Environmental Research Journal ISSN: 1935-3049

Volume 6, Number 2 © 2012 Nova Science Publishers, Inc.

FUSARIUM WILTS: AN OVERVIEW

F. I. Okungbowa1 and H. O. Shittu1,2

1
Department of Plant Biology and Biotechnology,
University of Benin, Benin City, Nigeria
2
Department of Molecular and Cellular Biology,
University of Guelph, Guelph, Canada

ABSTRACT
Fusarium species are soil borne vascular wilt pathogens, which are among the most
important phytopathogenic and toxigenic fungi. They are filamentous and belong to the
Class Ascomycetes and Family Hypocreaceae. Fusarium species typically produce
macroconidia and microconidia, as well as mycelia and chlamydospores that serve as
propagules in infecting host plants. The life cycle can be divided into dormant, parasitic
and saprophytic stages. Most species are harmless saprobes; some species are parasitic,
with some producing mycotoxins on plants. The pathogenic strains have high level of
host specificity which has led to the development of the “formae specialis” concept. Each
formae specialis can be further sub divided into races, on the basis of virulence in a set of
differential cultivars within the same plant species. Fusarium wilt is a major concern in
agriculture as it causes great economical losses in a wide variety of crops. The symptoms
of Fusarium wilt range from stunted growth, yellowing and wilting of the leaves, reddish
discolouration of the xylem vessels (visible inside the stem as lines or dots in cross
section) and white, pink or orange fungal growth on the outside of affected stems
(particularly in wet conditions), to root or stem decay.
There is remarkably little knowledge available about the molecular mechanism
and/or pathogenicity genes required by Fusarium species to cause disease and how hosts
combat or tolerate the pathogen. The genomes of some Fusarium species have been
sequenced and comparative genomic analyses have shown that pathogenic Fusarium
species consist of a larger number of proteins in the pathogenicity related protein families
such as transcription factors, hydrolytic enzymes, and transmembrane transporters which
play significant roles in pathogenicity, compared to non pathogenic species. In general,
the disease is difficult to control, as physical,chemical and cultural methods of control are
not only ineffective but also expensive.
The best method of control is breeding for resistant cultivars. Also, rhizosphere fungi
such as Trichoderma harzianum, T. asperellum, T. koningii, Penicillium spp. and
Streptomyces griseoviridis have been used to control the disease. This present review
gives a general overview of some common Fusarium wilts.


Corresponding author: fiokun2002@yahoo.com
84 F. I. Okungbowa and H. O. Shittu

INTRODUCTION
Presently, about 80% of plant diseases can be traced to fungal pathogens. Fusarium wilt
is a soil-borne fungal disease in which the water-conducting (xylem) vessels become blocked,
so that the plant wilts and often dies. Fusarium wilts are caused by pathogenic strains of
several species of Fusarium, including F. eumartii, F. oxysporum, F. avenaceum, F. solani,
F. sulphureum and F. tabacinum (Plant Health Research and Diagnostics, 2007) which are
usually very host-specific. However, the most commonly encountered culprit is F.
oxysporum.

Fusarium Species

Fusarium Schlechtendahl Emend. Snyder and Hansen is a filamentous fungus of the

Class Ascomycetes and Family Hypocreaceae (Pitt et al., 1994). It is a soil-inhabiting fungus
which is distributed worldwide. Some species of Fusarium are restricted to the tropics, some
are predominant in the temperate zones, while others are found in desert, alpine, and arctic
areas, where harsh climatic conditions prevail (Francis and Burgess, 1975). Many Fusarium
species are abundant in fertile cultivated and rangeland soils but are relatively uncommon in
forest soils (Jeschke et al., 1990). Fusarium species are often regarded as soil-borne fungi
because of their abundance in soil and their frequent association with plant roots, as either
parasites or saprophytes (Nelson et al., 1994). Its different species are considered to be some
of the most important plant disease pathogens, with some species producing mycotoxins
(such as fumonisins, zearalenones and trichothecenes) on plants which contaminate the seeds
and enter the food chain, affecting human and animal health, and are thus hazardous to
agricultural products, wildlife, livestock and humans (Balali and Iranpoor, 2006; Arif et al.,
2011; Wang et al., 2011).
The wide spread distribution of Fusarium species has been attributed to the ability of
these fungi to grow on a wide range of substrates and their efficient mechanisms for spore
dispersal (Nelson et al., 1994). One of the economic importance of Fusarium species over the
years is their role as plant pathogens, causing diseases such as crown rot, head blight, and
scab on cereal grains; vascular wilts on a wide range of horticultural crops (for example,
tomato, cucurbits and banana), root rots; cankers; and other diseases such as pokkah-boeng on
sugarcane and bakanae disease of rice (Booth, 1971).
The genus Fusarium currently contains over 20 species (Mueller and Beckman, 1988;
Wang et al., 2011). Some Fusarium species have a teleomorphic state (Booth, 1981). The
commonest species include Fusarium solani, F. oxysporum, F. equisetti and F.
chlamydosporum (Burgess et al., 1994; Chimbekujwo, 2000). Macroscopic and microscopic
features, such as colour of the colony, length and shape of the macroconidia, the number,
shape and arrangement of microconidia, and presence or absence of chlamydospores are key
features for the differentiation of Fusarium species (Larone, 1995; De Hoog et al., 2000).
Molecular methods, such as 28S rRNA gene sequencing, may be used for rapid identification
of Fusarium strains to species and sub species levels (Hennequin et al., 1999). Others are
polymerase chain reaction (PCR) based rDNA detection method (Lacmanova et al.,2009) and
detection of protein banding patterns by SDS-PAGE and esterase isozyme electrophoresis
(El-Kazzaz et al., 2008).
 Fusarium Wilts 85

Cultures of Fusarium species grown on Sabouraud Dextrose Agar at 25oC produce

woolly, cottony, flat or spreading colonies (Larone, 1995; Mui-Yun, 2003). Colony colour
from the top is white, cream, tan, salmon, cinnamon, yellow, red, violet, pink, or purple. On
the underside, the colour may be tan, red, dark purple, brown, or may also be colourless
(Nelson et al., 1994). During unfavourable conditions, the fungus produces sclerotia (singular
= sclerotium). A sclerotium is the organised mass of hyphae that remains dormant during
unfavourable conditions (Mui-Yun, 2003) and germinates later when favourable conditions
return and become a source of infection. Fusarium species typically produce both
macroconidia and microconidia from slender phialides (Nelson et al., 1994). Macroconidia
are hyaline, two- to several-celled, fusiform- to sickle-shaped, mostly with an elongated
apical cell and pedicellate basal cell. Microconidia are 1- to 2-celled, hyaline, pyriform,
fusiform to ovoid, straight or curved (Figure 1 a-c).

Figure 1. The three different spores produced by Fusarium oxysporum. a: microconidia; b:

macroconidia; c: chlamydospores.

FUSARIUM Wilts
As earlier stated, Fusarium wilts are caused mainly by F. oxysporum. This fungus
includes many important pathogenic species which are able to infect different plants causing
wilts in crops of economic importance. Strains of F. oxysporum are commonly isolated from
healthy roots. Strains from apparently healthy plants are termed non-pathogenic and are
interesting, since some of them can protect plants against the pathogenic strains (Shishido et
al., 2005). Several non-pathogenic strains of F. oxysporum, isolated from soils suppressive to
Fusarium wilts, have been selected as potential biological control agents.
86 F. I. Okungbowa and H. O. Shittu

Fusarium oxysporum is a complex species. It causes destructive vascular wilts in a wide

variety of crops (Namiki et al., 1994). The high level of host specificity of pathogenic strains
in F. oxysporum led to the development of the “formae specials” concept to enable better
differentiation of these morphologically similar strains (PADIL, 2011). The formae speciales
are distinguished by the ability of their members to cause a wilt disease on a limited
taxonomic range of host plants (Lievens et al., 2009). Some of the formae speciales are
further divided into subgroups, named races, on the basis of virulence to a set of differential
cultivars within the same plant species (Armstrong and Armstrong, 1981). Currently, there
are over 100 different formae speciales described, causing disease in a wide range of dicot
and monocot plant species. For example, Banana wilt; Panama wilt (F. oxysporum f.sp.
cubense), Fusarium wilt of cotton (F. oxysporum f.sp. vasinfectum), Fusarium wilt of sweet
potato (F. oxysporum f.sp. batatas), Fusarium wilt of Callistephus (F. oxysporum f.sp.
callistephi); Fusarium wilt of tomato (F. oxysporum f.sp. lycopersici), Fusarium wilt of date
palm (F. oxysporum f.sp. albedinis) and Fusarium yellows of common beans (F. oxysporum
f.sp. phaseoli).

Host Plants

Tomato and other solanaceous crops, sweet potato, legumes, cucurbits and banana are the
most susceptible plants (Miller et al., 2011), though it will also infect other herbaceous plants
as well as cotton, ornamentals and palms. Other hosts are Callistephus (China aster),
Dianthus (carnations, pinks), French/runner beans, hebe, peas. However, individual
pathogenic strains within the species have a limited host range, and strains with similar or
identical host ranges are assigned to the same formae speciales (f. sp.) (Armstrong and
Armstrong, 1981).

HOW FUSARIUM SPECIES CAUSE DISEASE

Fusarium species are soil borne pathogens, which attack the water conducting vessels of
host plants. In soil, fungal colonisation of plant roots has been traditionally studied by indirect
methods such as microbial isolation that do not enable direct observation of infection sites or
of interactions between fungal pathogens and their antagonists (Olivain et al., 2006). The
disease cycles of most Fusarium wilts are similar and resemble that of the Fusarium wilt of
tomato (Agrios, 2005). Like other vascular pathogens, such as Verticillium, the life cycle of
Fusarium species can be divided into dormant, parasitic and saprophytic stages (Beckman,
1987). The dormant stage comprises inhibition and germination of resting structures in soil.
The parasitic stage comprises penetration of roots, colonisation of the root cortex and
endodermis, movement to the xylem; colonisation of the xylem of stems and leaves, symptom
expression and, finally, death of the host. The saprophytic stage is the formation of resting
structures in the dead host (Schnathorst, 1981).
In the dormant phase, mycelia, chlamydospores, macroconidia and microconidia
(propagules) present in infested soil are inhibited from germinating because of mycostasis or
microbiostasis (Huisman, 1982). Reversal of inhibition of resting structures from germination
is non-host specific. The inhibition can be reversed when propagules come in contact with
 Fusarium Wilts 87

Root exudates released in the rhizosphere of a host plant (e.g. tomato), a non-host plant (e.g.
grass) or contact with pieces of fresh non-colonised plant remains (Steinkellner et al., 2008).
The exudates serve as rich source of carbon (sugar), nitrogen (amino acids) and organic acids,
which are generally known to stimulate spore germination (Nelson, 1991; Huisman, 1982).
However, what triggers the production of exudates and the actual role of exudates in the
germination of spore are not yet understood.
Fusarium species enter the parasitic phase when any of the propagules or germ tube of
spore, penetrates the host through cracks formed by emerging lateral roots, wounds or at the
root cap, root hairs or branch roots (Inoue et al., 2002; Rodríguez-Molina, 2003; Hardham,
2001; Wanjiru et al., 2002; Mandeel, 2007). The penetration process is likely enhanced by
certain hydrolysing enzymes secreted by Fusarium (Walter et al., 2009).There has been
report of an association with Fusarium wilt and nematode colonisation, where the nematodes
provide a potential entry point (wound) for the fungus (Morrell and Bloom, 1981).
Penetration is usually intercellular. Inside the root, the cortex is colonised by emerging
mycelia (Bishop and Cooper, 1983). From the cortex, the hyphae penetrate the endodermis
and invade the xylem vessels through the pits. The mycelia remain in the vessels where they
invade the plant in an upward direction (colonisation), through the stem and crown of the
plant (Rodríguez-Gálvez and Mendgen, 1995; Agrios, 2005). Effective colonisation is
genetically controlled (Inoue et al., 2002). Inside the xylem vessels, the mycelia produce
microconidia, which are released to travel upward in the transpiration stream, until trapped in
pit cavities or at vessel end walls. They germinate into new hyphae and penetrate adjacent
vessel elements to continue colonisation and increase infection (Schnathorst, 1981). At this
stage, Fusarium hyphae spread within the cell apoplast, which leads to significant cytological
alterations resulting in symptom expression (Walter et al., 2009). A combination of vessel
clogging by mycelia, spores (from the fungus) and gels, gums, tyloses and crushing of the
vessels by proliferating adjacent parenchyma cells from the host plant in an attempt to defend
itself plug vessels and is responsible for the breakdown of the water economy of infected
plant (Agrios, 2005; Moreau et al., 1978; VanderMolen et al., 1977). This gives rise to
wilting of lower branches, followed by the entire plant, which eventually leads to death.
The new spores can either be returned to the soil when the plant decomposes or
disseminated to new plants or areas by wind or water. In the process, conidia are also formed
in sporodochia on dead leaves, and hyphae and chlamydospores are also produced
extensively. The chlamydospores are returned to the soil, when the diseased plant residues
decay. They can remain viable in the soil in their dormant state for several years, and grow
upon germination by parasitic or saprophytic colonisation of a new host. Certain weeds are
symptomless carriers of Fusarium (Fassihiani, 2000).

SYMPTOMOLOGY AND EPIDEMIOLOGY OF FUSARIUM WILTS

The general symptoms of wilts caused by Fusarium are stunted growth, yellowing and
wilting of the leaves, reddish discoloration of the xylem vessels, visible inside the stem as
lines (if the stem is cut open lengthways) or dots (if it is cut across). Others are white, pink or
orange fungal growth on the outside of affected stems, particularly in wet conditions, root or
stem decay (Mueller and Beckman, 1988; Miller et al., 2011). The amount and severity of
leaf damage that is seen in the field depend on a number of factors, including the distribution
88 F. I. Okungbowa and H. O. Shittu

of inoculum of the fungal organism in the field, the degree to which the vascular tissue in
stems has been damaged by the fungus as it grows within plant tissue, the duration of the
fungal “attack” and ability of the plant to re-grow or retain leaves.
At the seedling stage or in young plants, cotyledons and leaves wilt and drop, leading to
bare stems. Early detection of Fusarium wilt can be difficult because early symptoms may
resemble some types of seedling disease and symptoms developing much later may be similar
to those of other diseases. For example, symptoms are easily confused with those of crown or
root rot, stem cankers, pest injury, drought, nutrient deficiency, bacterial and Verticillium
wilts (Hutmacher et al., 2003;Plant Health Research and Diagnostics, 2007; Elliot, 2009;).
Past research has shown that impacts of Fusarium can also be worse when infections are
combined with some types of plant stress that compromise plant health and growth, such as
high temperature stress or injury; nematode damage; root injury associated with fertilizer
“burn”; anaerobic conditions associated with over-irrigation; moderate to severe water
deficits (Morrell and Bloom, 1981; Plant Health Research and Diagnostics, 2007; Gunua,
2010).

DIFFERENCES BETWEEN FUSARIUM AND VERTICILLIUM

WILT SYMPTOMS
Vascular discoloration (brown staining of stem tissue) caused by F. oxysporum tends to
be darker and more continuous, whereas Verticillium causes more of a “flecking”or “spotty”
type of stain. The vascular discoloration tends to be seen lower in the plant stem in Fusarium
than what is seen with Verticillium (more in the lower stem, below the cotyledonary node and
upper tap root in Fusarium). Another interesting difference is that Fusarium wilt is favored
by warm temperatures while Verticillium wilt is favored by cool temperatures. This means
that Verticillium is typically more damaging following cool weather (organism is more active
in growth under cooler conditions), while the Fusarium organism is more active in warmer
weather. On many, but not all incidences, significant plant foliar and vascular tissue damage
occur at earlier growth stages in Fusarium than with Verticillium, resulting in more stunting
of plants with Fusarium. Yellow, necrotic areas are more likely to occur at outer edges of
leaves with Fusarium, while discoloration can spread across much of the leaf in Verticillium
(Hutmacher et al., 2003).

FUSARIUM WILTS OF SOME SELECTED PLANTS

Fusarium Wilt (Panama Disease) of Banana

Fusarium wilt (Panama disease) is the most serious disease of banana, threatening 80%
of the world's banana production, most of which is planted with the susceptible varieties. It
first became epidemic in Panama in 1890 and spread to Central American and the Caribbean
(Daly and Walduck, 2006).
Bananas are a staple food in the diet of millions throughout the subtropics and tropics,
and the spread of Panama disease could have devastating effects on both large scale
 Fusarium Wilts 89

production and subsistence farms. Fusarium wilt is a severe disease of banana plants caused
by the fungus Fusarium oxysporum f. sp. cubense (Foc). The fungus infects banana plants
through the roots and invades the plant’s water conducting tissues. Once Foc is introduced
into banana gardens, it remains in the soil making it impossible to grow susceptible bananas
in the same location for up to several decades. Foc is thought to have originated in Asia, and
then spread during the 20th century to become a major problem throughout most banana
production regions of the world (Daly and Walduck, 2006).
An important exception is the South Pacific, where Fusarium wilt is a new disease and
not yet widespread.
An infected plant is characterized by a strong yellowing of the leaves that remain erect
for 1 - 2 weeks. As Foc disrupts the plant’s water conducting vessels, leaves become yellow
(progressing from older to younger leaves). Some of the leaves may then collapse at the leaf
stalk and hang down at the pseudostem from the oldest to the youngest, and dry up (Figure 2).
Distinctive symptoms appear inside the pseudostem; numerous brown, red or yellow lines
running in all directions are visible in vertical section (appear as rings in cross-section). These
are the infected water conducting vessels. Smaller brown streaks or flecks appear in the corm,
at ground level. Later, all leaves turn yellow and die and internal rotting becomes extensive
and it emits a strong unfavourable smell. Splits may also appear in the pseudostem. Infected
plants usually do not produce fruit. Infected suckers growing out of diseased corms produce
plants that wilt and eventually die out. Leaf symptoms appear after the fungus has spread
through the corm. In younger plants, the first signs of infestation are to be found on the
unfurling leaf which turns yellow and dies off.

Figure 2. Early stage of Fusarium wilt of banana.

There is great strain variation in Foc. There are four recognized races of the pathogen
which are separated based on host susceptibility (Daly and Walduck, 2006). They are races 1,
2, 3 and 4. The first confirmed record was of a race 1 strain in the Northern Mariana Islands
in 1971. Race 2 affects cooking bananas in north Queensland and Africa. Race 4 is a very
serious quarantine threat to the Pacific, as it is spreading in the western half of the island of
New Guinea. Race 3 affects Heliconia spp., a close relative of banana, and is not considered
to be a banana pathogen. In addition to its potential impact on banana production in the
90 F. I. Okungbowa and H. O. Shittu

region, the spread of Foc into the island of New Guinea and elsewhere in the Pacific
endangers valuable germplasm resources.
Spread of the disease occurs mostly in banana planting material (suckers or rhizome
pieces). The best way to combat this disease is to prevent its introduction. Movement of
banana planting material out of infected regions should be completely prohibited.

Fusarium Wilt of Cotton

The causative fungus is F. oxysporum f.sp. vasinfectum (Fov). Yellowing, wilting,

defoliated plant, and plant death are the typical symptoms (Figure 3). If a stem is cut
lengthwise near the base, its vascular tissues below the bark exhibit a brownish discoloration
through the entire main stem. Root knot nematodes are most widely found in coarser-textured
soils such as sands or sandy loams, or in sand streak areas in other fields. Therefore,
incidence of Fusarium in cotton has generally been linked to these soil types, which support
higher populations of root knot nematodes (Hutmacher et al., 2003). In addition, many of
these sandy loam soils which are more susceptible to root knot nematode infestations have, in
the past decade, been planted to short-term or long-term perennial crops instead of cotton.
When the disease occurs at the seedling stage or in young plants, cotyledons and leaves can
either turn brown and dry right on the plant, or can wilt and drop, resulting in bare stems. In
mildly-affected or older plants, the lower leaves will show symptoms but the plant may
survive, but will have reduced vigor. In the most severely affected plants, leaves wilt and drop
and the plant may die. Fusarium wilt can affect cotton at any time during the growing season,
but is favored to some degree by warm weather.

Figure 3. Cotton plant infected by Fusarium oxysporum f.sp. vasinfectum

(Hutmacher et al., (2003).

Due to resistant spores and its ability to sustain itself on the roots of many plants and in
plant debris, it is nearly impossible to eradicate Fov from large production fields. However,
with preventative strategies, early detection, and containment of infested soil and plants, the
disease can be somewhat managed and dispersal limited or slowed.
In order to avoid increasing populations of Fov spores, general practices to follow are
using clean planting seed in root knot nematode affected fields, and improving control with
pre-plant fumigants if practical within the crop rotation.
 Fusarium Wilts 91

Another method is the use of nematode-resistant varieties under conditions of the Fov
that involves root knot nematodes. Biological control measures using bacteria are possible
(Chen et al., 1995). Fusarium which apparently does not require root knot nematode for
colonisation has been identified.

Fusarium Wilt of Sweet Potato

Once an important disease of potato in the USA, it has now spread to other countries like
Argentina, Brazil, China, India, Japan, Malawi and New Zealand. Although it is primarily
caused by F. oxysporum f.sp. batatas, sometimes strains of the tobacco pathogen (F.
oxysporum f.sp nicotianae) can cause wilt in susceptible potato (Loebenstein and
Thottappilly, 2009). Yellowing and wilting of the lower, older leaves and the vines turning
tan to light-brown are the typical symptoms. The dying vines have pinkish fruiting bodies of
the fungus.
The tubers produced by an infected plant have discoloured vascular tissues which may rot
upon storage. Fields are commonly infected through contaminated cuttings. Once in the field,
the fungus penetrates healthy plants through open wounds. Yield losses may be up to 50
percent, and are more likely under warm weather and in dry soils. Plants normally die within
a few days after visible symptoms appear in the plant (Gunua, 2010). The vascular tissues of
affected plants turn dark brown or black, especially close to the soil level. In addition to
resistance, other controls include crop rotation to lower soil disease pressure, selection of seed
roots from disease-free fields, and fungicide treatments (Clark and Moyer, 1988).

Fusarium Wilt of Tomato

The disease is caused by the vascular wilt fungus, F. oxysporum f. sp. lycopersici (Fol).
The fungus directly penetrates roots and colonises the vascular tissue (Inoue et al., 2002).
Other wilt pathogens of tomato are Verticillium albo-atrum (Pegg and Brady, 2002; Shittu et
al., 2009) and Pseudomonas solanacearum (Wokoma, 2008). Infestation often occurs on
mature plants after flowering and at the beginning of fruit set. Yellowing begins to appear on
one side of a leaf and then all leaflets become yellow on the other half of the leaf. As the
disease progresses, one side of the plant wilts and this process spreads to the other side as the
infection worsens (Figure 4a). An infected plant often dies before maturing. Full grown
tomato plants have the biggest problem with severe wilting; it is not as severe in younger
shoots (AVRDC, 2005). In seedling infection, the older leaves droop and curve downward,
vascular tissue darkens, and the plant wilts and dies. In older diseased plants, the leaves
yellow after blossoming. The vascular tissue in the stem is dark brown but the pith remains
healthy (Figure 4b). Fruit infection can occur, displaying the same brown vascular
discolouration.
Fusarium wilt of tomato is of worldwide importance where at least 32 countries have
reported its occurrence, which is particularly severe in countries with warm climate such as
United States, Australia, United Kingdom, Netherlands, Brazil, Mexico, Nigeria, Morocco,
Israel, Iraq and Vietnam (Mui-Yun, 2003). The disease can be associated with infection by
root knot nematode (Morrell and Bloom, 1981).
92 F. I. Okungbowa and H. O. Shittu

Figure 4. Fusarium wilt of tomato caused by Fusarium oxysporum f.sp. lycopersici. (a) Infested
farm land (b) Vascular discoloration of stem. (Photo courtesy of Clemson University, USDA
Cooperative Extension Slide Series, www.ipmimages.org).

The effect of Fol wilt on the photosynthetic ability of tomato was studied by Nogues et
al. (2002). During the first stage of disease development, Fol race 1 (Fol-1), wilt decreases
the rate of Carbon (IV) oxide (CO2) assimilation. Fol-1 wilt also decreases leaf area, thereby
causing a reduction in the ability of the tomato plants to capture photosynthetically active
radiation; hence there is a depression in the photosynthetic productivity of these infected
plants. Typically, the plant either does not produce fruit at all, or if it does, the fruit is
deformed. This leads to great economic losses. Fusarium wilt in tomato plants is favoured by
temperature of 28°C, especially during weather that is wet which allows it to spread more
quickly throughout the nearby tomato plants. An overview of the interaction between Fol and
tomato has been recently reviewed (Okungbowa and Shittu, 2011).

Fusarium Wilt of Palms

Palms have leaves attached directly to the crown. Fusarium wilt is a devastating disease
of certain species of palms that was first observed in the United States in 1970 and in
Australia in the early 1980s, when palms began to die at Centennial Park in Sydney ( Elliot,
2009;). It has also been reported in France, Greece, Italy and Japan (Elliot, 2009). It is likely
that more palms will die and that the disease will limit the use of certain palm species used for
landscaping. Palms affected by this disease are characterised by an unusual type of frond
death - fronds may die more rapidly on one side of the tree, or from the base or from the
centre of the tree. Most characteristically the pinnae and spines on one side of an individual
frond die first and the lower fronds die rapidly so that eventually only a few surviving fronds
form a spike at the top of the tree (Figure 5). Eventually the whole palm will die. Affected
fronds when removed from the plant will often show discolouration of the vascular bundles.
The fungus was thought to only be a significant problem in certain species of Phoenix
(Canary Island date palm), viz., P. canariensis and P. dactylifera. Glasshouse tests have
shown that P. reclinata can be infected by the fungus, but symptoms have been rarely
observed in the field. There is very little information on the factors that predispose palms to
this infection. It is more common on sandy soils, however it is not known whether clay soils
are unfavourable to the disease or whether it has not yet been introduced to palms on
such soils.
 Fusarium Wilts 93

The two commonest methods of spread of are by transplantation of infected palms or by

the use of tools that are unsterilized. Once a tree is infected, it will eventually die and this
may take as little as two months or up to several years (Elliot, 2009).

Figure 5. Fusarium wilt of Phoenix sp caused by Fusarium oxysporum f. sp. canariensis.

There are no effective fungicides and control is dependent on avoidance of the disease
and other sanitary practices. Palm trees are valuable plants. It can cost over $10,000 to replace
a large Canary Island date palm (Elliot, 2009). It is advisable not to plant Phoenix or
Washingtonia species of palms in areas where the disease is endemic. Two other fungi,
namely, Dothiorella and Gliolcadium can cause one-sided wilt and xylem discoloration also.
Therefore, molecular diagnosis is required to ascertain the organism causing the disease.
Besides Canary Island date palm, Fusarium oxysporum f. sp. canariensis attacks date palms,
Senegal date palms, wild date palms and California fan palms. Another strain of Fusarium
wilt, Fusarium oxysporum f. sp. albedinis, is called Bayoud disease and infects only date
palms--or Phoenix dactylifera--in Algeria and Morocco. In Central Africa and South
America, oil palms of the genus Elaeis succumb to Fusarium wilt of oil palm caused by
Fusarium oxysporum f. sp. elaeidis.

Fusarium Wilt of Cucurbits

The Cucurbitaceae plant family is affected by several vascular wilt diseases caused by
different formae speciales of the fungus F. oxysporum, which are morphologically similar,
but generally host-specific (Egel and Martyn, 2007). The most economically important of
these attack watermelon, muskmelon, or cucumber. Fusarium wilt of watermelon is one of
the oldest described Fusarium wilt diseases and the most economically important disease of
watermelon worldwide. It occurs on every continent except Antarctica and new races of the
pathogen continue to impact production in many areas around the world (Egel and Martyn,
2007). Consequently, Fusarium wilt of watermelon, caused by F. oxysporum f. sp. niveum
(Fon) is described here as an example of the group. Fusarium wilt of watermelon has been an
important factor in watermelon production in the United States since the late 1800’s. The
disease now occurs in all watermelon growing regions of the world and on every continent
94 F. I. Okungbowa and H. O. Shittu

except Antarctica. It is the most economically important disease of watermelons throughout

the world. While there are no economic loss data due specifically to Fusarium wilt,
significant losses continue in many areas of the world.
Six different formae speciales have been described that cause wilt in curcurbits among
which F. oxysporum f. sp. niveum (watermelon); F. oxysporum f. sp. melonis (muskmelon);
F. oxysporum f. sp. cucumerinum (cucumber) are the most economically important (Egel and
Martyn, 2007). While there are reports of cross infection between some formae speciales,
these are mostly laboratory and greenhouse phenomena and, in the field, the cucurbit wilt
fusaria are host-specific and rarely cross-infect. The biology, pathology, epidemiology, and
control are very similar among all of the cucurbit-infecting formae speciales. Three races of
F. oxysporum f. sp. niveum have been described – race 0, 1, and 2. Races are described based
on their ability to overcome specific resistance genes in a set of differential cultivars. Race 0,
first detected in Florida in 1963, is pathogenic only on watermelon cultivars with no
resistance genes and, therefore, is of little economic importance. Race 1 is the predominant
race throughout commercial watermelon regions in the U.S. and world. Most commercial
diploid cultivars have a high degree of resistance to race 0 and 1. Triploid (seedless) cultivars
are generally more susceptible to Fusarium wilt since there has been less time to breed
resistance. On the other hand, race 2 is highly aggressive to all current commercial
watermelon cultivars and hybrids and clearly is a distinct race. Race 2 was first observed in
Israel in 1973 and now occurs in the United States and several other countries. No
commercial genotypes have high resistance to race 2; however, an improved plant
introduction line from South Africa (PI-296341-FR) has high resistance to all three races. A
second PI line, PI-272769, also is reported to have resistance to race 2 (Egel and Martyn,
2007).

Fusarium Wilt of Cabbage

Fusarium wilt is caused by Fusarium oxysporum f. sp. conglutinans. Many crucifers

(members of the cabbage family) are susceptible to Fusarium wilt (RPD,1988). They include
cabbage, broccoli, Brussels sprout, cauliflower, Chinese cabbage, collard, kale, kohlrabi,
mustards, radishes, rape, rutabaga, seakale, turnips, and watercress. There are five strains or
races of the fungus known and described: Strain 1 infects cabbage, Brussels sprout
cauliflower, collard, and kale; strain 2 attacks radish; strains 3 and 4 are found on flowering
stock; and strain 5 is found on cabbage (Song et al., 1996). In thoroughly infested soils,
susceptible cabbage and radish varieties may be completely destroyed. Since cabbage is the
most commonly affected crucifer, the symptoms on this crop are the ones described here.
The first and most apparent symptom is a dull green to yellowish green colour of the
leaves of plants in the field, within a month after transplanting. The lower leaves develop a
one-sided warping or curling (Figure 6), with the yellow colour being more intense on one
side of the leaf midrib than on the other. The stem may be twisted toward one side.
Yellowing, browning, and withering of the leaves progresses up the plant. Affected leaves
drop prematurely, and growth is retarded. Very susceptible plants may die within a few
weeks, while others in the same field or garden may live for a month or more. A yellow to
dark brown discoloration can be seen in the water-conducting vessels in the stem, petioles,
 Fusarium Wilts 95

and veins of the leaves when they are cut through. The disease however, is almost completely
checked when the average soil temperature is below 61°F (16°C).

Figure 6. Fusarium wilt of cabbage caused by F. oxysporum f.sp. conglutinans.

Infected leaves drooping from plant (RPD, 1988).

Soil moisture and soil pH have little effect on Fusarium wilts. However, soil nutrient
status can critically affect symptoms expression; potassium deficiency leads to a much
intensified syndrome. The fungus invades the plant through the young rootlets or wounds in
the older roots at transplanting time or later (RPD, 1988). Dissemination of the fungus takes
place from seedbed to field or from one field or garden to another by infected transplants,
infested soil clinging to transplants, farm equipment, plant refuse, animals, surface-drainage
water, and wind. Occasionally, the fungus is carried long distances in seeds.
The best control measure is to plant resistant cultivars (Baik et al., 2010). There are two
types of resistance, A and B. Cabbage varieties with type A are uniformly resistant regardless
of the soil temperature while varieties with type B show a relatively high degree of resistance
when average soil temperatures are below 70°F (21°C) and when grown at optimum soil
fertility levels (RPD,1988). As the soil temperature increases, type B resistance breaks down.
At about 77°F (25°C) or above, type B-resistant plants become infected and killed while type
A-resistant plants remain unaffected. Type B resistance is found principally in the older, late-
maturing cabbage varieties. Most of the modern Fusarium-resistant cabbage varieties carry
type A resistance. Susceptible crucifers should not be planted in areas that are likely to
receive surface-drainage water from infested fields. Transplants should be gown in soil that
has been disinfested by steam or soil fumigant.

Genetics of Fusarium Species

The genomes of some Fusarium species have been completely sequenced. These include
genomes of the cereal pathogen, F. graminearum, which has a genome size of 36.2 Mb,
organized into 4 chromosomes (Cuomo et al., 2007); maize pathogen, F. verticillioides, with
a genome size of 41.7 Mb, organized into 12 chromosomes (Xu and Leslie, 1996) and tomato
pathogen, F. oxysporum f. sp. lycopersici with a genome size of 59.9 Mb, organized into 15
chromosomes (Ma et al., 2010). Comparative genome analyses have shown the presence of
96 F. I. Okungbowa and H. O. Shittu

mobile pathogenicity chromosomes in Fusarium (Ma et al., 2010) and that the genomes of
pathogenic Fusarium species consist of a larger number of proteins in the pathogenicity
related protein families, compared to non- pathogenic fungi. This region encodes transcription
factors, hydrolytic enzymes, and transmembrane transporters which play significant roles in
pathogenicity of the fungi (Cuomo et al., 2007). Also, Fusarium genomes contain a total of
46 secondary metabolite biosynthesis gene clusters, among which encode mycotoxins that
exhibit toxicity to humans and other mammals (Desjardins and Proctor, 2007; Ma et al.,
2010).
With the advancement in molecular techniques, several genes involved in Fusarium spore
germination, infection, colonisation and pathogenicity have been characterized. In F.
graminearum, the causal agent of the Fusarium head blight disease, studies have identified
and shown the expression of several genes associated with spore germination processes (Xu,
2000). Also, a secreted lipase encoded by FGL1 gene has been shown to be required for
infection of cereals (Voigt, 2005). With the use of forward and reverse genetic approaches,
the role of several genes which function as virulence factors of F. oxysporum f. sp. lycopercisi
(Fol) has been identified (Michielse and Rep, 2009). Martin-Urdiroz and coworkers (2008)
identified three genes (chs1, chs2 and chs3) in the genome of Fol, which encode structural
chitin synthases of class I, class II and class III, respectively. Using targeted gene disruption
by homologous recombination, the results suggest that chitinases may play a role in
pathogenesis. Other studies also implicated chitinases as pathogenicity factors of Fol (Madrid
et al., 2003; Martin-Urdiroz et al., 2008). The use of Agrobacterium-mediated insertional
mutagenesis to generate and screen several transformants for loss or reduction of
pathogenicity, coupled with complementation and gene knockout experiments, suggest that
the role of some transcription factor, chitin synthase V, developmental regulator FlbA,
phosphomannose isomerase and certain cellular processes are important in pathogenesis of
Fol (Michielse et al., 2009).

Fusarium Wilt Management and Control

Fusarium wilts are generally presumed to be monocyclic - that is, the disease does not
exhibit plant-to-plant spread during the season (Egel and Martyn, 2007). This is primarily
because there are no propagules capable of dissemination to other plants to cause secondary
infections that form above ground until very late in the season. However, the time of
appearance of symptoms and the rate of disease progression in plants may vary considerably
within a field, giving the appearance of secondary spread.
There is some evidence that suggests some Fusarium wilts, for example, Fusarium wilt
of tomato, may be a polycyclic disease capable of significant secondary spread during the
season (Egel and Martyn, 2007). Tillage practices, flooding or heavy rain, contaminated farm
equipment, and other cultural or environmental factors may be involved. Field-to-field spread
can occur when equipment and infected plants are moved from one field to another. It is
possible that macroconidia formed on the decaying vines on the soil surface could be blown
short distances and aid in the spread. Apart from total crop loss, other losses result from loss
in marketable yield i.e., fruit that is formed but cannot be sold because they are too small,
misshapen, low in nutrients, or may be cracked or sunburned.
 Fusarium Wilts 97

There also are hidden losses resulting from increased costs associated with roguing or
replanting dead plants, fumigation or other soil treatments, and fuel and labour as well as
considerable costs associated with preparing new land for production once an existing field
becomes unusable because it is infested with the fungus.
Several chemical fungicides such as prochloraz and carbendazim (Song et al., 2004),
Bavistin (Alam et al., 2010) and salicylic acid (Amel et al., 2010), are used to suppress the
disease by inducing resistance, but these chemicals have a negative impact on human health
and are hazardous to the environment.
The use of chemicals as the sole method of control may indeed result in non-target effects
on soil microorganism populations. A better alternative to chemicals are the soil microbes
such as Trichoderma harzianum, T. asperellum, T. koningii, Penicillium spp. and
Streptomyces griseoviridis residing in the rhizosphere of the plants and have the ability to
suppress the pathogens and stimulate plant growth by the production of phytohormones
and/or degradation of complex substrates (Osuide et al., 2002; Syed et al., 2010; Borrero et
al., 2011). This has been proved in tomato.
Several disadvantages are associated with these biocontrol measures. Biofungicides are
usually composed of living organisms and as a result, their efficacy may vary under a wide
range of environmental, cultural, and biotic conditions. Besides, several chemical fungicides
are effective against soil-borne pathogens and possess competitive advantages not yet
available with their biofungicide counterparts. Thirdly, conventional fungicides are often
cheaper and easier to use and their efficacy is constant except in very severe conditions. Due
to such difficulties, integrated pest management strategies offer bright opportunities of
success, provided that the mode of action of the various components is understood.
Cultivation of resistant varieties (the best option) is commonly practiced as well as
maintaining good hygiene (such as avoidance of contamination, during planting and seedling
transplanting, irrigation, and clearing of debris from previous year’s planting) (Jones and
Woltz, 1981). By modification of the soil pH and fertilizer composition, disease development
can be drastically reduced (AVRDC, 2005; Borrero et al.,2011).
Crop rotation is also used but it is generally ineffective due to the effective survival
strategies of the pathogen. There is the potential for the development of new races that may
overcome cultivar resistance (AAFC, Canada, 2006). The reports of Okungbowa and Edema
(2006) and Okungbowa (2011) have indicated the possible use of plant extracts for the control
of F. oxysporum.

CONCLUSION
Fusarium wilts remain a major problem all over the world causing huge losses in
economic crops, despite measures aimed at prevention and control. Although the use of
resistant cultivars proves to be the best method of control, new races of the pathogen can
develop.
As a result, alternative control strategies are being investigated some of which are
biocontrol methods. Further research aimed at determining the actual role of root exudates,
genetic control of spore germination as well as whether it is vascular occlusion or presence of
toxin that causes death of the plant, are of great necessity for a better understanding of the
biology of the organism.
98 F. I. Okungbowa and H. O. Shittu

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