Causes of rubber tree bark necrosis identified
The rubber tree, Hevea brasiliensis, is cultivated in many humid tropical countries for the latex it produces, from which is extracted natural rubber mainly used by the tyre industry. Asia alone provides almost 95 % of the world production, where the first producer is Thailand whose rubber industry earns a regular income for 10 % of the population. However, a disease is attacking rubber trees that causes irreversible drying-up of latex flow, and can affect up to 30% of trees in African, Asian and American plantations, causing marked falls in production and substantial economic losses. Termed “rubber tree bark necrosis syndrome” (RTBN), it was diagnosed in 1983 (4) in an industrial-scale plantation estate (Michelin company, Ivory Coast) by IRD researchers. The first investigations, conducted at the request of the plantation company, could not establish a link between RTBN and any pathogenic agent (fungus, virus, bacterium or mycoplasm).
Further research projects were launched at the end of 1999 by the IRD team and its partners (2) at the request of the rubber production sector and with its support (1). This complex syndrome was then tackled using a multidisciplinary approach (involving plant pathology, agricultural soil science, cell and molecular physiology, virology, and so on) and focusing on several different localities (3), which provided conditions for identifying its origin and activating mechanism.
Since the 1970s, the predominant basis of rubber cultivation has been propagation by grafting on tree stock. In 90% of cases, RTBN attacks the tree vascular tissues, starting right at the grafting point situated in the transition zone between the trunk and the roots, the collar. The first stage of the disease is not detectable because the first cells to undergo necrosis are located in internal tissues of the bark. The necrosis, however, extends steadily to the whole base of the trunk before travelling upwards, up to the tapping notch. At this stage, the notch no longer produces latex and the affected trees are then noticeable. When the outer bark becomes diseased, cracks begin to appear starting from it and then dead parts flake off.
Previous results prompted a search for pathogenic agents focused on viruses or viroid organisms that could be transmitted by the tapping knife. This line proved unfruitful. Any major influence of soil chemistry characteristics was also excluded. The research team subsequently favoured a hypothesis envisaging a multi-factor physiological cause. Investigations into the influence of the physical constraints of the soil then began. Evidence appeared of a clear correlation between the risks of the emergence of the disease and the strong mechanical resistance of soils which holds up water transport and absorption by the tree roots. This accentuated resistance, which can be the result of low porosity or induration of these soils, appeared here to be more specifically linked to ground compaction by bulldozers. The non-random distribution of diseased trees is consistent with the areas where bulldozer use has been most intense. Physiological observations showed moreover that the rubber trees hit by necrosis have poorer than normal root development. This anomaly, whether a result of poor stock/graft interaction or of genetic predisposition of the stock tree, causes supply of water and mineral salts to the tree to be low. This tendency is accentuated by complications that grafting engenders in the tree’s circulation vessels, particularly in the junction between the different sap-conducting vessels of the graft-carrier and graft. Eco-physiological analyses revealed that the RTBN-affected trees are in a state of water deficit. This is aggravated in times of drought (a climatic factor) or when trees are overexploited for tapping (human factor).
The combination of these different stresses induces necrosis (cell-death) in the collar of the tree, involving the disintegration of cell compartments, and a resulting release of large amounts of cyanide which the rubber tree tissues naturally contain. The effect of this poison, accumulating owing to the impaired metabolism, is to activate the necrosis. Water that rises towards the notch, drawn up by tapping, facilitates the upward diffusion of the cyanide and hence the spread of necrosis towards the upper trunk. The resulting deep disintegration of the trunk phloem and bark tissues explains the irreversible blockage of latex production.
Rubber tree bark necrosis –its appearance and development- therefore results from the accumulation of climatic and human-induced stresses and physiological malfunctions in the grafted trees. This multifactor approach has provided the first overall view of how the disease generates. However, grey areas remain to be explored. A genetic approach is now being applied, with the aim of finding early indicators of the disease that can make field detection as reliable as possible. The results acquired have provided the bases for recommendations on practical measures to take. These are already being applied and are an important new tool in plantation management.
Fabienne Doumenge (Montpellier) - DIC
(1) Institut français du caoutchouc (Paris), Michelin (Clermont-Ferrand), International Rubber Plantation Society (Paris), Socfinco (Brussels), in the context of a research agreement concluded with the IRD n°2454 (1999-2004).
(2) Abobo-Adjamé University (Ivory Coast), Instituto Valenciano de Investigaciones Agrarias (Spain), INRA (Avignon, Bordeaux), Cirad (Montpellier), Poincaré University (Nancy), Mahidol University (Thailand).
(3) Brazil, Cambodia, Cameroon, China, India, Indonesia, Ghana, Liberia, Malaysia, Nigeria, Republic of the Ivory Coast, Thailand.
4) NANDRIS D., CHRESTIN H., GEIGER J.P., NICOLE M. et THOUVENEL J.C., 1984. Occurrence of a phloem necrosis on the trunk of rubber tree. 75th Annual Conference of Rubber Research, Sri Lanka, September 1984, Colombo, in Proceedings p. 59.
Marie Guillaume | alfa