Anastomosis Grouping of Rhizoctonia solani Associated with Black Scurf and Stem Canker of Potato in South Africa.

Rhizoctonia disease (black scurf of tubers and stem canker) of potato (Solanum tuberosum L.) caused by Rhizoctonia solani Kühn was first recorded in South Africa in 1918 (3). Although the sclerotial form on tubers is one of the most common potato diseases in the country, it is not known which anastomosis groups (AGs) of R. solani are involved. Between 1999 and 2001, R. solani was isolated from 28 plant and 56 soil samples collected in 7 (Eastern Free State, Gauteng, KwaZulu-Natal, Limpopo, Mpumalanga, Northern Cape, and Sandveld) of the 14 potato-production regions of South Africa and screened for hyphal anastomosis with tester strains of R. solani AG-1 to AG-10 according to Carling et al. (1). Of the 411 isolates from tubers with black scurf symptoms, 408 were AG-3 and three were AG-5. Symptomless tubers yielded two AG-3 isolates and three AG-5 isolates. Of 39 isolates from symptomatic stems and roots, 32 were AG-3, five were AG-4, and two were AG-5. Of the 127 isolates obtained from soil, 86, 28, 7, 3, and 3 were AG-3, AG-4, AG-5, AG-7, and AG-8, respectively. More than one AG was isolated from five of the seven regions. Virulence of 40 isolates representative of the above AGs was determined in triplicate on sprouts growing from seed tubers of potato cultivar Up-to-Date in a sand/soil mixture as described by Carling and Leiner (2) but using cultures grown in cornmeal/sand instead of colonized agar disks as inoculum. Damage to sprouts (lesions, girdling, and death) was assessed after 28 days at 16 to 28°C according to the 0 to 4 rating scale (2). Chi-square analysis of the data indicated that AG-3 was the most virulent, with isolates from sclerotia on tubers and lesions on stems more aggressive than those from symptomless tubers or soil. AG-4 and AG-5 caused significantly less disease than AG-3, but none of the AG-7 and AG-8 isolates showed any virulence to potato sprouts. References: (1) D. E. Carling et al. Phytopathology 77:1609, 1987. (2) D. E. Carling and R. H. Leiner. Phytopathology 80:930, 1990. (3) E. M. Doidge. S. Afr. Fruit Growers 5:6, 1918.