Candidatus Phytoplasma palmae (lethal yellowing of coconut)
- Taxonomic Tree
- Notes on Taxonomy and Nomenclature
- Distribution Table
- Risk of Introduction
- Hosts/Species Affected
- Host Plants and Other Plants Affected
- Growth Stages
- List of Symptoms/Signs
- Biology and Ecology
- Seedborne Aspects
- Vectors and Intermediate Hosts
- Detection and Inspection
- Similarities to Other Species/Conditions
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Candidatus Phytoplasma palmae
Preferred Common Name
- lethal yellowing of coconut
Other Scientific Names
- Candidatus Phytoplasma palmae-related strains
- coconut lethal yellowing mycoplasma-like organism
- coconut lethal yellowing phytoplasma
- palm lethal yellowing phytoplasma
International Common Names
- English: coconut lethal yellowing; lethal yellowing; palm lethal yellowing
- Spanish: amarillamiento letal del cocotero; amarillez letal (Mexico); pudricion del cogollo (Cuba)
- French: pourriture du bourgeon terminal du cocotier
- PHYP56 (Coconut lethal yellowing phytoplasma)
Taxonomic TreeTop of page
- Domain: Bacteria
- Phylum: Firmicutes
- Class: Mollicutes
- Order: Acholeplasmatales
- Family: Acholeplasmataceae
- Genus: Candidatus Phytoplasma
- Species: Candidatus Phytoplasma palmae
Notes on Taxonomy and NomenclatureTop of page
According to phylogenetic analyses of 16S rRNA gene sequences, phytoplasmas (formerly known as mycoplasma-like organisms, MLOs) constitute a monophyletic clade of prokaryotes within the class Mollicutes most closely related to the genus Acholeplasma (Gundersen et al., 1994; Sears and Kirkpatrick, 1994; Seemüller et al., 1994, 1998). Within the phytoplasma clade, numerous groups (subclades) were also differentiated by these analyses. A phylogenetically based taxonomy of the phytoplasmas has been proposed (ICSB Subcommittee on the Taxonomy of Mollicutes, 1993) in which subclades are considered to represent distinct species (ICSB Subcommittee on the Taxonomy of Mollicutes, 1997). Names under the provisional taxonomic status ‘Candidatus’ (Murray and Schleifer, 1994) are being assigned to a reference strain within each primary group (Zreik et al., 1995; Davis et al., 1997; White et al., 1998; IRPCM Phytoplasma/Spiroplasma Working Team Phytoplasma Taxonomy Group, 2004; Harrison et al., 2011). The palm lethal yellowing (LY) phytoplasma (Florida strain) and coconut lethal decline (LDY) phytoplasma, a distinct, albeit closely related strain from the Yucatan peninsula, Mexico (Harrison and Oropeza, 1997) represented one (subclade VII) of 11 subclades of phytoplasmas originally resolved by Gundersen et al. (1994). Phytoplasmas associated with lethal yellowing-like diseases of coconut in eastern Africa (lethal disease, Tanzania) and western Africa (Awka disease, Nigeria; Cape St. Paul wilt, Ghana) were differentiated from the LY and CLD phytoplasmas. They were assigned to new subclades XII and XIV, respectively, in more recent phylogenetic classifications (Liefting et al., 1996; Tymon et al., 1998).
In a related classification scheme based upon similarity coefficients derived from RFLP analysis of PCR-amplified 16SrDNA sequences, phytoplasmas were delineated into 14 major groups (termed 16Sr groups) and 40 subgroups (Lee et al., 1993, 1998a, b). A total of 45 strain subgroups were resolved when RFLP data derived from less-conserved ribosomal protein genes were also considered in these analyses. Differentiation and classification of phytoplasmas has been augmented by computer-simulated RFLP analysis (Zhao et al., 2009) of 800 phytoplasma 16S rDNA sequences. Based on distinctive virtual RFLP patterns and calculated similarity coefficients, the phytoplasma strains were most recently classified into a total of 28 groups (Wei et al., 2007). Within the RFLP classification system, the LY phytoplasma has been assigned to RFLP group 16SrIV (coconut lethal yellows group), subgroup A (16SrIV-A). Within group 16SrIV, five other related phytoplasmas have since been assigned as subgroup members, namely, LDY phytoplasma (16SrIV-B) and Tanzanian coconut lethal disease (LDT) phytoplasma (16SrIV-C) (Lee et al., 1998), Texas Phoenix palm decline (TPPD) phytoplasma (16SrIV-D) (Harrison et al., 2002b), coconut lethal yellowing (LYDR-B5) phytoplasma (16SrIV-E) (Martinez et al., 2008) and Washingtonia decline (FP) phytoplasma (16SrIV-F) (Harrison et al., 2008).
DescriptionTop of page
Phytoplasmas are cell wall-less prokaryotes, too small in size to be resolved adequately by light microscopy methods. By transmission electron microscopy of ultrathin sections, phytoplasmas appear to consist of rounded to filamentous bodies bounded by a trilaminar unit membrane. These bodies contain granules the size of ribosomes and strands of DNA that apparently condense during specimen preparation (Thomas, 1979; Thomas and Norris, 1980). In phloem sieve tube elements of coconut palms, cells of the LY phytoplasma are generally 142-295 nm in diameter and may vary from 1 to 16 µm in length (Waters and Hunt, 1980).
DistributionTop of page
The disease is presently most active in the Caribbean; specifically, on the islands of Saint Kitts and Nevis (IPPC, 2012; Myrie et al., 2012); and has also been reported in Antigua (ProMED-mail, 2012). Areas currently affected in Saint Kitts include the northern and eastern portions of the island; the disease has been present on Nevis since 2005 (IPPC, 2012).
See also CABI/EPPO (1998, No. 264).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Benin||Present||CABI/EPPO and, 1998a|
|Cameroon||Present||CABI/EPPO and, 1998a|
|Ghana||Present||1937||CABI/EPPO and, 1998a|
|Kenya||Present||CABI/EPPO and, 1998a|
|Mozambique||Present||CABI/EPPO and, 1998a; EPPO, 2014|
|Nigeria||Present||1917||CABI/EPPO and, 1998a|
|Tanzania||Present||CABI/EPPO and, 1998a|
|Togo||Present||1937||CABI/EPPO and, 1998a|
|Mexico||Restricted distribution||1978||CABI/EPPO and, 1998a; McCoy et al., 1982; EPPO, 2014|
|USA||Restricted distribution||1937||CABI/EPPO and, 1998a; EPPO, 2014|
|-Florida||Present||CABI/EPPO and, 1998a; Thomas, 1979; EPPO, 2014|
|-Texas||Absent, unreliable record||CABI/EPPO and, 1998a; McCoy et al., 1980; EPPO, 2014|
Central America and Caribbean
|Antigua and Barbuda||Present||EPPO, 2014; IPPC, 2014; Myrie et al., 2014|
|Bahamas||Absent, formerly present||1946||CABI/EPPO and, 1998a; Howard and, 1983; EPPO, 2014|
|Belize||Restricted distribution||1994||CABI/EPPO and, 1998a; Escamilla et al., 1993; EPPO, 2014|
|Cayman Islands||Present||1834||CABI/EPPO and, 1998a; Howard and, 1983; EPPO, 2014|
|Cuba||Present||192*||CABI/EPPO and, 1998a; Howard and, 1983; EPPO, 2014|
|Dominican Republic||Present||1915||CABI/EPPO and, 1998a; Howard and, 1983; EPPO, 2014|
|Haiti||Widespread||CABI/EPPO and, 1998a; Howard and, 1983; EPPO, 2014|
|Honduras||Restricted distribution||1994||CABI/EPPO and, 1998a; Ashburner et al., 1996; EPPO, 2014|
|Jamaica||Present||1955||CABI/EPPO and, 1998a; Plavsic-Banjac et al., 1972; EPPO, 2014|
|Netherlands Antilles||Present||EPPO, 2014|
|Saint Kitts and Nevis||Restricted distribution||IPPC, 2012; EPPO, 2014|
|Guyana||Absent, invalid record||EPPO, 2014|
|Netherlands||Absent, confirmed by survey||NPPO of the Netherlands, 2013; EPPO, 2014|
|Australia||Absent, confirmed by survey||EPPO, 2014|
Risk of IntroductionTop of page
Lethal yellowing and related diseases pose a significant threat to global coconut production (Harries, 1978b). To discourage inadvertant spread of LY in the tropics, commercial movement of living palms and palm seeds from affected to unaffected areas is generally not permitted. However, quarantine requirements vary according to the specific geographic localities involved. Technical guidelines for the safe movement of coconut germplasm from LY-affected areas for research, but not for commercial purposes, have been developed under the auspices of the International Board for Plant Genetic Resources (IBPGR) (Frison et al., 1993).
Hosts/Species AffectedTop of page
Plant host range for LY phytoplasma (16SrIV-A) includes: Aiphanes lindeniana (Ruffle palm), Allagoptera arenaria (Kutze seashore palm), Caryota mitis (Burmese or clustering fishtail palm), C. rumphiana (Giant fishtail palm), Chelyocarpus chuco (Round leaf palm), Copernicia alba (Caranday palm), Corypha taliera (Buri palm), Crysophila warsecewiczii (Rootspine palm), Cyphophoenix nucele (Lifou palm), Dypsis cabadae (Cabada palm), D. decaryi (Triangle palm), Gaussia attenuata (Puerto Rican Gaussia palm), Howea belmoreana (Belmore Sentry palm), H. forsteriana (Kentia or Sentry palm), Hyophorbe verschaffeltii (Spindle palm), Latania lontaroides (Latan palm), Livistona chinensis (Chinese fan palm), L. rotundifolia (Footstool palm), Nannorrhops ritchieana (Mazari palm), Phoenix canariensis (Canary Island date palm), P. dactylifera (Date palm), P. reclinata (Senegal date palm), P. rupicola (Cliff date palm), P. sylvestris (Silver date palm), Pritchardia maideniana (Kona palm), P. pacifica (Fiji Island fan palm), P. remota (Remota loulu palm), P. thurstonii (Thurston palm), Ravenea hildebrantii (Hildebrants palm), Syagrus schizophylla (Arikury palm), Veitchia arecina (Montgomerys palm) and V. merrillii (McCoy et al., 1983; Eden-Green, 1997; Harrison and Jones, 2004; Harrison and Oropeza, 2008).
The LY phytoplasma (16SrIV-A subgroup) has also been experimentally transmitted to the following palm species: C. nucifera, P. canariensis, P. pacifica, P. thurstonii, T. fortunei and V. merrillii. Replicated transmissions to these palm species were achieved using the vector planthopper Haplaxius (syn. Myndus) crudus field-collected from palms in areas of high disease incidence in Florida, USA (Howard and Thomas, 1980; Howard et al., 1983, 1984).
Current knowledge of symptomless palm hosts include Thrinax radiata (Florida thatch palm) and Coccothrinax readii (Mexican silver palm) (Narvaez et al., 2006).
Although restricted primarily to the Arecaceae, the host range of the LY phytoplasma (16SrIV-A) also includes at least one non-palm host, namely the arborescent monocot Pandanus utilis (screwpine) (Thomas and Donselman, 1979; Harrison and Oropeza, 1997).
The host range of other coconut lethal yellows group (16rIV), subgroup phytoplasmas are as follows:
16SrIV-B subgroup - Acrocomia aculeata (coyol palm), C. nucifera (Roca et al., 2006);
16SrIV-C subgroup - C. nucifera (Lee et al., 1998);
16SrIV-D subgroup - Caryota urens (jiggery palm), P. canariensis (Canary Island date palm), P. dactylifera (date palm), P. reclinata (Senegal date palm), P. roebelenii (pygmy data palm), P. sylvestris (silver date palm), Pseudophoenix sargentii (buccaneer palm), Roystonea sp., Sabal mexicana (Mexican palmetto), Sabal palmetto (sabal or cabbage palm), Syagrus romanzoffiana (queen palm), S. romanzoffiana x Butia capitata (mule palm), Washingtonia robusta (Mexican fan palm) (Harrison et al., 2008, 2009; Rodriguez et al., 2010; Vázquez-Euán et al., 2011);
The host range of 16SrIV-D subgroup phytoplasmas includes the non-palm host Carludovica palmata (Panama hat or jipi palm) (Wei et al., 2007);
16SrIV-E subgroup - C. nucifera (Martinez et al., 2008);
The host range of subgroup 16SrIV-E phytoplasmas includes the non-palm hosts Cleome rutidosperma (fringed spiderflower), Cyanthillium cinereum (little ironweed cited as Vernonia cinerea), Macroptilium lathyroides (wild bushbean), Stachytarpheta jamaicensis (light-blue snakeweed) (Brown et al., 2008; Brown and McLaughlin, 2011).
16SrIV-F subgroup - Washingtonia robusta (Mexican fan palm), P. dactylifera (date palm) (Harrison et al., 2008).
Host Plants and Other Plants AffectedTop of page
|Aiphanes lindeniana (ruffle palm)||Arecaceae||Other|
|Allagoptera arenaria (Kutze seashore palm)||Arecaceae||Other|
|Borassus flabellifer (toddy palm)||Arecaceae||Other|
|Chelyocarpus chuco (round leaf palm)||Arecaceae||Other|
|Cocos nucifera (coconut)||Arecaceae||Main|
|Corypha taliera (Buri palm)||Arecaceae||Other|
|Corypha utan (gebang palm)||Arecaceae||Other|
|Crysophila warsecewiczii (Rootspine palm)||Arecaceae||Other|
|Cyphophoenix nucele (Lifou palm)||Arecaceae||Other|
|Dypsis cabadae (Cabada palm)||Arecaceae||Other|
|Gaussia attenuata (Puerto Rican Gaussia palm)||Arecaceae||Other|
|Howea forsteriana (paradise palm)||Arecaceae||Other|
|Hyophorbe verschaffeltii (spindle palm)||Arecaceae||Other|
|Livistona chinensis (Chinese fan palm)||Arecaceae||Other|
|Phoenix canariensis (Canary Island date palm)||Arecaceae||Other|
|Phoenix dactylifera (date-palm)||Arecaceae||Other|
|Phoenix reclinata (senegal date palm)||Arecaceae||Other|
|Phoenix sylvestris (east Indian wine palm)||Arecaceae||Other|
|Pritchardia maideniana (Kona palm)||Arecaceae||Other|
|Pritchardia remota (Remota loula palm)||Arecaceae||Other|
|Pritchardia thurstonii (Thurston palm)||Arecaceae||Other|
|Ravenea hildebrandtii (Hildebrants palm)||Arecaceae||Other|
|Roystonea regia (cuban royal palm)||Arecaceae||Other|
|Trachycarpus fortunei (chinese windmill palm)||Arecaceae||Other|
|Veitchia merrillii (christmas palm)||Arecaceae||Other|
|Wodyetia bifurcata (foxtail palm)||Arecaceae||Other|
Growth StagesTop of page Flowering stage, Fruiting stage, Vegetative growing stage
SymptomsTop of page
Palm lethal yellowing disease involves a prolonged latent (incubation), 'symptomless', phase. The time from primary infection to appearance of overt visible symptoms on young, non-bearing coconut palms has been estimated as between 112 and 262 days (Dabek, 1975). About 80 days prior to symptom appearance, growth of infected palms is stimulated. This is followed by a period of gradual decline and then complete growth inhibition about 1 month before the end of the incubation phase.
The early stages of LY on coconut palms are accompanied by numerous biochemical and physiological abnormalities in roots that include marked fluctuations in respiration, total sugars and reducing sugars (Oropeza et al., 1995; Islas-Flores et al., 1999; Martínez et al., 2000; Maust et al., 2003). Decreased respiration and increased root necrosis occur prior to the appearance of any visible symptoms in above-ground portions of palms (Eden-Green, 1976, 1982). The onset of symptoms also coincides with alterations in phloem flux rates (Eden-Green and Waters, 1982) and changes in water relations (McDonough and Zimmerman, 1979; Eskafi et al., 1986) due to irreversible suppression of leaf stomatal conductance (Oropeza et al., 1991; León et al., 1996). Reduction of photosynthetic capacity is marked by decreases in photosynthetic pigments, growth regulators and activity of enzymes of the carbon reduction cycle (Dabek and Hunt, 1976; León et al., 1996).
Visible symptoms on the highly susceptible Atlantic tall (also known as Jamaica tall) coconut ecotype chronologically include premature shedding of all fruit (nutfall) regardless of their developmental stage. Aborted nuts often develop a brown-black calyx-end rot reducing seed viability. Premature nutfall is accompanied or followed by inflorescence necrosis. This next symptom is most readily observed as newly mature inflorescences emerge from the ensheathing spathe. Normally light yellow to creamy white in colour, affected inflorescences are instead partially blackened (necrotic) usually at the tips of flower spikelets. As disease progresses, additional emergent or unemerged inflorescences show more extensive necrosis and may be totally discoloured. Such symptom intensification results in the death of most male flowers and an associated lack of fruit set.
Yellowing of the leaves usually starts once necrosis has developed on two or more inflorescences (Arellano and Oropeza, 1995) and discoloration is more rapid than that associated with normal leaf senescence. Beginning with the older (lowermost) leaves, yellowing progresses upward to involve the entire crown. Yellowed leaves turn brown, desiccate and die. In some cases, the advent of this symptom is seen as a single yellow leaf (flag leaf) in the mid-crown. Affected leaves often hang down forming a skirt around the trunk for several days before falling. A putrid basal soft rot of the newly emerged spear (youngest leaf) occurs once foliar yellowing is advanced. Spear leaf collapse and rot of the apical meristem invariably precedes death of the palm at which point the crown topples away leaving a bare trunk. Infected palms usually die within 3 to 6 months after the appearance of the first symptoms (McCoy et al., 1983).
LY symptomatology may be complicated by other factors. For example, non-bearing palms lack fruit and flower symptoms. Foliar discoloration also varies markedly among coconut ecotypes and hybrids. For most tall-type coconut palms, leaves turn a golden yellow before dying whereas on dwarf ecotypes leaves generally turn reddish to greyish brown.
Nutfall and inflorescence-necrosis are early stage symptoms common to all other palm species affected by LY disease. Differences may occur in the stage at which spear leaf necrosis appears. For edible date palm (Phoenix dactylifera), death of the spear leaf usually precedes foliar discoloration whereas for Adonidia and Veitchia species, the spear is usually unaffected until after all other leaves have died. Two patterns of leaf discoloration have been described. Leaves yellow before dying in species such as fishtail palms (Caryota sp.), round leaf palm (Chelyocarpus chuco), gebang palm (C. elata), fan palms (Livistona and Pritchardia sp.), princess palm (Dictyosperma album) and windmill palm (Trachycarpus fortunei). In most other susceptible species, leaves turn brown rather than yellow. Irrespective of species, however, foliar discoloration generally advances from the oldest to youngest leaves in the crown (McCoy et al., 1983).
List of Symptoms/SignsTop of page
|Fruit / premature drop|
|Growing point / rot|
|Inflorescence / blight; necrosis|
|Leaves / yellowed or dead|
|Roots / rot of wood|
|Seeds / rot|
|Whole plant / plant dead; dieback|
Biology and EcologyTop of page
Phytoplasmas are transmitted in a persistent (circulative-propagative) manner primarily by insect vectors belonging to the families Cicadelloidea (leafhoppers) and Fulgoroidea (planthoppers) (D'Arcy and Nault, 1982). The cixiid Haplaxius (syn. Myndus) crudus is a primary vector of palm LY in Florida (Howard et al., 1983, 1984; Eziashi and Omamor, 2010). Distribution of this planthopper species also coincides with the known geographic range of the disease (Howard, 1983) including the Caribbean region and North, Central and South Americas. Although this association strongly supports a role for H. crudus as a vector of LY elsewhere in the Caribbean region, successful transmissions of LY disease using this species in geographic locations outside of Florida have yet to be demonstrated (Eden-Green, 1995).
Two types of spread characterize primary outbreaks of palm LY disease. One involves the emergence of symptoms on one or two palms initially, followed by further local spread in a desultory pattern around this active focus of disease eventually claiming most susceptible palms within the locality. From this primary focus, a second type of spread occurs as a series of jumps of a few to 100 km or more, thus establishing new disease foci from which the local pattern of spread is repeated (McCoy, 1976). According to estimates of local palm-to-palm spread in Dade county, Florida (McCoy et al., 1983), each infected coconut palm served to inoculate 4.6 new palms during an 8-month period following the establishment of primary disease foci. Within 2 years, when the logarithmic stage of spread was well underway, each infected palm served as a reservoir of inoculum for infection of 9.3 new palms. At localized sites in south-eastern Florida, the apparent rates of spread of LY were generally lower among palms situated adjacent to the coastline compared with palms at inland sites under high cultural maintenance. Differences in rates of disease spread at different geographical locations have also been noted.
Seedborne AspectsTop of page
There have been several studies using PCR that have indicated the presence of phytoplasma DNA in embryos of some seed from diseased coconut palms (Harrison et al., 1996; Harrison and Oropeza, 1997; Cordova et al., 2003). A recent study by Oropeza et al. (2011) showed that LY phytoplasma DNA was isolated from embryos of fruits at different stages of development; although the presence of phytoplasma DNA in coconut embryo tissues suggests a potential for seed transmission there is no prior evidence to support seed transmission of LY (Romney, 1983).
Vectors and Intermediate HostsTop of page
ImpactTop of page
The Atlantic tall, the most prevalent coconut ecotype throughout the Caribbean region and Atlantic coast of the Americas (Harries, 1978a), is highly susceptible to LY disease. During the past three decades, at least 50% of Florida's estimated one million coconut palms and over 80% of Jamaica's five million coconut palms have been eliminated by LY (McCoy et al., 1983). Similar epidemic losses of coconut to LY continued along the Atlantic coasts of southern Mexico and Honduras (Oropeza and Zizumbo, 1997). Although rarely affecting palms less than 5 years old, the disease prevents any re-establishment of highly susceptible coconut ecotypes in LY-endemic locations such as Florida and Jamaica.
DiagnosisTop of page
Phytoplasmas are obligate parasites and cannot be cultured on standard microbial growth media, so identification methods have primarily relied upon visual symptom identification, transmission electron and fluorescent microscopy, and most recently, molecular detection using specific probes for DNA dot hybridization and phytoplasma 'generic' and 'specific' PCR primers followed by restriction fragment analysis or sequencing of the PCR products.
Transmission Electron and Fluorescent Microscopy
In the past, confirmation of field diagnoses had traditionally been based on locating the phytoplasma in palm tissues using transmission electron microscopy (TEM) (Beakbane et al., 1972; Plavsic-Banjac et al., 1972; Thomas and Norris, 1980). Phytoplasmas that are found in the phloem of coconut palms have been described as non-filamentous and filamentous, the previous averaging 295 nm in diameter and the latter averaging 142 nm in diameter and with a length of approximately 16 µm (Waters and Hunt, 1980). The pathogen is found most reliably in young phloem-rich leaf bases surrounding the apical meristem (heart tissues) of symptomatic palms (Thomas 1979; Thomas and Norris, 1980) and to a lesser extent in partially necrotic inflorescences and tertiary roots (Waters and Hunt, 1980). In most mature tissues, phytoplasma concentrations are generally below levels detectable by this diagnostic method.
Phytoplasma infections are characterized by an associated accumulation of DNA within the phloem which can be demonstrated by treatment of either fresh or chemically preserved plant tissues (Seemüller, 1976; Sinclair et al., 1992) with the DNA-binding fluorochrome DAPI (4',6'-diamidino-2-phenylindole, 2HCl). Phytoplasma cells appear as patches of blue-white fluorescence in phloem sieve tube elements of plants such as palms when tissues are examined under UV light by epifluorescence microscopy whereas sieve tubes of healthy palms are devoid of fluorescence and are usually invisible (Cardeña et al., 1991). Although this technique can be used for large scale diagnosis (Andrade and Arismendi, 2013) issues arise due to relatively high levels of false negatives in palms. False negatives are those samples that the phytoplasma titre is extremely low and/or the phytoplasma has accumulated in an uneven pattern throughout the plant.
Both TEM and DAPI detection systems only allow for the 'presence or absence' of phytoplasma within the plant sample, neither can determine the specific strain of phytoplasma that is causing the disease (Harrison et al., 1999).
Molecular detection of the palm lethal yellowing phytoplasma by DNA probe hybridization or PCR assays has largely replaced non-specific microscopic techniques as the preferred methods for disease diagnosis.
Used as probes in DNA dot hybridization assays, DNA fragments of the LY phytoplasma cloned from LY-diseased Manila palm or windmill palm (Harrison et al., 1992; Harrison et al., 1994a; Harrison and Oropeza, 2008) have been used to detect the lethal yellowing phytoplasma and permit detection and identification of the LY phytoplasma, and closely related strains, in extracts derived from palm heart tissues (Harrison et al., 1994b, c; Harrison and Oropeza, 1997; Tymon et al., 1997). However, these probes have also shown to vary in detection sensitivity and specificity (Harrison et al., 2008).
Southern blot hybridization has been used to analyse phytoplasma DNA restriction profiles and can provide a measure of genetic variability among closely related phytoplasma strains (Harrison et al., 1992, 2008).
Polymerase chain reaction (PCR) employing phytoplasma 'universal' primer pairs constructed from 16S ribosomal RNA (rRNA) gene sequences (Lee et al., 1993; Martinez-Soriano et al., 1994; Gundersen and Lee, 1996) has significantly improved phytoplasma detection. These assays readily amplify rDNA of most, or all, phytoplasmas. Digestion of the PCR products with selected restriction enzymes, a process known as restriction fragment length polymorphism (RFLP), provides a DNA fingerprint in the form of 16S rDNA fragment patterns that can be used to determine phytoplasma identity when resolved on agarose or by polyacrylamide gel electrophoresis (PAGE). These primers, however, have also identified non-phytoplasma target sequences. The latter PCR products are similar in size to PCR products from phytoplasmas, so the phytoplasma identity is not known (Harrison et al., 1999). Profiles resolved by PAGE after separate digestion of products with AluI, HinfI, TaqI or Tru9I endonucleases are especially useful for identification of group 16SrIV phytoplasmas (Harrison et al., 1999). They are also useful for distinguishing this pathogen from phytoplasmas associated with African coconut lethal decline diseases (Harrison et al., 1994a) and other recently recognized members of the LY phytoplasma group (Harrison and Oropeza, 1997; Cordova et al., 2000).
Group or subgroup-specific detection of phytoplasmas by utilizing primers for PCR based upon variable regions of the 16S rRNA gene or the 16-23S intergenic spacer region (SR) sequences of the phytoplasma genome permit selective amplification of rRNA gene sequences of 'Ca. Phytoplasma palmae' and related strains in a group-specific manner. Primers 503f and LY16Sr derived from the 16S rRNA gene of the LY phytoplasma selectively amplify a 928 bp rDNA product from the LY phytoplasma strains infecting coconut and Pandanus and from the YLD (Yucatan coconut lethal decline) and CPY (Carludovica palmata yellows) phytoplasmas (Harrison et al., 1999; Cordova et al., 2000). Strains can be further differentiated by AluI digestion of the resulting amplification products.
LY16Sf and LY16Sr also selectively amplify 16SrRNA gene sequences of the LY agent from mixtures with host palm DNA (Harrison and Oropeza, 2008). When used to reamplify products obtained by PCR employing universal primer pair P1 and P7, primer set LY16Sf/LY16Sr amplifies rDNA from the LY phytoplasma and related strains in a group (16SrIV)-specific manner (Harrison et al., 2002a). Polymorphisms revealed by HinfI endonuclease digestion of the rDNA products differentiated coconut-infecting phytoplasmas in Jamaica from those detected in Florida, Honduras and Mexico (Harrison et al., 2002a).
Exclusive detection of 16SrIV-A subgroup strains is possible by a PCR assay employing non-ribosomal primer pair LYF1/LYR1 permitting unequivocal identification of 'Ca. Phytoplasma palmae' (i.e. subgroup 16SrIV-A) in palms, Pandanus utilis, and the vector Haplaxius crudus (Harrison et al., 1994; Llauger et al., 2002).
Analysis of less conserved secA gene sequences has also been used to distinguish groups and subgroups of phytoplasmas (Hodgetts et al., 2008).
PCR allows for sensitive detection of the LY phytoplasma in inflorescence, spear leaf and trunk tissues and has made possible practical non-destructive sampling of palms for LY diagnosis.
Detection and InspectionTop of page
Because of a protracted incubation phase in palms (Dabek, 1975), visual examination for LY symptoms is insufficient to conclusively determine the disease status of palms. To date, no biological or serological tests for detection of the LY phytoplasma have been successfully developed. PCR is the most sensitive test currently available for phytoplasma detection although this diagnostic method is complicated by the unusually low pathogen titres in palm tissues. When symptomless, pre-bearing coconut palms were evaluated for natural infection by LY, monthly assessment of spear leaf samples by LY-specific PCR in a year-long study revealed phytoplasma titres reached detectable levels in these palms between 47 and 57 days prior to the appearance of visible foliar symptoms (Harrison et al., 1994c).
Similarities to Other Species/ConditionsTop of page
No single symptom is diagnostic of palm LY disease. Abiotic factors, such as nutritional disorders, may induce premature nutfall (boron deficiency) and foliar discoloration (potassium deficiency). Ganoderma butt rot (Ganoderma zonatum) shows progressive symptoms closely in-line with those of lethal yellowing, such as basal stem rot leading to canopy wilting, die off of lower leaves, and die off of the spear leaf (Broschat et al., 2010). In their advanced stages, coconut lethal declines due to Phytophthora bud rot (Joseph and Radha, 1975; Bennett et al., 1986; Uchida et al., 1992), red ring (Griffith, 1987) and hartrot (Parthasarathy et al., 1978; McCoy and Martinez-Lopez, 1982) all share a number of symptoms in common with LY disease. The geographic ranges of these diseases overlap in some areas of the western Caribbean region and may confuse field diagnoses. The appearance and chronological progression of symptoms (syndrome development) provide accurate identification of LY.
Elsewhere, phytoplasma-associated diseases of coconut resembling LY have been recognized in Nigeria (Awka wilt) (Ekpo and Ojomo, 1990), Ghana (Cape St. Paul wilt), Togo (kaïncopé disease) (Dabek et al., 1976), Cameroon (kribi disease) (Dollet et al., 1977), Tanzania and Kenya (Nienhaus et al., 1982). A previous lack of methods to directly compare the associated aetiological agents led to erroneous speculation about the origins and relatedness of these diseases (Howard, 1983; Maramorosch, 1996). Recent molecular comparisons, with the causative phytoplasmas of these diseases, have since clarified relationships, revealing the LY phytoplasma to be phylogenetically distinct from the African coconut phytoplasmas. Similarly, group 16SrXXII phytoplasma strains affecting coconut in West Africa (Wei et al., 2007) are also distinct from strains associated with coconut lethal disease in Tanzania and Kenya (Tymon et al., 1998; IRPCM Phytoplasma/Spiroplasma Working Team Phytoplasma Taxonomy Group, 2004) but very similar or identical to phytoplasmas affecting coconut in Mozambique (Mpunami et al., 1999; Bonnot et al., 2010).
Still other phylogenetically distinct phytoplasmas have been associated with coconut diseases elsewhere that include Kalimantan wilt in Indonesia (Warokka et al., 2006), coconut yellow decline in Malaysia (Nejat et al., 2009a, b, 2012), coconut (root) wilt (Manimekalai et al., 2010) and yellow leaf disease of Areca catechu (Ramaswamy et al., 2012) in India,Weligma coconut leaf wilt in Sri Lanka (Perera et al., 2012) and Bogia coconut syndrome in Papua New Guinea (Kelly et al., 2011).
Prevention and ControlTop of page
For coconut, the use of genetically resistant ecotypes and hybrids offers the only practical long-term solution to LY given our present understanding of the disease. Both the Malayan dwarf and the Maypan (Malayan dwarf x Panama tall) hybrid were thought to be resistant to LY and were used extensively for replanting in Jamaica and other countries affected by the disease. However, high mortality in both cultivars planted in LY-infected regions in recent years shows that these cultivars cannot be considered resistant to LY as previously thought (Broschat et al., 2002; Lebrun et al., 2008). Other hybrids have also succumbed to lethal yellowing disease in other countries, such as Ghana, where there was extensive plantings of the hybrid Malayan Yellow Dwarf x Vanatu Tall (MYD x VTT) which were used to replace palms that had succumbed to Cape Saint Paul Wilt of coconuts (Danyo and Dery, 2011; Danyo, 2011). Promising levels of resistance have been identified in other ecotypes such as Chowghat green dwarf, Cuban dwarf, Fiji dwarf, Red spicata dwarf, Sri Lanka yellow dwarf and King, but this resistance remains to be commercially exploited (Harries, 1995; Ashburner and Been, 1997).
In contrast to coconut, useful varietal resistance to LY in the commercially important edible date palm (Phoenix dactylifera) has not been demonstrated (Howard, 1992). With the exception of species of Pritchardia (Howard and Barrant, 1989), the relative susceptibility to LY of all remaining host palms, while varying among species, is generally lower than that of coconut palm (McCoy et al., 1983; Meerow, 1992). Numerous popular ornamental palm species are apparent non-hosts of LY and are recommended for landscape and amenity plantings in affected areas (Chase and Broschat, 1991; Meerow, 1992).
Eradication of infected palms does not lead to any measurable reduction in the spread of LY in highly susceptible coconut ecotype populations in newly affected areas. A reduction in the rate of spread of disease has been demonstrated by insecticide suppression of vector Haplaxius crudus populations (Howard and McCoy, 1980). Identified as poor breeding hosts of H. crudus, tropical forage grasses such as Brachiara brizantha, Chloris gayana or Hemarthria altissima used as groundcovers underlying palms provide an additional promising means of controlling vector abundance (Howard, 1989, 1990). Oxytetracycline-HCl (OTC), a systemic antibiotic treatment that is injected into the palm trunk on a quarterly basis, can be effective but they are not economical in large-scale nursery settings or coconut-producing regions (McCoy et al., 1976). However, in landscape and amenity plantings, this control measure can be utilized to control early stage symptoms of infection and can be used as a preventative treatment in healthy palms (Hunt et al., 1974; McCoy et al., 1982).
ReferencesTop of page
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