The main constraint in rubber plantations worldwide is the cessation of latex production because of two syndromes: (i) tapping panel dryness (TPD), a reversible physiological response to overexploitation; and (ii) bark necrosis (BN), an irreversible syndrome spreading from the collar toward the tapping cut. Early BN symptoms develop in the inner phloem tissues but never affect the cambium. Necrotic patches appear in the outer phloem, inducing bark cracking and peeling, but these alterations never lead to tree death. BN spreads gradually to neighboring rubber trees, and evidence of linear disease centers suggest that a pathogen may be involved, possibly transmitted by the tapping knife. Several previous etiological investigations (fungi, phytoplasma, bacteria, and virus) were performed (3) on leaves, bark, and latex using different methods (e.g., isolation, transmission, chemical treatments, and optic and electron microscope studies). Recent works focused on mechanically transmissible pathogens, such as viroid (2) or virus/double strand RNA, using RNA extraction (nonionic cellulose and appropriate ethanol concentrations) and treatment with RNase A, followed with sequential polyacrylamide gel electrophoresis (s-PAGE), reverse transcription-polymerase chain reaction (RT-PCR), degenerate oligonucleotide primer-PCR (DOP-PCR), and cloning and sequence analysis. While numerous viroid-like (between 250 and 400 nucleotides) and double strand virus-like (1,800 bp) low-molecular-weight RNAs were observed, no definite correlation was found with the BN status of trees. Sequencing of the various isolated RNAs only identified plasmids, nonpathogenic bacteria and yeasts, but none of the suspected pathogens. In addition, previous and recent transmission trials (tapping knife disinfection, bud grafting, bark implantation, and etc.) failed to confirm the involvement of a biotic agent. In conclusion, since these etiological investigations were inconclusive, a physiological disease is now suspected that involves exogenous stresses, nonoptimal vascular relations at the rootstock/scion junction and impaired cyanide metabolism (1,4).
References: (1) H. Chrestin et al. Plant Dis. 88:1047, 2004. (2) N. Duran-Vila et al. J. Gen. Virol. 69:3069, 1988. (3) D. Nandris et al. Eur. J. For. Pathol. 21:340, 1991. (4) D. Nandris et al. Plant Dis. 88:1047, 2004.