Submitted to: Sugarcane Pathology
Publication Type: Book / Chapter
Publication Acceptance Date: February 1, 2002
Publication Date: October 20, 2004
Citation: Grisham, M.P. 2004. Ratoon Stunting Disease. In: Rao, G.P., Saumtally, A.S., Rott, P., editors. Sugarcane Pathology Vol. III: Bacteria and Nematode Diseases. Enfield, NH: Science Publishers, Inc. p. 77-96. Technical Abstract: Ratoon stunting disease (RSD) of sugarcane is caused by the bacterium, Leifsonia xyli subsp. xyli, and has a worldwide distribution. The disease produces no characteristic external visual symptoms with the primary effect a mild to severe reduction in growth, particularly in the ratoon crops. In an infected sugarcane plant, a salmon pink discoloration may appear just below the growing point of a young cane and an orange red discoloration of the vascular bundles may appear at the nodes. Transmission of the pathogen from field to field or from one geographical area to another is by cuttings for propagation from infected plants. There is no evidence of insect vectors or seed transmission. Sugarcane is the only known natural host of L. xyli subsp. xyli. The xylem-limited bacterium is mechanically transmitted from infected plants to healthy plants in sap on tools and equipment during planting, harvesting, and cultivating the crop. Diagnosis sis primarily by laboratory techniques including light and electron microscopy, culture of the bacterium, serological tests, host induced responses, and DNA-based methods. The primary method of controlling RSD is to establish seed cane with a very low incidence of infection through either heat therapy or micropropagation of foundation plants followed by sanitation practices to reduce the reintroduction of the pathogen into healthy fields. Breeding for resistance to RSD is possible because of the recent development of diagnostic protocols that can be used to screen large numbers of clones economically. A multinational project has been established to map the L. xyli subsp. xyli genome and identify genes involved in pathogenicity.