Ramu stunt disease of sugarcane (ScRS) was responsible for large yield losses in commercial sugarcane varieties (interspecific hybrids of Saccharum spp.) in the Ramu Valley in northeast Papua New Guinea during the late 1980s. Losses were total in the cultivar Ragnar; Q90 and Yasawa were also affected but Cadmus and Q107 were resistant. Since that time, replanting with resistant cultivars has kept the disease under control. The disease spreads rapidly in susceptible cultivars, where it results in severe stunting of the cane and a yellow mottled striping of the leaves. Although several attempts have been made to detect a viral pathogen, no evidence for viral etiology exists and the causal agent remains unknown. With a nested polymerase chain reaction (PCR) of general phytoplasma primers from the 16S rDNA (1), phytoplasma-specific products were consistently amplified from the leaves of field-grown sugarcane, from sugarcane with ScRS symptoms grown in the glasshouse at IACR-Rothamsted, UK, and from samples of the putative vector collected at Ramu, the delphacid plant hopper Eumetopina flavipes Muir, which had been found to transmit symptoms of Ramu stunt in pot trials (2). Digestion of the amplimers with restriction enzymes RsaI and HaeIII gave profiles that matched those of members of the sugarcane white leaf (SCWL) phytoplasma group. The DNA sequence of the intergenic spacer region of the phytoplasma associated with ScRS showed a 95.98% homology with that of SCWL, suggesting that this newly discovered phytoplasma can provisionally be placed in this group. The 16S-23S intergenic spacer sequence has been submitted to GenBank (accession no. AF 106061). References: (1) C. P. R. Cronjé et al. Ann. Appl. Biol. 133:177, 1998; (2) L. S. Kuniata et al. J. Aust. Entomol. Soc. 33:185, 1994.