USDA-ARS Sugarcane Field Station, Canal Point, FL 33438, USA

Background and objectives
Ratoon stunting disease (RSD) is a major disease of sugarcane causing yield losses worldwide. In Florida, five percent yield losses have been estimated industry wide. The pathogen, Clavibacter xyli subsp. xyli, (Cxx) invades the vascular system and is spread by harvest equipment that is contaminated with Cxx while cutting infected plants that then cuts stalks of other plants. Our objectives were to initiate a screening program for RSD resistance, release RSD resistant cultivars from the variety development program at Canal Point, and demonstrate the effectiveness of RSD resistance in controlling the disease under commercial production.

Materials and methods
A tissue blot immunoassay [1] was used that identifies the Cxx colonized vascular bundles (CVB) in infected sugarcane stalks. The number of CVB indicates disease reaction; resistant clones have near zero with increasing number of CVB indicating increased susceptibility. Initial screening began at the second vegetative stage (Stage II) entailing 700-1000 clones and was repeated for clones advanced to each subsequent stage in the variety development program. Plants were inoculated at planting by cutting the stalks with knives dipped in juice crushed from infected stalks of CP 53-1, a highly susceptible cultivar, that supports high Cxx populations. At 9 to 10 months, five stalks were sampled from a single plot and the average number of CVB was determined. Susceptible clones were not advanced from Stage II. Screening of subsequent stages was similar except that four replications were planted and susceptible clones were not always discarded. RSD susceptible clones that were extremely high yielding clones were advanced because the industry uses hot water treatment to reduce RSD infection in vegetative planting material.

Results and conclusion
In 1997, susceptible clones entailed 35.6% of the 721 clones of CP 96 Series tested in Stage II, 16.2% of the 130 clones of CP 95 Series tested in Stage III, and 9.1% of the 11 clones of CP 93 Series tested in Stage IV of the variety development program. Parental clones influence frequency of RSD resistance of their progeny. Only 2.9% of the progeny of resistant cultivar, CP 72-2086, used as either male or female parent, were susceptible while 20.8% of the progeny derived from susceptible CP 86-1664 were susceptible. Of the seven cultivars recently released from the program, four were moderately resistant and two were resistant. In a test to monitor disease spread, RSD was restricted in plantings of resistant cultivars in comparison to that of susceptible cultivars, where RSD incidence increased in each successive ratoon. In the third ratoon crop the incidence was 76.2% for the highly susceptible cultivar, CP 53-1, 34.9% for susceptible cultivar, CP 72-1210, and 2.4% for resistant cultivar, L 60-25 [2]. When no other RSD control practice was used, the incidence in commercial growers fields varied by cultivar susceptibility. RSD incidence averaged 1.5% in CP 72-2086 in 28 commercial fields surveyed and 2.7% for CL 73-239 in 10 fields. These two cultivars have been grown for 10 years without any heat treatment and had ample time for natural infection to occur. Under the same conditions, the RSD incidence of susceptible cultivars CL 61-620, CP 70-1133, and CP 72-1210 was greater than 90% in grower fields. The RSD incidence in moderately resistant cultivars varied between these extremes. Heat treatments can eliminate Cxx in vegetative cuttings but re-infection rapidly takes place in susceptible cultivars. RSD resistant cultivars were obtained in the development program and resistant cultivars have been a practical control practice in Florida.

1. Harrison NA, Davis MJ, 1988. Phytopathology 78, 722-27.
2. Comstock JC, Shine, JM Jr, Davis MJ, Dean JL, 1996. Plant Dis. 80, 704-8.