19931 MARAMOROSCH:CADANG-CADANG t87 Principes,37(4), 1993, pp. r87-r96 The Threat of Cadang-CadangDisease Kenr Menerr,roRoscH Department ofEntomology, Cook College, New Jersey Agricuhural Experiment Station, Rutgers-The State Uniuersity, Neu Brunswick, Nl 08903 "milk") ABSTRACT (coconut and the palms provide the only shade and building material. of cadang-cadang disease In 1975 the viroid cause Cadang-cadang disease occurs and of coconut and other palms became established in the Philippines and Guam. The suspected occurrence of spreads currently.on Luzon and a number this disease on other Pacific inlands requires confir- of other Philippine islands, as well as on mation. Replanting with the early maturing Mawa Cuam. The diseasehas been suspected on cultivar, widely advocated in the Philippines, merely a few other Pacific islands recently. provides a temporary but inadequate remedy because this cultivar is susceptible to viroid infection. The HistoricalBackground spread of the disease could be controlled by proper "dying-dying," extension work, requiring the thorough decontami- Cadang-cadang means nation of tools used by plantation workers. Concen- or slowly dying in Bicolano, the language trated sodium carbonate solution can degrade RNA viroids, remaining stable and retaining its RNA- spoken in southeastern Luzon. The first destroying activity under tropical conditions. An well-documented outbreak of the disease extensive testing program for resistance to cadang- was noticed on San Miguel Island off Luzon Such a long-term program will cadang is imperative. in 1928. By 1933 nearly 257o of the require proper funding, commitment, trained person- nel and quarantined importation of coconut cultivars coconut palms had died there and the plan- from all parts of the world. tation owners approached Prof. Gerardo Ocfemia, a U.S. trained plant pathologist Cadang-cadang disease of palms, the and head of the Plant Pathology Depart- most devastating viroid disease known, is ment at the College of Agriculture in Los always fatal. In the Philippines, where the Banos. to helo control the disease. Since disease has killed more than 30 million no fungi or bacteria were found associated coconut palms, currently 1,000,000 palms with dying palms, Ocfemia (1937) con- succumb every year. The Philippines are cluded that the disease was infectious and the world's largest producer of coconuts most likely caused by a virus. Shortly and half of the country"s export income is thereafter the disease reached the main- derived from copra, the dried coconut meat land of Luzon Island. Before the Japanese from which coconut oil is extracted. This invasion in I 94 I , nearly half of the original oil provides the main source of fat in the 250,000 coconut palms on San Miguel had diet of the local population. Elsewhere died and the disease appeared in several coconut oil is used in soaps. margarines. provinces in the Bicol area of Luzon, as synthetic rubber, cosmetics and moistur- well as on some nearby islands. During izing compounds. Coconut palms also pro- World War II no further research was vide lumber, while leaves are used for carried out, but after the war the Philip- thatching, brooms, baskets and hats. The pine Government obtained active help from husk fiber is transformed into mats and the United States, through the Interna- carpets, and ropes are made from the yarn. tional Cooperation Administration (ICA). On many Pacific atolls the only potable By that time cadang-cadang was devas- liquid is provided by the coconut water tating plantations in the provinces of Albay, 188 PRINCIPES lVoL. 37 Sorsogon,Camarines Sur, and Camarines found as causative agents of other plant Norte, as well as on the islands of Samar, diseases(Romaine and Horst 1974; Yan Masbate,and Catanduanes.On SanMiguel Dorst and Peters 1974; Diener 1979, 90% of the palms were dead and the 1987). In 1975, Randles provided evi- remaining onesdied soonafterwards. Else- dence for the association of two RNA spe- where on Luzon the disease incidence cies with cadang-cadang disease. The ranged from IOTI ta 60To. ICA assigned establishment of the viroid etiology was Dr. Donald De Leon, an entomologistwho followed by intensive studies on the epi- had earnedhis Ph.D, at CornellUniversity demiology of the disease and rate of spread in 1933 and specializedin insect trans- as well as on certain measures to control missionof virusesand taxonomy.to study cadang-cadang. Surprisingly, by 1992 the the diseasein the Philippines(De Leon and diseasehas not yet entered the main coco- Bigornia1953). In 1953 the ICA abruptly nut growing areas in Laguna province' Its cancelledthe technicalassistance program spread in some areas appears to be very for cadang-cadangand perman€ntly aban- slow, yet in parts of Camarines Sur, where donedit under the pressureof U'S. soy- the incidence in 1956 was only 37o, some bean and corn oil producers' lobby. The areas are now heavily affected and up to Philippine Government turned for help to 70% of the palms are dying. the United Nations' Food and Agriculture Organization (FAO). During the following Symptomatology four decades,experts were sent by FAO to the Philippinesto study the devastating The cadang-cadang disease cannot be diseaseand to determineits cause,manner diagnosed authoritatively by symptoma- of spread,and possiblemeans of control. tology, but in an endemic area symptoms Indian,U.S., Australian, Cerman, and Ital- can assist in the detection of affected palms. ian experts were assistedby Philippine sci- On young leaves the earliest symptoms entistsfrom the Bureau of Plant Industry. are tiny, circular, translucent spots on the By 1960 the diseasereached Bondoc veins. On mature leaves the number and Peninsulain QuezonProvince, only a short size of the spots increases so as to impart distance from the solid stand of coconut a characteristic chlorotic pattern of the palms of Laguna Province (Maramorosch spots (Fig. l). On the lower surface of I 96 I Lessthan 100 palmsof the original mature coconut leaves appear irregular ). "water-soaked quarter million on San Miguel were still spots." Mature coconut standing and slowly dying. Strip surveys leaves display yellow streaks as a result of indicated that more than a million trees enlargement and fusion of adjacent spots. becameinfected every year (Maramorosch The veins and veinlets become cleared in 1964). a very characteristic, although not very Until i967 plant pathologistsdid not pronounced, way. The basal portion of the know of the existence of autonomously petiole of a healthy tree differs strongly replicating low-molecular-weightRNA from those of a diseased one, because the speciesthat could infect and damageplants. stipules of diseasedtrees remain attached In 1967 Diener and Raymer ( I 967) found to the base of the petiole, giving it a winged that potato spindle tuber diseaseis caused appearance. Nuts are produced only dur- by a free RNA. The following year Diener ing the early stages of the disease, but they (1968) demonstratedthat this RNA is sen- are smaller, rounded at the base or mis- sitive to ribonuclease.In I97l Diener shaped and scarified with brown streaks "viroid'n coinedthe name as a genericterm (Fig. 2). Nut bearing of diseasedtrees can for pathogenicnucleic acids of low molec- stop within 18 months, but occasionally ular weight. Viroids were subsequently the period is extended to 4-5 years. A r9931 MARAMOROSCH:CADANG-CADANG 189 comparison of healthy and diseased inflo- Epidemiology rescences shows an abundance of female florets (buttons) on the healthy and fewer The mode of spread of cadang-cadang on the diseased,that is reduced in size and has not been well elucidated. An aerial retains a characteristic upward position of vector has been suspected, but none ever its branches (Fis. 3). found or incriminated. Viroids that cause The fronds of diseased palms gradually potato spindle tuber, chrysanthemum stunt, assume an erect position in the crown (Fig. hop stunt, citrus exocortis, and other viroid 4), dry up, die, and drop off. This results diseasesare mechanically transmissible and in a gradual reduction in the total number do not require vectors to infect susceptible of fronds until a small, yellowish-green or plants (Diener 1979). Man is the actual yellow tuft is left at the apex of the trunk. vector in those diseases. Experimentally, Finally, the bud dies, falls off, and leaves the cadang-cadang viroids have been the crownless trunk standing. A plantation transmitted to coconut and other palms in this stage looks like a field of telephone mechanically (Randles 1985). There is no poles (Fig. 5). doubt that mechanical transmission could Coconut oalms seldom become diseased be responsiblefor the spread of the disease before flowering. In rare cases the disease under natural conditions. The fact that strikes before flowering sets in. The prog- young palms that have not yet commenced ress of the disease is slow, with a five to bearing nuts are very seldom infected might ten year interval between the appearance support this assumption. On the other hand, of first symptoms and the death of younger pollen transmission or long incubation peri- trees. In older palms this period may extend ods would also fit this observation. How- to l5-lB years. ever, pollen transmission could in no way The proper recognition of typical symp- explain the very rare infection of palms toms of the disease helps in field diagnosis before flowers are formed. Pollen trans- but it requires long practice and experience mission could hardly be responsible for the and cannot prove accurately cadang- very slow, perhaps not more than 500 cadang etiology. In an epidemic area, meters, spread of the disease in certain symptomatology is still adequate for rec- areas, while in others cadang-cadang ognizing the disease. However, the symp- seemed to have been able to jump from toms may differ slightly, depending on the island to island.