Abstract

Abstract Calonectria pseudonaviculata (Lombard, Crous, Wingfield & Wingfield) causes a severe blight disease on boxwood known as “boxwood blight”. Three isolates: 11-9-4a and CTWH1 - wild types from Connecticut landscapes, and FC1 - an isolate of 11-9-4a that was selected for ability to grow on up to 250 μg a.i./ml pyraclostrobin fungicide, were evaluated for sensitivity to nine fungicides belonging to the demethylation inhibitor ([DMI] propiconazole, tebuconazole, triflumizole, myclobutanil, tetraconazole) and strobilurin (pyraclostrobin, azoxystrobin, trifloxystrobin, kresoxim-methyl) groups. The effects of fungicides on mycelial growth and conidial germination were analyzed using in vitro assays. All DMI fungicides strongly inhibited radial growth, but did not prevent conidial germination. Of the strobilurins, only pyraclostrobin inhibited mycelial growth and conidial germination of the 11-9-4a and CTWH1 isolates within label use rates. Pyraclostrobin, kresoxim-methyl, and trifloxystrobin inhibited mycelial growth for 11-9-4a and pyraclostrobin and kresoxim-methyl for CTWH1. All strobilurin fungicides inhibited the conidial germination of 11-9-4a and FC1; only pyraclostrobin affected CTWH1. FC1 and CTWH1 exhibited reduced sensitivity to strobilurin fungicides for mycelial growth. For effective control of mycelial growth and conidial germination, and to reduce the risk of resistance development, fungicides from both FRAC groups should be used and integrated with other best management practices. Index words: fungicide resistance; Buxus; chemical disease management. Chemicals used in this study: azoxystrobin (Heritage 50 WG); kresoxim-methyl (Cygnus 50 WG); myclobutanil (Rally 40WSP); propiconazole (Procon-Z 14.3 L); pyraclostrobin (Insignia 20 WG); tebuconazole (Torque 38.7 SC); tetraconazole (Minerva 11.6 SC); trifloxystrobin (Flint 50 WG); triflumizole (Procure 480 SC). Species used in this study: boxwood (Buxus L.); boxwood blight (Calonectria pseudonaviculata).

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