Importance and management of fusarium wilt (Fusarium udum Butler) of pigeonpea - IJAAR

Int. J. Agr. & Agri. R.
Karimi et al. Page 1
REVIEW PAPER OPEN ACCESS
Importance and management of fusarium wilt (Fusarium udum
Butler) of pigeonpea
Rael Karimi1*
, James Otieno Owuoche2
, Said Nandy Silim3
1
Kenya Agricultural Research Institute (KARI), P.O. Box 340, Machakos, Kenya
2
Department of Crops, Horticulture and Soil Science, Egerton University, P.O. Box 536, Egerton,
Kenya
3
International Crops Research Institute for the Semi-Arid Tropics (ICRISAT), P.O. Box 39063,
Nairobi, Kenya
Received: 19 December 2011
Revised: 05 January 2012
Accepted: 09 January 2012
Key words: Pigeonpea, disease, distribution, management.
Abstract
Fusarium wilt (Fusarium udum Butler) is an important soil borne disease of pigeonpea [Cajanus cajan (L.)
Millsp], which causes significant yield losses in susceptible cultivars throughout the pigeonpea growing areas. The
soil borne fungus enters the host vascular system at root tips through wounds leading to progressive chlorosis of
leaves, branches, wilting and collapse of the root system. Temperature, soil type, water retentive nature of the soil
and nutrient availability has been shown to affect fusarium population. Disease management strategies have
emphasized on integrated disease management practices. Despite extensive pathological and molecular studies,
the nature and extent of pathogenic variability in F. udum has not been clearly established. Information on
characterization of F. udum is needed to help identify race differentials. In addition, there is limited knowledge
on the inheritance of fusarium wilt and other important traits in pigeonpea thus limiting specific cultivar
improvement. This paper reviews the literature on the distribution, symptomalogy, factors that affect its
development and control strategies of the disease.
*Corresponding Author: Rael Karimi  rlkarimi@yahoo.com
International Journal of Agronomy and Agricultural Research (IJAAR)
ISSN: 2223-7054 (Print)
Vol. 2, No. 1, p. 1-14, 2012
http://www.innspub.net

Introduction
Fusarium wilt (Fusarium udum Butler) is an
important soil borne disease of pigeonpea [Cajanus
cajan (L.) Millsp], which causes significant yield
losses in susceptible cultivars throughout the
pigeonpea growing areas. In India, the annual loss
due to this disease is estimated at US $71 million
(Reddy et al. 1993). Fusarium wilt causes economic
loss in pigeonpea of about 470, 000 t of grain in
India and 30,000 t of grain in Africa (Joshi et al.
2001). Kannaiyan et al. (1984) reported wilt
incidence (and range) in Kenya, Malawi and
Tanzania of 15.9% (0-90%), 36.6 (0-90) and 20.4%
(0-60%) respectively with annual loss estimated at
US $ 5 million in each of the countries. In
Tanzania, an incidence of Fusarium wilts as high as
96% has been observed (Mbwaga 1995). Losses due
to wilt in Kenya vary from negligible amount to
100% depending on the stage of the crop and
environmental factors (Kannaiyan and Nene 1981;
Sheldrake et al. 1984).
Although numerous control measures have been
suggested to alleviate the problem of wilt and
increase productivity of pigeonpea, their success
still remains low due to prohibitive cost of practices
and labour-constrained smallholder producers.
These practices are both resource and knowledge
intensive and small farmers often find it difficult to
control the disease especially when the rate of field
infestation is high. Research on disease
management strategies for F. udum may be
relevant to areas where the disease is important.
This paper reviews the literature on the distribution,
symptomalogy, pathogenecity, factors affecting its
spread and control strategies of the disease. The
paper also suggests priority areas for future
research.
Geographical Distribution of Fusarium wilt
The disease was first recorded by Butler (1906) in
India. Although the disease is more prevalent in
India, east Africa and Malawi where field losses of
over 50% are common, it also occurs in Bangladesh,
Grenada, Indonesia, Mauritius, Mynmar, Nepal,
Nevis, Venezuela, Trinidad, and Tobago (Kannaiyan
et al., 1984; Reddy et al., 1993; Marley and
Hillocks, 1996). Recently, this pathogen was
reported to be spreading in Southern Africa
reaching areas in Mozambique (Southern Zambezia
province) (Gwata et al., 2006). Although the
incidence and distribution information is not
available, the disease has also been reported in
Zambia (Reddy et al., 1993). Ghana is also included
in the distribution list but presence of the disease in
the country has not been confirmed (Reddy et al.,
1993). In Kenya, the disease was first reported in
1983 when the first released variety (Munaa) broke
down with Fusarium wilt and was withdrawn from
the farmers (Kimani, 1991). The disease is found in
all pigeonpea growing areas but incidences are high
in the eastern areas (Kannaiyan et al. 1984; Hillock
and Songa, 1993). In Tanzania the distribution
occurs around babati in the north in the southern
zone around Mtwara and along the coast near Dar
es Salaam (Hillocks, unpublished). Although the
Fusarium wilt has been observed in Uganda, the
present distribution and incidence of the disease is
not known.
Symptomatology
Being a soil-borne pathogen, Fusarium udum, the
fungus enters the host vascular system at root tips
through wounds leading to progressive chlorosis of
leaves, branches, wilting and collapse of the root
system (Jain and Reddy 1995). Although the
infection occurs in the early seedling stage,
symptoms are not visible until later in crop
developmental stages (Reddy et al., 1990; Hillocks
et al., 2000). The initial visible symptoms are loss of
turgidity in leaves and interveinal clearing. The
leaves shows slight chlorosis and sometimes
becomes bright yellow before wilting (Reddy et al.,
1990). Partial wilting of the plant as if there is water
shortage even though the soil may have adequate
moisture distinguishes this disease from termite
damage, drought, and phytophthora blight that all
kill the whole plant. Leaves are also retained on
wilted plants. Partial wilting is associated with
lateral root infection, while total wilt is due to tap

3
root infection (Nene, 1980; Reddy et al., 1993). The
most initial characteristic internal symptom is a
purple band extending upwards from the base of the
main stem. The xylem develops black streaks, and
this results in brown band or dark purple bands on
the stem surface of partially wilted plants extending
upwards from the base visible when the main stem
or primary branches are split open (Reddy et al.,
1990; Reddy et al., 1993). This band is more easily
seen in pigeonpeas with green stems than in those
with coloured stems. The intensity of browning or
blackening decreases from the base to the tip of the
plant. Sometimes, branches (especially lower ones)
dry, even if there is no band on the main stem.
These branches have die-back symptoms with a
purple band extending from tip downwards, and
intensive internal xylem blackening (Reddy et al.,
1993). When young plants (1-2 months old) die
from wilt, they may not show the purple band
symptom, but have obvious internal browning and
blackening.
Pathogenic races
The existence of variants/races of F. udum has been
reported and has been cited as a major drawback in
the development of pigeonpea varieties resistant to
Fusarium wilt (Okiror and Kimani, 1997). F. udum
isolates from the same site or diverse geographical
origins have been shown to exhibit high variability
in cultural characteristics (Reddy and Chaudhary,
1985; Gaur and Sharma, 1989) and virulence or
pathogenicity on pigeonpea genotypes (Soko et al.,
1995 ; Baldev and Amin, 1974; Shit and Gupta,
1978; Nene et al., 1981; Okiror, 1986; Gaur and
Sharma, 1989; Okiror and Kimani, 1997; Mayer et
al., 1998; Kiprop et al., 2002; Parmita et al,. 2005).
Baldev and Amin (1974) tested 10 isolates of F.
udum from various sources on 10 pigeonpea lines.
Only three genotypes showed resistance to all the
isolates. They also characterized these isolates as
the races of this fungus. In Malawi when 60 isolates
were inoculated onto the highly susceptible
pigeonpea line ICP 2376, all but seven isolates were
pathogenic (Soko et al., 1995). In a study to verify
diversity in F. udum on pigeonpea in Kenya using
several isolates of the fungus, Okiror and Kimani,
(1997) reported strong differences in growth habit,
morphology and high variability in terms of their
attack on various test cultivars used; and concluded
that the isolates are true variants of the pathogen.
Similar observations were made by Gaur and
Sharma (1989) using 18 pigeonpea varieties against
seven isolates of F. udum from India and Okiror and
Kimani (1997) using six pigeonpea genotypes
against 12 isolates of F. udum from Kenya. Kiprop et
al. (2002) observed differential reactions of seven
pigeonpea varieties to seventeen different isolates of
F. udum and concluded that five virulent groups
exist among Kenyan isolates. This variability was
confirmed by Songa et al. (1995) through field trials.
Songa et al. (1995) found that pigeonpea line ICP
9145, which was wilt resistant at Katumani (Kenya),
ICRISAT Asia Centre (India), and Malawi was
highly susceptible (71% wilt) at Kiboko (Kenya).
Variability of fusarium wilt reactions between
countries and even sites within the same country is
due to existence of different virulent isolate and
environmental influence (Songa et al., 1995; Hillock
et al., 2000). The high variation in cultural and
morphology characteristics of this pathogen could
be due to environmental conditions, age of the
isolates, subculturing, method of storage and
culturing conditions Kiprop et al. (2002). However,
according to Okiror and Kimani (1997) and Kiprop
et al. (2002) the wide variations in virulence
(pathogenecity) to different genotypes of pigeonpea
among F. udum isolates could be due to
environmental conditions and inoculation
techniques used. More work need to be done to
confirm these reports.
There has been conflicting reports on the diversity
of the pathogen using molecular markers.
Conflicting reports on the relationship between
cultural characteristics and the virulence of the
isolate are also available. While studies of genetic
diversity using isozyme markers revealed low
variation in F. udum isolates (Shit and Sen Gupta,
1980; Okiror and Kimani, 1997), Kiprop et al.
(2002) using AFLP reported high variability. Kiprop

4
et al. (2002) using 56 isolates from different
pigeonpea growing areas in Kenya observed that
cultural characteristics of F. udum appeared to be
independent of aggressiveness and no relationship
between aggressiveness and geographical origin of
the isolates used. Similar reports using isozyme
markers were made by Okiror and Kimani (1997)
who found no relationship between protein profiles
of 12 isolates of F. udum from three districts in
Kenya and their virulence. However, Shit and Sen
Gupta (1978) reported that isolates of F. udum
producing luxuriant mycelia growth were weakly to
moderately pathogenic (or aggressive). In order to
establish the extent of genetic variation of this
economically important fungus and relationships
with genetic and pathogenic traits, more isolates
from other countries and/ or geographical origins
should be assayed using other DNA based molecular
techniques.
The available reports on the differential reactions of
certain pigeonpea genotypes to different isolates
raises issues on whether isolates qualify to be called
races of F. udum or not. In the evaluation of
genotypic reaction of fusarium wilt conducted in
wilt sick plots in Kiboko (Kenya), Ngabu (Malawi)
and Ilonga (Tanzania), Gwata et al. (2006) recorded
different wilt incidences at Kenya (52.7%) and
Malawi (1.7%) for genotype ICEAP 00053 and
concluded that there was a differential host
response to the disease by the genotype between the
two locations. Similar findings in a similar study
involving an exotic cultivar (ICP 9145) screened for
resistance to the Fusarium wilt disease in Kenya and
Malawi were reported (Reddy et al., 1990).
According to Gwata et al. (2006) these differential
host response observed for genotype ICEAP 00053
and ICP 9145 between the two locations (countries)
suggests that probably, at least two different
pathogenic races of the disease exists in the African
region. Considering the mode of spread, more
studies need to be done to confirm the existence of
these two pathogenic races because the fact that
Fusarium wilt may carry-over as a contaminant of
pigeonpea seed (Nene 1981) suggests that there may
also be strains even from other different countries
in the Kiboko (Kenya) and Ngabu (Malawi) isolates.
However, apart from studies aimed at
characterizing F. udum isolates (Kiprop et al.,
2002), there are few reports attempting to
characterize the races of F. udum. Most of the
available reports relates different isolates to
different races (Gwata et al., 2006). This needs
further investigation to confirm whether an isolate
should be the same as a race.
Factors affecting infection and spread
Effect of Temperature on the development of
Fusarium wilt
Temperature has been cited as one of the weather
related factors that favour the development of the
wilt disease (Singh and Bhargava, 1981; Agrios,
2005; Ziska and Runion, 2007; Chand and Khirbat,
2009). In pigeonpea, Singh and Bhargava (1981)
observed highest fungal population at the soil
temperatures between 20-300C. In a study with
chick pea cultivars, Mina and Dubey (2010)
reported that the optimum temperature range for
growth and sporulation of the pathogen was 28–
30°C. This supported the earlier observations of
Landa et al. (2001) that optimum growth of F.
oxysporum f. sp. ciceris was at 24.5–28.5°C.
Observations by Landa et al. (2006) showed that
chickpea cultivar was moderately resistant to F.
oxysporium f. sp. ciceris when grown in
temperature regime of 21–24°C, but highly
susceptible at a temperature regime of 25–27°C.
Cooke and Baker (1983) in their review of the
biological control of plant diseases, noted that the
growth of Fusarium wilt pathogens is generally
maximimal at 280C, inhibited above 330C, and not
favoured below 170C. In a physiological study with
F. oxysporum f.sp. cubense isolates, the
temperature assay revealed that the optimum
temperature was 250C for all the isolates, no growth
was observed at temperatures of 5 and 400C, while
very little growth was observed at 10 and 350C
(Groenewald, 2006). Navas-Cortés et al., (2007)
through modelling reported positive correlation
between wilt severity and soil temperature.

5
However, according to Ben-Yephet and Shtienberg
(1997), the effect of temperatures on wilt occurrence
may vary in different pathosystems.
Nutrient status of the soil
The stage of growth, decrease or quiescence of
Fusarium population in soil depends on the
ecological balance and nutrient availability. Nene,
(1981) reported that the persistence of this pathogen
is influenced by soil type and nutrient status. High
levels of nitrogen fertilization in agricultural soils
generally lead to an increase in Fusarium wilt
development (Wolts and Engelhard, 1973; Wolts
and Jones 1973). Studies have also shown that the
form of nitrogen in the soil is important in the
development of fusarium wilt disease (Wolts and
Jones, 1973; Groenewald, 2006). Wolts and Jones
(1973) reported that F. oxysporum cultured on
ammonium nitrogen was more virulent than the
same fresh weight of the organism cultured on
nitrate nitrogen. In a study using F. oxysporum f.sp.
cubense (Foc), Groenewald (2006) observed that
Foc grew significantly better on the NO3-N medium
invitro than on a NH4-N medium. Similar results
were observed by Walker ( 1971) who reported that
high nitrogen and low potassium favoured the
disease, while low nitrogen and high potassium
retarded disease development. However, in a
different study, Byther (1965), observed reduced
disease incidence in the field fertilized with NO3-N
compared to fields fertilized with NH4
+-N. Effects
on nitrate and ammonium sources on disease were
apparently related to soil PH effects. Nitrate causes
an elevation in soil PH while ammonium causes a
reduction (Wolts and Jones, 1973). The nitrate form
of nitrogen becomes increasing unfavourable for the
disease with increasing rate of application, while the
ammonium form becomes more favourable as the
nitrogen application rate is increased. Relatively low
levels of calcium appear more conducive to disease
than normal levels.
Soil and soil pH
The amount of wilt incidence is influenced by water
retentive nature of the soil and the disease is
favoured by slightly acidic and alkaline soils with
sand content of more than 50% (Upadhyay and Rai,
1992; Hillock et al., 2000). Shukla (1975) observed
more Fusarium wilt inoculum in sand (94%) than in
heavy black cotton soil (18%). However, some soils
are suppressive to the pathogen due to their
physico-chemical characteristics (Upadhyay and
Rai, 1992). Sugha et al. (1994), found that a higher
soil PH reduced the disease incidences. Lower
disease incidence associated with a higher PH was
due to decreased availability of the micronutrient
that are essential for the growth, sporulation and
virulence of the pathogen (Jones et al., 1989).
Soil antagonists
The susceptibility pigeonpea cultivars to Fusarium
wilt is increased by the presence of certain
nematodes in the soil (Hillocks et al. 2000). The
association between Fusarium wilt and root-knot
nematodes is well established (Hillocks and Songa,
1993; Marley and Hillocks 1994; Marley and
Hillocks 1996). In India, reports have shown that
the cyst nematode, Heterodera cajani (Hasan 1984;
Sharma and Nene, 1989) and reniform nematode,
Rotylenchulus reniformis (Sharma and Nene, 1990;
Jain and Sharma, 1996) increase susceptibility to
the disease. Its growth is also influenced by soil
antagonists especially the bacterium Bacillus
subtilis that produces the antibiotic bulbiformin
(Pursey, 1989). The microflora have also been
reported to affect the pathogenecity of the fungus
(Upadhyay and Rai, 1987).
Susceptible pigeonpea cultivar
The disease begins in a field in a small patch which
enlarges with each successive year that a susceptible
cultivar is grown. Fusarium wilt is not seed borne
but it may be carried as a contaminant of pigeonpea
seed (Upadhyay and Rai, 1983). This may explain
why wilt is common in areas where the crop is
grown year after year making it more devastating in
small-scale farmers who retain their seeds.

6
Others
The main means of spread in a field is along the
roots of infected plants, movement of contaminated
soil, propagules carried in irrigation water, or rain
water run-off. Termites also act as agents of
dissemination. According to Okiror (1986), wilting
suddenly appears in ratooned crops probably
because of the continued use of ratooning knife
which acts as a carrier of inoculum from plant to
plant.
Inheritance
The knowledge of genetic inheritance is essential for
formulation of strategy on how to transfer the genes
into adapted susceptible varieties. Conflicting
reports have been made on the inheritance of
resistance to Fusarium wilt in pigeonpea.
Resistance to fusarium wilt has been reported to be
under the control of two complementary genes
(Parmita et al., 2005), single dominant gene (Pawar
and Mayee 1986; Pandey et al. 1996; Singh et al.
1998; Karimi et al. 2010), 2 genes (Okiror 2002),
major genes (Sharma, 1986; Parmita et al., 2005),
duplicate genes and even multiple factors (Mahotra
and Ashok, 2004) and a single recessive gene (Jain
and Reddy, 1995). Apart from dominant, recessive
and complementary gene action on the control of
Fusarium wilt (Kimani, 1991; Kotresh et al., 2006)
has been reported. Dominant epistatic gene
interaction and a single dominant gene play a
significant role in controlling resistance to wilt
(Parmita et al., 2005). Digenic and quantitative
genes that are resistant to Fusarium wilt have also
been observed (Odeny, 2001).
These differences may be due to several factors.
First, the sources and genetic background of the
resistant materials used in the above diferent
studies were different and this could have
contributed to the different findings. According to
Odeny (2001), genes for wilt are controlled
differently depending on the origin of the resistance
source used in a particular cross and the
background in which the gene is put. Secondly, the
inoculation methods used were different. Some of
the studies were carried out in the wilt boxes
(Kimani, 1991; Okiror, 2002) or field (Jain and
Reddy, 1995). In the field, the environmental and
edaphic factors may influence both the disease
severity and the expression of the resistance.
Disease control methods
Cultural method
Several cultural control practices are recommended
for restricting the severity of the Fusarium wilt of
pigeonpea. Crop rotation with sorghum [Sorghum
bicolour (L.) Moench], tobacco (Nicotiana tabacum
L.), or castor (Ricinus communis L.) every three
years has been found to free pathogen completely
from the field (Verma and Rai, 2008). Pigeonpea
intercropped with sorghum had only incidence of
24% wilt against 85% in sole crop treatment
(Natarajan et al., 1985). One-year break with either
sorghum or fallow reduced wilt to below 20%
(Verma and Rai, 2008). Application of nitrogen in
form of farmyard manure and green manuring with
Crotalaria juncea also reduce the incidence of wilt
disease considerably (Upadhayay and Rai, 1981;
Verma and Rai, 2008). Upadhyay and Rai (1981)
reported a significant reduction in pigeonpea wilt
incidence under mixed cropping with Crotalaria
medicaginea. Solarisation of the field during
summer period reduces the Fusarium inoculum
(Reddy et al., 1993). However, limited studies have
been conducted to understand the effect of cultural
practices such as intercropping and rotation on the
disease, with the aim of developing integrated
disease management practices.
Effects of chemical control on Fusarium Wilt
in pigeonpea
Several chemicals have been recommended for the
management of Fusarium wilt (Singh, 1998). Seed
treatment with a mixture of benomyl and thiram at
equivalent rates completely eradicate the fungus
(ICRISAT, 1987; Reddy et al., 1993). Ingole et al.
(2005) also observed that a combination of
carbendazim + thiophanate (0.15 + 0.10%) was
effective in reducing the Fusarium wilt. Seed
treatment with 4g Trichoderma viride formulation

7
+ 3 g thiram kg-1 seed and application of 2 kg T.
viride formulation with 125 kg farm yard manure
ha-1 has also been reported to control the disease
(Verma and Rai, 2008). Addition of boron (Bo),
manganese (Mn) or zinc (Zn) and methyl bromide
(CH3Br) to the soil effectively controls Fusarium
wilt (Perchepied and Pitrat, 2004). This report was
supported by Mandhare and Suryawanshi (2005)
who recommended the application of Trichoderma
as a seed treatment and soil application for
managing Fusarium wilt of pigeonpea. Sinha (1975)
observed a significant control of the disease by
Bavistic applied as a soil drench at 2gkg-1 of soil
days before inoculation of pigeonpea with Fusarium
udum. Antibiotics griseofulvin and bulbiformin
have been reported to be effective in controlling the
disease. Control of the pathogen by organic
amendments and by application of trace elements to
the soil has also been reported (Reddy et al. 1990).
However, none of the fungicides have been found to
give adequate protection against Fusarium wilt
disease (Lemanceau and Alabouvette, 1993; Pandey
et al., 1996; Singh 1998) as the pathogen is
primarily a soil inhabitant. Besides killing the non-
target beneficial microorganisms in soil, the
frequent application of fungicides to the soil causes
environmental hazards causing water and soil
pollution.
Biological control
In view of the adverse effect of fungicides to the
environment and increasing interest in sustainable
agriculture, biological control has been reported as
an attractive possibility for management of soil-
borne plant pathogens. Reports have shown that
supplementing the soils with fungal or bacterial
antagonists reduces incidences of Fusarium wilt
(Bapat and Shar, 2000; Singh et al., 2002; Anjaiah
et al., 2003; Mandhare and Suryawanshi, 2005;
Maisuria et al., 2008). Numerous rhizobacteria
have been used as biocontrol agents (Pusey, 1989;
Upadhyay, 1992; Bapat and Shar, 2000; Siddiqui et
al., 2005; Siddiqui, 2006; Siddiqui and Shakeel,
2007). Soil amendment with Trichoderma
harzianum at all pathogen levels has been reported
to give a disease control of 22% -61.5% (Prasad et al.
2002). Studies on antagonism, found that
Aspergillus niger, Aspergillus flavus,
Micromonospora globosa and Aspergillus terreus
highly suppressed the population of F. udum
(Upadhyay and Rai, 1981). In a different study on
tomatoes (Lycopersicon esculentum), Khan and
Khan (2002) observed that root-dip application of
Bacillus subtilis, Pseudomonas fluorescens,
Aspergillus awamori, Aspergillus niger and
Penicillium digitatum resulted in significant decline
of Fusarium oxysporum f.sp lycopersici population
in the rhizosphere. In a bio-control experiment,
Anjaiah et al. (2003) reported that inoculation of
pigeonpea and chick pea seeds with Pseudomonads
aeruginosa (PNA1) significantly reduced the
incidence of fusarium wilt in naturally infested soil.
Soil antagonists are also known to suppress the
development of wilt through induction of resistance
(Upadhyay and Rai, 1981; ICRISAT, 1987;
Upadhyay, 1992). For large scale management,
Mahesh et al. (2010) recommended integrated
management (systemic fungicide, biocontrol agent
and FYM) as the most effective treatment of
Fusarium udum.
Host plant resistance
The deployment of cultivars with resistance to
Fusarium wilt remains the most effective means of
control. The search for sources of resistance to wilt
in pigeonpea began as early as 1905 in India.
Subsequently screening has been conducted in
many locations in India, Malawi and eastern
African. Through evaluation of local landraces,
extensive world collections, introductions and
segregating populations of pigeonpea,
resistant/tolerant pigeonpea lines have been
identified (Kimani, 1991; Kimani et al., 1994; Songa
et al., 1995; Silim et al., 2005; Gwata et al., 2006;
Karimi et al., 2010). The release of many resistant
lines indicates the abundance of available resistance
to Fusarium wilt within the genus Cajanus. The
most successfully adopted wilt-resistant cultivar in
Africa was ICP 9145 which in the mid 1990s
accounted for around 20% of pigeonpea production

8
in Malawi (Babu et al., 1992; Reddy et al., 1992).
According to Hillocks et al. (2000), the resurgence
of pigeonpea wilt as a problem in Malawi, has been
due to a combination of the lack of a sustainable
seed production system to make ICP 9145 widely
available to farmers, introgression between local
susceptible types and ICP 9145, nematode-induced
susceptibility and consumer preference for the
cooking qualities of local, wilt susceptible cultivars.
In Kenya where ICP 9145 has also been tested, it has
not shown the high level of wilt resistance expected.
This may be due to a loss of resistance as a result of
segregation in ICP 9145 or some other
environmental factor in Kenya.
Kenyan elite germplasm ICEAP 00040 is another
widely adopted and adapted variety in Africa.
Observations from wilt-sick plots (Bayaa et al.,
1997) at Kiboko (Kenya), Ngabu (Malawi) and
Ilonga (Tanzania) research stations where the
disease pressure was considered to be high,
indicated that disease incidences for ICEAP 00040
were consistently low (<20.0%) at all three
locations (Gwata et al., 2006). Because of its ability
to withstand the high disease pressure, wide
adaptability and high yield potential, ICEAP 00040
has been attractive to pigeonpea farmers in the
region extending from the semi-arid lowlands of
eastern Kenya (50S) to Mozambique (250S) and was
subsequently released in 1995 for commercial
production in Kenya and later in 2003 both in
Malawi and Tanzania (Silim et al., 2005). ICEAP
00040 has large, cream grains that are preferred by
the farmers and markets in the region.
In spite of stupendous success achieved through
sustained breeding efforts over the last decade as
evidenced from commercially accepted resistant
pigeonpea varieties (Reddy et al., 1992; Gwata et al.,
2006), very few resistant cultivars are with the
farmers. This is due to lack of effort to breed
varieties that are both wilt resistant and farmer
acceptable. For instance, in India, wild relatives
have been reported to possess many agronomically
important traits such as resistance to pests and
diseases (Reddy et al., 1996; Sharma et al., 2003),
salinity tolerance (Subbarao et al., 1991) and high
protein content (Saxena et al., 1996), all of which
would be useful in cultivated pigeonpea. However,
no effort has been made to transfer these useful
genes from wild relatives to cultivated pigeonpea.
Specific cultivar improvement has been difficult due
to the limited knowledge on the inheritance of
important traits and lack of understanding on the
level of inter- and intra-specific genetic diversity. As
different needs and opportunities arise, pigeonpea
breeders need to incorporate new genetic sources
using various breeding methods aided with modern
tools such as biotechnology. Diffusion of the
improved varieties has also been limited by lack of
good quality seeds. The use of own saved seed by
farmers makes production of improved varieties
(self pollinated crops like pigeonpea) seeds
uneconomical, thus undermining the incentives for
private sector investment in commercial production
and marketing of such seeds.
Future research needs
Development of well adapted resistant pigeonpea
varieties offers the most efficient and economical
method for control of Fusarium wilt. Several
genotypes within the pigeonpea germplasm have
been identified. The resistant genotypes need to be
combined with high yield and consumer-preferred
agronomic traits so that they can be adopted by the
farmers. Knowledge on mode of inheritance for both
resistance to fuasium wilt and other agronomic
traits need to be well understood. Mapping of the
Fusarium wilt resistance genes in the already
identified resistant lines is recommended. This will
help shorten the development of the resistant
pigeonpea cultivars and the pyramiding of the wilt
resistance with other traits, particularly through the
use of marker-assisted selection.
Studies to characterize the races of F. udum in
pigeonpea in Africa should be done. This will help
identify the presence of different races of Fusarium
udum. It will also confirm whether the isolates are
the same as races.

9
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