a major limiting factor of sweet potato production in recent years. The disease was harmful to commercial root-used varieties of sweet potato, TN57 and TN66, as well as vegetable-used variety, TN71. It suggested that the majority of sweet potato cultivars in Taiwan were not resistant to this disease. The symptoms of this disease included yellowing of leaves, necrotic lesions on vine, and wilting of the sweet potato plants. The pathogen might grow from cankers on the vines down into storage roots, having brown wet rot lesions on the skin of storage root, and caused to severe yield loss and storage disease problems. The fungus generated two types of conidia from stromataic pycnidia on infected vines. The disease seedling was a major inoculum source. Therefore, good quality of seedlings would be an important factor to control the foot rot of sweet potato in the field. It was recommended that the field with the foot root disease should be rotated with rice annually or being flooded for more than 2 wk after harvesting season, and it could eradicate the pathogen as well as avoid the infection of foot rot disease next season. In the chemical control, the result showed that Carbendazim + Hexaconazole and Thiabendazole were effectively inhibited mycelial growth. From all the experimental data, possible integrated control strategies to the disease include (1) cultivating certified healthy seedling, (2) eliminating all disease-infected plants in the field, and (3) adopting flooding treatment or rotation of rice and non-host crops prior to planting season to reduce the pathogen density of the field.

(Key words：Sweet potato (Ipomoea batatas), Foot rot diseases, Phomopsis destruens, Disease control)

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圖一、甘藷基腐病之病徵。A、莖基部藤蔓出現褐化乾枯現象。B、病原向下擴展導 致塊根腐爛情形。C、甘藷病株藤蔓上產生黑色之子座式柄子器。D、罹病藷塊縱剖

面顯示組織褐化腐爛具濕臭味。

Fig. 1. Symptoms of foot-rot on sweet potato. Infected stem foot exhibiting browning and dying symptoms (A) and rot extending to diseased tuber (B). (C) Black stromatic pycnidia erumpent on infected stem. (D) Cross section of diseased tuber with tissue brown and rot symptoms⁽¹²⁾.

A B

C

D

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圖二、甘藷基腐病菌之分生孢子與菌落形態。A、單胞、透明無色、圓筒狀或卵 形、兩端有圓形油滴之甲型分生孢子 (α-conidia)。B、單胞次紡錘型，遠端凸尖 或略為鈍圓，而基端略呈截頭狀，並且一邊略彎之丙型分生孢子 (γ-conidia)。標 尺＝10 μm。C、甘藷基腐病菌於 PDA 培養基上於 25℃ 培養 20 天後的菌落 形態。

Fig. 2. Conidial shape and colony morphology of Phomopsis destruens. (A) α-conidia one-celled, hyaline, oblong or oval, with 2-guttulated. (B) γ-conidia clavate to

subcylindrical, one end actue or obtuse, the base somewhat truncate, and one side slightly curved. Bar= 10 μm. (C) Colony morphology of P. destruens cultured on PDA at 25℃ for 20 days ⁽¹²⁾.

A

B C

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圖三、甘藷基腐病菌對不同甘藷品種致病性之影響。

Fig. 3. Effect of sweet potato variety on the incidence of foot rot disease caused by Phomopsis destruens.

圖四、罹病種苗、健康種苗、田間罹病藤蔓及罹病土對甘藷基腐病發生之影響。

Fig. 4. Effect of diseased seedling, healthy seedling, diseased stem and infested soil on the incidence of foot rot disease caused by Phomopsis destruens.

Variety

TN-10 TN-17 TN-31 TN-57 TN-64 TN-66 TN-68 TN-71 TN-72 TN-73 0

20 40 60 80 100

Disease incidence (%)

Treatments

A B C D

Disease incidence (%)

0 20 40 60 80 100

120 A:Healthy seedling + Autoclaved peat moss B:Healthy seedling + Infested soil

C:Healthy seeding + Diseased stem in healthy soil D:Diseased seeding + Autoclaved peat moss

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表一、淹水處理時間對甘藷基腐病發生之影響

Table 1. Flooding treatment on the foot rot disease incidence of sweet potato caused by Phomopsis destruens

Disease incidence (%)^z Flooding time Diseased Tuber Diseased Stem

1 week 0.0 13.3

2 weeks 0.0 0.0

CK 30.0 26.7

z Disease incidence (%) = (Number of plants which showed symptom of foot rot/10) × 100%.

表二、不同殺菌劑對 Phomopsis destruens SPPD-11 及 SPPD-17 分離株菌絲生長之影響 Table 2. Effect of different synthetic fungicides on mycelial growth of Phomopsis destruens

SPPD-11 and SPPD-17 isolate

Fungicide

Inhibition (%)^z

1 ppm 10 ppm 100 ppm

SPPD-11 SPPD-17 SPPD-11 SPPD-17 SPPD-11 SPPD-17 62.5% Cyprodinil +

Fludioxonil (WG) 66.5 c^y 74.3 bc 40.2 c 70.6 b 88.3 ab 86.8 b 23% Azoxystrobin (SC) 72.0 c 50.8 d 73.7 b 46.9 c 79.7 b 68.4 c 23.7% Iprodione (SC) 10.8 d 28.6 e 22.9 c 47.7 c 26.6 c 47.7 d 40% Thiabendazole (WP) 100.0 a 69.4 c 100.0 a 100.0 a 100.0 a 100.0 a 39.5% Fluazinam (SC) 85.9 b 81.9 b 92.2 ab 89.5 b 100.0 a 100.0 a 34.5% Carbendazim +

Hexaconazole (WP) 100.0 a 100.0 a 100.0 a 100.0 a 100.0 a 100.0 a LSD (P = 0.05) 6.9 8.1 23.8 15.4 16.0 5.7

z Inhibition (%) = [(Diameter of mycelial growth on PDA without fungicide - diameter of mycelial growth on PDA with fungicides)/diameter of mycelial growth on PDA without fungicide] × 100.

y Means within a column followed by the same letter are not significantly different at 5% by LSD test.

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