Evaluation of fungicide resistance in Sclerotinia minor and strategies for chemical control of sclerotinia blight of peanut

TR Number



Journal Title

Journal ISSN

Volume Title


Virginia Tech


Testing several registered and experimental fungicides in the laboratory and field has resulted in the identification of two compounds possessing high levels of fungitoxicity to Sclerotinia minor, the causal agent of Sclerotinia blight of peanut. The two fungicides, ASC-66825 and RH-3486, are thought to have a different chemistry than the dicarboximide fungicides. The ED₅₀ value (dose required for 50% inhibition of mycelial growth) of ASC-66825 and RH- 3486 was 0.004 µg/ml and they were 45 times more fungitoxic to mycelial growth on glucose yeast extract agar (GYEA) than iprodione. At simulated field rates (1.12 kg/ha), none of the experimental fungicides effectively inhibited sclerotial formation in soil-plate assays, whereas all the dicarboximide fungicides (chlozolinate, iprodione and vinclozolin) significantly inhibited sclerotial formation. No cross-resistance was detected between the dicarboximide fungicides and ASC-66825 or RH-3486. During three years of field tests, RH-3486 controlled Sclerotinia blight of peanut significantly better than iprodione. The spray adjuvant, pinolene (Nu-Film-17®), significantly improved the performance of iprodione (Rovral®) over 5 years of field tests. Average yields from plots treated with iprodione and pinolene were 365 kg/ha higher and disease incidence 15% lower than plots treated with iprodione alone. Applying fungicides to experimental microplots infested with a pathogenic, dicarboximide-resistant isolate of S. minor (B-83-T2) indicated that fungicides still provided disease control in a field situation. Disease incidence was suppressed 96, 55, 62, 25 and 20% in microplots infested with isolate B-83-T2 and 97, 83, 33, 67 and 30% in plots infested with a sensitive isolate (S-2), following treatments with RH-3486, vinclozolin, iprodione, PCNB and dicloran, respectively. Sclerotia of S. minor from peanut fields treated with dicarboximides and other fungicides for leafspot control did not show field resistance to iprodione in spite of an in vitro resistance rate of 6.3% in GYEA tests containing 2 µg/ml of iprodione. Field resistance to iprodione does not seem to be a major threat to control of Sclerotinia blight of peanut with iprodione in Virginia. The use of chlorothalonil for leafspot control has been correlated with an increase in the incidence of Sclerotinia blight. Excised peanut stems obtained from plots exposed to field applications of chlorothalonil produced larger lesions after inoculation with S. minor, than stems from untreated plots. Treatment of excised stems with chlorothalonil just prior to inoculation did not enhance lesion development. However, cultures of S. minor conditioned on GYEA containing chlorothalonil at 10 µg/ml were more pathogenic on excised stems than unconditioned cultures. Chlorothalonil may increase the aggressiveness of S. minor by enhancing organic acid production without greatly inhibiting fungal growth.