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Review of studies on the cadang-cadang disease of coconut.

II. Background of the Studies

After World War II, the government of the United States sent a survey mission to the Philippines in order to find how the country could be helped and how much assistance should be allocated to raise it from the massive destruction of the war. The attention of the mission from the Mutual Security Agency (US MSA) was called to the alarming decimation of coconut in the Bicol Region; hence, the agency recommended an allocation of funds for a more detailed study of the disease. A few plant pathologists were commissioned to assess the situation. (Apparently those who presumed that the disease was pathogenic in nature inadvertently overlooked the fact that the word "disease" connotes a physiological condition).

Having decided that a fungus or bacterium was not involved, the plant pathologists suggested exploring the likelihood of a virus. The suspicion was based in part on the paper of Gerardo O. Ocfemia (1937), who called attention to the mottled leaves, necrosis of the bud, stunting, and failure to produce fruits. These characteristics are common to viral disease, such as abaca mosaic and bunchy top of abaca, with which he had some familiarity.

More plant pathologists came under the sponsorship of the International Cooperation Administration (US ICA, the later name for US MSA). Subsequently, the task was assumed by the Food and Agriculture Organization and the United Nations Development Program (FAO/UNDP).

A list of non-Filipino experts who kindly lent time and effort in the study of the problem is given in Table I.

Many of the experts stayed for one year, studying the problem. A few (such as K. Heinze, H. Petzold, M. K. Corbett, R. Marwitz, F. J. Park, A. O. Reinking, Y. Tokushige, and B. Plavsic-Banjac) visited for about one week in order to become acquainted with the problem and to secure samples. There were people whose commitments were in other fields but who nevertheless, in their desire to help, took time to look into the problem. These were G. C. Kent, K. P. V. Menon, M. V. D. Pieris, C. S. Reddy, H. W. Schapenseel, W. H. Tyner, H. R. von Uexkull, and E. P. Wallihan. On the other hand, W. C. Price and A. N. Nagaraj stayed for a few years; and J. W. Randies made a series of short visits over a period of 11 years, as leader of the group at the Waite Agricultural Research Institute (Waite ARI), Australia.

There was active interest in the problem in the late 1940s to 1970s, but it is apparently waning in the 1990s, judging from the few papers lately published on it. This current review attempts to prevent interest in other subjects from eclipsing interest in cadang-cadang.


III. Symptoms of Cadang-Cadang

The most obvious phenomenon is the successive death of coconut trees until the whole patch is laid bare.

Other than this fact, the scientists and technologists proposed various symptoms centered largely on the leaves, because they are most readily visible. Calica and Bigornia (1960), Calica (1961), and Bigornia (1977) did pioneering studies and arrived at the following group of symptoms.


From a distance, it is noted that the lower two-thirds of the crown of leaves is yellowish bronze, while the upper one-third is dark green. The yellowish bronze color results from the yellowish spots with irregular size and shape. These yellowish spots are characterized by distinct margins; first appearing as tiny, circular, lemon-yellow spots on the third or fourth leaf from the spear leaf; they are olivaceous or water-soaked when viewed by reflected light and bright translucent yellow when viewed by transmitted light; they increase in size and number as the leaf matures, and may coalesce to form larger spots and/or streaks; each spot has no necrotic center.

The leaves from diseased palms are smaller; they dry up much faster than do those from healthy palms. There is a gradual decrease in the rate of frond production resulting in the reduction of the size of the crown, ultimately forming a tuft of few leaves, after which death follows.


Stipules are persistently attached to the frond and accumulate at the base of the crown.


Coconut palms that become diseased before flowering bear leaves that are spread somewhat farther apart than on healthy trees of the same age. Thus the leaf scars are more widely spaced. The reverse is true on trees affected after fruiting. On these, the scars are closer together than those lower down the trunk, or those on healthy trees. The trunk is sometimes tapered, but in the majority of cases tapering is not evident.


There is a gradual reduction in the frequency of infloreseence produced and the number of flowers. On mildly diseased palm, the nuts are numerous and big. However, the nuts on severely diseased palms are round and smaller in size, but the meat appears normal in thickness and texture. Nuts are often scarified and the stigmatic point is constricted.


Finally, Calica (1961) cautioned, no one of these symptoms, taken singly, is sufficiently unique to be of diagnostic value in identifying the disease. On the contrary, each one of these symptoms, whenever applicable, should be considered as an essential part of the syndrome characteristic of cadang-cadang-affected coconut trees.


In many studies, almost exclusive emphasis is given to the water-soaked spots because the spots are reminiscent of the mottling in some virus diseases such as the corn mosaic. And besides, the symptoms (other than those on leaves) such as profuse stipules below the crown of leaves and the leaf-scars do not appear before the trunk has become visible.

Disappointingly, the water-soaked spots are not unique to coconuts affected by cadang-cadang. Earlier, Velasco and Fertig (1956) observed water-soaked spots in their coconut seedlings not affected by cadang-cadang. It seemed that the spots were a result of deficiency in some building block or photosynthate.

Moreover, there is no general agreement on the characteristic of the water-soaked spot; thus Nagaraj (1967) enumerated many kinds of water-soaked spots, even among plants outside the cadang-cadang area, which differ from each other only in their measurement. He considered only spots measuring 0.13-0.5 mm in diameter as specific to cadang-cadang. This distinction may not be valid, however, because he observed that spots can coalesce and form bigger spots and streaks.

IV. Proposed Theories on the Cause of Cadang-Cadang

Some of the major theories on the probable cause of cadang-cadang were (1) virus, (2) soil or nutritional imbalance, (3) physical stress such as typhoons, (4) microorganisms such as fungi, bacteria, and nematodes, (5) phytotoximia due to secretions of aphids or Marasmius sp., and (6) mycoplasma-like organisms.

Other, minor theories were also proposed from time to time. In his report of 1937, Ocfemia mentioned that farmers suspected the following causes: (1) presence of hard pan close to the surface of the soil, (2) poor drainage, (3) unadaptable site for coconut, (4) poor soil, (5) root parasite, and (6) individual vitality of trees.

Price (1958) added insect injury and root rot as two other causes. Moreover, Maramoroseh (1961) mentioned the belief of farmers that typhoon, eruption of Mayon Volcano, and introduction of cattle herd to coconut groves as contributing factors in the spread of cadang-cadang.

Only the virus/viroid theories and the theory on nutritional imbalance will be taken up here. The virus/viroid theories have grown dominant over the other theories because extensive effort was exerted to explore and prove them. On the other hand, some interesting findings have, of late, been reported regarding nutritional imbalance.

V. Field Surveys

Most field surveys seemed to proceed from the initial claim that the disease started in 1926 in San Miguel Island, Tabaco, Albay. Perhaps this ignored the claim of farmers that coconut palms suffered massive dying-off in 1914 in Nabua, Camarines Sur, and in 1919 in Calolbon, Catanduanes (Calinisan, 1948; De Leon, 1951; De Leon & Bigornia, 1953). The course of spread was traced by Celino (1947), as follows: "The cadang-cadang disease was first observed in 1928 just outside the Estate of the Agusan Coconut Company (now Gancayno Estate) on San Miguel Island, Tobacco, Albay. It spread gradually following a pattern of known virus diseases... to the provinces of Albay, Sorsogon, Camarines Sur, Camarines Notre, Catanduanes, Masbate, and Samar. The disease was also observed in some municipalities of Quezon."

Bigornia (1977) estimated that the zone of spread was 600 km long and 270 km wide, with San Miguel Island near the center.

Zelasny (1979) made another geographical survey, especially in the border areas of cadang-cadang occurrence such as Quezon, Camarines Norte, Western Samar, Eastern Samar, and Leyte.

In addition to these surveys regarding area of spread, other surveys were concerned with increasing severity. For example, Reinking (1950) estimated that in the Estate of the Agusan Company, only 116,000 sick trees remained standing in 1947, out of 260,000 trees planted in 1924. He further reported that the extensive survey in May and June of 1950 showed that the disease was most serious in Sorsogon and Albay, ranging from 50% to 100%. The disease was less severe in Camarines Sur and Camarines Norte. A similar estimate of De Leon (1952) was 19% in Albay, 11% in Sorsogon, and 5% in Camarines Sur. De Leon and Bigornia (1953) reported a massive increase - from 1.3 million trees in 1951 it rose to 3.2 million trees in 1952. In their epidemiological plots and strip surveys, Calica and Bigornia (1953) reported that there was an estimated increase of 15% infestation in just eight months (November 1951 to July 1952), but only 3% in the following 12 months.

Among the different age groups, disease was more severe among trees 25 years and older than among trees less than 25 years old (Sill et al., 1964).

In apparent refutation of Holmes's (1961) suggestion that weeds serve as a reservoir of the virus, Price and Bigornia (1972) argued that failure to find a correlation between disease incidence and weed control strongly suggests that the disease spreads from coconut to coconut.

The foregoing estimates of percentage increase in infestation did not specify the stage of decline. By way of improvement, Price (1958), Nagaraj (1967), and Zelasny and Niven (1967) categorized the diseased condition into early, medium, and late stages. However, each of these stages was not characterized so as to differentiate one from another. Perhaps the categories were simply personal estimates of density of water-soaked spots and reduction in the size of the crown. The danger here is that the expectation of the researcher, or the hypothesis he tries to confirm, might influence his estimate.

In an apparent attempt to confirm the pathogenic nature of the disease, each newly discovered area of infestation was considered to be a new case of infestation, and hence an indication of spreading. This ignores the alternative possibility that the newly discovered area had been infested all along, even before it was discovered, and was thus a case of the disease being widespread. This latter point was stressed by Zelasny et al. (1982). The following extended quotation gives an insight into their reasoning:

The hypothesis that the disease [cadang-cadang] originated on San Miguel Island (Tobacco, Albay) around 1930 and then spread quickly to other parts of the Bicol has been advanced frequently during the last 20 years. However, old records and recent studies on the distribution of the disease contradict this theory.

When the records collected by Bigornia et al. (1960) and Fajardo (1953) were compared with the present distribution of cadang-cadang, it became clear that the area containing the disease has not increased significantly during the last 20 to 30 years.

These observations suggest that cadang-cadang is endemic to Bicol and adjacent areas. As the area containing the disease has not increased significantly since the 1950s, it seems unlikely that the disease has spread from San Miguel to areas several hundred kilometers away between 1930 to 1950. The sequence of cadang-cadang reports from San Miguel (1931), Bicol provinces (1948 to 1950), Masbate, Northern Samar and the southern tip of Samar (1953) and Quezon province (1958 to 1960) gave the impression of a rapid spread of the disease, but obviously the most serious outbreaks (as in San Miguel) were noticed first and small isolated groups of infested palms (as in Quezon province) were found last.

VI. Attempts to Transmit the Virus

Since 1937 when the virus theory was proposed, plant pathologists had been running transmission experiments to prove that the disease was infective. Those who spent time and effort in this attempt were Celino, Bigornia, Calica, de Leon, Fajardo, Price, McWhorter, del Rosario, Holmes, Protacio, Sill, Nagaraj, and Nitzany.

Celino (1947) first reported some success in transmitting the disease with needle pricks. He reported his procedure as follows: "On June 1, 1946, the infected pinna was held firmly against the base of the unfurled healthy leaf of a 3- to 4-year-old seedling and pricked in succession. On August 12 or after an incubation period of 77 days, one of the inoculated seedlings showed symptoms of cadang-cadang." He placed the incubation period at 30 to 130 days.

Another claim of successful mechanical transmission came from del Rosario and Quiaoit (1962). The inoculum was needle-pricked into the stem or petiole, or rubbed into the leaf in the presence of 300 mesh Carborundum. Forty days after inoculation, 16 out of 88 coconut seedlings developed minute yellow dots, which later became water-soaked.

To verify these claims, Sill (1964) repeated the procedures. At the end of his study, he reported that "the expert is of the opinion based upon these negative results and other observations, that it is premature to state that cadang-cadang is a virus disease."

In reviewing the research efforts on coconut cadang-cadang, Bigornia (1977) said:

Research workers at Guinobatan Experiment Station [among whom are Bigornia, Calica, Protacio, Pizarro, Rillo, Pableo, Retuerma and Price together with other FAO consultants] conducted separately or in collaboration with each other, numerous inoculation experiments using similar or identical techniques and methods used by Celino and del Rosario. In a number of tests, other techniques and refinements were used. Mechanical transmission experiments carried out were: pin-pricking with and without various buffers; rubbing of abrasives with buffers; purified sap inoculation; three types of injection methods using hypodermic syringe, gravity injection and hypospray injection. In all these experiments involving several thousand coconut seedlings and trees, as well as other palm species and weeds, no conclusive and positive transmission was obtained by the workers, One plant in the hypospray experiments of Price et al. developed true cadang-cadang symptoms, but the validity of the cause of infection is still doubtful.

Transmission with various insect vectors were also tried. The latter line of experiments was rather extensive involving no less than 100 insect species on 5,000 coconut test plants. The experiments are still in progress with no symptoms thus far produced among test plants.

VII. The Viroid Hypothesis

The following notes were excerpted from Coconut Research and Development: Research on the Cadang-Cadang Disease of the Coconut Palm (AG:DP/PHI/523). This is a report prepared for the Government of the Philippines by the Food and Agriculture Organization (1982) of the United Nations, acting as executing agency for the United Nations Development Programme. The report was based on the work of W. C. Price, J. W. Randles, B. Zelasny, G. Boccardo, and N. A. Mohamed, conducted from 1971 to 1982.

Details are being quoted so that the reader can appreciate the extensive work done, the involved biochemical procedures, and the sophistication of modern science.


Randles et al. (1977) reported as follows: "Inoculation was by high pressure injection (Panjet injection technique) combined with either rubbing with Carborundum or slashing of petioles with a razor. The appearance of leafspotting symptoms on the young fronds of the RNA-positive inoculated palms between 19 to 22 months after inoculation suggests that the agent may have been transmitted as a result of transferring the RNA (ccRNA-1 and ccRNA-2) by the inoculation procedure."


(1) Age of inoculated seedlings: "Younger seedlings are more susceptive than older ones." (2) Preconditioning: "As earlier results had shown that darkening increased the susceptibility of seedlings, all test plants are now routinely kept in the dark for 72 to 96 hours before inoculation." (3) Source of inoculum: "Inoculum should be taken from palms at the early stage of disease, containing the fast ccRNA variant." (4) Amount of inoculum: "Usually 10 seedlings are inoculated with RNA-extracts from 1 kilogram of diseased leaves."


Batches of 250 g fresh, chopped leaves are blended in 750 ml of 0.1 ml SDS for 1 to 2 minutes at 4 [degrees] C. After clarification at 10,000 g for 10 minutes at 4 [degrees] C, extracts were pooled and macromolecules were precipitated by the addition of polyethylene glycol (PEG) 6000 to 5% (w/v), stirring and leaving at 4 [degrees] C for 2 hours. The pellet, collected by centrifugation at 10,000 g for 10 minutes, was resuspended in 50 ml of [1% SDS, 25 ml phenol and 25 ml chloroform]. After blending for 2 minutes at high speed the suspension was stirred for 1 hour and then the emulsion was broken by centrifugation at 8,000 g for 10 minutes. The aqueous phase was re-extracted twice with chloroform/phenol. After the last centrifugation, three volumes of ethanol were added to the aqueous phase and the solution was left overnight at -20 [degrees] C.

The ethanol-insoluble precipitate was collected by centrifugation at 10,000 g for 10 minutes; the pellet was dried and re-extracted with SDS-phenol-chloroform. After another ethanol precipitation, drying and resuspension in 0.1 M sodium acetate, ccRNA was precipitated with CTAB to remove further impurities (mainly carbohydrates) washed and resuspended in 0.1 M sodium acetate. LiCl was added to 2M to remove single stranded RNAs and the final pellet was obtained by ethanol precipitation. This pellet was either resuspended in sterile SSC [sodium chloride-sodium citrate] buffer for inoculation, or in 0.01 M sodium acetate + 5% sucrose for electrophoresis.


The technique involves the initial separation of the major species by electrophoresis, under non-denaturing conditions, in 5% polyacrylamide gels. The ccRNA bands are cut out and the strips of gel can either be frozen or layered immediately on to a 5% denaturing gel containing 8M urea. This effectively separates the linear and circular forms and also removes traces of any other nucleic acids. The required bands are then cut out and layered on to 3.3% acrylamide non-denaturing gel in a Bio-Rad preparative elution apparatus. The purified RNA is electrophoresed through the gel and eluted from the bottom, the elutant being constantly monitored by a spectrophotometer. The RNA peak is collected, precipitated with ethanol and the purified RNA is collected as a pellet.

Based on the kinetics of digestion with nutleases and by thermal denaturation studies, it was decided that RNA-1 molecule has both double- and single-stranded regions. Other biochemical procedures led to the conclusion that ccRNA-1 has a looped or (hairpin) secondary structure, stabilized by base-pairing. Its buoyant density (1.62 g/[cm.sup.3]) falls between the expected values for single-stranded and double-stranded RNA.

Under the electron microscope ccRNA-1 and ccRNA-2 are found to be circular single-stranded molecule comprising 310 [+ or -] 3 nucleotides and 438 [+ or -] 5 nucleotides; their molecular weights were estimated to be 1.05 and 1.49 x [10.sup.5] daltons).


However, despite the impressive studies, Bigornia (1977) was of the opinion that "until in-effectivity of the RNAs is conclusively demonstrated through experimental transmission, the characterization of the ccRNA-1 and ccRNA-2 and their more or less constant association with diseased condition can only be regarded as indirect supporting evidence for the viroid hypothesis of cadang-cadang."

It may be relevant to recall at this point that the water-soaked spots (which Randles and colleagues use as criterion for successful transmission) are not unique to cadang-cadang. Hence, this criterion may not be reliable indication of infection. Perhaps it would be necessary to grow the seedlings (which were positively inoculated with ccRNA) into bearing trees to find if, besides the water-soaked spots, they would produce the other symptoms in the cadang-cadang syndrome.

The use of coconut seedlings in the transmission experiments may be given some allowance on the claim that this facilitates the turnover of laboratory space. But Sill et al. (1964) observed that cadang-cadang is more often associated with older trees.

VIII. Nutritional Imbalance as a Cause

One curious comment against nutritional imbalance as a possible cause follows: "Nevertheless and in spite of all the evidence to the contrary, a few people fanatically adhere to this hypothesis, although their own field trials and those of others completely failed to substantiate their claims."


However, there were a few compelling reasons which made "a few people fanatically" search the soil for the cause of cadang-cadang. They include geographical limits, differences in rates of dying-off, different effects of fertilizers, and transplant recovery by locality.

1. Geographic Limits

There seems to be some natural barrier that stops cadang-cadang from proceeding northward beyond Tulay-na-Lupa, Labo, Camarines Norte, despite the heavy infestations in the adjacent fields of Daet and Mercedes towns. Another barrier seems to prevent the disease from invading the town of Imelda, Camarines Norte, from the neighboring diseased towns of Vinzons and Paracale.

2. Rate of Dying-Off Differs per Locality

The rate of attrition varies from one locality to another. In this regard, Sill (1964) quoted the report of Hans Rothkirch to his company as follows: "When I first saw this area [Paracale and Jose Panganiban] in 1946, about 1% to 2% of the trees were infested; in 1960 infestation had increased to approximately 3%, and today [1964] it is still about the same. What is surprising is the fact that only about 15 kilometers from this area - around Vinzons and Tali-say - large areas of coconuts have been practically wiped out by cadang-cadang during the past 10 to 12 years."

3. Rate of Dying-Off Differs by Age

The age of trees when they succumb to cadang-cadang varies from place to place. Trees in certain groves, such as those in Baao, Camarines Sur, are productive and grow to about 20 m tall before they succumb to the disease; while in some places such as those in Ligao, Albay, trees start to die off at 2-3 m tall, or before they attain bearing age. Incidentally, Sill et al. (1963) observed that cadang-cadang is largely a disease of old trees.

4. Effects of Fertilizers

Some fertilizers may ameliorate and others may aggravate the disease. In one experiment, Velasco et al. (1965) found that ammonium nitrate, applied for three years, aggravated production of water-soaked spots, bronzing of leaves, and death of trees. On the other hand, ammonium phosphate, applied at sites adjacent to the ammonium-nitrate plots, arrested deterioration from the disease and made the palms very productive. This was taken to mean that the nitrate form of the putative soil constituent was soluble whereas the phosphate was not - that is, assuming that an exchange reaction occurred between the applied fertilizer and the soil fraction that contains the constituent.

5. Recovery of Transplants According to Locality

Transplants vary in growth and production according to the health status of their new site. In 1969, Velasco et al. (1983) transplanted two comparable sets of 3-year-old coconut plants of various disease rating: one set to a known diseased area and the other set to an area which was estimated to be not diseased. The pairs contrasted markedly in growth and nut production. In 20 years the trees in the former site out-yielded those in the latter; but two trees had died in the former and none in the latter.


The search for the putative soil constituent that is related to cadang-cadang was handicapped by the lack of a criterion and procedure. The workers could not decide whether to search for a deficient essential element in plant nutrition, a highly toxic element present in minute amount, or a mildly toxic element with which the plant could exist for a long time without sustaining detrimental effects. Like the "imaginary invalid" they seized upon each "unusual" soil constituent, suspecting that it had all the qualities of the culprit. The question that they had to wrestle with was, How many negative results of analysis would impel them to drop the suspect as irrelevant? They felt uneasy, lost in a sea of uncertainty (Velasco, 1980).

Then they happened to play around with tannin, as indicator for a broad spectrum or elements. Their curiosity was piqued when they got a soil extract that formed a precipitate with tannin. This darkened upon exposure to light. It was soluble in feebly acid tartrate solution and insoluble in ammoniacal tartrate solution. These characteristics suggested the presence of either manganese or cerium. Manganese occurs widely, even in nondiseased area, so the attention became focused on cerium and, with it, the broad group of rare earths. The group does not occur often and widely; hence it might be associated with an unusual disease, such as cadang-cadang. However, when the soil samples from the diseased area were analyzed for the rare earths, equivocal results were obtained. It was only when the workers learned to remove the iron in the extract that they saw consistent differences in rare-earths contents between the diseased and the non-affected samples (Velasco et al. 1977).


Hand-in-hand with the attempts to analyze the soil, there were efforts to utilize some plants in pinpointing some detrimental soil constituent and, conversely, in finding the effects on cultured plants of some soil isolates.

1. Search for Indicator Plants

A survey was made of some abnormal plants growing in diseased and non-affected regions in the hope of finding a species whose abnormality was closely associated with the manifestation of cadang-cadang on coconut. (Abnormality was reckoned in terms of chlorosis and/or crinkling of leaves, die-back, stunting, and generally thin and non-succulent condition). There were several species that were abnormal in the diseased area (Bicol Region) and healthy in the non-affected areas (Laguna and Quezon). However, they grew normally when cultured in potted soil from Bicol and watered with Hoagland's solution. Apparently the abnormality was due in part to lack of some essential nutrient in the original soil, which was supplied by Hoagland's solution. Hence, the worker did not settle for an indicator plant from among those found abnormal.

To determine which fraction of the soil could be held suspect in the cadang-cadang problem, extracts from affected and non-affected soil samples were fractionated into groups according to a scheme of separation in qualitative analysis: i.e., insoluble chlorides (Group I, silver-mercury), insoluble acid sulfides (Group II, copper-arsenic), insoluble alkaline sulfides (Group III, iron-aluminum), and the residue from these treatments (Group IV, alkaline earths, and Group V, alkalies). The diluted fractions were added to Hoagland's culture solution and used in maintaining okra (Abelmoschus esculentus) in sand culture. Unhappily, the results did not give a distinct indication as regards the fraction which could be suspected of being associated with cadang-cadang.

2. Effects of Rare Earths on Some Annual Species

When the rare earths were found in soil analysis as a suspected culprit in the cadang-cadang problem, the workers decided to find out if the group would elicit some unique effect on some annual species. The search for a short-lived indicator plant was deemed important because the coconut, being a perennial, was expected to take years before giving a definitive reaction.

Lanthanum and cerium were taken to represent the rare earths. Observations were made on the effects of their dilute solution (5, 10, 20 ppm) on the germination and early growth of tomato, sweet pepper, and mungbeans. (Chromium was incidentally added in the study because it was found in appreciable levels in the soil of some diseased coconut groves. This was to find if its effect would interfere and/or would get confused with those of the rare earths).

Alejar et al. (1988) found marked stimulating effects of the elements on the growth of shoot and root of the test plants; but there was no unique effect that would single out a species as promising indicator of a particular element among those studied.

3. Effects of Rare Earths on Coconut

Although hoping to find a short-lived species as indicator plant, the workers were confirmed in the thought that the ultimate criterion of relevance to cadang-cadang of any treatment should be shown on the coconut itself. Hence, treatment of the coconut with lanthanum, cerium, and chromium was started in 1985, hand with the study of their effect on annual species. Preliminary results on the coconuts showed that some of the symptoms of cadang-cadang as observed in the field were duplicated by the treatments (Velasco et al., 1993). To wit, with lanthanum the leaflets tended to be brittle; there was profuse and persistent stipules; the trunk grew fast in the early stage of treatment and rather slowly in the late stage and close together in the late stage. The crown of leaves became decidedly parted at the latest period of observation.

With cerium, most of the above-mentioned symptoms produced with lanthanum were noted, except the stimulation of growth of the trunk and the farther spacing of the leaf scars.

The brittle leaflets were readily observed in the palm treated with chromium.

IX. Acknowledgment

The writer gratefully acknowledges the assistance from the Instituto Cervantes de Manila in improving the Resumen.

X. Literature Cited

Alejar, A. A., R. M. Macandog, J. R. Velasco & Z. N. Sierra. 1988. Effects of lanthanum, cerium and chromium on germination and growth of some vegetable species. Philipp. Agric. 71 (2): 198-197.

Bigornia, A. E. 1977. The virus and viroid theories on cadang-cadang. Philipp. J. Coconut Stud. 2: 7-12.

Calica, C. A. 1960. Symptomatology of coconut cadang-cadang. Proceedings of the Coconut Seminar,

17-18 March 1960, Guinobatan Experiment Station, Guinobatan, Albay.

-----. 1961. Cadang-cadang of coconut in the Philippines: current studies in aetiology. Meeting of FAO Technical Working Party on Coconut Production, Protection, and Processing, 27 November-2 December 1961, Trivandrium, India. FAO Regional Office, Bangkok.

----- & A. E. Bigornia. 1960. Symptomatology of the yellow mottle decline (cadang-cadang) of coconuts. DANR. Bur. Pl. Industr., Manila.

Calinisan, M. R. 1948. Methods employed by the coconut farmers in the Bicol region to control cadang-cadang diseases. Philipp. PI. Industr. J. 1948: 3-5.

Celino, M. R 1947. Progress report on experimental transmission of cadang-cadang disease of coconut. Philipp. J. Agric. 13: 109-113.

De Leon, D. 1951. Report on studies of a disease (yellow mottle or infections kadang-kadang) on the coconut tree in the Philippines. Mimeograph. [Cited in Price, 1958.]

-----. 1952. Kadang-kadang disease of coconuts in the Philippines. Foreign Agric. Washington, D.C. 16(5): 103.

----- & A. E. Bigornia. 1953. Coconut kadang-kadang disease in the Philippines and experimental control program. U.S. Operation Program in Philippines.

Del Rosario, M. A. & A. R. Quiaoit. 1962. Studies on the virus aspect of cadang-cadang of coconut: 1. Transmission and serology. Phil. Agric. 45(9): 477-480.

Fajardo, T. G. 1953. Study on coconut diseases; 1. Report on certain observation and experiments on the study of cadang-cadang and other maladies of coconuts in the Philippines. Proc. 8th Pacific Sci. Congr. 6-B: 215-226.

Food and Agriculture Organization. 1982. Cadang-cadang research 1971-1982. FAO Report No. 523. FAO/UNDP Coconut Research and Development Project, Rome.

Holmes, F. O. 1961. Correlation of cadang-cadang disease in coconut with certain diseases in weeds. FAO PI. Protect. Bull. 9(8): 148-152.

Maramorosch, K. 1961. Report to the government of the Philippines on the cadang-cadang disease of coconut. FAO Rep. No. 1333. FAO, Rome.

Nagaraj, A. N. 1967. Report to the government of the Philippines on cadang-cadang disease of coconut. UNDP Rep. No. RA 2376. FAO, Rome.

Ocfemia, G. O. 1937. The probable nature of cadang-cadang disease of coconuts. Philipp. Agric. 26(4): 338-340.

Price, W. C. 1958. Report to the government of the Philippines on the yellow mottle decline (cadang-cadang) of coconut. FAO Rep. No. 850. Expanded Technical Assistance Program, FAO, Rome.

----- & A. E. Bigornia. 1972. Evidence for the spread of cadang-cadang disease of coconut form tree to tree. FAO PI. Protect. Bull. 20(6): 133-135.

Randles, J. W., G. Boccardo, M. A. Retuerma & E. P. Rillo. 1977. Transmission of the RNA species associated with cadang-cadang of coconut palm and insensitivity of the disease to antibiotics. Phytopathology 67: 1211.

Reinking, O. A. 1950. Preliminary report on the cadang-cadang disease and on soil deficiency trouble of coconut in the Philippines. PI. Disease Rep. 34(10): 300-304.

Sill, W. H., Jr., A. E. Bigornia & R. P. Pacumbaba. 1964. Incidence of cadang-cadang disease of coconut trees of different ages and its relationship to practical control. Philipp. J. P1. Industr. 29(3-4): 87-100.

-----. 1964. Report to the government of the Philippines on cadang-cadang disease of coconut. FAO Report No. 1861. FAO, Rome.

Velasco, J. R. 1980. In quest of certainty: odyssey into the cadang-cadang problem. Trans. Natl. Acad. Sci. Techn. (Philipp.) 2: 78-96.

----- & S. N. Fertig. 1956. Progress report; sand culture experiment with coconut. Philipp. Agric. 39(9): 540-548.

-----, E. Pantastico, C. S. Canoy, C. L. Barile & D. B. Guevarra. 1965. Fertilization of coconuts in the Bicol Region. Philipp. Agric. 49: 573-588.

-----, L. E. Domingo, Z. N. Sierra & F. F. Coronado. 1977. Rare earths in coconut groves affected by the cadang-cadang disease. Philipp. J. Coconut Stud. 2(2): 1-16.

-----, C. S. Canoy & Z. N. Sierra. 1983. Comparative performance of coconuts transplanted to cadang-cadang affected and non-affected areas. Philipp. Agric. 66(4): 417-438.

-----, R. S. Atienza & Z. N. Sierra. 1993. The effects of the rare earths and chromium on the growth of coconut. Philipp. Agric. 76(1): 49-71.

----- & A. A. Alejar. 1996. Relations between the rare earths and cadang-cadang. In press.

Zelasny, B. 1979. Report on ecological studies on the cadang-cadang disease on coconut palm. Coconut Research and Development Project. FAO Rep. No. 523. [Also published in Acta Phytopath. Acad. Sci. (Hungary) 14: 115-126.]

----- & B. S. Niven. 1980. Duration of stages of cadang-cadang disease of coconut palm. Pl. Disease 64:841-842.

-----, J. W. Randles, G. Boccardo & J. S. Imperial. 1982. The viroid nature of the cadang-cadang disease of coconut. Sci. Filipinas 2: 45-63.
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Author:Velasco, Jose R.
Publication:The Botanical Review
Date:Apr 1, 1997
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