Lethal Yellowing of Palms
R. E. McCoy, editor
Agriculture Mi_ m
Institute of Food and Agricultural Sciences
University of Florida, Gainesville
F A. Wood, Dean for Research
R. E. McCoy, F. W. Howard, J. H. Tsai,
H. M. Donselman, D. L. Thomas, H. G. Basham,
R. A. Atilano, F. M. Eskafi, Lizbeth Britt,
and Mary E. Collins
R. E. McCoy; F. W. Howard, J. H. Tsai, H. M. Donselman, D. L.
Thomas, H. G. Basham, R. A. Atilano, and F. M. Eskafi
University of Florida, Institute of Food and Agricultural Sciences,
Agricultural Research and Education Center, 3205 S. W. College
Ave., Fort Lauderdale, FL 33314
Lizbeth Britt, Tree Specialist, Dade County Department of Environ-
mental Resource Management, 909 S. E. 1st Ave., Miami, FL
Mary E. Collins, Horticulturist, The Fairchild Tropical Garden,
10901 Old Cutler Road, Miami, FL 33156.
TABLE OF CONTENTS
Chapter 1-Lethal Yellowing of Palms: Introduction, List
of Susceptible Species, and Symptomatology 1
Chapter 2-The Search for a Causal Agent:
Mycoplasmalike Organisms and their
Association with Lethal Yellowing. 23
Chapter 3-Distribution and Epidemiology of Lethal
Yellowing Disease 32
Chapter 4-Physiological Aspects of Lethal Yellowing:
Water Relations, Protein Assays,
and Free Arginine Levels 49
Chapter 5-Transmission of Lethal Yellowing:
Historical Studies 56
Chapter 6-Biology of Myndus crudus and Evidence
Implicating It as a Vector of Lethal Yellowing 65
Chapter 7-Control of Lethal Yellowing:
Resistance and Chemotherapy 73
Literature Cited 92
Trade names of chemicals, where used, are for the purpose of providing
specific information. No endorsement of products is implied, nor any criti-
cism of products not named.
Cover Photo: Lethal yellowing diseased coconut palms, Miami, Florida,
Courtesy of D. L. Thomas.
We wish to thank James V. DeFilippis for photographs of insects, Ronelle
C. Norris for micrographs of palm tissue, and Beverly E. Benner for graphics.
We also thank Jose Amador and William F. Theobold for photographs, Donna
S. Williams for editorial assistance, and Betti J. Patterson and Janie Greene
for manuscript preparation.
LETHAL YELLOWING OF PALMS:
INTRODUCTION, LIST OF SUSCEPTIBLE
SPECIES, AND SYMPTOMATOLOGY
Lethal yellowing (LY) is a pandemic disease of coconut palm' which
has a high potential to become an international threat to palm trees.
Since 1955 LY has destroyed hundreds of thousands of coconut and\
other palms in southern Florida. The disease has been present in
certain islands of the Greater Antilles for at least 100 years and in
West Africa for at least 50 years, destroying coconut production
wherever it has occurred. LY affects coconut palm, at least 30 addi-
tional species of palms, and possibly common screwpine, Pandanus
utilis Bory, a palm-like member of the family Pandanaceae. Some
authors (e.g., 71, 110, 158) refer to LY-type diseases of palms other
than coconut as "lethal declines." LY-type diseases that affect differ-
ent palm species and Pandanus in different localities are very sim-
ilar, and in this bulletin these diseases are collectively referred to
Palms are an important part of the Florida landscape (Fig. 1). They
provide the tropical atmosphere which distinguishes south Florida
from other areas of the United States. The Florida nursery industry
is one of the world's leading producers of ornamental palms for land-
scape and interior plantings (Fig. 2).
The coconut palm is a leading crop throughout the humid tropics. A
great variety of commercial products are derived from the copra
(meat), oil, fiber, and wood of the coconut. Large portions of the \
populations of many countries are dependent on coconut production
as a livelihood and consider the coconut fruit a staple food item. In
general, smallholders, rather than large agribusinesses, are the prin-
cipal producers of coconuts (133). In addition to being a source of cash
income for such people, coconut palms furnish many products for local
use, such as cooking oil, coconut meat, fiber, and coconut water, all of
which have an importance in everyday life that is difficult for resi-
dents of countries outside of the tropics to fully appreciate. There
1. Hortus Third (4) was followed for common names of palms used in text.
Scientific names are given in Tables 1 and 2. Scientific names are used in text
for species for which common names are not provided in Hortus Third.
.-. ... W
Fig. 1. Coconut palms, Fort Lauderdale beach. These are of the 'Jamaica
Tall' cultivar, which is widely planted in Florida and the Caribbean region
and is highly susceptible to lethal yellowing.
Fig. 2. Field grown Manila palms in a Florida nursery. Florida ranks
second in the United States in wholesale nursery production.
are certain tropical islands where human life is made possible only by
the presence of coconut palms (125, 133). It was recently estimated
that two-thirds of the world's coconut palms are of varieties that are
susceptible to LY (62).
As the coconut palm is a basic part of life in much of the humid
tropics, the date palm, which is also susceptible to LY, is an essential
plant in the arid tropics. The date palm has been interwoven with the
culture of the Middle East for at least 5,000 years (21, 47, 133). It is
the only palm species grown as a commercial food crop in the United
States, and LY now threatens this industry (113, 114).
In response to the urgent need for research on LY indicated by the
disease outbreak in Miami in 1971, the University of Florida Agri-
cultural Research and Education Center in Fort Lauderdale initiated
a program of investigation into the etiology, epidemiology, and con-
trol of LY. This bulletin synthesizes current knowledge of LY, re-
ports research progress at Fort Lauderdale, and discusses the poten-
tial for developing improved methods of managing the disease.
Palms Resistant or Susceptible
to Lethal Yellowing
The term lethal yellowing (LY) was first used to denote a specific
disease of coconut palms in Jamaica (124), and was subsequently
applied to diseases of identical symptomatology in coconut palms in
other countries (see Chapter 2). Most of the research effort on LY in
Florida and elsewhere has been concentrated on coconut palms, since,
prior to the last decade, there was very little indication that other
species were susceptible. This is partly due to the importance of the
coconut palm as a commercial crop in tropical countries, to its pre-
dominance as a landscape tree in southern Florida, and also, to the
scarcity of exotic ornamental palms in the LY-affected coconut grow-
ing areas in the Caribbean, West Africa, and the Florida Keys. About
20 exotic and 5 native species of palms are commonly planted for
landscaping purposes in south Florida. Many additional palm species
are represented in two large living collections at the USDA Sub-
tropical Horticulture Research Unit (Chapman Field) and Fairchild
Tropical Garden, both in the Miami area, and in private collections.
The first evidence of an apparent extension of LY to species other
than coconut palm in Florida was the rapid decline and death of
palms of three other species widely planted in the LY-affected area of
Coral Gables-Manila palm (Fig. 3), Fiji fan palm, and Thurston
palm (Fig. 4) (130). Parthasarathy (129) observed m~scolasmalike
organisms (MLO) in phloem elements in tissue samples from Fiji fan
palm and Manila palm. By 1974, MLO had been observed in tissue
Fig. 3. Lethal yellowing diseased Manila, or Christmas palm, left, healthy,
right. The Manila palm is one of the most popular ornamental palm species
and is highly susceptible to lethal yellowing.
samples of eight additional palm species present in the LY-affected
area and apparently affected by the same disease (157). By 1983, at
least 30 species could be associated with the presence of MLO (158,
159) (Table 1).
An effort has been made to keep the list of susceptible species
current in order to implement quarantine regulations. Reports of
field diagnoses of LY symptoms in species new to the list have been
followed by electron microscopic examination of phloem tissue sam-
ples from the diseased palms. LY was detected in three species in
1973, and in eleven additional species in 1974. Since that year, the
number of additional species per year has declined. LY had been
detected in the more common and/or highly susceptible species dur-
ing the first three years of the epidemic. Since then, less susceptible
or rarer species have been reported.
Several of the palms listed in Table 1, while susceptible to LY, are
actually highly resistant and are recommended for replanting. These
include Cabada palm, Chinese fan palm, and Senegal date palm.
Palm species that have escaped LY are tentatively classified as im-
mune. A list of these palms is presented in Table 2.
Susceptibility of Palm Species in Fairchild Tropical Garden
Fairchild Tropical Garden (FTG) has one of the largest palm col-
lections in the world. LY has been present in FTG since 1973. Records
on plants in FTG were examined, and a list of genera and species was
compiled. Only palms that were growing outdoors in the display area
and that were at least two years of age [the presumed minimum
susceptible age (13)] were included in the study. These included 4,005
palms belonging to 113 genera and 386 species. The palm collection
included the 30 species known to be susceptible to LY. Of these,
palms of 18 species died of LY between 1973 and 1981.
Fig. 4. Lethal yellowing diseased Thurston palm, left, and healthy palm,
Table 1. Palm taxa susceptible to LY1, popularity in landscaping in southeastern Florida, and relative susceptibility rating.
Popularity Relative LY
as a susceptibility
Scientific Common landscape in
name name plant2 southeast Florida3
A inhnnp linrdniana R +
(H. Wendl.) H. Wendl.
(Gomes) O. Kuntze
Arenga engleri Becc.
(Mart.) L. H. Bailey
Borassus flabellifer L.
Caryota mitis Lour.
H. E. Moore
Cocos nucifera L.,
Corypha elata Roxb.
(Bory) H. Wendl. &
Drude ex Scheffer
(0. F. Cook) Becc.
Cluster fish-tail palm
Puerto Rican gaussia palm
Table 1. Continued.
Popularity Relative LY
as a susceptibility
Scientific Common landscape in
name name plant2 southeast Florida3
(C. Moore & F. J. Muell.)
(Jacq.) R. Br. ex Mart.
(W. Griffith) J. E. T. Aitch.
Neodypsis decaryi Jumelle
Hort. ex Chabaud.
P. dactylifera L.
P. reclinata Jacq.
P. sylvestris (L.) Roxb.
Pritchardia affinis Becc.
Belmore sentry palm
Spindle palm '
Chinese fan palm
Canary Island date palm
Senegal date palm
Wild date palm
Table 1. Continued.
Popularity Relative LY
as a susceptibility
Scientific Common landscape in
name name plant2 southeast Florida3
P. pacifica Seem. & Fiji fan palm C ***
P. remote Becc. -R +
P. thurstonii F. J. Muell. & Thurston palm C ***
Pritchardia spp. ***
Ravenea hildebrandtii -R +
H. Wendl. ex Bouche
Trachycarpus fortunei Windmill palm M **
(Hook.) H. Wendl.
Veitchia merrillii Manila palm, Christmas C **
(Becc.) H. E. Moore palm
Veitchia, other species4 R *
1. Includes only species for which an association with MLO has been demonstrated by electron microscopy.
2. C = Common; R = Rare; M = Moderate distribution.
3. Ratings based on combined field estimates by H. M. Donselman, F. W. Howard, and R. E. McCoy.
*** highly susceptible, ** moderately susceptible, slightly susceptible, + susceptible, but too rare outdoors in southeast Florida to estimate
4. Other species: V. montgomeryana H. E. Moore, V. arecina (Becc.), and V. species = Sunshine palm.
Table 2. Common and scientific names of ornamental and economically
important palm species that are not known to be susceptible to LY.
African oil palm
Areca palm, cane palm
Cuban royal palm
European fan palm
Florida royal palm
Hispaniolan royal palm
Puerto Rican hat palm
Pygmy date palm
Elaeis guineensis Jacq.
Chrysalidocarpus lutescens H. Wendl.
Sabal palmetto (Walt.) Lodd. ex Schult. &
Roystonea regia (HBK) O. F. Cook
Chamaerops humilis L.
Roystonea elata (Bartr.) F. Harper
Roystonea hispaniolana L. H. Bailey
Butia capitata (Mart.) Becc.
Thrinax morrisii H. Wendl.
Ptychosperma macarthurii (H. Wendl.) Nichols
Acoelorrhaphe wrightii (Griseb. & H. Wendl.)
H. Wendl. ex Becc.
Bactris gasipaes (HBK) L. H. Bailey
Sabal causiarum (0. F. Cook) Becc.
Phoenix roebelenii O'Brien
Arecastrum romanzoffianum (Cham.) Becc.
Coccothrinax argentata (Jacq.) L. H. Bailey
Ptychosperma elegans (R. Br.) Blume
Arenga pinnata (Wurmb) Merrill
Thrinax radiata Lodd. ex Schult. &
Washingtonia robusta H. Wendl.
Washingtonia filifera (L. Linden)
Losses due to LY at FTG were not typical of the losses seen in south
Florida in general. For instance, the most striking difference was the
loss of only three of 99 Manila palms from 1973 to 1977. During this
period there was a nearly total loss of the three species of Pritchardia
known to be susceptible to LY and a loss of 70 of the 129 coconut
palms. At least 10 cultivars of coconut palm were present in FTG, and
resistance in some of these, such as the 'Malayan Dwarf (58, 59, 60,
124, 138, 152), accounts at least partly for the survival of this species.
Fourteen of 25 Arenga engleri Becc. succumbed in FTG, whereas a
local nursery lost an entire block of about 500 field grown A. engleri to
LY. Between 1973 and 1975 a total loss of Nypa fruticans occurred at
and near FTG. Symptoms were similar to LY; however, MLO were
not observed in electron microscopic observations.
A possible explanation for the relatively small losses in species
such as V. merrillii in FTG is that plant diversity there is relatively
high. In a mixed planting, nonsusceptible palms, if attractive to the
insect vector, would act as barriers to disease spread. In general,
however, the relative susceptibilities of species of palms determined
in the study at FTG agree with estimates based upon field observa-
tions of H. M. Donselman, F. W. Howard, and R. E. McCoy (Table 1).
Native Distributions of LY-Resistant
and Susceptible Palm Species
Of the 30 palm species susceptible to LY, only four are of New
World origin. Of these species, Allagoptera arenaria, Aiphanes lin-
deniana, and Arikury palm are native to South America, and Puerto
Rican gaussia palm is native to Puerto Rico. The numbers of palm
species originating from different floristic regions were determined
and are summarized in Table 3. Although a possible association
between LY and Roystonea sp. of Haiti was reported by Leach (86),
LY has not been reported as affecting Roystonea spp. in Jamaica,
Cuba, or Florida (71, 75, 76). Thus, the hypothesis that LY is almost
entirely a problem of certain Old World palms is supported. Other-
wise, no clear relationship between LY susceptibility and biogeo-
graphical origin has emerged among the species studied. Palm spe-
cies from 20 floristic regions were evaluated. Palms representing 12
widely scattered regions were susceptible. There also is no pattern
evident in the botanical relationships of LY-susceptible species.
Moore (121) pointed out that LY attacks species of genera in 7 of 15
major taxonomic groups.
Symptoms of Lethal Yellowing
The first symptom of LY in mature coconut palms is the premature
dropping of most or all of the coconuts regardless of size (Fig. 5).
This is termed "shelling." Most of the fallen nuts will have a brown
or black water-soaked area immediately under the calyx on the stem
end. Shelling of "buttons" or small nuts of 3 to 4 cm diameter is a
Table 3. Palm species affected by lethal yellowing (LY) grouped by the
floristic regions' within which they are naturally distributed, and
numbers of species exposed to and lost to LY at Fairchild Tropical
Garden during 1973-1977.
Number Number Number
Species of of lost
affected species palms2 to LY
by LY in FTG in FTG in FTG
Caribbean 2 127 1,442 3
Pacific North America 0 9 63 0
Venezuela and Guiana 0 5 32 0
Amazon & Southern Brazil 2 38 406 1
Andean 0 5 33 0
4 184 1,976 4
Madagascar 5 18 209 18
African-Indian Desert 2 4 28 2
African Savannah 0 10 97 0
Humid Tropical Africa 2 5 77 1
Macronesia 0 1 21 0
Mediterranean 1 1 31 0
10 39 463 21
Malaysian 1 68 734 3
Continental Southeast Asian 0 8 178 12
New Caledonian 0 6 41 0
Australian 1 13 136 0
Melanesian and Micronesian 1 10 177 70
Polynesian and Hawaiian 7 8 37 30
Sino-Japanese 2 8 98 1
New Zealand 0 5 20 0
Indian 4 18 145 10
16 144 1,566 126
1. Floristic regions modified after Good (46).
2. Includes only palms two years of age or more between January 1971 and January
normal occurrence and should not be considered a symptom of LY.
This stage of development is the least reliable for accurate diagnosis /
The next symptom to develop is the blackening of new in-
florescences (flower stalks) (Fig. 6a). This may be observed as they
break through the spathe (the structure in which the inflorescence is
enclosed) and is quite distinctive because the inflorescences of
Fig. 5. Premature dropping of coconuts, or "shelling," the earliest symptom
of lethal yellowing of coconut palms.
healthy trees are a creamy white to yellow in color (Fig. 6b). Most of
the male flowers will be dead on the blackened inflorescences, and no
fruit will set on such flower stalks.
Next, the leaves turn yellow, usually beginning with the oldest or
lower leaves and advancing upwards through the crown (Figs. 7, 8).
In some cases, a single leaf in mid-crown will turn yellow first, giving
a characteristic "flag" appearance (Fig. 9). Yellowed leaves are nota-
bly turgid; they are not flaccid as in the case of wilt diseases. Leaves
that have become yellow ultimately turn brown, desiccate, and hang
down. Such leaves fall readily, or are easily pulled off (Fig. 10).
Death of the bud occurs about halfway through the yellowing
sequence. The newly emerged spear leaf will collapse and may bd
seen hanging down within the crown (Fig. 11). Finally, the top of the
tree falls away, leaving a bare trunk or "telephone pole." Infected
trees usually die within 3 to 6 months after appearance of the first
symptoms. McCoy (97) devised a LY severity rating based on these
symptoms (Table 4). This rating system is useful as a means of
standardizing studies of LY disease. A similar rating system was
devised by Eden-Green in Jamica (35).
Palms Other than Coconut
In other palms, early symptom stages generally are similar to those
for the coconut palm-that is, the premature dropping of fruit
(shelling) and the blackening or necrosis of new inflorescences. The
stage at which spear leaf necrosis occurs and the form of foliar dis-
coloration differs for individual species (Table 5). In general, leaf
discoloration due to LY falls into two distinct categories: those in
which the leaves turn a golden-yellow before dying and those in
which the leaves turn a reddish to greyish-brown. Palms in the first
symptom category, yellowing of leaves, are coconut, gebang, Pritch-
ardia, arikury, windmill, princess, and spindle palms. The symptoms
in these palms are similar to those of coconut palm, with yellowing
beginning in the lower leaves. Often, one specific leaf will turn before
any others, giving a "flagging" appearance. The leaves remain yellow
Table 4. Coconut lethal yellowing severity rating scale.
Category rating Symptoms
0 Healthy or incubating
1 Nutfall only'
primary 2 One necrotic inflorescence'
3 Two or more necrotic inflorescences'
4 Yellowing in lower leaves only
yellowing 5 Yellowing in lower and middle leaves
6 All leaves yellowed, spear leaf good
7 Spear leaf dead, some green leaves left
dying 8 Spear leaf dead, all leaves yellow
9 Palm dead (telephone pole)
1. May or may not have one yellow flag leaf in center of crown.
Fig. 6a. Coconut inflorescence showing necrosis and retention of dead male
flowers, an early symptom of lethal yellowing.
Cr ^ 3
Fig. 6b. Healthy male and female flowers and fruits (coconuts) of a 'Jamaica
Tall' coconut palm.
qrIW am p-wr~
I ~ 1~,(
Fig. 7. Yellowing in lower leaves (Rating 4).
for various lengths of time before turning brown and dying. Some
leaves have a tendency to break at the leaf base junction and hang
down somewhat like a collapsed umbrella. Leaves may cling to the
tree instead of falling to the ground. Yellowing generally advances
from the older to the younger leaves.
The remaining susceptible palms on the list fall into the second
symptom category, i.e., a browning appearance of fronds. The Ma-
nila palm is perhaps the best example of this group (Fig. 3). The first
two symptom stages in this palm are similar to symptom develop-
ment in LY-affected coconut palms. Frond discoloration is not as
Fig. 8. Yellowing in all leaves (Rating 6). This is the same palm as in Fig. 7,
photographed one month later.
dramatic nor is it as easily detected in the early stages of development
as in coconut or Pritchardia palms.
First evidence of infection is a brownish "water mark" along the
margin of the pinnae or leaflets. Browning extends to the rest of the
frond over a period of days, resulting in a dried-out appearance. As in
other LY-affected palms, the older leaves tend to break easily at the
junction of the leaf-base and the midrib, whereas younger fronds tend
to break within the lower region of the pinnae. Unopened in-
florescences may have a distorted or twisted appearance. Death of the
bud follows, and the entire top falls away resulting in a bare trunk.
Table 5. Symptom development of lethal yellowing in five palm species.
Immature Inflorescence Leaf Spear leaf Root tip
Palm fruit drop necrosis discoloration necrosis necrosis
Phoenix spp. '
. 7 .
Fig. 9. Crown of a 'Jamaica Tall' coconut, showing a yellow "flag leaf," which
is often a symptom of lethal yellowing.
Fig. 10. Late stage of decline (Rating 8). This is the palm shown in Figs. 7
and 8; the photograph was taken one month after Fig. 8.
The palmyra, cluster fish-tail Chrysalidocarpus cabadae H. E. Moore,
and the three species of Phoenix palms (Fig. 12) all show "brown-
ing" symptoms similar to that just described for the Manila palm.
The spear leaf usually dies about midway through foliar yellowing
in coconut palm; however, in Pritchardia and Phoenix palms, spear
leaf necrosis is the first visible symptom. Once the spear leaf dies,
death of the crown follows, ending in a falling away of the top of the
tree with only a trunk remaining.
Fig. 11. Collapse and necrosis of spear leaf (Rating 7).
Fig. 12. Lethal yellowing of Canary Island date palm. Courtesy J. Amador,
Texas A & M University.
Diagnosis of LY disease is particularly difficult with palms that are
not old enough to bear flowers and fruits, and with palms grown
under unusual conditions, such as in experimental cages. Damage by
insects, mites, cold, fungal and bacterial pathogens, or nutrient de-
ficiencies can cause symptoms resembling those of LY. In ex-
perimental work in which accurate diagnosis is essential, diagnoses
by symptomatology must be confirmed by electron microscope ex-
amination for MLO in the phloem tissue.
THE SEARCH FOR A CAUSAL AGENT:
AND THEIR ASSOCIATION WITH
Early Attempts to Discover
the Causal Organism
A coconut disorder reported on Grand Cayman Island in 1834 (80)
may have been lethal yellowing (LY). This is the earliest known
reference to the disease. Even with the long recorded history of LY,
its cause was not determined until 1972 when laboratories in the
United States, Great Britain, and Germany observed mycoplasma-
like organisms (MLO) within the phloem of LY-diseased coconut
palms (5, 65, 131). The failure to identify the LY pathogen before that
date is not a reflection upon the quality or quantity of prior research,
for many eminent scientists had spent years of intensive research on
the disease. Much of the information accumulated by these research-
ers still serves as a basis for present studies on LY.
The first concerted effort to investigate LY was initiated in 1880 by
a group of Cuban biologists led by D. Filipe Poey, an eminent zoolo-
gist of that period. Various species of insects and fungi were in-
vestigated as possibly causing LY (28). It is interesting to note that
these early probes into the nature of LY were made during a period in
which the science of plant pathology was in its infancy.
Investigations of Bacteria and Fungi
From the late 1800's until the 1970's various workers studied
bacteria or fungi as possible causal organisms, because symptoms
included a necrosis of juvenile tissues and a soft rot within the crowns
of affected palms (2, 67, 80, 151). Martyn (93, 94) could find neither
bacteria nor fungi in microscopic examinations of tissues at the onset
of necrosis. Bacteria were isolated from rotting heart tissues, but all
pathogenicity tests failed to reproduce LY. He theorized that LY
initiates a breakdown of young tissue by the action of some toxic
substance carried through the conducting vessels of affected palms,
which in turn allows attack by saprophytic bacteria. Mijailova (120)
reported preliminary results from work in Cuba that suggested the
involvement of a fungus, Verticillium sp., as a causal agent; however,
this was not confirmed by later work. Studies of possible relationships
between fungi or bacteria and LY continued into the 1970's with
results that have supported Martyn's (94) conclusions that these
organisms do not cause LY but are secondary invaders (14, 55, 66, 86,
109, 124, 139).
Investigations of Soil Factors
The failure to isolate causal fungi or bacteria from LY-affected
palms prompted investigators to consider soil factors that might
initiate the disease. The hypothesis that plant nutrients may have
some involvement in the LY syndrome was based on the repeated
observation that the most vigorous palms in a stand were the first to
succumb to LY (9, 86, 92, 93, 124). Leach (86) noted that soil con-
ditions greatly affected the incidence of LY because the rate of spread
differed on various soil types. He concluded that susceptibility was
probably due more to the host nutrient status than to any direct effect
on a potential parasite. Bruner and Boucle (9) noted in Cuba that
healthy coconut palms planted in soil where trees had died of LY
remained healthy for indefinite periods. Nutman and Roberts (124)
noted in Jamaica that not only were vigorously growing palms more
susceptible to LY, but that the only escapes from the disease showed
symptoms of nutrient deficiency or adverse growth, such as pencil
Although the literature contains many observations that palm
vigor increases susceptibility to LY, none of several studies could
correlate LY with the excess or deficiency of any particular chemical
element? or plant nutrient (14, 17, 44, 78). Innes (78) could find no
relationship between disease incidence and the manganese content of
leaf tissues, and he felt that it was improbable that a nutrient de-
ficiency would cause the symptoms of LY. By comparing chemical
analyses of diseased and healthy palms, Chen (17) found that dis-
eased palms showed an imbalance in their mineral nutrition, but he
concluded that it was highly unlikely that nutrient deficiencies or
toxicities per se were causes of LY. Experiments were conducted to
determine whether any soil-borne organism, particularly nematodes,
could transmit LY (14, 85, 93). Martyn (93) attempted transmission
by burying roots from diseased palms among those of healthy palms.
No transmission occurred. Latta (85) further discounted any involve-
ment by nematodes. In his experiments, palms were grown in soil
collected from around the roots of diseased palms, and nematodes
extracted from the soil and roots of diseased palms were placed
around the roots of healthy plants.
The Viral Hypothesis
S With the lack of supporting evidence that fungi, bacteria, nema-
todes, or nutrients were causative of LY, early investigators were left
With only one conclusion-that LY had a viral etiology. Several
researchers favored a virus hypothesis (9, 11, 13, 20, 54, 55, 92, 124,
L--`-Many virus diseases of plants are transmitted by Homoptera or
other winged insects. The pattern of LY spread observed in many
studies (9, 14, 20, 54, 73, 92, 94), indicated that an air-borne vector
transmitted the pathogen. LY tends to spread from areas of high
incidence to small, localized foci, oftentimes at a distance of several
miles (8, 14, 68, 92, 93, 141; see Chapter 6). The newly formed LY foci
are frequently diffuse, with symptomless palms intermixed with
diseased palms. A marked increase in the incidence of LY following
violent storms was noted in Cuba (28), Jamaica (93), and the Domini-
can Republic (19). Experimental evidence favoring an air-borne in-
sect vector was also obtained with caging studies (66). Coconut palms
were protected against LY by caging them in insect-proof enclosures,
but contracted the disease when the cages were removed.
Other lines of evidence supporting a viral etiology for LY came
from anatomical studies. Nutman and Roberts (124) observed that
leaves from LY-diseased palms contained a higher number of
binucleate cells than did healthy palms, and they pointed out that
this cytological condition was similar to that reported for some virus
disease. Carter (13) noted a blockage of translocation associated
with a phloem necrosis in the trunks of diseased palms and concluded
that such abnormalities might well be caused by virus infection.
A report of mechanical transmission of LY came from a group of
Florida researchers who claimed success by using mechanical
transmission techniques of virology (92, 132). However, these results
could not be repeated in Jamaica (55), even when attempted by the
Florida scientists in Jamaica (139), nor were they repeatable by other
workers in Florida (R. E. McCoy, personal communication), and it has
been concluded that some agent other than the LY pathogen was
,J It is understandable that early LY researchers ascribed a viral
etiology to the disease, because at that time diseases which are now
known to be associated with MLO were thought to comprise a special-
ized group of virus diseasesjThe size range of MLO is just at the
resolving power of the light microscope, and this group of microor-
ganisms went unrecognized as plant pathogens until 1967 when they
were first observed in diseased plants with the aid of an electron
microscope (30). Within four years of that date, MLO were seen in
LY-diseased coconut palms by researchers in three separate laborato-
ries (5, 65, 131). Shortly after that, it was determined that lethal
declines of other palm species were associated with MLO (129, 157).
and Lethal Yellowing
Evidence Linking MLO to LY in Coconut Palms
The LY pathogen eluded discovery until 1972 when the presence of
MLO within the phloem vascular tissue of coconut palms affected by
LY was reported (5, 65, 131) (Fig. 13). There are two lines of evidence
linking mycoplasmas to lethal yellowing. First, MLO have con-
sistently been detected in diseased but not healthy palm tissue from
Florida (129, 157, 158, 159), Jamaica, (5, 65, 131), and Africa (27, 31,
32) by researchers in nine separate laboratories in the United States,
France, England, Germany, and Jamaica. This is not a chance
observation but a consistent occurrence. The MLO can be seen in
LY-diseased palms before tissue breakdown and secondary bacterial
rot occur. Healthy palms and palms affected by diseases other than
CW = host cell wall. Line = 2.0 rm.
Fig. 13. Electron micrograph of a sieve tube element (SE) from a young leaf
base of a princess palm infected with mycoplasmalike organisms (arrows).
CW = host cell wall. Line = 2.0 Rm.
LY do not contain MLO. Repeated isolations made from dying coco-
nut tissue early in the development of LY show these tissues to be
free of any bacteria or fungi. As the dead and dying tissues are
exposed to the air, they are rapidly colonized by bacteria, fungi, and
the larvae of many insects. Death of the palm occurs when the bud is
killed in a putrid, foul-smelling, soft rot associated with a large
number of bacteria of the Erwinia and Pseudomonas groups and
assisted by numerous burrowing maggots.
SThe second factor linking MLO to lethal yellowing is the antibiotic
response of diseased palms. Mycoplasmas and MLO are sensitive to
tetracycline antibiotics, and insensitive to penicillin. Shortly after
the outbreak of LY in Miami, tetracycline antibiotics were tested
against the disease. LY symptom development was suppressed as a
result of these first limited tests in LY-affected coconut palms. This
encouraged more extensive testing, which eventually demonstrated
the therapeutic value of oxytetracycline and the ineffectiveness of
penicillin in the treatment of LY (96, 97, 98, 99, 100, 101, 102, 104,
106, 108, 110, 111, 112). This was strong evidence that MLO caused
LY. The effectiveness of oxytetracycline against LY was confirmed
simultaneously by independent work in Jamaica (77) and later in
Africa (155) Antibiotic treatments were soon developed as a disease
management tool (See Chapter 7). s
The Association of MLO with Palms Other than Coconut
Following the outbreak of LY on the Florida mainland in 1971, and
the associated epidemic loss of coconut palms, unusual losses of other
palm species were noted in areas where LY was severe. Lethal
yellowing was suspected in these additional palm species, but the
problem of LY diagnosis was complicated by two factors: many of the
palms were not in reproductive cycles and, therefore, could not show
fruit or flower symptoms; and some of the affected species did not
show the characteristic yellow leaf color of affected 'Jamaica Tall'
coconut palms. The only other means to diagnose LY was to de-
termine whether the dying palms contained MLO. Initial electron
microscope studies did identify MLO infection in dying members of
two popular palm species, the Manila palm and the Fiji fan palm
(129). Therefore an intensive electron microscopic investigation was
initiated by the University of Florida to determine the possible
association of MLO with additional declining palm species in the
Information on the location of dying palms other than coconut was
solicited from the Florida Department of Agriculture's Division of
Plant Industry, the University of Florida's county Extension Service
offices, and Fairchild Tropical Garden, as well as from members of
the Palm Society and citizens of southern Florida. The decline of some
palms that were reported was attributed to causes other than LY.
Butt rot caused by Ganoderma infection and bud infestations by palm
weevils were commonly encountered. When neither of these nor other
recognized causes of palm declines could be detected, the palms were
sampled to determine whether they contained MLO. Whole palm
crowns were collected in the field and brought to the laboratory where
they were further dissected. Tissue samples were taken from young,
unemerged leaf bases within 3 cm of the apical meristem and pro-
cessed for electron microscopy (157) (Fig. 14).
MLO were observed in phloem tissue from declining palms of 28
identified species and several palms that were identified to genus, i.e.,
at least 30 species (Table 1). These organisms were never found in the
healthy palms that served as controls for this study. MLO were also
found to be associated with declining Pandanus utilis (160).
Mycoplasmalike organisms were found most readily in the young
leaf bases that contain the greatest concentration of functional sieve
elements, and the success of finding MLO decreased sharply as pro-
gressively older leaf bases were examined. The only exception to the
low concentration or apparent absence of MLO in mature tissue was
noted in diseased coconut palms where MLO were readily seen in
"flag" leaves, the first leaves to turn yellow. Even within the younger
tissues the MLO concentration was generally low; many diseased
palms had MLO in less than 5% of the vascular bundles. Infre-
quently, samples were examined that contained MLO in over 50% of
Fig. 14. Leaf bases dissected from the growing point of a coconut palm. The
third to fourth smallest leaf bases are most likely to contain MLO.
the vascular bundles. The numbers of MLO varied considerably
among different plants, but some species, such as the Canary Island
date palm and the windmill palm, contained considerably more MLO
than other species.
Healthy control palms were examined for most of the species stu-
died, and the data strongly support the hypothesis that MLO are the
organisms responsible for the death of these species of palms. Posi-
tive therapeutic responses to oxytetracycline by declining arikury,
Pritchardia, windmill, and coconut palms, and successful results
in the preventive treatment of Manila palms with oxytetracycline
(110), provide additional support. Furthermore, the similarity of
symptom expression, and the close chronological and geographical
coincidence of the various palm declines with LY, indicate that all
these palm maladies are caused by the same pathogenic MLO. Fi-
nally, transmission of MLO to coconut, Manila, and Pritchardia
palms in the same cage (Chapter 6) further suggests that all these
palm maladies are caused by the same organism.
What Are the Mycoplasmas?
Man's acquaintance with mycoplasmas began with the great
pleuropneumonia epidemic of cattle which swept through Europe in
the last century. The organism causing this disease was present in
the lungs of affected animals, but it could not be cultivated in the
laboratory, and the fact that it passed through bacterial-proof filters
led early investigators to classify it as a virus. A major breakthrough
came when the pleuropneumonia organism was finally cultivated in
artificial media (123). The character of this agent could then be
determined. It was found not to be a virus but a cellular organism. It
was smaller than any bacterium, and its shape was variable, ranging
from small round bodies to filaments. Research on the mycoplasmas
accelerated in the 1950's, and over 60 species in 3 genera were found
in human and animal infections. As a result, the mycoplasmas were
considered unique and were placed in a separate biological class
between the bacteria and the viruses.Simply put, the mycoplasmas
are the smallest and simplest cellular organisms known. They have
no cell wall, no nucleus, and no internal structures other than DNA
and ribosomes (Fig. 15). Mycoplasmas have been grown in artificial
culture, but their nutritional requirements are exacting, and in
many cases, years passed before medical researchers found the proper
combination of nutrients to support their growth. Because they have
no cell wall as do the bacteria, the mycoplasmais are immune to
penicillin, which kills by inhibiting bacterial cell wall synthesis.
Mycoplasmas are, however, susceptible to tetracycline antibiotics,
Fig. 15. High magnification electron micrograph of mycoplasmalike orga-
nisms in a sieve element of a coconut palm. Arrows point to unit membranes
of typical MLO. Line = 0.1 p.m.
and these are the drugs of choice for treating maladies such as
mycoplasmal pneumonia in humans.
Characteristics of Plant Diseases Associated with MLO
Because of common symptom characteristics, the plant yellows
diseases had been set apart as a distinct group well before Japanese
workers found MLO in diseased plants in 1967 (30). The character-
istic symptoms are yellowing, stunting, and aberrations of the
phloem, or food conducting system. In addition, most yellows diseases
result in sterility; that is, flowers are not formed, are aborted, or are
transformed into leafy structures. Before MLO were shown to be
associated with plant diseases, these symptoms were thought to be
caused by virus infections because they were manifested principally
in living, growing tissues, and, as already stated, no other organisms
were consistently found with these diseases. Although no virus parti-
cles were seen in the yellows diseases, it was already known that
phloem viruses were particularly difficult to purify. Therefore the
inability to find the so-called "yellows viruses" was considered to be a
reflection of the "state of the art" of virus purification at the time.
Since 1967, MLO have been found associated with over 100 plant
In order to be classified as a true mycoplasma, an organism must
first be grown on culture media and then undergo an array of diag-
-nostic tests for growth requirements and serological affinities to
other mycoplasmas. Because the MLO associated with most plant
diseases, .including LY, have defied cultivation attempts, these
organisms must be called "mycoplasmalike" for the present.
DISTRIBUTION AND EPIDEMIOLOGY OF
LETHAL YELLOWING DISEASE
The distribution of LY by countries is generally considered to be as
follows: the Cayman Islands, Jamaica, Cuba, Haiti, the Dominican
Republic, New Providence Island (Bahamas), United States (Florida,
Texas), Mexico (Quintana Roo), Ghana, Togo, Cameroon, and possi-
bly Nigeria and Tanzania (88, 126, 156). Early literature on LY and
similar palm diseases was often based on uncertain diagnoses. It is
now known that at least four diseases of coconut palms in the Carib-
bean were at one time considered to be a single disease which was
most commonly known as "bud rot." In addition, injury caused by
unfavorable weather conditions, lightning, insects, and nutritional
deficiencies may have sometimes been misdiagnosed as "bud rot."
Thus, an evaluation of the reports of LY, particularly in the earlier
literature, must proceed cautiously, and conclusions based on this
literature must often be tentative.
A destructive disease of coconut palms was observed in the Cay-
man Islands in 1834 (Fig. 16). Authors generally consider this to be
the earliest record of LY (e.g., 80, 89, 93, 124, 150). The disease
destroyed many coconut palms on Grand Cayman Island around the
turn of the century (57, 80). Other than these records, there is a
paucity of published information on LY in the Cayman Islands, and
there has been no attempt to confirm the field diagnosis by showing
an association of the disease with MLO.
Since the 1800's commercial coconut production in Jamaica has
been concentrated on the western, northern, and eastern coasts. LY
apparently destroyed a large number of coconut palms near the
southwest coast in the 1870's and continued to be endemic in parts of
western Jamaica for several decades (93). During this early period,
some observers reported finding cases of the same disease in scattered
TROPC OF CANCER
Fig. 16. The Caribbean Basin including Florida, the Bahamas, the western islands of the Caribbean, and the northeast tip of
the Yucatan Peninsula.
localities in the eastern part of the island (80). These reports are
questionable, and might have been based on misdiagnoses. In the
1940's and early 1950's LY was still destructive in the western
districts of Jamaica, spreading generally westward from Montego
Bay. The disease was also present near Falmouth, but was more
scattered (94, 124).
During the period of the 1940's and 1950's a number of field com-
parisons of symptoms were made between similar diseases of coconut
palms in the Caribbean and West Africa. On the basis of these
observations, the disease that was concentrated on the west end of
Jamaica was termed "unknown disease" (57, 78,94) or "lethal yellow-
ing" (124) to distinguish it from similar diseases, particularly bud
rot, caused by the fungus Phytopthora palmivora Chee, and bronze
leaf wilt. The latter is restricted to northern South America and the
extreme southern islands of the Caribbean and is now known to be a
LY had spread over most of the western half of Jamaica by 1952. In
1961, LY was discovered near Buff Bay in the eastern end of Jamaica,
more than 110 km from the nearest LY case. The disease destroyed
an estimated one million coconut palms in eastern Jamaica during
the next 20 years (139), and four million by 1979 (39) (Fig. 17).
The LY disease of Jamaica is considered to be identical to LY in
Florida and other areas of the Americas. The symptoms are the same
(15, 167), and MLO have been associated with the disease (5, 65, 77,
131). The rate of spread of LY in Jamaica is similar to that of LY in
A disease called Pudrici6n del cogollo (bud rot) was found in Cuba
at least as early as the 1870's when it was observed near the city of
Matanzas on the northern coast and within 8 years had extended to
Cienfuegos on the south coast. Around 1890 it had reached the
Baracoa district, an 80 km strip of the eastern coast where coconut
production was the principal industry. The disease was so destructive
that many coconut plantations were converted to banana farms. The
disease spread to western Cuba, and destroyed coconut plantations
throughout that region. It was said that the commercial coconut area
did not extend throughout the northern coasts because of the sup-
posed prevalence of bud rot there in "early times" (80).
By the 1940's coconut plantations had been virtually destroyed.
Except for the Baracoa district, plantations tended to consist of a few
dozen trees. Production still centered in the Baracoa district, but the
annual exportation of coconuts from this district was only 2% of what
it had been 36 years previously (9).
Fig. 17. A coconut palm plantation in Jamaica devastated by lethal
Pudrici6n del cogollo was present in many localities in Cuba and on
the Isle of Pines during the 1960's (29, 120). On the basis of detailed
studies of the symptoms of Pudrici6n del cogollo, Mijailova (120)
pointed out that the disease in Cuba showed symptoms that Leach
(86) associated both with LY in Jamaica and with bronze leaf wilt in
Venezuela, and suggested that Pudrici6n del cogollo of Cuba was
separate from diseases of coconuts reported in other localities.
However, some symptoms of bronze leaf wilt are similar to those of
LY in Jamaica, and for many years these two diseases were thought
to be identical. On the basis of observations during 8 years of LY
research in Florida, the symptoms of LY can vary considerably, and
symptoms that Leach (86) considered restricted to bronze leaf wilt
may often be seen in coconut palms with LY. To complicate matters,
bronze leaf wilt was apparently used interchangeably with Cedros
wilt and the symptomatology described in early literature is con-
On the basis of comparative studies of the symptoms of Pudrici6n
del cogollo and those of LY in Jamaica and Florida, and the geo-
graphic proximities of the three regions, it has been tentatively
concluded that Pudrici6n del cogollo of Cuba is identical to LY (20,
63, 167). If it could be established that MLO are associated with the
Cuban disease, the evidence for the co-identity of these diseases
would be stronger.
Leach (86) compared "unknown disease" (later termed lethal yel-
lowing) of Jamaica with a disease of coconut palms in Haiti and
concluded on the basis of symptoms that they were identical. The
disease had been present in the Cap Haitien region since at least the
1920's and 1930's. An epidemic disease of coconut palms reported in
the 1880's may have been LY (86, 141).
In the 1940's, LY appeared in Gonaives, a distance of 70 km from
Cap Haitien, and destroyed all but a few of the approximately 8,000
bearing coconut palms in and around that town. New outbreaks were
also seen in localities on the northern coast. Leach (86), who had
become familiar with LY in Jamaica, considered the disease in Haiti
to be highly "virulent". This was, of course, before LY had spread
from the west end to become epidemic in eastern Jamaica.
Ciferri and Cicaronne (19) compared the symptoms of a disease
observed as early as 1925 (18) in the Dominican Republic with the
bronze leaf wilt of Venezuela (now considered physiological in origin)
and the "bronze leaf wilt" of Jamaica (now termed LY), and concluded
that the disease most closely resembled the latter. It appears, then,
that LY may have been present in the Dominican Republic much
earlier than recent authors (143) have reported. Cases of LY were
diagnosed by Carter in 1962 in several sites on the north coast
(Dajab6n, Bajabonico, San Marcos, Imbert, Puerto Plata, and Sosia)
(D. H. Romney,3 personal communication). In 1969, it was reported in
the regions of Dajab6n and Puerto Plata (143, 144). In 1970, Romney3
(personal communication) diagnosed several dozen cases near Sosfia
and observed hundreds of dead trees in that area that were presum-
ably killed by LY. However, he found no cases of LY in the Dajab6n
region. He pointed out that the patchiness of coconut plantings in the
northern parts of the D. R. could possibly have slowed or prevented
the spread of LY. The main commercial coconut growing region is in
Samand Province, about 160 km from the easternmost case di-
agnosed by Romney. LY cases were scarce or absent in the Dominican
Republic in 1980 (75).
Leach (86) observed "unknown disease" on New Providence Island
in the Bahamas in 1946 and stated that it appeared to have been
3. National Coconut Development Project, Dar es-Salaam, Tanzania
present there for 20 years in a localized area. He stated that the most
extensive coconut plantings were on Andros and Eleuthera Islands,
but that these islands were free of the disease. G. H. Gwin4 (personal
communications) made a limited survey in 1974 and found 11 cases
United States (Florida)
A lethal disease that affected 30 coconut palms on Key West in
1937 may have been LY (92). In 1938 and 1939 an epidemic of
Pudrici6n del cogollo (probably LY) destroyed 18,000 coconut palms
in Havana Province, Cuba, which is about 145 km across the Straits
of Florida from Key West (9); possibly, infected vectors were blown to
Key West from Cuba. Between 1955 and 1960 LY occurred in an
epidemic on Key West, destroying about 15,000 (75%) of the coconut
palms (92), and persisted until 1968 (147). Since then, few coconut
palms in Key West have succumbed to LY (R. H. Zerba,5 personal
In 1969, LY was observed on Key Largo, about 160 km from Key
West (137). Since then, LY has spread in a desultory pattern in the
Keys, appearing and in some cases recurring on some islands, while
other islands populated with coconuts have not been affected (Fig.
18). LY was first reported on the lower east coast in Miami in 1971,
and had been reported as far north as Palm Beach County by 1973
(103, 148). Since then, LY has continued to spread erratically within
the lower east coast area as far as northern Palm Beach County and a
strip of the coast at the southern border of Martin County. About
100,000 coconut palms and thousands of other palms of LY-
susceptible species have been destroyed on the southeast coast.
The east coast from Stuart northward has remained free of LY. A
few cases were reported in the Clewiston area (Hendry County) in
1976 and a total of fewer than 15 LY cases have been reported in the
vicinity of Naples (Collier County) (Charlie Lowery," personal com-
munication). Lee County, which has about 30,000 coconut palms, has
not had a case of LY. The distribution of LY in Florida appears to be
related to the distribution of relatively high populations of the insect
vector, Myndus crudus Van Duzee along the southeast coast (68).
4. Florida Department of Agriculture, Division of Plant Industry, Miami
5. University of Florida, Cooperative Extension Service, Key West 33050
6. University of Florida, Cooperative Extension Service, Naples 33940
I Co. 270N
LOT TE GLADES UPITER
F LEE HENRY PALM BEACH C EST PALM BACH
\y ___ c M-POMPANO BEACH
NAPLE COLLIER Co.. a I. LAUDERDALE
EAPL E 0 llOLLYWOOD 260N
O MIAMI IAMI BEACH
MONROE Co 0
BYv WT o O
Fig. 18. Southern Florida, showing range of coconut palms (hatching) and
current distribution of lethal yellowing disease (cross-hatching).
United States (Texas)
A disease believed to be identical to LY was recently reported in
Canary Island date palm and date palms in the lower Rio Grande
Valley of Texas (113, 114) (Fig. 12). Coconut palms are not grown in
Texas. Between 1978, when the disease was first noticed in Browns-
ville on the coast, and 1980 when it was first diagnosed, the disease
moved inland about 70 km. The disease has not yet been reported
from the Mexican side of the Valley, probably because ornamental
palms are less common on that side (Dale Myerdirk,7 personal com-
The Texas disease is believed to be identical to LY for four
reasons: (1) Canary Island and date palms are susceptible and (2)
Washington palms, queen palms, and cabbage palmettos appear to be
immune, as in Florida (113, 114); (3) the symptoms, and the pattern
and rate of spread are similar in both localities; and (4) MLO have
been observed in sieve tubes of the phloem.
For decades LY was conceived of as a disease primarily of coconut
palms and limited to two general areas, West Africa and the greater
Caribbean basin. It is now known that LY affects date palm, Canary
Island date palm, Senegal date palm, Chinese fan palm, and windmill
palm, all of which are cold-hardy species grown in northern Florida
and states bordering the south Atlantic and Gulf coasts. Until re-
cently it was questionable whether the disease could spread on the
mainland beyond the relatively warm coconut belt of southern
The Texas outbreak has raised new concerns regarding the poten-
tial further spread of LY, because it demonstrates that LY can affect
date palms in the absence of coconut palms. Thus, the threat to the
date-growing regions of Arizona and California, and to parts of north-
ern Florida and other southeastern states where cold-hardy palms
are grown as ornamentals, now seems more plausible.
In January 1982, LY was diagnosed in dying palms at the north-
eastern tip of the Yucatan Peninsula (R. E. McCoy, unpublished).
The disease had been noted about one year previously, during which
time some 70% of the coconut palms on the island of Cancun were
lost. The disease was also present on the mainland in Puerto Juarez.
This significant outbreak is the first occurrence of LY on mainland
Ghana and Togo
LY has been known in both Ghana (as Cape St. Paul wilt) and
neighboring Togo (as Kaincop6 disease) since 1932 (Fig. 19). Cape St.
7. Research Leader, Boyden Fruit and Vegetable Entomological Labora-
tory, University of California, Riverside 92521
Cape Three Points N
Fig. 19. West Africa, showing localities mentioned in the text.
Paul wilt destroyed about 100,000 coconut palms in the general area
of the communities of Keta and Cape St. Paul, Ghana, between 1937
and 1959 (87). In 1968, the disease was reported about 450 km further
east in the region of Cape Three Points (1), and as of 1976 was highly
active in the Keta area (27).
Between 1937 and 1941, Kaincop6 disease was limited to an area
near the village of Kaincop6, Togo, where it killed about 1000 coconut
palms. From 1947 to 1954, 4000 coconut palms were killed. The
disease spread rapidly between 1954 and 1959, killing about 40,000
coconut palms. Another rapid extension of the disease took place from
1961 to 1964. By 1974, the disease had spread eastward nearly to the
border of Togo and Benin (154). The spread and distribution of the
disease was shown in detail by Bachy and Hoestra (3) and Steiner
An LY-type disease known as Kribi disease was observed in 1937
near Ebodie: by 1975 it had spread north from this initial focus 80 km
to Londji and south about 20 km to a locality near the border of
Equatorial Guinea. There is evidence that the disease may also be
present in the latter country. Kribi disease can eliminate 90% of a
stand of 100 to 200 coconut palms within 2 to 3 years following initial
A disease similar to those described above broke out in the vicinity
of Awka, Nigeria, in 1951. A similar epidemic resulting in the death
of about 5000 coconut palms occurred in the same area in 1917 (9).
Relationship Between LY of the Americas
and of West Africa
The West African diseases have important similarities with LY as
it is known in the Americas. 'West African Tall' or 'Typica' is the
principal coconut palm cultivar in this area, and is basically the same
or very similar to the 'Jamaica Tall', which is the principal cultivar in
the Caribbean region. Both cultivars are highly susceptible to the LY
diseases of their respective regions (52, 53, 61, 62). The symptoms of
LY reported from the different localities of Africa and the Americas
are identical (95, 103, 126). MLO have been observed in sieve tubes of
phloem tissue samples from palms infected with the LY disease in
Ghana (27), Togo (27, 31), and Cameroon (32). Oxytetracycline treat-
ments of coconut palms infected with Kaincop6 disease (Togo) re-
sulted in disease remission (155), further supporting the hypothesis
that the African LY diseases are caused by a mycoplasma.
There are two important differences between the West African
LY-type diseases and LY of the Caribbean: (1) the 'Malayan Dwarf'
cultivar is highly susceptible to LY in West Africa, but highly resist-
ant to LY in the Americas (1, 32, 58, 170); (2) the pattern of spread of
LY in Africa has been described as suggesting a soil-borne, rather
than an air-borne vector (154). An air-borne vector of LY has been
indicated in the Americas (8, 14, 66, 103). In Florida, an insect,
Myndus crudus Van Duzee, has been demonstrated to be a vector of
LY (74, Chapters 5 and 6). Regarding the differences noted between
LY in Africa and in the Caribbean area, three possibilities are
suggested: (1) two different species or strains of MLO may be in-
volved; (2) the 'Malayan Dwarf' coconut palms grown in West Africa
may represent a different genetic line than those grown in the Carib-
bean area; and/or (3) the vectors of LY in Africa and the Caribbean
area may be different.
Epidemiology of Lethal Yellowing
The first cases of LY on the Florida mainland were found in late
1971 in the city of Coral Gables in Dade County (Fig. 18). About 50
diseased palms were seen at that time. By the end of 1972, 2000
palms had been affected in a limited area of greater Miami. However,
by the autumn of 1973 the number of palms affected by LY was
estimated to be close to 20,000, approximately 5% of the entire
coconut population of Dade County. Losses in Dade County
approached 50% by the end of 1974 and reached 75% by the end of
Lethal yellowing not only spreads rapidly, but it kills rapidly.
Affected trees are dead within 3 to 5 months of the first visible
symptoms. Since the causal MLO is considered to be an obligate
parasite, the dead trees can no longer serve as inoculum sources.
Therefore any epidemiological analysis must consider rate of re-
moval of infectious trees in calculating the propensity for spread of
this disease. Rates of spread calculated simply on cumulative num-
bers of infected palms will vastly underestimate the actual tree-to-
tree rate of spread of LY, since a majority of the infected trees will
already be dead (removed from the epidemic) within 6 months of
Epidemiological analysis has been used as a tool for measuring the
degree of disease suppression in control experiments (111), and can
be used for determinations of the degree of resistance in various host
cultivars (166). Epidemiological analysis of the data available on the
LY epidemic in Florida has brought about increased understanding
of the disease process, particularly vector relationships, and allowed
estimations of the durations of the latent and infectious periods of the
Spread of Disease
The apparent infection rate of any disease as defined by Van der
Plank (166) is based on the cumulative numbers of visible infections
in the population. The differential equation used to describe epidemic
dx/dt = rxt(1-x) (eq. 1)
where the change in proportion of disease, x, with time, t, is propor-
tional to a rate value r. The apparent infection rate, r, is the "speed-
ometer" of the epidemic and is defined as the slope of the line obtained
In [x/( x)] (eq. 2)
against time. The proportion of disease, x, present at any time is
divided by a factor, (1 x), to account for the fact that we are dealing
with a finite population that cannot become more than 100% infected.
Spread of Lethal Yellowing
During the first two years of the LY epidemic in Dade County, the
Florida Department of Agriculture's Division of Plant Industry (DPI)
kept accurate records on the occurrence of each case of LY as it was
found as well as its location. These records, involving close to 20,000
individual cases of disease, were used for epidemiological analysis.
Both apparent infection rates based on proportional analyses and
disease dispersal gradients based on spatial analyses have been
calculated. Additionally, a number of manipulations of these two
basic approaches to the study of disease spread have allowed some
insights into the factors driving the LY epidemic.
Using the data supplied by DPI and assuming a coconut palm
population for Dade County of 350,000, an apparent infection rate of
0.21 logits per month was derived. Plotting data transformed by
equation 2 against time (Fig. 20) produced a coefficient of linear
regression of 0.98 (103). When this line was projected into the future,
it closely approximated actual disease spread through the point at
2 A -90
0 0- -50 2
S-2 1 m
1971 1972 1973 1974 1975 1976
Fig. 20. Spread of lethal yellowing of coconut in Dade County, Florida
based on monthly counts of diseased palms (circles) made by the Florida
Department of Agriculture and Consumer Services. Line is fitted by linear
regression of actual counts (correlation coefficient = 0.98, population = 3.5
x 105 trees). Dashed portion is projection. Triangles represent later esti-
mates of actual disease spread.
which 90% of the population had been lost. The rate then slowed
below that predicted, possibly due to two major factors. First, the
release of the antibiotic oxytetracycline-HCl (OTC) for LY control in
the autumn of 1974 slowed the rate of LY spread. By the time use of
the treatment became widespread in mid-1975, 75% of the coconut
palms in Dade County were dead and a majority of those left were
incubating infection. However, many of the remaining 5% had re-
ceived OTC treatment through 1978-80. The other factor affecting
LY spread as predicted by apparent infection rate is the effect of
removals. By the late stages of the epidemic the numbers of standing
symptomatic trees (inoculum sources) was very small, the majority of
trees having been removed from the epidemic by death.
Effect of Removals
The apparent infection rate is based on the cumulative number of
visible infections. It does not take the effect of removals into account.
Since LY diseased palms are usually dead 4 months after the appear-
ance of symptoms, equation 1 can be corrected for removals by using
only the number of palms actually showing disease at any one time
dxldt = rk [xt (xt (1-xt) (eq. 3)
where i denotes the infectious period of the diseased palms, i.e., that
time for which the tree is contagious, and rk is the infection rate
corrected for removals. For an area in Dade County having an appar-
ent infection rate of 0.30 logits per month the rk value was calculated
to be 0.48 logits per month, a spread rate some 1.7 times faster than
accounted for in considering cumulative visible infections.
Calculation of Absolute Values ofLY Spread Based on rk
The infection rates r and rk are based on proportions rather than
absolute values or actual numbers in a population. This allows com-
parisons of disease spread in different populations whose total num-
bers may vary. However, in the case of the Dade County LY epidemic,
both the absolute population values and the calculated infection
rates were available. By converting the proportions of disease pres-
ent at different time intervals to absolute values and accounting for
both infectious period (effect of removals) and latent period (time
from infection until infectious), actual tree-to-tree spread values
were determined. These values are seen to vary with the proportion
of the population infected. In the first 8 months of the epidemic, when
only a small portion of the population was infected, each infected tree
served to inoculate 4.6 new trees. By the fall of 1973, when the
logarithmic stage of spread was well underway, each infected tree
served to infect 9.3 new trees because of the greater predominance of
inoculum in relation to the remaining uninfected palms. By mid-
stages of the epidemic this number decreased to 3.5 new trees per
diseased tree. Late in the epidemic this number was reduced to 0.3
new trees per infected tree because of the tremendous impact of
removals in reducing the amount of inoculum available to incite new
Spatial Analyses-Dispersal Gradients
Dispersal gradients of LY were calculated by Britt (7) through
spatial analyses of disease incidence data for a 200 square mile area
of greater Miami. The LY incidence data provided by DPI were
plotted on an area map, and the locations of the diseased palms were
converted to digital coordinates to facilitate computer analysis. The
base line population of healthy palms in 1971 was estimated from
aerial photographs by counts of 'Jamaica Tall' palms in representa-
tive blocks (124 blocks per square mile) for each one of the 200 square
mile quadrats in the study area.
Dispersal gradients, as defined by Gregory (51) and Gould (48),
were calculated from the regression of the log of the cumulative
number of infected trees per unit of ground area, x, against the log of
distance from source, y. The equation
log y = a + b log x (eq. 4)
where b = the infection gradient and a = average incidence,
assumes that the gradient varies with the distance from source of
infection and not with the amount of disease. Steep gradients indi-
cate the enlargement of existing foci while shallow gradients indicate
the development of new foci. Cumulative infections were determined
for 10 concentric rings, each 1 mile (1.6 km) wide, around the original
source of infestation in Coral Gables. Regression was performed for
cumulative infections per square mile against distance in miles from
the source, for six time periods of 4 months each, beginning in
September 1971 (Fig. 21).
Interpretation of dispersal gradients shows that b values (slopes of
the regression equations) varied greatly for the different time
periods. The steepest gradients (- 2.66 and 2.23) occurred during
the first 8 months of the epidemic when infections were concentrated
at the source and few daughter foci had developed. A more shallow
gradient (- 1.51) developed during period III (8 to 14 months), in-
dicating the beginning of a "jump spread" pattern of new focal de-
I -9 9T
I .5 I I I I
.7 0 .8 1.6 2.4 3.2
(.5mi.) (1mi.) (2mi.) (5mi.) (11mi.) (24mi.)
log e of distance (miles)
Fig. 21. Dispersal gradients for six time periods (four months each) mea-
sured at one-mile increments around the initial focus of infection in Dade
velopment. In periods IV through VI dispersal gradients are greatly
flattened, indicating the development of more diffuse foci throughout
the study area.
Innovation curves, developed by plotting the percent infected trees
per square mile in each concentric ring with distance from source in
S 0.1 I
0.025 \ \\ ]
MILES 1 2 3 4 5 6 7 8 9 10 11
KM 1.6 3.2 4.8 6.4 8.0 9.6 11.2 12.814.416.1 176
Fig. 22. Innovation curves of the percent of palms infected per square mile
against distance from source.
miles (Fig. 22), indicate the development of daughter foci. The U-
shaped gradients in periods III through VI indicate the approach to
other sources, i.e., the daughter foci, at distances of 8 to 11 miles (12.8
to 17.6 km).
The rapid spread of LY on the Florida mainland has been analyzed
by McCoy (103) and Britt (7). In general, approximately 2 years after
the first cases of LY in any area of a few city blocks, all the coconut
palms were dead or dying. McCoy (103) reported that the apparent
rate of spread, r, was lower on shoreline sites, and this has been
verified by Steiner (154) for Kaincop6 disease in Africa. The pattern
of spread of LY in the Florida Keys has not been numerically ana-
lyzed; however, the pattern of spread in the islands has been erratic,
and seldom have coconut palms on any site been totally eradicated as
on the mainland. The reason for this disparity has not been deter-
The first 8 months of the LY epidemic in Miami was basically
manifested in primary focus development. Disease developed in ran-
dom contagion around this focus. The steep diffusion gradient indi-
cates that the number of infected palms dropped off rapidly with
increased distance from the source of inoculum. However, the in-
crease in number of infections and in number of foci in period III is
predicated by the number of infected palms in period I, assuming a 6
to 8-month latent period of LY. That is, the increase in number of LY
foci in period III came from inoculum and vector insects present in
period I. The "source" trees of period I were already dead (removed)
by the beginning of period III.
Lethal yellowing is a definite threat to coconut and date palm
production worldwide. Its rapid spread in the Caribbean and Florida
attest to this fact. The occurrence of LY or a very similar disease in
Africa emphasizes this international threat. Epidemiological analy-
ses of LY incidence data in Florida, Jamaica, and Africa have
brought about increased understanding of the disease process and
can serve as tools in control studies.
PHYSIOLOGICAL ASPECTS OF LETHAL
YELLOWING: WATER RELATIONS,
PROTEIN ASSAYS, AND
FREE ARGININE LEVELS
Relatively little information is available on the physiology of
lethal yellowing. Studies on the mineral content of healthy and
diseased palms have revealed few or no differences (44). Dabek and
Hunt found that detached, yellow pinnae became green after treat-
ment with gibberellic acid or copper, zinc, or iron salts (25). This led
tlTem to suggest that a hormonal imbalance might, in part, be re-
sponsible for the symptoms of LY. They also reported that exoge-
nously applied amino acids greatly increased the longevity of de-
tached healthy pinnae, but not of diseased pinnae, suggesting a
decreased rate of protein metabolism in LY-affected leaves (23).
Studies on the water relations of LY-diseased palms were initiated
by McDonough and Zimmermann (115). They reported that the diur-
nal fluctuation in water potential normally observed in healthy
palms was absent in diseased palms, and this phenomenon could be
observed in apparently healthy palms up to 2 weeks prior to the first
visible symptom expression. Healthy palms exhibited xylem pres-
sures ranging from an average of 1 bar (- 105 Pa) at night to 10
bar (- 1005 Pa) at midday. Diseased palms seldom exhibited pres-
sures lower than 4 bar ( 405 Pa), suggesting that stomatal closure
might be involved.
To corroborate these earlier studies using more sensitive tech-
niques and to tentatively identify the sites at which inhibition of
water transport occurs, the movement of solutions through healthy
and LY-diseased coconut palms was determined by injection of
radioactive 32P phosphate. Leaf tissues were sampled at intervals,
and relative amounts of 32P were determined with a gas-flow propor-
tional detector. When petiole bases of mature leaves on apparently
healthy palms were injected with 32P solution, activity was detected
in distal leaflets within 30 minutes. In palms with LY, transport was
absent or greatly reduced. When palms were injected in the trunk,
peak activity in leaves from the control plant reached 1000 counts per
minute after 4 hours, while no activity was detected in leaves from
the diseased palm over the 5 days of the experiment. When 32P was
supplied to palms through roots, activity was detected after 24 hours
in the apparently healthy palm and was not detected after 5 days in
the diseased palm.
To measure uptake of solutions by roots, a symptom-free and a
diseased 4-year old coconut palm were removed in the dry season
from 20-gallon drums in which they had been growing. Soil was
removed by washing the root mass in running water for 24 hours,
with care being taken to minimize root damage. The roots were
placed in drums containing 18 gallons (68 L) water to which 32P had
been added, and leaf samples were taken at intervals. Activity was
detected after 24 hours in the apparently healthy palm and was not
detected after 5 days in the diseased palm.
Stomatal openings were determined in the field by the silicone
impression method of Zelitch (174). Impressions were taken from
each of two medial leaflets from a mid-age and young leaf. The
transverse separation between guard cells was measured on 100
stomata on each impression. Stomata were rated as "open" if sepa-
ration was at least 2 pm. Stomata were closed on leaves of diseased
palms. Mean percent stomata open were 84 10 (healthy palm),
45 + 10 (early stage LY), and 1 1 (late stage LY). Resistance to
diffusion of water vapor from leaves was also higher (p < 0.002) in
diseased palms as measured by a diffusion resistance autoporometer.
Palms in early and intermediate disease stages had no significant
difference in diffusion resistance between yellowed and green leaves
from the same plant. Yellowed leaves from flag-leaf stage palms had
diffusion resistance comparable to that in diseased palms, whereas
non-yellowed leaves from the same palms showed diffusion resist-
ance comparable to that in healthy palms. Stomatal impressions
indicated that physical closure of stomata does indeed occur.
The data presented here, along with the earlier dye conduction
studies of Dabek (22) and Carter (12), clearly show that xylem trans-
port is reduced in coconut palms with LY. Both root necrosis and
vascular obstruction occur in palms with early-stage LY. Eden-
Green reported that root necrosis is coincident with the onset of
general yellowing of the crown in most instances, but follows the
earliest detectable symptoms by 10 to 30 days (38). Stomatal closure,
on the other hand, is detected in both symptomatic and asymptomatic
leaflets of yellow flag leaves before root necrosis occurs. Further,
stomatal closure is near its maximum throughout the crown as soon
as symptoms become systemic. This pattern suggests that stomatal
closure may be the primary factor in the restriction of water move-
ment in diseased palms.
Isoenzyme and Protein Studies
Antigenic comparisons of phloem sap derived from healthy and
diseased palms were reported by Charudattan and McCoy (16,107).
They reported the presence of a common antigen in phloem sap from
diseased coconut and Manila palms that was not present in exudate
from healthy palms, indicating that a characteristic protein might be
present in diseased tissues. Electrophoretic analysis of proteins from
healthy and diseased Manila palms, reported herein, has verified the
presence of a characteristic protein; however, it has not been detected
in coconut tissue.
In these studies, bud tissues were taken from mature coconut and
Manila palms with symptoms of LY, frozen in liquid nitrogen, lyo-
phylized, and ground in liquid nitrogen. Sodium dodecylsulfate-
protein extracts were prepared and electrophoresed on 5-15% linear
gradient polyacrylamide gels. Gels were stained with coomassie bril-
liant blue for protein analysis or were assayed for esterase, malate
dehydrogenase, lactate dehydrogenase, glucose-6-phosphate dehy-
drogenase, acid and alkaline phosphatases, 'a' and 'b' glucoisidases,
and ribonuclease. Tissues taken from healthy coconut and Manila
palms were run concurrently. Petiole base material from coconut
produced 28 to 30 bands on SDS gel electrophoresis, but no difference
in band patterns between healthy and LY material was apparent.
Gels from samples of petiole bases of Manila palms with LY showed a
characteristic protein band at Rf 0.78 0.1 (Fig. 23). This band was
detected in all the diseased palms sampled and was not apparent in
samples from healthy palms. There was a general increase in inten-
sity for this characteristic band as symptom severity increased (Fig.
24). Regression analysis indicated significant increase of adjusted
band intensity with increasing symptom severity (P < 0.003), with a
regression coefficient of 0.88.
The characteristic protein band in diseased Manila palms is clearly
an early indicator of LY. The intensity of the band is weakest in
palms showing the earliest visible symptoms. This suggests that the
characteristic protein may be present at a low concentration in dis-
eased palms prior to the onset of visible symptoms. However, since
the palm must be sacrificed to collect petiole base tissue, it would be
impossible to determine experimentally if this characteristic protein
could be detected in palms before the development of visible symp-
Three-year-old Manila palms grown in 18-gallon containers were
stressed by various means in an attempt to detect alterations in the
physiological systems which mimicked the LY disease state. Drought
stress was induced by withholding water for 30 days. Stressed palms
developed drooping, somewhat brittle leaves, but petiole bases
qrw -W T:
D H D H D H
Fig. 23. Proteins isolated from bud tissues of diseased (D) and healthy (H)
Manila palms. Arrow indicates unique protein from diseased tissue.
appeared normal. Palms held in the dark for 30 days developed
chlorotic leaves and had petiole bases of normal appearance. Palms
subjected to traumatic injury by striking the stem with a hammer in
the region of petiole bases developed an early stage bud rot after 7
days, but had no foliar symptoms. Palms held in the cold (4C) for 3
days, then for 4 weeks in a 50% shade house, developed no visible
symptoms. Controls were: (1) field-collected LY-diseased Manila
palms, showing browning and desiccation of leaves in the lower half
of the crown and an early stage secondary bud rot, and (2) healthy
container-grown Manila palms. The characteristic band was faintly
container-grown Manila palms. The characteristic band was faintly
" c-,~Lr Y- QCLI~
~ .7~A. i~ltt.
gi*l~- g a
Fig. 24. Protein bands isolated from Manila palms manifesting from 0,
healthy, to 3.5, severe, symptoms of lethal yellowing. Arrow denotes char-
acteristic protein band.
'-' ~- -~1IR
visible in two of three drought-stressed palms in duplicate gels of
duplicate SDS-protein preparations. The characteristic band was
absent in all other preparations, and with the exception of the
marker band in diseased and drought-stressed trees, all protein com-
ponents in all samples migrated at the same rate as components
present in the healthy palms.
In the isoenzyme assays, up to five esterase, three peroxidase, one
ribonuclease, and one alkaline phosphatase isoenzymes were de-
tected in various samples. Other enzymes were not detected by the
system used, and no consistent differences between diseased and
healthy tissue were observed.
Free Arginine Levels in Susceptible
and Resistant Palm Cultivars
In attempts to determine physiological factors related to the resist-
ance or susceptibility of palms to LY, a study was made of the free
amino acid distribution patterns in foliage of 18 species and varieties
of palms (Table 6) (Barcelon, McCoy, and Donselman, 1983, J. Chro-
matog. 260:147-155). In addition, phloem exudates collected from
three species and varieties of palm were examined. Evaluations were
made for 28 different amino acids by two-dimensional thin layer
chromatography of dansylated leaf or sap extracts after chloroform
extraction to remove non-polar organic components (Barcelon, M.,
1982, J. Chromatog. 238:175).
A correlation was observed between the presence of free arginine
and susceptibility to LY. Arginine was readily detected in samples
from susceptible palms and was not detected in palms apparently
immune to LY. Intensity of arginine spots on the chromatograms was
greatest in the most susceptible varieties, i.e., 'Jamaica Tall' coconut
and Thurston palms. No apparent relationship to LY was evident for
any of the other amino acids assayed in these tests.
The potential significance of these results lies in the fact that
species of the genus Mycoplasma that do not utilize sugars for growth
depend on arginine as a major source of energy (Razin, S., 1978,
Microbiol. Revs. 42:414). Should the correlation between the pres-
ence of arginine and LY susceptibility be verified, it could serve not
only in the formulation of media for growth of the causal MLO, but as
a quick biochemical means of screening new palm cultivars for resist-
ance to LY.
Table 6. Detection of free arginine by thin layer chromatography of ex-
tracts from palms resistant or susceptible to lethal yellowing.
Suscepti- Relative arginine level2
Scientific name rating' foliage phloem sap
Arecastrum romanzoffianum 0 nd3
Crysalidocarpus lutescens 0 nd
Phoenix roebelenii 0 nd
Ptychosperma elegans 0 nd
Roystonea regia 0 nd
Sabal palmetto 0 nd
Washingtonia robusta 0 nd
Carpentaria acuminata 0 + nd
Cocos nucifera 'Malayan Dwarf' 1 + -
Cocos nucifera 'Maypan' 1 nd
Caryota mitis 2 + nd
Arikuryroba schizophylla 2 + nd
Phoenix dactylifera 'Deglet Noor' 2 + nd
Phoenix dactylifera 'Halawi' 2 + nd
Veitchia merrillii 2 + + + +
Cocos nucifera 'Jamaica Tall' 3 + + + +
Pritchardia thurstonii 3 + + nd
Wallichia disticha nd4 + + + nd
1. 0 = apparently immune, 1 = resistant, 2 = moderately susceptible, 3 = highly
2. Intensity of fluorescence of monodansyl arginine on TLC plate: = not detected,
+ = faint, + + = definite, + ++ = bright.
3. nd = not determined.
4. Palm very rare in Florida. Not examined for MLO, but most specimens in LY-
affected areas have died.
TRANSMISSION OF LETHAL
YELLOWING: HISTORICAL STUDIES
Early Investigations on the Role of Insects
As early as the 1880's it was suspected that insects were in some
way associated with LY. Some early observers in Cuba suggested
that LY was possibly caused by toxins injected into coconut palms by
certain insects that fed on them. Species of beetles (Coleoptera), true
bugs (Heteroptera), and scale insects (Coccoidea) were suspected by
various workers (28). A second early notion concerning a possible
relationship between insects and LY was based on the belief that a
fungus or bacterium associated with the decaying bud of palms in
later stages of disease was the causal organism. Many kinds of
insects are attracted to decaying plant material; they burrow in and
feed on the plant material or the decay fungi, or prey on other insects
attracted to the site. Flies (Diptera) are the insects most consistently
found around decaying palm buds. Since there was evidence by the
turn of the century that certain flies spread human diseases (50), flies
were the first insects to be singled out by workers in Cuba as possible
vectors of LY (80, 151). Observations by Johnston in 1912 of the
erratic spread of the disease in coconut plantations strengthened
suspicions that an insect vector might be involved; this author pro-
posed flying insects or birds as the probable modes of spread.
The Beginning of the Modern Phase
Bruner and Boucle in 1943 suggested on the basis of their observa-
tions of the spread of LY in Cuba that the disease was probably
caused by a virus and that the vector was probably either a species of
thrips (Thysanoptera) or a species of the order Homoptera. Thrips
known to occur on coconut palms in Cuba were not leaf-feeders, but
were associated with the flowers or were predaceous. Since LY could
attack young coconut palms that had not developed flowers, these
authors concluded that a homopteran was probably the vector. Of the
Homoptera, they discounted the scale insects, because although some
species were common on coconut palms, no species of scale insect was
known to transmit viruses. Their prime suspect was an unidentified
species of aphid that, although uncommon on coconut palm, was the
only homopteran in Cuba other than scale insects that completed its
life cycle on this host (8).
Bruner and Boucle's report probably had little influence on LY
research during the following three decades. Most of the work was
carried out in Jamaica, and researchers in that country were either
unaware of the Cuban work, or possibly considered that the diseases
in the two countries were different. They arrived independently at a
theory similar to that of Bruner and Boucle, based on detailed
observation of the symptomatology and pattern of spread (14, 124).
Although the virus-insect vector theory was questioned by some
authors (e.g., 94, 120, 141), the theory was generally favored by
researchers from the 1940's through the 1960's (e.g., 14, 19, 20, 54,
Early Transmission Experiments
Beginning in the early 1960's transmission tests were initiated in
Florida and Jamaica. The work in Florida was reported in Florida
Division of Plant Industry Biennial Reports. Much of the work
accomplished in Jamaica from 1962 to 1971 is contained in record
books and unpublished reports; however, Johnson and Eden-Green
published an excellent review of this work (79).
Transmission trials during this period were based on the hypoth-
esis that LY was caused by a virus. Thus, auchenorrhynchous
Homoptera leafhopperss and planthoppers and their relatives) were
emphasized because many virus diseases of plants are transmitted by
species of that taxonomic group. Whiteflies (Aleyrodidae) were also
intensively investigated. In addition, species of scale insects and
mealybugs, aphids (Aphidae), true bugs (Heteroptera), thrips, and
flies (Diptera: Ortalidae) were tested. A million or more insects were
involved in these tests. Species of mites (Acarina) were also tested,
and experiments were conducted to determine whether nematodes
could transmit the LY agent, or cause LY directly.
Evidence was obtained that the disease was transmitted by an
insect. Caged palms into which insects were not introduced but which
were in areas of high LY incidence did not contract the disease until
after the cages were removed (66, 139). Although transmission ex-
periments in Jamaica conducted during the 1960's neither conclu-
sively implicated a vector of LY nor entirely eliminated any species
as a possible vector, progress was made in developing experimental
techniques, and demonstrating the feasibility of the relatively large
scale and long term experiments required for this phase of palm
disease research. In addition, experimental transmission was
apparently accomplished with at least four out of a total of 373 test
palms used in these experiments. These apparent successes were in
experiments involving mixtures of different insect species containing
auchenorrhynchous Homoptera and, in three cases, were restricted
to the latter group. Of particular interest are the results of an experi-
ment conducted by K. Heinze and M. Schuiling in which one and
possibly two palms exposed to mixtures of Omolicna cubana Myers
and Myndus crudus Van Duzee plus unidentified species from the
undergrowth of coconut plantations, contracted LY. Similar results
were obtained by R. K. Latta and P. McKenzie with mixtures of
Cicadellidae and Fulgoroidea (79). These results were discounted
because they could not be repeated, there were tears in the cages, and
the infection rate was thought to be too low for the numbers of insects
introduced into cages.
Johnson and Eden-Green (79), however, in discussing populations
and movements of auchenorrhynchous Homoptera in relation to LY
infection rate in Jamaican coconut plantations, pointed out that
transmission of LY by insects could have occurred in these tests.
They also reported that M. crudus, although not identified in trans-
mission tests prior to 1969, was present in collections from the areas
where the tests were conducted and may have been involved in some
Whiteflies were suspected as possible vectors because in Jamaica
several species complete their life cycle on coconut foliage. During
the 1960's these insects were tested by different workers. In one
experiment in 1967 involving Aleurodicusjamaicensis Cockerell and
possibly other species, one and possibly two coconut palms appar-
ently became affected by LY (79). A whitefly of this same genus, A.
dispersus Russell, was under scrutiny as a possible vector of LY in
Key West, Florida, and transmission experiments had been con-
ducted with this insect (91). In 1971, this species was reported to be
spreading from Key West eastward along the Keys; meanwhile there
was an outbreak of LY on Key Largo. Thus, whiteflies became prime
suspect vectors of LY (169). Attention shifted from whiteflies, how-
ever, when experiments with whiteflies were repeated and no trans-
mission occurred (36). A reappraisal of the whitefly transmission
experiments cast further doubt that these insects transmitted the
disease inside cages. In Florida, the distribution of A. dispersus is
spotty, and palms which have been inspected frequently and been
determined to be free of this insect have contracted LY (F. W.- Ho-
ward, unpublished observations). When it was discovered in 1972
that MLO were associated with LY, emphasis on these insects was
dropped, as no whitefly has been reported to be a vector of this type of
By the early 1970's no possible mode of transmission had been
entirely rejected. Experimental and observational evidence disfa-
vored transmission by nematodes or other soil inhabiting organisms,
and favored transmission by an airborne insect. It had been suspected
by many investigators since the 1940's that LY was caused by a virus
that was transmitted by a species of Homoptera. Throughout the
1960's auchenorrhynchous Homoptera had been intensively investi-
gated as suspected vectors. The discovery of the association of MLO
with LY in 1972 further focused attention on this taxonomic group of
Taxonomic Relationship of MLO Vectors
Known vectors of MLO-associated plant diseases are insects in the
order Homoptera (83, 163). Taxonomic relationships within this
order may be summarized for the purpose of this bulletin as follows
Suborder Coleorrhyncha-a small primitive taxonomic group confined to
the Southern Hemisphere.
Superfamily Cicadoidea. Families: Cicadidae (cicadas), Membracidae
(treehoppers), Cercopidae (froghoppers, spittlebugs), Cicadellidae
Superfamily Fulgoroidea (Planthoppers). Families: Delphacidae, Der-
bidae, Cixiidae, Flatidae, plus 16 additional families.
Superfamilies: Psylloidea psyllidss), Aleyrodoidea (whiteflies), Aphi-
doidea (aphids, phylloxerans and relatives), Coccoidea (scale insects
The vast majority of insect species known to be vectors of MLO
diseases belong to the family Cicadellidae. A few vector species
belong to the Delphacidae and Cixiidae and one to the Psyllidae.
Species of Coccoidea and Aphidoidea have been reported as vectors of
MLO-associated plant diseases, but these reports are unsubstanti-
Potential Vectors of LY
According to results of field surveys in Jamaica since 1972, five
species of Fulgoroidea were found to be commonly associated with
coconut palms (145, 146). In southern Florida, two fulgorids, Myndus
crudus and Cedusa inflata Ball, and one membracid, Idioderma vires-
cens Van Duzee, constitute the common coconut palm-associated
Auchenorrhyncha (69, 72, 73). Myndus crudus (Fig. 25) is the only
auchenorrhynchous species commonly found on coconut palms in
Fig. 25. Myndus crudus Van Duzee, a planthopper implicated as a vector of
both areas and has been extensively tested as a vector of LY (See
Chapter 6). Cicadellidae are occasionally collected from palms in
Florida and Jamaica (39, 69, 73, 145, 146); however, in Florida, even
small palms growing in tall grass infested with cicadellids are usu-
ally free of these insects (F. W. Howard, unpublished observations).
Annotated List of Potential Vectors
in Addition to M. crudus
A Myndus sp. near crudus is known from two male specimens
collected in July 1980 from foliage of 'Malayan Dwarf' coconut palms
near Maimon on the north coast of the Dominican Republic. One
female, probably of this same species, was also collected there (75).
The population of Myndus sp. was apparently low at the time these
collections were made. Myndus crudus has not been reported from
the Dominican Republic or neighboring Haiti. Thus, Myndus sp. may
replace M. crudus as the vector of LY on this island. Further field
studies should be conducted in these two countries.
Cedusa inflata has been collected from 21 species of palms in
Florida (73), from several palm species in the Dominican Republic
(75), and, without host data, in Cuba (127). Cedusa sp. near flavida is
found on coconut palms in Jamaica (145). However, both C. inflata in
Florida and Cedusa sp. near flavida in Jamaica occur in small, local-
ized populations. Even if the species were capable of transmitting LY,
they would be relatively unimportant as vectors. No species of Der-
bidae has been implicated as a MLO vector (163).
Omolicna sp. (cubana complex). The taxonomy of this complex
needs clarification (J. P. Kramer,8 personal communication). Omo-
licna cubana has been reported as common in Jamaica and was
present in mixtures of insects that may have transmitted LY in
experimental cages (79). Species of this complex were collected on
palm foliage in the Dominican Republic (75) and rarely from palms in
Idioderma virescens Van Duzee has been collected from the foliage
of several palm species in Florida (69, 73) and the Dominican Repub-
lic (75). It has been reported from Cuba (127) and Bimini Island,
Bahamas (117). Idioderma varia was reported in coconut plantations
in Jamaica (40), but this record is questionable and has not been
verified by a specialist in this taxonomic group.
In one test in Florida a total of 32 Idioderma adults were collected
over a 12-month period from Manila palms in the LY epidemic area.
They were caged on a 0.5-m tall Pritchardia eriostachya palm, which
later died, but no MLO were detected in EM examination of this
palm. No membracid species has been implicated as a vector of a
MLO disease (163).
Chlorotettix minimus Baker is common on grasses in warmer re-
gions of the Western Hemisphere. This species has been collected on
palms in Florida (73) and in the Dominican Republic (75). Although
seldom found on palms, C. minimus is the most common cicadellid on
Hortensia similis Walker is widely distributed in the Americas
(118). It was collected on coconut palm foliage in the Dominican
8. Smithsonian Institution, Washington, D.C.
Republic (75), and in Florida is common on grasses, but rare on
palms. It is abundant in the undergrowth in coconut plantations in
Jamaica and has been tested as a possible vector of LY in Jamaica
and Florida with negative results (39, 79, 161).
Graminella spp. are generally grass feeders. In Florida we have not
observed species of this genus feeding on palms, but have occasion-
ally found damaged specimens that appeared to be species of Gram-
inella in sticky traps in palms. Three Graminella species, G. nigri-
frons Forbes, G. cognita Caldwell, and G. floridana Delong and Mohr,
are found abundantly on bermudagrass in south Florida, and they
were often found in rotary flight trap samples near palms (173). A
specimen of G. cognita Caldwell was collected from a coconut palm in
the Dominican Republic (75). In a test in Florida G. nigrifrons and G.
cognita were given 48 to 120 hours acquisition access period (AAP) on
LY-affected coconut palms, or were injected with phloem exudate or
triturated meristem tissues collected from LY-affected Manila
palms. The injected insects were kept on corn plants for 10 to 19 days
incubation period (IP), after which they were caged on Pritchardia,
coconut, or Manila palms. No disease symptoms were observed. Spe-
cies of Graminella have also been tested for LY transmission in
Jamaica (79) with negative results. Graminella nigrifrons is a vector
of the corn stunt spiroplasma (81, 122).
Dalbulus maidis (Delong and Wolcott) is another vector of corn
stunt spiroplasma (122). One specimen of D. maidis was collected
from a coconut palm in the Dominican Republic, but there is no
evidence from more extensive observations in Florida and Jamaica
that this species is associated with palms. However, an experiment
was conducted in Florida to test this insect as a potential ex-
perimental vector of the LY agent. Two groups of D. maidis were
caged on LY-affected palm leaves for a 24-hr AAP. At the end of the
AAP, 377 and 2097 leafhoppers were caged on potted sweet corn for
14 to 20 days IP, followed by transfer to a Manila and a coconut palm.
Neither of these test palms developed LY symptoms during 18
months of observation.
Peregrinus maidis Ashmead was also tested as an experimental
vector. Three groups ofP. maidis (300, 600, and 600) were allowed to
feed on LY-affected palm tissue. After 2 to 7 days AAP, the insects
were transferred to potted corn plants for 14 to 20 days IP. Only 10,
159, and 163 insects were recovered, respectively. These were caged
on one 2-m tall coconut palm and two 2-m tall Manila palms. No
symptoms were observed during 18 months of observation.
Oncometopia nigricans Walker has been found in coconut groves,
and was found to feed on Manila and coconut palms (43). Transmis-
sion tests with this insect in Florida were negative (161).
Spangbergiella vulnerata is abundant on St. Augustinegrass and
other grasses under coconut plantings both in Jamaica and Florida
and has been proved to feed on palms. Spangbergiella leafhoppers
from stock colonies were caged on spear leaves of LY-affected coconut
palms for a 2 to 5 day AAP and were then transferred to three 2-m tall
coconut and three 1.5-m tall Manila palms. None of the test plants
developed LY symptoms after 18 months.
Several groups of Macrosteles fascifrons StAl totaling 6680 adults
were allowed to feed on detached fronds of diseased coconut and
Manila palms for 5 to 9 days AAP. The surviving insects were then
transferred to young coconut and Manila palms after 2 to 3 weeks on
corn plants. Longevity of M. fascifrons on coconut and Manila palms
is presented in Table 7. No transmission resulted. M. fascifrons fed or
injected with phloem exudate from diseased coconut palms were
placed on aster, celery, and coconut or Manila palms, but no symptom
development was observed. Inoculum processed from the lyophilized
meristem of a diseased Manila palm was also injected into M. fasci-
frons nymphs. The insects were kept on oat plants, Avena sativa L.,
for 7 days prior to transferring to Pritchardia, coconut, or Manila
palms. No transmission resulted.
Table 7. Longevity of Macrosteles fascifrons on palms.
Longevity on palm (days)
Test plant No. of insects Max. Mean
Coconut palm 70 33 9.3
Coconut palm 142 24 9.7
Manila palm 208 38 6.7
Manila palm 110 43 -
Palm aphids (Cerataphis variabilis (Hille Ris Lambers) are
phloem-feeders associated with many species of palms. This insect
has strong host preferences and is only rarely found on the LY-
susceptible 'Jamaica Tall' coconut and Manila palms, but may build
up high populations on 'Malayan Dwarf' coconut palm. For this
reason, and because aphids rarely, if ever, transmit MLO, the palm
aphid is an unlikely LY vector. However, several attempts were
made to transmit the LY agent with this aphid. Many technical
difficulties were encountered during the course of the transmission
trials. These were mainly due to a high mortality rate in transferring
the insects from one palm to another. Colonies were reared on
'Malayan Dwarf' palms. The early instar nymphs were transferred
by a camel hair brush, and winged adults were transferred by means
of an aspirator or by attaching the cut spear leaves which were
colonized by the aphids to LY-affected leaves for 5 to 7 days AAP.
Only about 5% of several thousand transferred aphids survived after
AAP. Furthermore, only about 1% of those were successfully trans-
ferred to two coconut and two Manila palms. No symptoms were
noted during 10 months observation in a screenroom.
BIOLOGY OF MYNDUS CRUDUS AND
EVIDENCE IMPLICATING IT AS A
VECTOR OF LETHAL YELLOWING
Myndus crudus is the most common auchenorrhynchous homop-
teran on coconut palms in Florida (73) and Jamaica (145). Its range
generally coincides with LY-affected areas in Florida and it has been
found on all but the rarest of the palm species susceptible to LY.
Adults of this planthopper feed on palm foliage, but oviposit on soil
(37). Nymphs develop underground and feed on the roots of grasses,
most notably, St. Augustinegrass.
Although M. crudus was included in early transmission tests in
Florida (161, 162) and Jamaica (26, 37), the LY pathogen was not
transmitted. Because field evidence favored M. crudus as a vector of
LY, studies of its biology, and transmission tests under experimental
conditions different from those of previous tests, were initiated.
Biology of Myndus crudus
Eggs are whitish, about 0.15-0.20 x 0.5-0.6 mm. They are laid
near the soil surface on plant parts or underneath debris (37, 164,
175). Eggs hatch in 19.5 0.8 days at 24C and 11.0 days at 30C
There are five nymphal instars (Fig. 26). Tsai and Kirsch (164)
reported an average of 61.3 days from egg eclosion to the last
nymphal molt at 24C, and 41.5 days at 300C. Nymphs kept at 15C
did not develop into adults. Nymphs are found aggregated in the soil
in "nests" lined with a flocculent material which they secrete from
ducts on the abdomen. Usually five to eight nymphs are observed in a
nest. Nymphs are usually within a few cm of the soil surface, but have
been found as deep as 20 cm (175).
Adults (Fig. 25) are 4.0 to 4.8 mm long, the females being slightly
larger and longer lived than the males. Female to male ratios have
been reported as 1:1 and 1.7:1; this ratio probably varies with season
and environmental conditions (135, 164, 175). Mating has been
observed on palm fronds (175, and F. W. Howard, unpublished
observations). Adults can live up to 50 days on palms (164).
Fig. 26. A nymph (immature stage) of Myndus crudus. The nymphs live
underground and feed on the roots of grasses.
Myndus crudus is a phloem feeder (43, 168). The species is
apparently almost entirely restricted to monocotyledonous host
plants. In Colombia, nymphs of M. crudus (as Haplaxius pallidus)
were collected from roots of eight species of grasses (Poaceae) and one
species of sedge (Cyperaceae). Adults were collected from Heliconia
bihai L.f. (Heliconiaceae) and Carludovica palmata Ruiz and Pav.
(Cyclanthaceae) as well as from palms (116, 175). Seven species of
grasses and one species of sedge were found to be hosts in Florida. In
addition, nymphs were found to feed on roots of Verbena scabra Vahl.
(Verbenaceae) (164). Myndus crudus has been collected from 26 spe-
cies of palms (73, 134) and from Pandanus utilis (F. W. Howard,
unpublished) in Florida. Palms and several species of grasses are
hosts ofM. crudus in Jamaica (33, 34, 37). Grasses have been used to
rear M. crudus in the laboratory (37, 165).
Certain palm species and varieties are more attractive to M. cru-
dus adults than others. 'Golden Malayan Dwarf' coconut palms are
more attractive than 'Green Malayan Dwarf' or 'Jamaica Tall'
varieties (164). Young coconut palms are more attractive than young
date palms, but no difference in numbers of M. crudus visiting ma-
ture coconut and Canary Island date palms has been detected (69).
Relatively high numbers ofM. crudus adults have sometimes been
observed on coconut palms, Pritchardia spp., Washingtonia spp.,
Sabalpalmetto, Acoelorraphe wrightii, and Veitchia merrillii, but the
insect has been observed only occasionally on certain other palms,
e.g., Chrysalidocarpus lutescens, Arecastrum romanzoffianum,
Caryota spp., and Latania spp. These apparent host preferences have
not been confirmed experimentally, however (F. W. Howard, unpub-
Eden-Green (37) found that St. Augustinegrass was the most reli-
able grass for rearing M. crudus nymphs for experiments. Reinert
(135) reported that higher numbers of adults were collected in sweep
net samples from St. Augustinegrass than from bermudagrass or
Seasonal and Diurnal Activity
Myndus crudus flies actively all year in southern Florida (173).
Reinert (135) collected adults in sweep net samples from grasses
throughout the year, and found that nymphal populations varied
little throughout the year on bahiagrass, but during cooler months
were greatly reduced on St. Augustinegrass. In general, it is possible
to find high numbers of M. crudus on palms at any time of year in
southern Florida. The eyes of M. crudus become adapted to darkness
or light through a distal-proximal migration of eye pigments (Fig.
27); thus, the species flies actively by day and night (70).
Field Evidence for Myndus crudus
as an LY Vector
Myndus crudus was described by Van Duzee from specimens col-
lected in eastern Jamaica in 1907 (82). It was not listed as present in
the fauna of coconut plantations by LY researchers in Jamaica until
1969, but in re-examining the field collections of these researchers,
Johnson and Eden-Green (79) found a long series of specimens of this
Myndus crudus (as M. pallidus Caldwell) was collected in Miami,
Florida, as early as 1934 (10), but almost nothing was known about
this species until the 1970's. A survey of auchenorrhynchous insects
on and among coconut palms in southern Florida was initiated soon
after the discovery of MLO associated with LY. Similar surveys were
undertaken in Jamaica to augment information already accumu-
lated during the 1960's. It was determined that both in Florida (172)
and in Jamaica (145), M. crudus was the most abundant auchenor-
rhynchous insect associated with coconut palms. This circumstantial
Fig. 27 Cross sections of compound eyes of Myndus crudus: (top) light-
adapted eyes, (bottom) dark-adapted eyes.
evidence for a vector of LY was immediately followed by biological
studies and transmission experiments with this insect (26,33, 34,37,
38, 161, 162).
In further survey work in Florida, M. crudus was the only auche-
norrhynchous insect which was collected in all localities where LY
had been reported, was collected from all but the rarest LY suscepti-
ble palm species (73), and was found to be the most abundant auche-
norrhynchous insect on mature Canary Island date palms (69). Based
on simultaneous sampling in and outside the area affected by LY in
Florida, populations of M. crudus were about 40 times greater inside
the affected area (i.e., the southeast coast) than in LY-free areas (68).
Where certain insecticides were applied bi-weekly for 15 months to
Manila palms in Hollywood, Florida, populations ofM. crudus were
reduced and the rate of spread of LY was diminished. These results
were further interpreted as evidence that an insect, possibly M.
crudus, was the vector of LY (72, Chapter 7).
Myndus crudus has been reported from diverse localities in north-
ern South America, Trinidad, Central America, and Mexico (82). It
was recently found in the Rio Grande Valley of Texas in a survey
initiated after LY was reported in, that area (119). Myndus crudus
was collected on Grand Cayman Island in 1938 (41) and by W. B.
Ennis, Jr.9 in 1979. It is known from diverse localities in Jamaica and
Cuba (82). All three islands have been affected by LY for many years
The relative abundance ofM. crudus on palms in Florida compared
to other species of Auchenorrhyncha is indicated by the two following
examples. (1) Insects visiting 60 Manila palms that served as the
untreated controls of an insecticide experiment in Hollywood, Flor-
ida, were sampled by applying an adhesive substance to five pinnae of
each palm. The average numbers of auchenorrhynchous insects per
five pinnae for 15 months total sampling were 11.2 M. crudus, 0.08 1.
virescens, and 0.06 others (mostly cicadellids) (72). (2) In a three-
county area of southern Florida, 20 x 20 cm sticky traps were
exposed for 30 days in the crowns of 16 mature Canary Island date
palms and 16 mature coconut palms. Average numbers of auchenor-
rhynchous insects on sticky traps in Canary Island date palms
were: 42.0 (range 1-541) M. crudus, and 0.6 I. virescens; on sticky
traps in coconut palms, 11.2 (0-59) M. crudus, and 0.4 I. virescens.
Fewer than 10 cicadellids in too poor a condition for identification
were present in samples (69). Similar sticky trap samples in a plant-
ing of 4-year old coconut palms caught an average of about 28 M.
crudus and 0.8 C. inflata; I. virescens was not collected.
9. University of Florida, AREC, Fort Lauderdale, Florida 33314
During the past 5 years about 200,000 live specimens ofM. crudus
have been field collected for transmission experiments. The numbers
collected vary considerably at different times and localities, but in
some habitats it was possible during any time of the year for a skilled
collector to capture 200 to 800 live specimens from palms within a few
hours. I. virescens and C. inflata were seldom encountered.
Transmission Tests with Myndus crudus
Early Tests with Myndus crudus
An exhaustive series of controlled acquisition and transmission
experiments was conducted with M. crudus in Florida (162). Adult
and nymphal instars were allowed to feed on diseased coconut palms,
on excised palm hearts and roots, and through membranes on phloem
sap collected from diseased coconut palms. Insects were caged on
2.5-m tall coconut palms in a screenhouse; however, very few test
insects survived more than 3 weeks on the test palms. None of the
palms tested developed LY symptoms after a year in a screenhouse.
Additional tests used phloem sap from LY-diseased Manila palms,
either injected into M. crudus or fed through a membrane. Again no
transmission occurred. Attempts to transmit LY from coconut to
Manila palms and vice versa were also unsuccessful, as were
attempts to transmit LY to periwinkle [Catharanthus roseus (L.) G.
Don.]. In all, over 70,000 M. crudus were used in these tests, but no
verifiable transmission occurred. Nevertheless, because circumstan-
tial field evidence indicated that M. crudus was a likely vector ofLY,
additional transmission experiments were undertaken.
Replicated Transmission Test
Ten cages were constructed at the Agricultural Research and
Education Center in Fort Lauderdale in September 1978 (Fig. 28). A
long term experiment was planned because LY has an estimated
incubation period of 114 to 450 days (7, 24, 103, 139). A field-grown
'Jamaica Tall' coconut palm about 5 years old was planted in the
center of each cage. One or two Manila palms each estimated to be 5
years old were transplanted from pots into each cage. One Thurston
palm was planted in each of six cages. All palms were obtained from
LY-free areas. Two species of grasses were established as ground
cover in the cages: bahiagrass (Paspalum notatum Flugge) was
seeded into the dirt floor of the cages, and St. Augustinegrass stolons
free of insects were sprigged into the cage floor. Five cages that
S ":''- '- ,-... '" ""- "
r S -1 '- .
Fig. 28. A coconut palm with lethal yellowing in one of five cages into
which Myndus crudus from lethal yellowing-affected areas had been
received introductions ofM. crudus (i.e., treatment cages) alternated
with five cages used as controls.
Beginning on October 23, 1979, each treatment cage received
about 850 M. crudus per month from LY-affected areas. This number
was similar to or lower than the numbers of these insects that natu-
rally visit palms outdoors in LY-affected areas. For example, an
average of 22 M. crudus were observed resting on 4-year-old 'Jamaica
Tall' coconut palms in the LY-affected planting where most of the
M. crudus were collected for this study (69). The flight habits of M.
crudus have not been studied, but palms from which all of the M.
crudus were removed were quickly reinfested (F. W. Howard, unpub-
lished observations). Assuming that insects fly to a new palm only
once per day, 660 M. crudus may visit a 4-year old coconut palm
during a 30-day period, and the actual number is probably greater
Palms with symptoms of lethal yellowing were removed from the
cages and diagnoses were confirmed by electron microscopic (EM)
examination for the presence of MLO (74, 157, 158, 159). The experi-
ment was terminated after 34 months, at which time the coconut
palms had grown too large for the cages. At least one palm in every
treatment cage contracted LY (Howard, Norris, and Thomas, unpub-
lished). In two of the treatment cages palms of all three species
contracted LY. Three of five coconut palms, five of seven Manila
palms, and two of three Thurston palms in the treatment cages
contracted LY, and MLO were observed in bud tissue sections from
all of these palms. Healthy Thurston palms from control cages were
saved for additional experiments. All other healthy palms were re-
moved from cages, and sections were made of bud tissue for examina-
tion by EM. MLO were not observed in any of these palms.
These results provide strong evidence that M. crudus is a vector of
the MLO that causes LY. They also serve as evidence that the dis-
eases of these three species of palms are caused by the same
These experiments differed from previous LY transmission experi-
ments in the following ways: in addition to coconut palm, palms of
other species were used as test plants; grasses were planted in the
cages as alternate hosts to attempt to increase the longevity of the
insects; the insects were captured using a technique that reduced the
possibility of injuring them (in many previous experiments aspira-
tors were used); insects were introduced throughout the year, rather
than during a limited period; higher numbers of the suspected vector
were introduced into the cages; and insects were captured from symp-
tomatic as well as from symptomless palms.
CONTROL OF LETHAL YELLOWING:
RESISTANCE AND CHEMOTHERAPY
Control of lethal yellowing is possible through an integrated pro-
gram utilizing the measures of resistance, protection, eradication,
and quarantine. Although no permanent chemical cure is known for
LY or any MLO-associated plant disease, the antibiotic oxytetracy-
cline can bring about a remission of LY and may be administered
protectively to healthy palms. Chemotherapy may be used to main-
tain susceptible palms in the landscape while resistant palms are
being cultivated. Ultimately, host plant resistance is the best means
for dealing with LY. Eradication of diseased palms, in itself, has
never stopped LY; however, it is presumed that the rapid removal of
affected palms will slow the apparent rate of spread to healthy palms
(See Chapter 3). Quarantine is a regulatory measure designed to
prevent the inadvertent movement of infected palms or vectors to
disease-free areas. Each of these measures is currently recommended
for control of LY in Florida. This chapter will discuss resistance,
chemotherapy, and an alternative approach, vector control.
The Search for Resistant Palms
Data on resistance of palm species and cultivars to LY has been
derived from observations in established plantings affected by the
disease. Work in Jamaica established the level of resistance of
numerous coconut cultivars. Most notable among these is the
'Malayan Dwarf' (Fig. 29) (58,59,60,63,124,170,171). The 'Jamaica
Tall' cultivar had been the foundation of the Jamaican coconut indus-
try, and was practically the only variety grown in Florida. It is one of
the most susceptible cultivars to lethal yellowing, and millions of
these palms were killed after the outbreaks of the disease in Jamaica
and Florida during the last two decades. Fortunately, an estimated
70,000 seeds of'Malayan Dwarf' coconut palm had been imported to
Jamaica prior to 1951 (170). It was not known at that time that they
were resistant to LY; their chief advantage was that they come into
bearing at an earlier age than 'Jamaica Talls.'
Fig. 29. "Green form" of the 'Malayan Dwarf' coconut palm at the Florida
Division of Forestry's Miami Seed Orchard. These are vigorous growers and
are highly resistant to lethal yellowing.
The 'Malayan Dwarf' Coconut Palm
As lethal yellowing spread through the eastern end of Jamaica, it
was discovered that while 90% or more of the 'Jamaica Tall' coconut
palms were killed wherever the disease occurred, less than 5% of the
'Malayan Dwarf' coconut palms were affected. The Jamaican coconut
industry has been converting to resistant cultivars (49,64,138,
149,152); presently, nearly a million 'Malayan Dwarf' coconut palms,
and about 50,000 resistant hybrids are being planted each year to
replace 'Jamaica Tall' coconut palms killed by LY in Jamaica (140).
Approximately 200,000 'Malayan Dwarf' palms have been estab-
lished in Florida (Fig. 30).
'Malayan Dwarf' coconut palms have been grown in south Florida
for over 25 years, although most individuals in this area are less than
10 years old. Three color forms are cultivated-"golden" or "red,"
"green," and "yellow." The majority are of the golden form, so named
because of the golden color of the petioles and coconuts. The golden
'Malayan Dwarf' has a less intense green coloration of the leaflets
than most coconut palms, and unless properly fertilized, exhibits
what might be called a "hungry look." The 'Malayan Dwarf' does
need extra care, similar to that given other ornamentals and fruit
crops; in contrast, the 'Jamaica Tall' coconut palm grows very well in
sandy soil with little fertilization. However, once established, the
Fig. 30. Management of lethal yellowing disease in Palm Beach by inter-
planting resistant varieties among the susceptible 'Jamaica Tall' coconut
palms and, at the same time, injecting the Jamaica Talls to maintain them
until the new palms are large enough to serve as replacements.
'Malayan Dwarf' does well in Florida, as demonstrated by the vigor-
ous growth and healthy appearance of many older palms of this
variety planted on the mainland and in the Florida Keys.
Since August 1979, the Jamaican Coconut Industry Board has
agreed to export the green 'Malayan Dwarf' in large quantities. This
form establishes more readily, and grows more rapidly during the
first 5 years than the golden or yellow forms. The green form more
closely resembles the 'Jamaica Tall' and does not have the yellow cast
of the golden, although some people prefer the golden specifically for
its coloration. Resistance to lethal yellowing is the same in all three
Spear Leaf Necrosis of 'Malayan Dwarf' Coconut Palms
One problem of 'Malayan Dwarf' palms in Florida has been a spear
leaf necrosis that begins at or near the point at which the spear leaf
emerges from the sheath of the preceding leaf base. The necrosis
advances up and down the spear leaf and eventually engulfs the bud,
killing the palm. The other leaves of affected palms often appear
normal, although a wilt sometimes accompanies the spear leaf necro-
In some cases, inadequate nutrition, poor drainage, or cold injury
have appeared to be the causes of, or at least contributing factors to,
deaths in this coconut palm cultivar. Studies were initiated to deter-
mine the relationship of fungi to spear leaf necrosis. The most fre-
quently isolated fungi from palms at locations in southeastern Flor-
ida were Acremonium spp. and Fusarium moniliforme. Of 10 dying
palms, Acremonium spp. and F. moniliforme were found in eight and
five palms, respectively. F. moniliforme was isolated from necrosing
spear leaves, while Acremonium spp. was found in brown lesions on
young or primordial leaf bases or in brown vascular traces near the
bud. Inoculation trials with these fungi are in progress to determine
if they play a role in the spear leaf necrosis affecting'Malayan Dwarf'
The 'Maypan' Coconut Palm
Until recently the 'Malayan Dwarf' coconut palm has been the only
LY-resistant coconut palm commercially available in Florida. The
'Maypan' (Fig. 31), an F, hybrid cross between 'Malayan Dwarf' and
'Panama Tall,' grows very rapidly during the first 4 or 5 years, often
surpassing 'Malayan Dwarf' of the same age by several meters.
Establishment after transplanting is also more rapid than for the
'Malayan Dwarf'. 'Maypan' resistance to LY is high (86-96%), and
the palms begin to bear after 5 years (64). The color of the 'Maypan' is
more like that of the 'Jamaica Tall' and may be preferred to that of
the golden and yellow forms of the 'Malayan Dwarf.' Its faster growth
rate and greater adaptability to different habitats and poorer soils
are advantages over the 'Malayan Dwarf' in Florida. The disadvan-
tage of the 'Maypan' is that seednut production is dependent on hand
pollination of each individual floret. Homeowners cannot reproduce
'Maypans' by seed because seedling coconut palms from 'Maypans'
are variable; they exhibit everything from LY resistance to suscepti-
bility and may resemble 'Malayan Dwarfs,' 'Panama Talls,' or in-
termediates in this respect.
Other Resistant Coconut Cultivars
In Florida, several additional LY-resistant coconut cultivars are
under evaluation. These non-hybrids may be used to increase the
genetic diversity of coconut palms in the state. Some varieties which
are highly resistant to LY in Jamaica are not suitable for commercial
copra production. Since this is not a concern for coconut palms
planted for their landscape value, they may prove to be suitable for
use in Florida. Trial plantings of cultivars such as 'King,' 'Ceylon
Dwarf,' 'Red Spicata,' and 'Fiji Dwarf' are being evaluated for LY
resistance, adaptability to southern Florida, and their aesthetic qual-
ities. A small planting of commercial date palm varieties is also being
maintained in resistance trials at the Fort Lauderdale AREC.
Resistant Palms Other Than Coconut
Fortunately many palm species are resistant to LY (Table 2)
(71,76). Many of these are commercially available in Florida (Table
7), while production of others may require obtaining seed from wild
plants, palm collectors, or specialized nurseries. The state tree of
Florida, the cabbage palmetto, is widely planted and available in
large sizes at a reasonable cost. In south Florida the royal palm is
used as a street tree and is suitable for planting in large areas. The
paurotis palm, with its small diameter multiple trunks, is easily and
effectively incorporated into most tropical landscapes.
Two species of thatch palm and the similar silver palm are native
to south Florida(4). These are slow growing and rarely available from
nurseries. The thatch and silver palms are well adapted to the coral
based soil of south Florida and tolerate a wide range of soil condi-
tions. They respond well to good horticultural practices. Many of the
introduced palms that are readily available from nurseries are LY
Table 7. Selected palm species resistant to LY that are available in Florida nurseries.
or cane palm
Pygmy date palm
1. For scientific names, see Table 2.
20 m Pinnate Fast growing, produces trunk 3rd or 4th year, edible coconuts 4th or 5th year.
Golden, yellow, and green forms available (Figs. 29, 30). For horticultural
practices, see IFAS Fact Sheets OH46, OH48, OH49, and OH55.
20 m Pinnate Fast growing. More vigorous than 'Malayan Dwarf'. A "tall" variety (Fig. 31).
6 m Pinnate Palm forms a clump. May be used as a screen. Requires good fertilization.
20 m Palmate Native, highly adaptable to different sites, very cold-hardy.
2 m Pinnate Dark, glossy leaves and form of palm very attractive if good horticultural
practices are followed.
3 m Pinnate Cold-hardy. Better adapted to northern than southern Florida.
7 m Pinnate Palm forms a clump. Damaged by frost.
12 m Palmate Forms a lump. Grows best in moist soils.
12 m Pinnate May suffer nutrient deficiencies in southeastern Florida. For horticultural
practices see IFAS Fact Sheet OH49.
30 m Pinnate Fast growing. One of most impressive palms for street plantings.
10 m Pinnate Highly adaptable. Tall, slender palm lends "South Pacific" appearance
to landscape. Leaves cold-tender.
20 m Palmate Fast growing. Very popular in California. Recommended for street
plantings in Florida.
1. For scientific names, see Table 2.
Fig. 31. 'Maypan' hybrid coconuts in Jamaica. This hybrid is vigorous and
adaptable to many soils. It is highly resistant to lethal yellowing, and has
some of the graceful appearance of the 'Jamaica Tall.'
Treatment of Lethal Yellowing
Chemotherapy tests initiated shortly after the discovery of MLO in
LY-affected palms indicated that tetracycline group antibiotics
would suppress symptom development if injected prior to the expres-
sion of systemic foliar yellowing (96). Experiments done concurrently
in Jamaica (77) and later in West Africa (155) also proved tetracy-
cline to induce remission of lethal yellowing. Subsequent tests
showed that the antibiotic gentamicin would also induce disease
remission, but that penicillin and streptomycin were ineffective (97).
Since mycoplasmas are known to be sensitive to tetracycline, but not
to penicillin, these differential evaluations provided additional evi-
dence for a mycoplasmal etiology of LY.
Experimental Treatment Programs
The initial chemotherapy treatments for LY were undertaken to
provide additional evidence for a MLO etiology of the disease. How-
ever, the results of these tests were sufficiently dramatic that two
expanded programs were initiated to precisely determine the ther-
apeutic and protective benefits of oxytetracycline (OTC) treatment.
The effect of OTC dose was evaluated by treating 140 carefully
selected diseased trees in severity stages ranging from primary to
moderately advanced with doses ranging from 0.5 to 20 g active
ingredient (a.i.) OTC per tree (101). Ninety percent of the palms in
the earlier or pre-yellowing stages of disease responded to all dosage
levels. Approximately 50% of these exhibited a full remission; that is,
they stopped all symptom development for the following 4 to 7
months. The remainder exhibited some continued symptom develop-
ment, even while producing new growth, i.e., showing partial remis-
sion. Palms with early yellowing symptoms responded to doses of 6 g
or higher, but the response ratio was only about 25%. In consequence,
the recommended therapeutic dose is 1 to 3 g OTC per tree when
treated prior to the occurrence of foliar yellowing. Treatment of trees
with yellowed fronds is discouraged, although particularly valuable
trees may be given doses of 6 g or more with the understanding that a
response may not be forthcoming. Since the remission lasts from 4 to
7 months, these treatments must be repeated at 4-month intervals, or
even sooner if symptom development is not arrested.
The preventive effects of OTC treatment were evaluated in a large
scale test involving 2078 healthy palms treated over a 16-month
period in areas of high LY incidence (111). The apparent rate of
spread of LY, monitored in adjacent treated and untreated blocks of
palms, was shown to be decreased by as much as five times in the
treated blocks. The preventive treatments consisted of doses of 1 to 3
g of OTC repeated at 4-month intervals.
A number of classes of compounds were tested for their effect on
LY. These included antibiotics, systemic fungicides and insecticides,
plant growth regulators, and heavy metals. Only tetracycline group
antibiotics were effective in inducing symptom remission, although
the antibiotic gentamicin also showed promise as a chemother-
apeutant. Table 9 lists the materials tested for their effect on LY and
the response obtained. All materials were screened for their effect on
a minimum of five diseased palms in the primary stages of symptom
A number of methods have been evaluated for treating coconut
palms with OTC. These fall into several general categories: injection
of aqueous solutions, implantation of solid tablets, foliar sprays, and
soil drenches. Of these categories, only injection of aqueous solutions
has consistently proved to be of therapeutic value and regularly
produces detectable foliar residues of OTC (98,102,104,110). Foliar
Table 9. Response of lethal yellowing affected trees treated in pre-yellowing
stages of symptom expression to different chemical agents.
Compound Response' Compound Response
oxytetracycline base + benomyl -
oxytetracycline-HCl + thiabendozale -
tetracycline base + dexon -
tetracycline-HCl + nystatin -
gentamicin-S04 + Insecticides
spectinomycin-S04 carbofuran -
spectinomycin-HCl aldicarb -
erythromycin-P04 Heavy Metal Salts
penicillin-G CuC12 -
chloramphenicol CuS4 -
Plant growth regulators
indole acetic acid -
1. Positive response = remission; negative = no effect-all trees died.
sprays and soil drenches have not induced disease remission, and
subsequent evaluations of foliage for OTC residues have been nega-
tive. Trunk implantations of solid tablets have also not resulted in
detectable foliar residues; however, this technique has been ther-
apeutically effective at about half the success rate achieved with
trunk injections (100,110).
A number of methods exist for injecting aqueous solutions into
palms. Most of these involve injection of the trunk (100), although
injection of frond bases petioless) has also been evaluated (105). The
sites for injection are holes drilled approximately 5 cm deep into the
trunk at a convenient working height. Only one injection site is
necessary each time a palm is treated. Liquid may be applied to the
hole either through gravity infusion or under pressure produced by
compressed air or by hydraulic pump. Trunk injection by gravity
infusion is made simply by connecting a solution reservoir by a piece
of tubing to the hole drilled in the tree. This apparatus may be readily
made at home from a plastic milk or bleach bottle and some plastic
tubing. Plastic infusion bags are also available commercially at
nominal cost. This method is recommended for the homeowner who
has only one or two trees to treat. One-half liter of solution will
usually be taken up overnight by this method.
Two compressed air-powered injection methods have been utilized.
The MaugetR injector, which is commercially available, is used to
inject small quantities of concentrated solutions of OTC (Fig. 32). It is
recommended that the Mauget injection capsules be left on the tree
for 1 week, and then discarded. Although we originally recommended
that only 1 g a.i. of antibiotic be injected per Mauget capsule (99), we
have found no adverse effect in using 2 g a.i. OTC per capsule and this
amount is now recommended as a therapeutic or preventive dose. The
second air pressure method, which has only been used experimen-
tally and has many variations, involves a pressurized solution reser-
voir of 1.0 or more liters capacity connected by a quick-connect
coupling to a hollow lag screw through which the injection is made.
The OTC dose, dissolved in ca. 0.5 liter water, is contained in the
reservoir, which is pressurized to approximately 100 p.s.i., either at a
filling station, or by hand pump, compressed air bottle, or portable
compressor. Pressure tanks have been made or modified from com-
pressed air bottles, fire extinguishers, and metal or plastic pipe, and
fittings capable of withstanding the pressure involved. Approxi-
mately 50 minutes to 1 hour is required to make an injection by the
pressure tank method.
Hydraulically actuated injections are widely used in large scale
treatment programs in Florida because of their labor saving capacity.
Approximately 1 minute is required to inject a concentrated dose of
OTC with the Minute TreeTM injector. These injectors, made from
modified grease guns or hydraulic jacks in which the hydraulic fluid
is replaced by OTC solution, generate very high pressure which
rapidly forces the solution into the tissue. The unique property of the
patented Minute Tree injector is that a smooth needle is used to inject
the solution into a hole of the same diameter as the needle. The
pressure generated by the injection seals the tissue around the needle
to prevent backflow. The Dade County Parks Department has used a
hydraulic injection probe with a rubber tip which is placed in an
injection hole of the same diameter. When pressure is applied, the
rubber tip swells and seals the hole, preventing backflow. The major
problem with hydraulic injectors is that the very high pressures
generated cause internal tissue damage, such as splitting and the
formation of pockets of necrotic tissue in palms. A repeat hydraulic
Fig. 32. The Mauget injector, a disposable plastic capsule that is highly
effective for injection of antibiotics into palms.
injection may leak out of a previous injection site if an internal crack
is produced between the sites. Because of the tissue damage pro-
duced, hydraulic pressure injections are now discouraged, although
they are still favored by some groups because of their rapidity of
Use of the same injection site for subsequent treatments has been
discouraged because of the localized necrosis surrounding the site.
However, at least one field applicator has observed that gravity feed
injections may be made repeatedly at the same site using a PVC tube
permanently inserted into an injection hole of ca. 2.5 cm diameter.
The effectiveness of this technique has not been clearly established.
Translocation of Injected Antibiotic
The systemic movement of OTC has been monitored by bioassay
of tissues sampled from various portions of injected palms
(98,100,102,104). The bioassay is relatively simple and can detect
concentrations of active antibiotic as low as 0.2 parts per million in
coconut foliage. Mature coconut palms trunk-injected with 6 g a.i.
OTC in 1 liter of water by the pressure tank method accumulated
relatively uniform concentrations of OTC throughout the crown of
the tree, even though only one injection site was used (104). Max-
imum foliar concentrations in the range of 8 to 10 gg/g were found in
the most actively transpiring fronds within 3 days of injection. The
lower senescing fronds and the unopened spear leaf had much lower
OTC levels, as did nontranspiring fruit, trunk, and root tissues.
Foliar OTC levels declined over a 6-week period with an approximate
half-life of 14 days. The pattern and rapidity of distribution indicate a
xylem transport pathway of the introduced antibiotic. The anasto-
mosing vascular network existing in the trunks of palms (176)
accounts for the uniform distribution obtained with a single injection
site. Injection of 1% acid fuchsin at the base of a coconut palm several
days prior to felling verified that, with increasing height, the dye
became uniformly distributed in vascular bundles throughout the
trunk cross sectional area.
Use of Oxytetracycline in Florida
The coconut palm is grown in Florida almost exclusively for its
aesthetic value as a landscape plant. No other tree can generate the
tropical atmosphere engendered by this palm. Because Florida relies
heavily on the tourist trade for revenue, the maintenance of its
tropical appearance is of great importance. As such, LY, with its
potential to eradicate the coconut palm, poses a detriment to the
economy of the area (42), and has, therefore, created a great deal of
As a result of this interest and after completion of the field tests just
described, a non-restricted pesticide registration was granted for the
use ofoxytetracycline-HCl (TerramycinR, Pfizer Inc., New York City)
for LY control by the United States Environmental Protection
Agency, in June 1974. This constituted the first federal registration
of an antibiotic to control any plant disease associated with a myco-
plasmalike agent. Oxytetracycline-HCl became commercially avail-
able in September 1974 and its use by private individuals and by civic
agencies was initiated.
The entry of another company into the market with a similar
formulation of oxytetracycline-HC1 (Uri-Tet"', Key Pharmaceutical,
Miami, Florida) created competition and reduced the price of the
antibiotic to the public. In addition, the Florida Department of Agri-
culture and Consumer Services developed a plan to purchase bulk
quantities of antibiotic on a bid basis and distribute it to municipal
agencies at an additionally reduced cost. Approximately one million
grams of oxytetracycline-HC1 were distributed yearly by this pro-
gram in the first 4 years of operation. Also, it is estimated that 20,000
g per year of antibiotic have been purchased privately. At an average
dose of 2.0 g per tree, three times per year, this amounted to about
150,000 trees being treated in south Florida.
Since its approval, the pattern of use of OTC in Florida has varied
from area to area. Every municipal agency faced with the loss of
coconut palms to LY has evaluated the pros and cons of establishing a
control program and come to separate decisions. Some cities or coun-
ties have programs to treat all coconut palms within their bound-
aries, while others have programs to treat only public-owned trees.
Some have made antibiotic and injection equipment available to the
public at little or no expense in the form of do-it-yourself kits, and
some agencies have done nothing. Most agencies have instituted
equally important programs to replant with the lethal yellowing
resistant 'Malayan Dwarf' coconut. In addition to these, the Florida
Department of Agriculture and Consumer Services developed a pro-
gram to treat all coconut palms within a 100 meter radius of any new
outbreak of LY outside of Dade, Broward, and Palm Beach counties
in an attempt to reduce or prevent spread of this disease into pre-
viously non-affected areas.
Safety of Antibiotic Use
The safe use of antibiotics in the control of a plant disease is an
important factor for consideration. These clinically important com-
pounds should receive as little exposure to the environment as possi-
ble. Also, the persons applying the compounds and the consumers of
the treated plants should be protected from any potential adverse
effects. Tetracycline toxicity to humans is not a major factor; rather
the development of antibiotic resistance in the normal human mi-
croflora is to be avoided inasmuch as possible. Transfer of this resist-
ance to other strains of bacteria could reduce the usefulness of the
antibiotic in human medicine.
Environmental exposure is minimized in treating LY by confining
the tetracycline within the trees by direct injection. As with any
pesticide, applicators should wear protective clothing. The EPA has
stipulated that fruit from treated coconut palms should not be used
for food or feed purposes. Even so, the amounts of OTC in coconut
fruit are extremely low (102). When carefully used according to label
directions, OTC is safe and will have little untoward effect on the
Possibilities of Controlling
Lethal Yellowing Through Control
of its Insect Vectors
The rate of spread of vector-borne plant diseases depends in part on
the population density of the vector or vectors. However, few insect-
borne plant diseases have been effectively controlled by controlling
their vectors. Methods of reducing the chances of LY transmission
should become increasingly apparent as more information becomes
available concerning the biology and life cycle of the vector and the
conditions under which transmission takes place.
Reinert (134) tested the effectiveness of a number of insecticides
against M. crudus. He found that certain insecticides were effective
in reducing populations of this insect on grasses and palms. Because
of the high reproductive capacity and mobility of planthoppers, and
the rapid degradability of present day insecticides, a single applica-
tion of an insecticide to a palm would not be expected to have more
than a short term effect.
In another test, Manila palms were sprayed with insecticides effec-
tive against M. crudus (134) in order to determine the effect that
maintaining low population levels ofM. crudus would have on spread
of LY. There were about 500 palms in each of three treatments
(diazinon, dimethoate, and untreated experimental controls). Treat-
ments were made biweekly for 14 months. Myndus crudus popula-
tions were reduced by the insecticide treatments. After waiting one
year from the initiation of biweekly spraying to allow for the disease
incubation period, the apparent rate of spread (See Chapter 3) of LY
diminished 50-75% in the plots where palms were sprayed. Un-
treated plots showed a slight increase in apparent rate of spead (72,
F. W. Howard, unpublished data).
Although these data showed that insecticides could reduce the
spread of LY and provided information on the spread of the disease
and the insects that might be involved, the rate of spread was not cut
sufficiently for practical measures to be recommended. A 50% reduc-
tion in apparent rate of spread will double the time required to kill all
the palms in the test. Treatment of larger areas and of grasses where
M. crudus nymphs develop might have given a better response.
However, such an indefinite broadcast spraying of insecticides in an
urban area is totally infeasible and would not be justified by the
Possibilities for Biological Control
Biological control utilizes organisms that control pest species
naturally through predation or parasitism. These "natural enemies"
include microorganisms, fungi, and invertebrate and vertebrate
animals. Many factors are involved in the art and science of biologi-
cal control, and the field has not advanced to the point at which it is
universally effective. Several species of spiders, red imported fire
ants, lizards, and tree frogs prey on M. crudus. A fungus, Hirsutella
citriformis Speare, occasionally attacks M. crudus (Fig. 33). Species
of parasitic mites, Leptus sp. and Erythaeus sp. (Erythraeidae), have
been rarely seen on M. crudus (Fig. 34). All of these natural enemies
have been observed in LY-affected areas (F. W. Howard, unpublished
observations). Thus, by themselves they are ineffective in preventing
the spread of the disease. Future research may eventually result
in the discovery of natural enemies that can effectively control
Host Plant Resistance
Natural host plant resistance offers a solution to many pest prob-
lems. For example, the natural resistance of American grape root-
stocks to a destructive species of aphid saved French vineyards over
100 years ago (128). These rootstocks are still used effectively in
France. Host plant resistance is the sole method of combating pests of
Fig. 33. Myndus crudus adult infected by a fungus, Hirsutella citriformis.
..." .. .. ,. .....'
*" al l : .' :il ....." ":" .,,II' i
,I~ .: ~li' 5 % 'li
Fig. 34. Myndus crudts adult parasitized by an erythaeid mite (arrow.)
many crops. In other crops it is used in concert with other control
The 'Malayan Dwarf' coconut palm is resistant to LY, as are many
other varieties and species of palms; palms resistant to the disease
may or may not be resistant to the vector itself. Since M. crudus feeds
on both grasses and palms, there is interest in natural resistance in
both these hosts. Turfgrass breeders are constantly working towards
improved grasses. Florida could become a less suitable environment
for LY if resistance to the vector could be bred into grasses widely
planted in landscape associations with palms.
Current Recommendations for Control
of Lethal Yellowing
Great strides have been made in lethal yellowing research in the
past decade. When LY first appeared on the Florida mainland in late
1971, the cause, physiology, mechanism of spread, and chemical
control measures for this disease were unknown. Multinational in-
vestigations have revealed the consistent association of MLO with
LY and the response of LY to tetracycline antibiotics. Additionally,
insect associations have been elucidated and a vector pinpointed. As
a result, control measures are now available that will allow palms to
be reestablished and maintained as an integral part of the Florida
In Florida, antibiotic treatments are recommended as a part of a
disease management scheme in which a transition is made from
susceptible to resistant palms. The treatments may be used to sup-
press LY symptoms and keep taller palms alive for a few years,
during which time plantings of LY resistant palms can be estab-
lished. It is not recommended that injection programs be carried out
indefinitely, nor are injection programs recommended in the absence
of replanting programs. LY resistant palm species and varieties offer
the only long term solution to this disease problem.
The planting of a diversity of palm varieties or species that have
natural resistance to the disease is the best means of combating LY.
Many species of ornamental palms are resistant, and can be success-
fully grown in Florida. In Jamaica LY has been managed by convert-
ing coconut plantings to resistant varieties and hybrids. During
recent years, about one million 'Malayan Dwarf' and 'Maypan' coco-
nut palms have been planted annually in Jamaica (140). Assistance
to the grower from the Jamaican Coconut Industry Board has been
important in bringing about this conversion (49,64,138,149,152).
Antibiotic treatments of palms are not used in Jamaica. Some re-
planting with resistant coconut varieties has been initiated in other
tropical countries affected by LY (63).
Harries (62), taking into account the world distribution of coconut
varieties, estimated that two-thirds of the world's coconut palms are
susceptible to LY. Coconut growing areas from northern South
America and Central America through Mexico are threatened be-
cause of the presence of M. crudus in these localities (82). Whether
M. crudus is present in palm-growing areas in California, other
southwestern states, and states other than Florida and Texas border-
ing the Gulf of Mexico has not been investigated.
The Division of Plant Industry (DPI), Florida Department of Agri-
culture and Consumer Services, implements regulatory measures
designed to prevent the spread of LY to new areas. In general the
movement of LY-susceptible plant material from the regulated (LY-
affected) zone to areas outside of this zone is not permitted, although
such material can be certified for shipment under certain conditions.
Persons who wish to move such material between counties in Florida,
or from this state to another area, should be aware of current LY
regulations. These can be obtained from DPI personnel.
In early stages of disease spread, eradication can play an important
role in slowing the epidemic spread of LY (See Chapter 3). In the late
stages of epidemic development, eradication would play a less valu-
able role as a control measure. The major drawback to the eradication
of diseased palms for LY control is that LY has a long latent period,
thus making it impossible to diagnose diseased palms until months
after they have become infected. Eradication alone cannot control
LY; however, in conjunction with the measures of protection and
resistance it can contribute to the comprehensive management of
this devastating disease.
PUBLICATIONS ON LETHAL
YELLOWING AND ITS MANAGEMENT
The following publications can be obtained from your County Coop-
erative Extension Service or by writing to the Department of
Ornamental Horticulture, 1545 HS/PP Bldg., University of Florida,
Gainesville, Florida, 32611.
University of Florida, Cooperative Extension Service, Fact Sheets:
Donselman, H. M. 1981. Lethal Yellowing of Palm Trees in Florida. Fact
Donselman, H. M. 1981. A Fertilization Program for the Coconut Palm. Fact
Donselman, H. M. 1981. Palms Resistant to Lethal Yellowing for South
Florida. Fact Sheet OH48.
Donselman, H. M. 1981. The Carpentaria Palm-A New Palm for South
Florida. Fact Sheet OH56.
Donselman, H. M. 1981. Nutritional Deficiencies of Palms in Florida. Fact
Donselman, H. M. 1981. Planting a Palm Tree. Fact Sheet OH46.
Donselman, H. M., and R. A. Atilano. 1981. Treating Cold-Damaged
Ornamental Palms. Fact Sheet OH50.
University of Florida, Agricultural Experiment Stations, Circular:
McCoy, R. E. 1974. How to treat your palm with antibiotic. University of
Florida, Agricultural Experiment Stations, Circular S-228.
1. Addison, E. A. 1978. The Cape St. Paul wilt disease in Ghana: the
present position. (Abstr.) Proc. 3rd Meeting Int. Counc. Lethal Yellowing,
Univ. of Florida, Agric. Res. Cent., Ft. Lauderdale. Publ. FL-78-2:7.
2. Ashby, S. F. 1920. Notes on two diseases of the coconut palm in Jamaica
caused by the fungi of the genus Phytopthora. W. Indian Bull. 18:61-73.
3. Bachy, A., and H. Hoestra. 1958. Contribution A l'6tude de la "Maladie
de KaincopC" du cocotier au Togo. Ol1agineux 13:721-729.
4. Bailey, L. H. (Staff of L. H. Bailey Hortatorium). 1976. Hortus third, a
concise dictionary of plants cultivated in the United States and Canada.
Macmillan, New York. 1290 pp.
5. Beakbane, A. B., C. H. W. Slater, and A. F. Posnette. 1972. Mycoplas-
mas in the phloem of coconut, Cocos nucifera L., with lethal yellowing
disease. J. Hortic. Sci. 47:265.
6. Borror, D. J., D. M. Delong, and C. A. Triplehorn. 1976. An introduction
to the study of insects. 4th Ed. Holt, Rinehart, and Winston, New York.
7. Britt, L. L. 1981. A study in spatial diffusion: lethal yellowing in Cocos
nucifera. M. A. Thesis, Univ. of Miami. 115 pp.
8. Bruner, S. C., and L. Boucle. 1943. La enfermedad conocida por "pudri-
ci6n del cogollo del cocotero en Cuba." Rev. Agric. 26:132-141.
9. Bull, R. A. 1955. Bronze leaf wilt of coconut palms in Nigeria. J. West
African Inst. of Palm Res. 3:70-72.
10. Caldwell, J. S. 1946. Notes on Haplaxius Fowler with descriptions of
new species (Homoptera: Cixiidae). Proc. Ent. Soc. Washington 48:203-206.
11. Carter, W. 1964. Present status of research on lethal yellowing dis-
ease of coconut palm in Jamaica. FAO Plant Prot. Bull. 12:67-69.
12. Carter, W., ed. 1965. FAO lethal yellowing disease project: a compila-
tion of data derived from the FAO mission from June, 1962-June, 1965.
Coconut Industry Board, P. O. Box 204, Kingston 10, Jamaica.
13. Carter, W. 1966. Susceptibility of coconut palm to lethal yellowing
disease. Nature (London) 212 (5059):320.
14. Carter, W., and J. R. R. Suah. 1964. Studies on the spread of lethal
yellowing disease of the coconut palm. FAO Plant Prot. Bull. 12:73-78.
15. Carter, W., R. K. Latta, and J. R. R. Suah. 1965. The symptoms of
lethal yellowing disease of coconut palms. FAO Plant Prot. Bull. 13:49-55.
16. Charudattan, R. and R. E. McCoy. 1975. Antigenic difference in
phloem exudates of healthy and lethal yellowing diseased coconut palms.
Proc. Amer. Phytopathol. Soc. 2:71.
17. Chen, R. A. 1966. Nutritional aspects of lethal yellowing in coconuts.
Trop. Agric. (Trinidad) 43:211-218.
18. Ciferri, R. 1929. Phytopathological survey of Santo Domingo, 1925-
1929. J. Dept. Agric. Porto Rico 14:5-44.
19. Ciferri, R., and A. Ciccarone. 1949. Observaciones sobre la enfermedad
de la hoja bronceada del cocotero en Venezuela. Rev. Fac. Agron. Medellin
20. Corbett, M. K. 1959. Disease of the coconut palm. Principes 3:5-13.
21. Corner, E. J. H. 1966. The natural history of palms. Weidenfeld and
Nicholson, London. 393 pp.
22. Dabek, A. J. 1973. Some physical and anatomical aspects of the lethal
yellowing disease of coconut. Ph. D. Thesis. University of West Indies, Kings-
ton. 331 pp.
23. Dabek, A. J. 1974. Biochemistry of coconut palms affected with the
lethal yellowing disease in Jamaica. Phytopathol. Z. 81:346-353.
24. Dabek, A. J. 1975. The incubation period, rate of transmission and
effect on growth of coconut lethal yellowing disease in Jamaica. Phytopathol.
25. Dabek, A. J., and P. Hunt. 1976. Biochemistry of leaf senescence in
coconut lethal yellowing, a disease associated with mycoplasma-like orga-
nisms. Trop. Agric. 53:115-123.
26. Dabek, A. J., and H. Waters. 1980. Attempts to transmit coconut lethal
yellowing disease with palm-feeding Fulgoroidea in Jamaica, 1977-79.
(Abstr.) Proc. 4th Meeting Int. Counc. Lethal Yellowing. Univ. of Florida,
Agric. Res. Cent., Ft. Lauderdale. Publ. FL-80-1:13.
27. Dabek, A. J., C. G. Johnson, and H. C. Harries. 1976. Mycoplasma-like
organisms associated with Kaincope and Cape St. Paul wilt diseases of
coconut palms in West Africa. PANS 22(3):354-358.
28. De La Torre, C., 1906. La enfermedad de los cocoteros. Rev. de la
Faculdad de Let. y Cienc. (Havana) 2:269-281.
29. Diaz-Silveira, M. F., and P. T. Mijailova. 1973. Los nematodos y su
relaci6n con la "pudrici6n del cogollo" del cocotero en Cuba. Acad. Cien.
Cuba, Serie Agric. 29:1-11.
30. Doi, Y., M. Teranaka, K. Yora, and H. Asuyama. 1967. Mycoplasma-
or PLT group-like microorganisms found in the phloem elements of plants
infected with mulberry dwarf, potato witches' broom, aster yellows, or
Paulownia witches' broom. Ann. Phytopathol. Soc. Japan 33:259-266.
31. Dollet, M., and J. Giannotti. 1976. Maladie de Kaincop6, presence de
Mycoplasmes dans le phlo6me des cocotiers malades. Ol1agineux 31(4):169-
32. Dollet, M., J. Giannotti, J. L. Renard, and S. K. Ghosh. 1977. etude
d'un jaunissement 16tal des cocotiers au Cameroun: la maladie de Kribi.
Observations d'organismes de type mycoplasmes. Ol6agineux 32(7):317-
33. Eden-Green, S. J. 1973. Some attempts to rear potential leafhopper
vectors of lethal yellowing. (Abstr.) Principes 17:156.
34. Eden-Green, S. J. 1974. Quelques tentatives d'6levage de cicadelles
vecteurs potentiels du Jaunissement Mortel. (Abstr.) Olagineux 29:143.
35. Eden-Green, S. J. 1976. Disease scoring scale for lethal yellowing. pp.
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