PLANT PATHOLOGY

Crop Diseases and their Management

Professor Y.S.Ahlawat
Division of Plant Pathology
Indian Agricultural Research Institute
New Delhi-110012

(30-04- 2007)
CONTENTS
Wheat Diseases
Rice Diseases
Maize Diseases
Sorghum Diseases
Bajra Diseases
Sugarcane Diseases
Groundnut Diseases
Sunflower Diseases
Mustard Diseases
Pigeonpea Diseases
Soybean Diseases
Gram Diseases
Lentil Diseases
Cotton Diseases
Potato Diseases
Tomato Diseases
Brinjal Diseases
Chilli Diseases
Vegetable Crucifer Diseases
Vegetable Cucurbit Diseases
Pea Diseases
Bean Diseases
Mango Diseases
Apple Diseases
Papaya Diseases
Citrus Diseases
Peach and Pear Diseases
Guava Diseases
Grape Diseases
Sapota Diseases
Ber Diseases
Custard Apple Diseases
Coconut Palm Diseases
Management of Plant Diseases

Keywords
Crop disease, symptom, pathogen, control, disease cycle, economic importance


Wheat Diseases
1. Rusts of Wheat
The rusts of wheat belong to genus Puccinia, family Pucciniaceae, order Uredinales and class
Basidiomycotina. Wheat suffers from three rust diseases namely stem, leaf and stripe rust.
Stem rust caused by P. graminis, leaf rust caused by P. recondita but currently P. triticina
was suggested to be the preferred name, yellow rust of wheat is caused by P. glumarum but
later changed as P. striiformis. Rust fungi which are morphologically identical but attack
different host genes are known as special forms (formae specialis) for example, P. graminis
on wheat is Puccinia graminis f. sp. tritici, P. recondita as Puccinia recondita f. sp. graminis
and P. striiformis as Puccinia recondita f. sp. graminis. In each special form of these rusts
are several pathogenic (physiological) races which can be detected on different varieties of
the same species by inoculation and these varieties are known as differential hosts.

The rust fungi, being an obligate pathogen, must be cultured on living host plants under
controlled condition in a glasshouse. Black and brown rust pathogens complete their life
cycle on two hosts. For P. graminis tritici, wheat is the primary host and barberis is the
secondary or alternate host. P. graminis tritici completing their life cycle on two hosts is
known as heteroecious rust. This rust pathogen produces five different stages/spores to
complete the sexual cycle and the stages are: pycnial, aecial, uredial, telial and basidial.
Urediospores and teliospores are formed on wheat and basidiospores, pycniospores and
aeciospores on alternate host (barberis). Such rusts are known as macrocyclic or long cycled
rusts.

2. Black or Stem Rust of Wheat
Stem rust of wheat is worldwide in its distribution and affects wheat wherever it is grown. It
caused enormous losses to wheat production all over the world. This disease has caused
greater damage than any other disease of wheat crop. In dry areas, the disease developed in
epiphytotic form during wet season. Losses were higher in spring wheat areas of North
America than winter wheat areas because of relatively high summer precipitation in spring
wheat areas and the the plants exposed to longer period of favourable summer conditions.
Now stem rust is largely under control worldwide.

Symptoms: The stem rust pathogen attacks all the above ground parts. In addition to wheat,
this pathogen also infects its alternate host barberis (Barberis vulgaris). The black or brown
colored elliptical blisters or pustules develop on upper and lower surfaces of leaves, stem and
leaf sheaths of wheat generally parallel to their long axis and known as uredia (Fig.1a).











(b)Leaf Rust
(P. recondita)
(a)Stem Rust
(Puccinia
graminis tritici)
(c)Stripe Rust
(P. striiformis)

Fig 1. Three rusts of wheat
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These uredia are 1-3 mm wide and upto 10 mm long in size. The epidermis of the infected
plants is ruptured releasing a powdery mass of brick red coloured uredospores. Later in the
season these pustules turn black due to abundant production of shiny black teliospores
alongwith the uredospores but finally the uredia are transformed into black colored telia
forming teliospores. All the affected parts are ultimately covered with uredia or telia filled
with either urediospores or teliospores or both. Stem rust is favoured by humid conditions
and warmer temperatures of 15 to 35 C. Uredia contain upto 10000 urediospores.

The basidiospores infect barberis, the alternate host. On barberis, symptoms are developed on
affected leaves as yellowish to orange colored spots. Later on the upperside of the leaves
appear minute black colored bodies known as spermagonia or pycnia having nector. Horn-
like or cup shaped aecia appear below pycnia or sometimes next to them. The host tissue
swollen in and around the infection and whitish aecial wall protrudes at the margin of aecia.
Aeciospores can also be a source of inoculum of wheat stem rust and can infect wheat similar
to uredospores wherever alternate host is found.
Pathogen: Puccina graminis tritici (pers.) Erikss. Henri =Puccinia graminis f. sp. tritici is the
causal pathogen.
Disease Cycle: Wheat, barley, triticale and a few related species are the primary hosts for P.
graminis f. sp. Tritici .The pycnia and aecia develop on alternate hosts, Barberis vulgaris L.
and Mahonia spp. wherever they are found.The pathogen completes its life cycle on two
hosts, wheat and barberis being its heteroceous nature. The uredo and teleuto stages are found
on wheat, barley or some grasses and pycnial and aecial stages on alternate hosts. The life
cycle is given in (Fig 1a-1).
















Fig 1a-1. Life and disease cycle of Puccinia graminis tritici
(Source: Courtesy of V. Brewater)

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The uredospores are brown, thick walled with spines and measure 25-30 X 17-20 m. They
germinate through the germ tube when come in contact to a proper host. The germ tube
produces appressoria which in turn develop the infection peg. The infection pegs enter the
host through stomata and finally hyphal strands develop and hyphae spread intercellularly.
When fully established, the uredosori are developed, which erupt releasing the uredospores.
Uredospores spread from field to field of wheat through winds.

At late in the season the telia are produced in mature uredial sori. The teliospres are dark
brown, two celled and wedge shaped with thick walls measuring 40 to 60m x 18 to 22m.
Teliospores are dicaryotic (n = n) and remain with the straw after harvesting where
karyogamy occurs and the teliospores become diploid (2n). The teliospores germinate after a
long resting period and exposer to freezing temperature. They undergo meosis producing a
four celled basidium. Each cell produces a single haploid basidiospore (1n) which is hyline
and travel through wind and infects barberis bush resulting the production of a pycnium (1n).
The picnium produces receptive hyphae and picniospores of a single mating type (+or -) that
serves as female and male gametes of the fungus. Pycniospores of one mating type must be
transferred to the receptive hyphae of the opposite mating type to initiate aecia and
aeciospores development which is normally done by insects or splashing rains. Aeciospores
are dicaryotic (n+n) and are produced in aecia on the lower surface of barberis leaves below
the pycnia.

Aeciospores are hydroscopically released from the aecia, travel by wind and infect wheat
resulting in the production of dicaryotic uredia with uredospores. The asexual stage is
repeated several times during the season. However, the sexual stage is not found in India
because of nonavailability of proper alternate host (s). In India, disease develops by air borne
uredospores which needs free moisture and temperature above 20 C for spread. The pathogen
perpetuates in Nilgiri hills during off season and becomes air borne. If peninsular and central
India has rainfall during November then epidemics are severe. Late infection causes less
damage in north India.

Control: Control of wheat stem rust has been achieved through the development of rust
resistant varieties. Genetic analysis of five bread wheat cvs. Hd 2135, HD 2160, HD 2189,
HD 2285 and Vaishali with four selected pathotypes 21, 21A-2, 40-1 and 117A of Puccinia
graminis f. sp. tritici showed the presence of three dominant and one recessive gene for
resistance in HD 2135, two dominant and one recessive genes in HD 2160, four dominant
genes in HD 2189, three dominant and two complementry recessive genes in HD 2285 and
five dominant genes in Vaishali. Test of allelism confirmed the presence of Sr 8a and Sr 30 in
HD 2135 and HD 2160; Sr 8a in HD 2189; Sr5 in HD 2285 and Sr5 and Sr8a in Vaishali.
World wide resistance genes of stem rust (Sr genes) have been identified from Triticum and
related genera and incorporated in agronomically superior cultivars.

The cultivation of slow rusting varieties will be useful for certain regions. Therefore,
commercial wheat varieties were evaluated for slow rusting phenomenon. Wheat cvs. HPW
42, Hs 207, and GW 190 showed slow rusting to both stem and leaf rusts. Among durum
wheat cvs. HI 8316, HI 8381 and HD 4633 are slow ruster to stem rust.

Eradication of alternate host (barberis) from countries where it plays role in rust recurrence
helped in controlling black rust. In India, the inoculum survives on self sown wheat at hills.
Therefore, resistant varieties should be grown in hills as eradication of self sown plants is
practically impossible. Use of early maturing varieties and early sowing is also helpful to
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avoid damage due to black rust since this rust appears late in the season. Excessive irrigation
increases the susceptibility to uredospores. Therefore, irrigation schedules recommended for
a variety or cultivar must be followed.

Seedling and adult plant resistance and use of slow rusting varieties/cultivars are another area
of interest to minimize the losses caused by stem rust. Slow rusting means the ability of a
cultivar to retard rust development. This phenomenon is governed by genes. Several Sr genes
are associated with slow rusting on wheat by stem rust pathogen.

Single foliar spray of new systemic fungicides such as Bayleton, Diniconazol can control
stem rust. For the efficient use of fungicides mathematical prediction model to forecast stem
rust based on environmental variables have been developed. The linear prediction equation
developed for stem rust (Y=29.3733 +1.820X1 +1.7735X2 +0.2515X3) may be useful in
estimating the severity of the disease and thereby giving enough time to decide the economic
use of fungicides for the disease management. In this equation, Y, X1, X2 and X3 were
expected disease severity after one week, prevous disease severity, minimum temperature and
maximum relative humidity in the next week.

3. Brown or Leaf Rust of Wheat
Leaf rust of wheat is found in all the wheat growing countries. In India, this rust appears in
northern and eastern part of the country in wheat crop earlier than yellow or black rust and
causes much higher damage than other rusts. Epidemics due to this rust have been
experienced in North western region during the year 1971-72 and 1972-73 causing losses in
wheat production to the tune of eight and ten lakh tones respectively. Similary, during the
year 1985-86 and 1986-87 this rust appeared in a severe form in North western states of India
especially on late sown wheat.

Symptoms: As the name indicates the first symptom of the disease is the appearance of
minute, round, orange sori, irregularly distributed on the leaves but occasionally they may
appear on stem, leaf sheath and spikes. These sori are irregularly distributed on both the
surfaces of leaves (Fig.1b). Maximum numbers of sori are seen on the flag leaf towards late
in the season. Initially these sori are bright orange in colour but become brown at maturity.
The epidermis is ruptured over the pustules and brown powder of large number of
uredospores can be seen on the leaf surface. The affected leaves become yellow. At the time
of maturity of the crop, the telia are formed on the lower surface of leaves. Telia are lead gray
or black in colour and are covered with epidermis. The affected plants remain dwarfed and
develop shrinkled grains. During severe infection plants may die before maturity.

Pathogen: Puccinia recondita Roxb. Ex Desm =Puccinia triticina Pers = Puccinia recondita
f. sp. tritici is the causal organism. It is hererocious rust. The uredial and telial stages appear
on wheat and some grasses. The alternate host is Thalictrum speciosissimum where the
fungus produces its sexual gametes (pycniospores and receptive hyphae). In India, The
alternate host does not to play any role.

Disease Cycle: Infection normally takes place from the inoculum survives on self sown
wheat or grasses or overlapping of crops. Puccinia recondita attacks a wide number of
grasses but it is primarily a pathogen of wheat. The rust inoculum survives on volunteer (self
sown) wheat. The inoculum comes from volunteers in the form of uredospores. The pathogen
over-summers in low and mid-altitudes of Himalayas and Nilgiri hills. Primary infection
develops from wind deposited uredospores in eastern Indo-gangetic plains in middle of
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J anuary where it multiplies and moves westward by March. Temperature of around 20C with
free moisture (rain or dew) causes epidemics. Uredospores germinate 30 minutes after
contact with free water and temperature of 15 C to 25 C.











Fig 1b-1: Life and disease cycles of Puccinia recondita
(Source: Courtesy of V. Brewater)

The germ tube grows along the leaf surface until it reaches to a stomata ; an appresorium is
then formed, followed immediately by the development of penetration peg and a sub-stomal
vesicle from which primary hyphae develops. A haustrial mother cell develops resulting in
additional haustrial mother cells. The mycelium produces uredia where uredospores are
developed. Maximum sporulation is reached in about four days following infection under
favourable temperatures.

Uredospores are orange to dark red, echinulate, spherical and usually measure 20 to 28 m.
The telia are rare but when formed are found mostly on the under surface of leaves and do not
rupture the epidermis of the host. The sori are divided into compartments by means of
lengthy paraphysis among the teliospores. They are developed with unfavourable conditions
or senescence. They are dark brown, two celled with thick walls and rounded or flattened at
the apex. The teliospores remain under the epidermis with the leaves. Pycnial and aecial
stages of the pathogen are similar to P. graminis tritici and are known to occur on 11 species
of Thalictrum. The life cycle of the pathogen is shown in (Fig 1b-1).

Control: The control strategies described under black rust of wheat are also applicable for
the management of leaf rust. In India, several races of leaf rust have been identified with
variable virulence. Genetic analysis for leaf rust resistance in nine cultivars viz. HD 2402,
HD 2643, HI 1077, HP 1731, PBW 343, UP 262 UP 2338, WH 147, and WH 542 with
pathotypes 77-2, 104-2 and 106 showed the presence of one dominant gene for resistance in
HD 2402, one dominant and one recessive gene in HI 1077, PBW 343, UP 262 and WH 542;
two dominant and one recessive resistant gene in HP 1731 and UP 2338 and three dominant
independent resiatance genes in HD 2643. Test of allelism confirmed the presence of leaf
rust resistant gene Lr1 in HD 2643, Lr13 in HD 2329 and Lr 14a in HI 1077 and UP 262.
6

Cultivars HI 7747, HI 8461, HI 8488, HI 8490, HD 4637 and HD 4645 are slow ruster to leaf
rust.

The linear prediction equation developed for leaf rust is:
(Y=-83.531 +1.522X2 +1.753X3).

4. Yellow or Stripe Rust of Wheat
Yellow rust of wheat is a major disease of wheat especially during winter or early spring or at
high elevations. In India, this is an important disease because wheat is a winter crop. This rust
pathogen infects wheat and barley in indogangetic plains. In Delhi and areas of Punjab this
rust appears in the month of J anuary-February. The disease is more damaging in northen and
eastern parts of the country than southern and western regions.

Symptoms: The disease symptoms appear as pin head-like light yellow coloured sori in
between the leaf veins and appear like a stripe (Fig.1c). In severe conditions, the sori may
also develop on other parts of the plant such as lemma, stalk, glumes, awns and even on
grains. When the infection is severe these sori may coalesce and the whole leaf show yellow
powder on its surface due to release of urediospores in large numbers and yellow powder of
these spores can be seen even on ground near the plants. Late in the season the dull black
coloured telia appears on leaves, stalk and glumes. Like uredium they also develop in a line
and covered with a membrane which does not burst like black rust. The light and shreveled
grains are formed on affected plants and such plants remain stunted.

Pathogen: Puccinia striiformis West = Puccinia glumarum Schmidt Erikss & Henn is the
causal pathogen.

Disease Cycle: Puccinia striiformis is a pathogen of grasses, and cereal crops, wheat, barley,
triticale and rye. No alternate host of P. striiformis could be confirmed as yet under natural
conditions. Puccinia striiformis is most likely hemiform rust in that the life cycle seems only
to consist of the uredial and telial stages. The uredospores require the lowest temperature as
compared to other wheat rust pathogens (minimum 0C, optimum 11 C and maximum 23 C)
for their development. In areas near the equater, yellow rust tends to cycle endemically from
lower to higher altitude and return following the crop phenology. In more northern latitudes,
the cycle becomes longer in distance with moving from mountain areas to the foothills and
plains. The pathogen spreads through air borne uredospores, when temperature is 10-20C.
Pathogen survives in the cool temperature of hills and the primary infection takes place by
middle of J anuary in the foot hills and submountaineous parts of north western India. Also
infection comes from across the western border; hence the probability of evolution of new
races increases in this area. Yellow rust from Nilgiri hills can not come out of the zone due to
high temperature in the peninsular and Central India.

Puccinia striiformis consists of Uredial and telial stages. Uredia develop uredospores on
wheat which are yellow to orange in colour, more or less spherical, echinulate and 28 to 34
m in diameter. Teliospores are dark brown, two celled and similar to size and shapes to
those of P. triticina. Uredospores are the only source of inoculum for wheat, and they
germinate and infect at cooler temperatures. In India, several pathogenic races in P.
striiformis are known to occur.

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Control: Most of the presently recommended varieties are resistant. Major emphasis should
be given to host resistance and cultivation of resistant varieties is the main strategy for
management.

Rust Reccurrence in India: Mehta from 1920 to 1950 studied the perpetuation of rusts in
more detail and systematic manner. He conclusively proved that the Barberis species found
in India do not play any role in the perpetuation of stem rust in India. Similarly it has been
proved that Thallictrum species occurring in the hills are also not playing any role in the
perpetuation of stem rust.

Mehta has shown that high temperature during summer in Indian plains followed by rains,
wheat rusts in general, can not survive. They oversummer in cooler climates of hills on self
sown wheat plants, ratoon tillers and also on summer crop grown in Nilgiri and Palini hills in
south India. He later concluded that stem rust of wheat spreads from the sub-Himalayan
ranges to the plains of India and asserted that central Nepal forms the most dangerous foci
of infection of this rust. Possible role of grasses in the hills in the annual reccurrence of stem
rust could not be established although some of the grasses were susceptible to Puccinia
graminis tritici under natural and glasshouse conditions in the hills and plains of India.
Until early 1970s, rusts were one of the major causes of economic losses to wheat production
Extensive wheat disease surveys conducted by the Indian Agricultural Research Institute
showed that the stem rust ( P. graminis f. sp. tritici ) is introduced from Nilgiri and Palini
hills of South India and spread every year northwards because of tropical cyclones that
crosses coastal Andhra Pradesh and Tamil Nadu late October-November. The northernly
winds associated with rain efficiently transport and wash down the inoculum over central
India where one month crop is available. The fixed path between Nilgiri and Palini hills to
Narmada and Tapti river belt is known as Puccinia path.

Initially, Mehta had shown the movement of leaf rust both from north and south Indian hills.
Later, J oshi and his team supported this view and further demonstrated that leaf rust ( P.
recondata ) spreads both from southern and northern hills. It is introduced from Nilgiri and
Palini hills and is established in the plains of Karnataka and Tamil Nadu in South India. The
rust population from southern foci moves northwards towards Maharashtra and Madhya
Pradesh. The spread of leaf rust over the Indo-Gangetic plains is predominantly from the
warmer north-eastern region and is influenced by the number of rainfall during winter month.

Stipe rust (P. striiformis) is a major problem only in cooler parts of the country especially
north and north-western region. Its infection in south, central and eastern parts remains
isolated and seldom become a serious threat to wheat. In north India, the inoculum moves
from northern hills and get established in the plains of Punjab, Hariyana and western Uttar
Pradesh. In the foot hills and northern Indian plains stripe rust spread much faster by
uredospores than leaf rust due to favourable cool temperature but the spread after February is
checked due to rise in temperature and this time the telial stage is developed which does not
play any role in the spread of the disease.

A national stretagy for vertical resistance (VR) and adult plant resistance (APR) genes
deployment has been proposed along Puccinia path for managing stem and leaf rusts. In
this strategy, vertical resistance genes in different epidemiological sub-zones are deployed to
minimize the possible break down of the cultivars from virulent pathotypes.


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5. Loose Smut of Wheat
Loose smut is a common disease of wheat throughout the world wherever wheat is grown.
The disease incidence depends from variety to variety and the environment conditions prevail
during crop season especially during flowering time. Cool, humid climate accompanied by
light showers favour the loose smut infection. In India, disease incidence is more in northern
areas than in southern parts where wheat is grown. Wheat yield is reduced in proportion to
the smutted heads. In India, loose smut causes 3-4 per cent loss in yield annually

Symptoms: The plants produce smutted spikes which are easily recognized at the time of
heading by their characteristic dusty black appearance of the ears (Fig.2). The smutted spike
emerged from the boot leaf a few days (1-3 days) earlier than those of healthy plants but in
some varieties smutted and healthy heads emerge simultaneously. The infected plants are
stunted and produce less tillers in some varieties such as sonalika. All the spikelets of a
smutted ear are filled with black powdery mass of spores. The spore mass is covered with a
delicate silvery membrane of host origin which usually ruptures before the complete
emergence of ears from the sheath exposing dark, olive brown powdery mass of spores in
place of normal spikelets. The chaff and grains are completely transformed into black
powder. The spores are blown away by the wind and by the harvesting time of crop, bare
rachis remains of the smutted heads.










Fig 3. Karnal bunt (Neovossia indica) of Fig 2. Loose smut of wheat

Pathogen: Ustilago tritici (Pers.) Rostr. =Ustilago segetum var. tritici is the causal pathogen
of the disease and belongs to the family Ustilaginaceae, order Ustilaginales and class
Basidiomycotina. The mycelium in the seed is hyaline, septate and dikaryotic. It grows
alongwith the plant and turns brown near maturity of plant. The cells of the mycelium are
turned into brown spherical teliospores which are carried to healthy plants by wind.
Disease Cycle: It is a seed borne disease and hence the primary inoculum comes from
contaminated seeds. The mycelium remains dormant in the embryo of seed and cause
infection to the next year crop. Maximum infection of loose smut fungus takes place during
flowering time. The olive black teliospores from smutted heads are carried by wind, rain or
insects to the open flowers of healthy heads. These spores are thick walled, echinulate and
measure 5-9 m. On the healthy spikelets the spores germinate quickly by forming a
germtube which develops into basidium or promycelium with four uninucleate cells.
Diplodization takes place between compatible cells of promycelium by means of short and
long conjugation tubes. The resulting diploid cells produce binucleate hyphae. These hyphae
invade the stigma and pistil and finally reach the young embryo in the seed. Penetration may
also occur directly to embryo cells. Infection is favoured by cool, humid conditions during
flowering period of the host plant.
Control: The best method available is the use of certified seed and seed treatment with
chemical like carboxin (Vitavex 75WP @ 2.5/ kg seed), carbendazim (Bavistin 50WP @
9

2.5g/kg seed), tebuconazol Raxil 2DS @ 1.25g/kg seed) if the disease level in the seed lot is
high. If it is low to moderate, treat the seed with a combination of Trichoderma viride @
4g/kg seed and half the recommended dose of carboxin.These are systemic fungicides and are
absorbed by seed or in growing plants. Before these chemicals were investigated hot water
treatment was in use and was very good method of controlling wheat smut specially in
countries like India where summers are bright sunny and temperature rises upto 45 C. To
carry out hot water treatment, the seeds are socked in ordinary water on a sunny bright day
from 8 a.m. to 12 noon (The mycelium inside seed become active) followed by exposure to
sun from 12 noon to 4 p.m. to dry (The active mycelium is killed by heat). Early roughing of
infected plants in the field must be done.

The studies on the inheritance revealed that resistance is controlled by single dominant gene
or by few genes. However, wheat breeding efforts in this direction are not adequate. As a
result existing high yielding wheat varieties are susceptible to loose smut. Some promising
strains of wheat viz, HD 2197, HD 2203, HD 2221, HD 4502, HD 4549, HI 7483, HI 7525,
HI 7595, HI 7717, HI 8073, NP 789, NP 791 MACS-9, E 559, E 140, E 3320, WR 29, BW 7,
BW 11, VL 428, VL 639 HDR 43, K 8027, HS 87, HB 1364, DL 108-3 etc. are reported to
possess fairly good degree of resistance. These strains can be used as resistance donors for
breeding for loose smut resistance.

6. Karnal Bunt of Wheat
Karnal bunt was first reported by Mitra in 1931 from Karnal, a place now in Haryana state of
India from where the name Karnal bunt originates. This fungal disease is causing severe
losses to wheat in India, Pakistan, Mexico, Iraq, Afganistan and a few states of southwestern
United States. Karnal bunt was found in traces and in isolated pockets of northwestern region
of India earler and was considered a disease of minor importance till 1974. The surveys in
India undertaken later showed that KB can cause losses upto 20% in susceptible cultivars
such as WL 711 and WG 357 etc. Karnal bunt has been listed as quarantine pest in 21
countries. In addition to yield losses, the quality of grain is also deteriorated directly affecting
its market and export value .The quality of the flour from wheat mixed up with infected
grains and the finished product like chapati. etc. are fishy in odor. This odor is due to the
production of a chemical, trimethylamine by the fungus. Wheat containing 3% bunted grains
is unfit for human consumption. Affected grains however, appear nontoxic.

Symptoms: Karnal bunt is principally a disease of grains. The (grains are either partially
affected or in severe cases the whole grain is converted into black powder of bunt spores
(Fig.3). In a stool all the ear heads are not infected and in an ear all the grains are not
infected. In severely infected spikelets, the glumes spread apart, forming a greater angle with
the main axis and bunted grains may fall down on the ground. Initially the smut sorus is
covered with a membrane (pericarp) but when it brust black masses of spores are exposed,
resulting in bunt smell. The spores may blow off or may fall on ground and thus the inoculum
is not resticted to only infected fields but can spread to distant places.

Pathogen: Tilletia indica Mitra or Neovossia indica (Mitra) Mundkur. Mitra reported the
causal organism of Karnal bunt as Tilletia indica but later in 1944 Mundker renamed it as
Neovossia indica.The bunt pathogen belongs to genus Tilletia = Neovossia, family
Tilletiaceae, order Ustilaginales and class basidiomycotina. The Karnal bunt affects wheat,
durum wheat, triticales and rye (susceptible only by inoculations). Five pathogenic
populations viz, KBAg-1, KBAg-2, KBAg-3, KBAg-4, KBAg-5 are known to exist in N.
indica. The teliospores of these pathotypes differ in the arrangement of surface rodlets and
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can be divided into three broad groups (1) rodlets compact and regularly arranged (2) rodlets
loose and irregular and (3) exines very loosely and irregularly arranged. KBAg-2 is virulent
and contains highest contents of lipids, nitrogen, protein sugars and also has linolenic acid
while less aggressive isolate KBAg-6 have lesser amount of these constituents and does not
have carpic and pentadecenoic acid and thus both the isolates behave differently.All these
isolates showed different Rf values in polyacrylamide gel electrophoresis analysis.

Disease Cycle: Mitra reported the karnal bunt as soil borne disease but now its airborne
nature has been well established. The fungal spores are also carrired as contaminent on farm
equipment, operational tools or by man moving from milling places. The spores remain
viable in soil, wheat straw and farm yard manure for several years (2 to 10 years). The source
of primary inoculum is either soil or seed contaminated with teliospores. The teliospores are
spherical to oval, reticulated with curved spines and measure 22-49 um in diameter. Each
teliospore consists of three layers, perisporium, episporium and endosporium.

Teliospores in the soil germinate at suitable temperature (15 to 25 C) and moisture. This
condition normally prevails during February and first week of March in North Indian plains.
Each teliospore produces promycelium on germination which produces as many as 110-185
primary sporidia at its tip. The primary sporidia are sickle shaped and were considered to be
the infective entities. But now it has been established that two kinds of secondary sporidia-
allantoid and filiform types play an important role in the disease cycle of the pathogen. The
allantoid sporidia are only pathogenic and filiform sporidia help in the multiplication of
inoculum on host/soil surface. Mature teliospoes contain a single diploid nucleus which
divides meotically into two as the promycelium emerged. The daughter nuclei further divide
mitotically and their number increases. Simultaneosly the sporidial initials are formed at the
tip of promycelium which elongate and become filiform. The nuclei move towards the tip and
finally the nucleus migrate into the sporidial initial. The mature sporidia are sickle shaped,
detach from promycelium and then carried to the flower either by wind currents or by water
splash. The sporidium elongates and the nucleus undergoes mitotic division producing two
nuclei. The two nuclei become separated by a septum making the sporidium bicelled. The
majority of sporidia are binucleate. The sporidia germinate and the germ-tube penetrates the
developing grain through stigma or through the ovary wall. Normally infection takes place at
the time of anthesis. Majority of grains are partially affected but in severe cases whole grain
may be infected.

Control: Karnal bunt is difficult to control due to its mode of perpetuation. The control
measures in the field are: to avoid sowing of highly susceptible cultivars in the endemic
areas; use of disease free seed; avoiding excessive nitrogen fertilizers or irrigation
particularly at flowering time and avoiding the late planting. Crop rotation and use of plastic
mulches (soil solarization) is also helpful in management of the disease.

Seed treatment with fungicide may reduce the incidence but is not effective to eliminate the
complete infection as the pathogen is soil borne. Since the disease is air borne also, one foliar
spray by fungicide, propiconazole (Tilt 25EC20.1%) should be given at the time of anthesis.
Integration of one spray of propiconazole with one spray of bioagent fungus, Trichoderma
viridae (0.4%) gives almost cent percent control. The bioagent spray should be done before
earhead emergence followed by spray of chemical at start of earhead emergence. Use of
resistant varieties is the most effective method for controlling the disease. Among the present
day varieties, PBW 502 is resistant while the others show various degree of susceptibility.

11

7. Powdery Mildew of Wheat
Powdery mildew is a destructive disease when it appears in severe form. For example, in
Canada the infection of the disease was observed up to 80 percent during years of heavy
infections. In India, the disease is mostly confined to northern and southern hills but
sporadically appear in plains and foothills of the country.

Symptoms
The symptoms start as superficial greyish small patches of white cottony growth on leaves,
stem, sheath and even on ear. The patches may appear on both surfaces of the leaves. The
white cottony growth can cover the whole leaf and other aerial parts of the plant (Fig.4). The
white patches turn into brownish to dull tan colour late in the season due to formation of
cleistothecia. The mildew colonies are surrounded with chlorotic or yellow areas resulting
decease in photosynthetic rate. The affected leaves die off prematurely. The cleistothecia
remain on wheat debris. At times, development of the ears is checked partially or wholly.

Pathogen: Erysiphe graminis f. sp. tritici =Erysiphe graminis var. tritici (D.C.) E. Marchel.
The fungus belons to family Erysiphaceae, order Erysiphales and sub-division Ascomycotina.
E. graminis is an obligate parasite. Primary mycelium of the fungus forms appresorium and
haustoria. Each haustorium is divided into finger-like structures which enter in the epidermal
cells and supply food to the mycelium. Conidiophores develop on the mycelium which
produces conidia or oidia in a basipetal manner. The mature conidia at the top are released
first and others are released in the succession and blown away by wind currents to healthy
plants and cause infection. This asexual cycle of the fungus is repeated several times during
the crop season. At the end of the season, the sexual parts develop at the tips of mycelium.
Two opposite mating type which are uninucleate fuse together and dikaryotization takes
place. The dikaryotic cells develop secondary mycelium. A series of cells on this mycelium
form ascogenous hyphae and convert into cleistothecia.The cycle is repeated till the death of
the invaded cell.
The cleistothecium is globose in the beginning but later depressed and its colour is also
changed from white to brown or black. Each cleistothecium contains 9 to 30 oval shaped asci
which are pedicellate. In each ascus there are 8 ascospores or sometimes four which are
formed when affected leaves are dried. Several physiological races are present in the
pathogen worldwide.

Fig 5. Helminthosporium blight of wheat












Fig 4 Powderu mildewq of
wheat (Erysiphe graminis f.sp.
tritici)


12

Disease Cycle: The cleistothecia of the pathogen remain attached to the infected straw after
the crop is harvested. The pathogen survives the off season in the cleistothecial stage. Under
favourable conditions, the ascospores are released ( December-J anuary ) bring about primary
infection, secondary infection is by air borne oidia which reach to the crop by wind and
develop typical mildew colonies, sporulate (asexually) and infect newly developing wheat
leaves. The infection is favoured by the temperature (15-20 C) and high relative humidity. As
the crop matures and temperature rises, the pathogen produces perithecia which remain
dormant in straw and debris after harvest to provide the primary source of inoculum for the
next season.

Control: Based on analysis of powdery mildew samples on 11 Pm lines (differential set) 41
pathotypes were recognized in the country. Different Pm genes combinations were found
effective against powdery mildew and should be utilized for breeding resistant varieties.
However, present day varieties are not resistant to powdery mildew. Hence, the disease
severity is more in some pockets. Avoid excessively dense stands by using adequate seed.
Powdery mildew fungi are unique among the plant pathogens showing high response to
sulphur and related fungicides. Several systemic fungicides such as benlate (0.1 %),
kerathane (2 lb /ha) etc. can control powdery mildew through foliar sprays. Seed dressing and
soil drenching with 0.01 % calexin was also found effective. One spray of propiconazol (Tilt
25EC@0.1%) on disease appearance is highly effective.

8. Alternaria Blight of Wheat
Alternaria blight causes significant yield losses in wheat in the Indian subcontinent, from
where it originates and has spread throughout the world. The disease was considered as minor
but the increase in the severity of leaf blight may be due to new cultural practices and use of
new germplasm. In India, The epidemic of the disease was observed during 1964 65 and
1965-66 in eatern Uttar Pradesh. It causes severe damage to certain wheat varieties and
reported to have acquired severe proportions in the recent past.

Symptoms: Wheat plants with Alternaria blight are affected when they are 45-50 days old.
The symptoms appear as discoloured, oval lesions on the lower surface of leaves (Fig5). The
disease progresses upwards, lesions enlarge and coalesce to irregular, dark blotches, often
with chlorotic margins. However, youngest leaves are not usually affected. Heavily infected
fields show a brunt appearance, even from a distance. Severely infected seeds are discoloured
and shriveled. During humid weather the pustules are covered with black spores and most of
the leaves of severely affected plants become dry. A temperature around 25C, coupled with
high humidity, favours the disease.

Pathogen: Alternaria triticina Prasada and Prabhu is the causal organism of the disease. The
genus Alternaria belongs to family Dematiaceae, order Hyphomycetales, class
Hyphomycetes and division Eumycota. The mycelium of the fungus is colourless in the
beginning but later turn deep olive. The conidiophores are 17 28 m. long and 3 -6m
wide. The conidia developed on conidiophores in acrogenous succession. Conidia are
irregularly oval, ellipsoid conical, generally tapering into a beak, 15 -92 x 8-35 m, with 1 -
10 transverse septa and 0-5 longitudinal septa, light brown to dark olive buff becoming
darker with age. Two physiologic races were found in the pathogen.

Disease Cycle: Wheat is the only host of Alternaria blight. The disease is seed as well as soil
borne. The inoculum survives as conidia on the surface of seeds and also as deep seated
mycelium in seeds. The conidia germinate on the lower surface of the leaves at temperature
13

of 5-35 C but the optimum temperature for germination is 25 C with 100 % humidity. Large
numbers of conidia develop on affected leaves in dark, dispersed by wind and infect healthy
plants. The maximum infection takes place when the crop is 45-50 days old.

Control: Only certified seed must be used and shriveled seeds should be discarded. The seed
infection can be eliminated by keeping the seeds in cold water for 4 hours followed by 10
minutes in hot water at 52 C. Seed treatment with Vitavex @ 2.5 g/kg or with 0.2 % Rovral
can remove the seed infection. One spray of Fungicide, propi-conazol (Tilt 25EC@0.1%) can
control the disease. To manage soil infection the crop debris must be brunt. Only
recommended doses of fertilizers should be used. In NP 52 a pair of recessive genes governs
resistance and two pair in NP 824 and NP 809. Presently, no wheat variety is resistant to
Alternaria blight.

9. Yellow Ear Rot of Wheat
The disease is popularly known as tundu disease and vernacularly known as tanan. This
disease was first reported from Punjab province of India. Now the disease is known to occur
in India, Egypt, China and Australia.The disease occurs in the prence of a nematode known
as ear cockle nematode, Anguina tritici and a bacterium, Corynebacterium michiganensis
tritici and never observed individually. There is no grain formation in the ears of affected
wheat. The disease incidence ranges between 0.5 to 50%. Sporadically, it is reported to be
very serious in some places in Bihar and some eastern U.P. districts. The disease incidence
depends on the degree of contamination of wheat seeds with galls at the time of sowing.

Symptoms: The symptoms appear as twisting and crinkling of lower and middle leaves of
affected plants (Fig.6). A slime is produced which cover the whole ear and other parts of the
plant like glume and stem resulting sticking of these parts together. Because of twisting and
sticking, the growth of affected plant is retarded and stem becomes deformed. Near maturity
of the crop, oozing of the slime is visible from tissue of affected plants under humid
conditions. However, if the weather is dry the slime becomes hard and turns to dark yellow or
brown in colour. Most of the grains in the ear are converted in to galls due to nematodes. The
nematodes serve as a vector of the yellow ear rot pathogen. The disease occurs only in the
presence of ear-cockle nematode, Anguina tritici. For the maximum expression of yellow rot
disease disease a combination of 0.4 optical density of the bacterium and 10 larvae of the
nematode is required.

Pathogen: Clavibacter tritici, a bacterium which belongs to genus Clavibacter, class
Thallobacteria, division Firmicutes and Kingdom Prokaryotae is the causal organism.The
bacterium is a gram-positive type, nonmotile and pleomorphic in nature. In synthetic
medium, it develops yellow pigmented colonies.

Disease Cycle: The disease is developed only when both nematode (Anguina tritici) and
bacterium (C. tritici) are present in plant. The bacterium alone is not capable to produce the
disease. Under favourable conditions of low temperature of 10-15C and high humidity (70-
100%) the bacterium multiplies and expresses itself in the form of yellow slimes on the
leaves of young plants. It has been observed that for the maximum expression of the disease a
combination of 0.4 optical density of the bacterium and 10 larvae of the nematode is required.
The causal bacterium remains in and around nematode galls. When seeds contaminated with
galls are sown, The galls swell due to moisture in the soil and nematodes come out from
swollen galls. The bacteria attached to these galls also move with nematodes either already
attached to nematode body insiside the galls or stick to them while nematodes coming out of
14

the galls. Thus both the pathogens infect the host simultaneously and cause their own disease.
The nematodes convert the grains into galls and these galls along with the bacterium are
harvested with the crop. The cycle is repeated when such seeds are used.
Control: The disease is managed by the use of certified seed, removal and burn of affected
ears and summer ploughing of affected fields to kill the nematodes by natural heat during
May-J une. The galls from mixed seed can be removed by brine-water treatment as for ear
cockle disease (next disease).







Fig 6. Yellow ear rot symptoms of wheat

10. Ear Cockle Disease of Wheat
Ear cockle nematode is a parasitic nematode and found throughout the world wherever wheat
is grown.The ear cockle nematode is still common in Eastern Europe, parts of Asia and
Africa. It is widely distributed in most of the wheat growing parts of India and cause
considerable loss to the crop annually. It is mostly found in some parts of northern India
especially the states of Bihar, J harkhand, eastern U.P. and Chhatisgarh








Fig 7. Ear cockle disease of wheat in field
Symptoms: The first symptom is the basal swelling of the stem at the ground level with a
whitish tinge. Infected seedlings are severely stunted and show characteristic basal
enlargement of the stem, rolling, twisting and crinkling of leaves (Fig.7). As the plant does
not have erect leaves, it remains stunted. The nematode infesting seedlings show profuse
tillering which starts earlier than healthy ones. This increase number of tillers does not
necessarily means an increase in the number of ear-heads, only few are only the productive
tillers. The nematode juveniles reach upto the growing point and start feeding
ectoparasitically and reach upto the developing ear. On initiation of the leaf primordia these
nematodes act as endoparasite and initiate production of galls preferably on staminate tissue.
The galls and the grains develop side by seed in the same floret. Number of galls produced in
15

a spikelet varies from 1 to 5 seedgalls in the beginning are greener and smooth but later turn
brown or black as the head matures. Diseased heads are shorter than healthy ones and remain
green longer than healthy heads. The galls are shed off the heads more readily. In case of
severe infections the plant may die prematurely.

Pathogen: Anguina tritici (Steinbuch) Filipjev is the causal pathogen and belongs to family
Anguinidae, order Tylenchida, class Secernenitea, and phylum Nematoda in the kingdom of
Animalia. This is one of the few parasitic nematodes that infects above ground parts of the
plant. The pathogen is a large nematode about 3.2 mm long and 120 m in diameter. The
nematode lays its eggs and produces all its juvenile stages including adult stages in seedgalls.
The seedgalls contain thousand of infective J 2 juveniles. These juveniles come out of seed
galls on receiving moisture when seeds are sown and infect the growing point in the plumule.

Disease Cycle: Ear cockle disease perpetuates year after year through the seed contaminated
with cockles or nematode galls. The seed contaminated with cockles or galls when sown, the
galls absorb water from the soil, become soft and liberate the second stage juveniles which
infect the seedling. In temperate countries the galls which fell down during the harvest of the
crop are considered as one of the sources of inoculum but in India such a situation is not
functional. In India, during rainy season juveniles emerge and perish in the absence of host
plants. The juveniles enter the seed, both at brush and embryo ends. J uveniles entering seed
embryo can reach the growing point of seedling and start feeding as ectoparasitically. On
initiation of floral primordial, the juveniles become endoparasitic and start producing galls.
The juveniles in the developing galls undergo three successive moults and developed into
males and females. The number of adult nematodes in a gall vary depending on the size of
gall ( 16-85). Each fertilized female lays eggs in hundreds inside the gall. The adults die soon
after oviposition. The eggs hatch and develop into second stage juveniles. Near maturity of
the crop each gall may contain upto 12000 juveniles in anhydrobiotic stage in which the
organism does not show any visible sign of life and metabolic activity is hardly detected. The
second stage juveniles are resistant to dessication and can survive in the galls upto 30 years.
They produce only one generation per year.

Control: The disease can be controlled by using certified seed, free from galls. The seed can
be cleaned by sieving or by seed floatation in fresh water. The seed lots are floated in 2-5%
brine solution. The galls, which float on the surface, can be easily separated and destroyed
away from the field. The seeds thus cleaned should be washed with clean water and used for
planting.No resistant variety has been found except one cultivar Saber beg in Iraq. Since
floatation is a very effective method to control, chemical or biological approaches has not
been tried much. Crop rotation in affected fields is also recommended.

Diseases of Rice
1. Blast Disease of Rice
Blast disease of rice is one of the earliest known plant diseases. Now it is of worldwide
occurrence wherever rice is grown. In India, blast disease occurs in rice crop of all the states
where rice is commercially grown. The disease is quite common in areas of high rainfall and
in irrigated areas where the crop is highly doses with nitrogen. Several epidemics due to blast
have been experienced in different parts of the world resulting losses in yield from 50 to 90
percent. In India, the yield loss during the year 1960-61 was estimated to 2,66,340 tonnes.

16

Symptoms: The blast symptoms appear on leaves and other above ground parts of rice plants
although leaves and the neck of the panicle are more commonly affected.. The affected leaves
developed water soaked, boat shaped white to grey lesions (Fig.8). The lesions may be from
0.5 cm to several centimeters in size and they are surrounded by a yellowish halo. The lesions
enlarge and coalesce with each other covering the whole leaf surface and the leaves
subsequently die off. Other parts of the plant such as stem, leaf collar, stem nodes and
occasionally the internodes are also affected. On stem nodes, brown to black lesions are
formed and cover 1 to 2 cm on both sides (Fig.9). After the heads are emerged, the fungus
attacks the peduncle neck node, which is girdled. This stage is known as neck infection which
is most destructive. If neck infection is at an early stage, the panicles become erect and grains
do not fill but if the infection is late, the grains are partially filled. However, in such a
situation the panicle base is broken due to grain weight and and weaking of neck tissue. Such
panicles hang down (Fig.9) and are visible in a rice field even from distances.













Pathogen: Pyricularia oryzae Cavara (It is not distinguishable from P. grisea (Cooke) Sacc.)
The pathogen belongs to family Moniliaceae, order Moniliales and sub-division
Deuteromycotina.
Fig.9 Node and Neck Blast symptoms of Rice

Fig.8. Leaf symptoms of
Rice Blast

Perfect or Teleomorphic stage is Magnaporthe grisea Kato and Yamaguchi (This stage has
not been found in nature but developed experimentally in the laboratory). In nature, most of
the pathogen isolates are of the same mating type (male) and do not cross with each other.
The teliomorphs were produced in the laboratory by crossing appropriate isolates. The
pathogen produces septate, branched, and hyaline to olivaceous mycelium which is localized
in lesions. The conidiophores emerge from the leaf through stomata or by rupturing the
cuticle. The conidiophores bear terminal pear shaped or pyriform conidia having 1 to 3 septa
but majority is biseptate. The conidia develop in succession and each cell of the conidium is
uninucleate. Conidia measure approximately 20-25 X 8.5-9.5 micron. The pathogen produces
several toxins such as piricularin, and alpha picolinic acid etc.The blast pathogen have
several physiologic races. In India, about 32 races have been reported but races 3(1C3) and
1(1D1) are more virulent.
17

The perfect stage of the pathogen is Magnaporthe grisea (Hebert.) Barr. which belongs to
ascomycotina. Perithecia of this fungus occur singly or in groups without apparent stroma.
The asci are beak-shaped, cylindrical to subclavate containing fusiform hyaline four celled
ascospores. The asci arose from the base of perithecium and measure 7-10 X 55-90 micron.
Ascospores measure 4-7 X 17-24 micron.

Several physiological races are recognized in P. oryzae based on infection types developing
on different hosts by artificial inoculation. Cytological studies have shown that the
chromosome number in nuclei varies from 2-12. The pathogenicity of individual conidia
continues to segregate in each generation. Asynchronous division, nondisjunction and lagging
chromosome appear to be the cause of differences in chromosome numbers. The unusual
nuclear behaviour explains the pathogenic variability in blast fungus.

The nature of rsistance in rice varieties due to blast has been studied over the past 50 years.
Silicification of the epidermal cells of rice plant is considered to confer resistance against
blast as it prevents the entry of the pathogen. Heavy nitrogenous manuring decreases silicate
accumulation in rice plants which makes the plants susceptible to the pathogen. Rice plants
have several prohibitins which are phenolic in nature. The nitrogen nutrition greatly
influences the concentration of prohibitins and their oxidation. In a resistant variety browning
reaction or necrotic response is due to irreversible oxidation of polyphenols of the host tissue.
There is an increase in the hydrogen peroxide level of the infected tissue leading the rapid
death of infected tissue. The blast pathogen produces a few toxins such as alpha picolinic
acid, piricularin and pyriculol. Phenolic compounds detoxify alpha picolinic acid while the
resistant tissues detoxify piricularin to non-toxic substances.

It appears that there are several genes confer blast resistance to rice varieties. The higher is
the degree of resistance of a variety, the fever are the races of the pathogen that would be
virulent to that variety. The rice varieties fall under the botanical group of japonica, indica,
javanica and glaberrina differ in their genetic behaviour nd can provide potential for breeding
new blast resistant varieties of rice.

Disease Cycle: The pathogen overseasons as mycelium and conidia on rice straw and seed
from contaminated crops. The inoculum may also survive on graminaceous weeds near the
crop or on overlapping crops of rice. The pathogen produces and releases conidia in
abundance at a favourable temperature and relative humidity of 90% or more. The conidia
can be formed at temperatures between 15 and 32 C but the optimum is between 20 and 28 C.
The mature conidia are released by wind and reach to the healthy plants. On landing to the
healthy plants, the conodia adhere by producing mucilage at their tips. Conidia germinate in
the presence of free water through a germ tube. The germ tube produces an appresorium
which produces and accumulate melanins which help the appresorium to penetrate the host.
The infection may also take place through stomata. Seedlings and young leaf tissues are
comparatively more susceptible to infection. Under favourable conditions, new lesions may
develop within 4 to 5 days after infection. Newly formed conidia are released within hours
and continue for several days. Low temperature (about 20C) and excessive dew during night
may increase the intensity of the disease. Most of the conidia are released after midnight to
sunrise. This cycle is repeated several times till the crop is harvested or temperature rises

Control: Th grows resistant varieties is the best option. The registant genes have been
identified in more than 13 rice cultivars. However, the resistance is break down due to
appearance of new races. Therefore, resistant varieties need to be developed more frequently.
18

Rice cultivars like J ava, Vani, Akashi, IR-8, IR-36 etc. are some of the promising resistant
cultivars. Other methods like use of certified seed, burning of rice remains from the field,
early sowing, avoid excessive doses of nitrogen and use of fungicides are also helpful in
controlling the blast disease. Several fungicides are being used for controlling rice blast viz;
mancozeb, edimfos, benomyl carbendazim and antibiotics such as blasticidin -S and
kasugamycin at 20 ppm.. Systemic fungicides, pyroquilone and tricyclozone were found to
provide better control as these fungicides interfere in melanin production by the appresorium
thereby inhibiting the entry of the pathogen to the host plant. Rabcide 20% solution @ 1.5
kg/ha spray can control both leaf and neck blast.

2. Brown Spot Disease of Rice
Rice brown spot is a historical disease because it caused a major outbreak in Bengal in India
in 1942 when approximately two million people died of starvation. The disease is widely
distributed in India, especially in West Bengal, Orissa, Andhra Pradesh and Tamil Nadu.

Symptoms: The symptoms first appear as brownish spot on
leaves and glumes of the plant. The disease causes blight of
seedlings. On seedlings, the pathogen produces small, brown
lesions, which may girdle the coleoptile and cause distortion
of the primary and secondary leaves. In some cases, pathogen
may also infect and cause a black discolouration of rootsatt.
Infected seedlings are stunted or killed. On the leaves of older
plants, the pathogen produces circular to oval lesions that are
grey at the centre and brown at the borders measuring about
0.5-2mm X 2-5mm (Fig.10). On moderately susceptible
cultivars, the pathogen produces tiny, dark specks. When
infection is severe, the lesions may coalesce, killing large
areas of affected leaves. The pathogen causes main damage
by attacking the leaves at seedling stage. At times the neck
region may be infected causing similar symptoms to those of
neck blat caused by P. oryzae. The affected plants become weak and the yield is drastically
reduced. The grains show a black discoloration.
Fig.10. Brown spot of rice

Pathogen: Helminthosporium oryzae Breda [Syn: Bipolaris oryzae Breda de Hann)
Shoemaker] is the causal pathogen which belongs to family Dematiaceae, order Moniliales
and sun-division Deuteromycotina. The perfect stage is Cochliobolus miyabeanus Ito and
Kubribayashi. C. miyabeanus belongs to the subdivision Ascomycotina, the sac fungi. The
brown mycelium is inter or intracellular in the host. The conidiophores are multiseptate upto
600m long and 4-8 m wide and develop singly or in bundles (generally 17). Conidia are
generally curved, boat or club shaped with 6-14 septa, 63-153 x 14-22 m and often with a
minute, slightly protruding hylum, by which they are attached to conidiophores. The conidia
are born singly and successively at regular intervals on the upper part of the conidiophore in a
sympodial manner.The conidia are dispersed by the wind. These spores are asexual; they do
not rise from sexual crosses, but rather act as a method of dispersing the pathogen. A
consequence of this is that the pathogen can spread rapidly in devastating epidemics. The
conidia germinate readily, producing germ tubes mostly from both the end cells.
The perithecia of the perfect stage pathogen (C. miyabeanus) are globose with the outer wall
dark yellowish brown and parenchymatous, and with ostiolar beak.The asci are cylindrical,
slightly curved and contain 4-6 ascospores. The ascospores are hyaline, long cylindrical with
6-15 septa and measuring 6-9 X 240-268 micron.
19

Disease Cycle: The fungus overwinters mainly in infected plant parts. The pathogen is not
soil borne. This disease occurs naturally on as many as 20 different wild species of Oryzae. A
few collateral hosts like Digitaria sanguinalis, Echinochloa colona, Pennisetum typhoides
Setaria italica and Cynodon dactylon, on which the pathogen is recorded, may serve as a
source of primary inoculum. The conidia carried through infected rice seeds are are also the
primary source of inoculum. The conidia germinate on the emerging seedlings and produce
several generations asexually as the plants grow. They are blown away by wind and cause
infection to the new crop and thus serve as the source of secondary infection. The optimum
temperature for the germination of conidia is 25-30C and humidity 90% or above. If
seedlings are affected crop yield is drastically reduced. The pathogen can spread fast and may
cause devastating epidemics.

Control: As the disease incites discolouration of the tissues, phenolic prohibitins present in
rice tissues are associated with disease resistance. The reducing agents such as ascorbic acid
and glutathione enhance the tissue susceptibility. The pathogen produces a toxin, obliobolin.
The varieties, BAM-10, CO-20, and IR-36 etc. are some of the resistant varieties. Plants
growing in good nutritional conditions are generally resistant to the disease. The
susceptibility to infection appears to be a deficiency in available silicon. Preventive treatment
of the field with calcium silicate may be used in deficient soil. Seed treatment may ward off
the seedling blight phase.

3. Bacterial Blight of Rice
The blight disease is widely prevalent in Asian countries including India. With the
introduction of rice variety Taichung Native-1 (TN-1) in India the disease spread rapidly as
TN-1 is highly susceptible to rice blast. The disease is now found in all the rice growing areas
of the country both on indigenous and exotic varieties. The disease was not considered
serious until 1962 when epidemics broke out in Bihar and other parts of North India.
Epidemics of this disease were also witnessed in non-traditional rice growing areas of Punjab
and Hariyana.

Symptoms: Symptoms appear on the margins of leaf blade and sheath as small, linear, water-
soaked areas that soon elongate and coalesce into irregular, narrow, yellowish and brownish
stripes. Droplets of white exudates are found on the stripes. During severe infection, the
leaves become yellow and start dying from the tip downwards. Small lesions are also seen on
the kernels. As the disease progresses, several lesions may coalesce to form straw brown
large lesions or blighted portions (Fig.11).







The disease develops mainly in rainy and humid weather and becomes more severe at the
time of grain formation. If seedlings or young pants are infected they show wilting a stage
Fig.11. Bacterial Blight of Rice caused by
Xanthomonas oryzee
20

known as Kresek stage. This stage commonly occurs within 3-4 weeks after transplanting of
the crop. Leaf blight phase is the most predominant form of the disease occurring between
tillering and heading stage of the crop. When the affected leaves are cut and immersed in
clear water in a test tube a turbid ooze of the bacterium, streaming from the vascular bundles
can be seen.

Pathogen: The bacterium, Xanthomonas oryzae pv oryzae = X. campestris pv oryzae
(Ishiyama) Dye is the causal organism. The bacterium is rod shaped 1-2 x 0.5 -0.8 m in size
occurring singly or in pairs, gram-negative, aerobic and non-spore forming with a polar
flagellum which helps in movement. The bacterial cells are surrounded by mucus capsules
which are soluble in water and precipitated by acetone. It is a kind of heteropolysacchride.
Wax yellow coloured bacterial colonies are formed on synthetic media. It does not produce
indole, nor does it reduce nitrate, and it may or may not liquefy gelatin and produce H2S. The
pathogen is found in several strains. Five different pathotypes have been identified in J apan
but in India only two pathotypes have been reported based on the reaction on international set
of differentials.

Disease Cycle: The blight disease of rice is a vascular disease. The primay infection may
result from the inoculum overwintering in seed or in crop residue or on overlapping crops. It
may also survive in soil. The primary inoculum may also be build up from soil or plant
stbbles and debris and can infect nursery seedlings. The bacterium infects some grasses like
Leersia spp. which might play a role in the spread of the pathogen. It is disseminated through
irrigation water and wind-borne rain. The bacteria enter in the host through roots, stem near
ground or hydathodes in leaves. After infection it becomes systemic in the vascular bundles
and move upward. The disease spreads fast at a temperature of more than 25 C with a
combination of rainy weather or in crops where excessive fertilizer is used.

Control: Control measures are the use of resistant cultivars, certified disease free seed and
crop rotation. A mere soaking of seed for 8 hr in Ceresan (0.1%) and steptacycline-crude
agricultural preparation (3g in 1100 litre of water) is effective to eradicate seed infection.
Spraying with copper fungicides alternatively with streptocycline (250 ppm) is effective in
controlling bacterial blight. Varities like TKM-6 and IR-42 and Chinsurah Boro II are
tolerant to disease.

4. Sheath Blight of Rice
Sheath blight is one of the serious diseases of rice and sometimes important to other cereals
as well. It is found worldwide wherever rice is grown. The banded leaf blight symptoms of
this disease have been reported from Uttar Pradesh.

Symptoms: The symptoms develop as large, irregular, and oval to elliptical, green grey,
water- soaked lesions on the sheath of leaves and have a straw coloured centre and a wide
reddish brown margin (Fig.12). These lesions first develop near the water line on sheath or
lower leaves when plants are in the late tillering or early internode elongation stage. These
lesions usually develop just below the leaf collar about 1/4 inch wide and 1/2 to 1.1/4 inch
long. With age, the lesions expand and the centre of the lesions may become bleached with an
irregular tan to brown border. Seedlings and mature plants are blighted when humidity
exceeds 95% and temperature in the range of 15-35C. Disease development progresses very
rapidly in the early heading and grain filling growth stages during period of frequent rainfall
and overcast sky. The grains in the lower parts of penicle are poorly filled. Additional losses
result from increased lodging or reduced ratoon production due to reduced carbohydrate
21

reserves. Near maturity of the plants dark brown coloured sclerotia are produced superficially
on or near the lesions and easily fell down on soil.

Fig.12. Sheath blight of rice





Pathogen: Rhizoctonia solani Kuhn. is the causal organism. The perfect stages is Hypochnus
sasakii Shirai =Corticium sasakii (Shirai) Matsumoto =Thanatephorus cucumeris (Frank)
Dark.The pathogen belongs to order Mycelia Sterilia of the sub-division Deuteromycotina.
The mycelium is colourless when young but turn yellowish to light brown with age, consists
of long cells and produces branches at the right angles to the main hypha and have a cross
wall near the junction. The sclerotia are flattened on the lower side and are loosely attached
and easily dislodge from the plant. The basidia are 10-15 x 7-9 and the sizes of
basidiospores are 8-11 x 5-6.5. The pathogen grows over a wide range of temperature, the
optimum ranging from 28-30C.

Disease Cycle: The primary source of inoculum comes from sclerotia and they survive
between the crops. When the rice crop is planted, the sclerotia float on the surface of flooded
water and infect the plants near the water line. Sclerotia can survive one to several years in
soil. Further spread takes place by rain, irrigation and tools carrying soil contaminated with
the pathogen. The infection can take place with a temperature ranging from 15 to35 C and
95% humidity. The pathogen can infect and survive on certain weed hosts which may also
serve as the source of inoculum for further spread of the disease. The mycelium grows inside
the tissues in all directions, initiating secondary spots, in turn producing sclerotia on the
spots. The disease is highly destructive during humid and warm temperatures. High dose of
nitrogenous fertilizers make the tissue more susceptible to the disease while high potassium
induces resistance to the disease.

Control: New vaieties and changing cultural practices often combine many of the factors that
favour disease development. In recent years, wide acceptance of susceptible varieties,
because of their high yielding potential, has contributed greatly to the rapid increase in the
incidence of sheath blight. To manage the disease, application of heavy doses of nitrogen
should be avoided as it predisposes plants to infection. Close transplanting of rice plants and
wet and poorly drained fields for cultivation of rice should be avoided. The fields may be
kept clean with grasses and weeds. Other measures like crop rotation, multching during
summer, biological control may be helpful. Resistant varieties if available should be used and
foliar fungicides may be economical for reducing sheath blight infection. In heavily infected
patches, soil drench with 0.1% wet Ceresan will be useful.

5. Tungro Disease of Rice
Tungro disease is most destructive to rice in countries of Southeast Asia. Outbreaks of the
disease are common in one part or the other in India. In severe cases of infection or infection
during early stages of plant growth the yield loss may be as high as 100%. The damage
22

depends on the variety used, plant stage at the time of infection, strain of the causal virus and
environmental conditions.

Symptoms: Affected plants show discoloration of the leaves which begins at the leaf tip and
move down to the lower leaf portion (Fig.13). Young infected leaves show interveinal
chlorosis and incomplete emergence. The tillering is reduced and plants become stunted. The
flowering on infected plants may be delayed and most panicles are sterile or with partially
filled grains with dark brown spots. The symptoms may be confused with nitrogen and zinc
deficiencies or water stress or insect damage or other virus diseases like grassy stunt and
orange leaf.

Pathogen: Tungro disease is associated with rice tungro bacilliform virus (RTBV) and rice
tungro spherical virus (RTSV) (Fig.13). Both the viruses appear responsible to cause
infection simultaneously by the leafhopper, Nephotettix virescens (Distant). RTBV can not be
transmitted by leafhopper vector in the absence of RTSV. RTBV particles are bscilliform in
shape measuring 100 to 130 nm in length and 30 to 35 nm in width and contain ds DNA of
8.3 kb. RTSV particles are isometric and 30nm in diameter and contain ssRNA of about
12kb.

Disease Cycle: The inoculum of the virus survives on rice or some wild relatives in the
nature from where the infection takes place to the rice crop plants by the leafhopper vector.
The vector can acquire the virus while feeding on infected plants within a feeding period of
minimum 30 minutes and transmit it immediately when feed to healthy plants for a few
minutes. After acquisition of the virus the leafhopper can transmit the virus from 5 to 8 days
and after that become nonviruliferous or no virus is retained by the vector and would require
reacquisition feeding.

Fig.13. Tungro disease of rice and its associated virus particles








Control: Planting of resistant varieties either to vector or virus is the most economical means
of managing the disease. The resistant varieties to the virus are now available in India and
neighboring countries. Eliminating the hosts of the viruses and vector and to destroy stubbles
after harvest is also advisable.





23

Diseases of Maize
1. Stalk Rots of Maize
Stalk rots are caused by several fungi and bacteria which affects the plants near maturity.
Losses from stalk rot vary region to region and are estimated 10 20 %. Losses are caused
either by poor filling of the cobs or due to lodging of affected plants. The following pathgens
are associated with stalk rot of maize.

Bacterial Pathogens: Pseudomonas avenae sub-sp. avenae Manns.
Enterobacter dissolvens (Rosen) Brenner et al. =Erwinia dissolvens (Rosen) Burkholder
Erwinia carotovora sub-sp. carotovora (J ones) Bergey et al. =E. chrysanthemi pv. Zae
(Sabet) Victoria et al.

Fungal Pathogens : Colletotrichum graminicola (Ces.) G.W. Wils., Telemorph: Glomerella
graminicola (Politis), G. tucumenensis (Speg.) Arx & E. Muller.
Physoderma maydis (Miyabe) Miyabe
Diplodia maydis (Berk.) Sacc.
Fusarium moniliforme J . Sheld var. subglutinans Wollenweb & Reinking
Gibbrella zeae (Schwein) Petch. (Anamorph: Fusarium graminearum Schwabe.
Setophaeria turcica (Luttrell) K.J . Leonard & E.G.Suggs (Anamorph : Exserohilum turcicum
(Pass.) K.J . Leonard & E.G. Suggs =Helminthosporium turcicum Pass.
Pythium aphanidermatum (Edson) Fitzp.
Rhizoctonia solani Kuhn. =R. zeae Voorhees =R. solani sub sp. sasakii
Cochliobolus heterostrophus (Drechs.) Drechs. Anamorph: Bipolaris maydis (Nisikado &
Miyake) =Helminthosporium maydis (Nisikado & Miyake).
Fusaium spp., Mucor sp., Spicaria spp. & Rhopographus zeae Pat.

Symptoms: Stalk rot and ear rot are the two important phases of the disease. In stalk rot,
symptoms appear after a few weeks of pollination as premature dying of lower leaves which
turn into dull grey appearance (Fig.14). The internodes become soft and appear tan to brown
from outside and pink or reddish inside. The pith is completely rotten and the stalk may
lodge. Plants may die if harvesting is delayed. In ear rot, ears may rot completely and a
pinkish mold can be seen between ear and husks.

Pathogens: Gibberella zeae; Diplodia zeae; Fusarium species and Colletotrichum
graminicola are the major pathogens involved in the rot complex but G. zeae dominates in
the complex. The fungus produces ascospores in perithecia, mycelium, or chlamydospores in
infected plant debris. G. zeae also produces mycotoxins which are toxic to human and
animals.

Disease Cycle: The pathogens survive in soil from one growing season to another. The
spores are blown off by wind into the base of leaf sheath and cause infection either by
directly penetrating into the host or through wounds caused by insects such as stem borer.
Conidia are produced on infected plant parts and serve as secondary inoculum. The disease is
favoured by wet weather near or after silking. Higher plant density, high nitrogen and low
potash doses and early maturity of hybrids also favour the disease.

Control: The preventive measures for disease management are use of resistant varieties, low
plant density, proper fertility practices, insect control and timely harvesting.

24

2. Downy Mildews of Maize
Downey mildews are found worldwide but they cause serious diseases in Asia and Africa on
maize and other grain crops. These diseases cause considerable losses to the yield under
favourable conditions of fungal growth. These diseases cause severe damage to hybrid maize
like Ganga-3 etc. Several mildews are known as mentioned below:
1. Brown stripe mildew caused by Sclephthora rayssiae Kenneth et al. var. zeae Payak &
Renfro.
2. Crazi top downy mildew caused by Sclephthora macrospora (Sacc.) Thirumalachar et al.
=Sclerospora macrospora Sacc.
3. Green ear downy mildew caused by Sclerospora graminicola (Sacc) J . Schrot.
4. Philippine downy mildew caused by Peronosclerospora philippinensis (W.Weston)
C.G.Shaw
5. Spontaneum downy mildew caused by Peronosclerospora spontanea (W.Weston) C.G.
Shaw. =Sclerospora spontanea W. Weston.
6. Sorghum downy mildew caused by Peronospora sorghi (Weston & Uppal) C.G.Shaw =
Sclerospora sorghi Weston and Uppal.
7. Sugarcane downy mildew caused by Peronosclerospora sacchari (Miyake0 Shirai & Hara
=Sclerospora sacchari Miyake
Symptoms: The symptoms appear on younger leaves as white or light green stripes which
soon become white or light yellow on most of the leaves of affected plants. The sporangia
develop on branched sporangiophores which emerge in groups from the plant tissues through
stomata. A white mat of the fungal growth can be seen on the lower or both the surfaces of
leaves during wet weather. The stem may also be affected if infection occurs during early
stages of plant growth.

Pathogens: Sclerophthora rayssiae, Peronosclerospora maydis; P. philippinensis; P. sorghi
and P.sacchari are commonly distributed downy mildew pathogens.These pathogens belong
to the group Oomycetes and family peronosporaceae. The first two pathogen attacks maize
but the rest two are the pathogens of sorghum and sugarcane respectively but also infect
maize.

The S. rayssiae produces sporangia at the tips of sporangiophores at their branches.
Sporangia are white in colour in the beginning but turn to greyish light brown later. The
sporangia germinate by protruding a germ tube and finally produce zoospores at higher
temperature. The P. philippinensis fungus produces numerous hyaline, thin walled,
ellipsoidal conidia on dichotomously branched conidiophores.

Disease Cycle: Downey mildews are soil and seed borne in nature. The spores in the soil or
on seeds germinate through a germ tube and infect plant tissues through roots or collar
region. This is called as primary infection. The infection becomes systemic and reaches at the
upper parts of the plants. The fungus develops sporangia in large numbers on the younger
leaves of affected plants. The sporangia blown away by wind or through rain water or insects
and infect healthy plants. This is the secondary spread of the disease where they form
zoospores which cause the secondary infection.

25

Control: The control of mildew diseases is difficult. The sprays with systemic fungicides
such as metalaxyl and propamocarb etc. can be used to manage the disease. However, the
best control is to use resistant varieties or hybrids, if available.

3. Leaf Spots of Maize
Leaf spots of maize are caused by several bacteria and fungi and they develop their respective
symptoms on leaves of maize plants. Leaf spots of various sizes are caused by different
pathogens.The following bacteria cause leaf spot symptoms on maize plants.

Bacterial leaf spot caused by Xanthomonas campestris pv. Holicola (Elliott) Dye; Chocolate
spot caused by Pseudomonas syringae pv. Coronafaciens (Elliott) Young et al.; and holcus
spot caused by P. syringae pv. Syringae Van Hall.

The following fungi causing spots or lesions on leaves are: Brown spot caused by
Physoderma maydis (Miyabe) Miyabe; Curvularia leafspot caused by Curvularia species
such as C. clavata P.C. J ain; =C. maculens (Bancroft) Boedijn (telemorph : Cochliobolus
eragrastidis (Tsuda & Ueyama) Sivanesan ; C. lunata (Wakk) Boedijn (telemorph :
(Cochliobolus lunatus R.R. Nelson & Haasis) ; C. pellescens Boedijn (Teliomorph :
Cochliobolus pellescens (Tsuda & Uema) Sivanesan ) ; Gray leafspot caused by C. zeae-
maydis Tehon & E.Y. Daniels ; Didymella leaf spot caused by Dodymella exitalis (Morini) E.
Muller ; Phaeosphaeria leafspot caused by Phaeosphaeria maydis (P.henn) Rane, Payak &
Renfro =Sphaerulina maydis P. Henn and zonate leafspot caused by Gloeocercospora sorghi
Bain & Edgerton ex Deighton. Leaf spots are also caused by several species of Alternaria
such as Alternaria alternata and A. tritici. Zonate leafspot, grey leaf spot and brown leaf spot
are important and described in this chapter.

4. Zonate Leaf Spot
The disease symptom appears as oval and black brown lesions near the leaf veins. These
spots enlarge and may coalesce and cover the leaf surface. Affected leaves may die and fall
down. The pathogen, Gloeospora sorghi develop slimy masses of conidia on the surface of
lesions which are dispersed by wind or rain. High temperature and humidity favour the
disease development more rapidly. When the lesions are old , small sclerotia are formed in
the infected tissues and survive overseason in infected tissues or contaminated seeds and
become the primary source of inoculum when the crop is sown. The disease can be managed
by using certified seed, crop rotation and the use of fungicides like benomyl, Bordeaux
mixture, maneb etc.

5. Grey Leaf Spot
The disease is caused by Cercospora zeae-maydis. The leaf spots are brown, narrow and
long which become ash grey in humid weather. The lesions may coalesce covering the whole
surface of the leaf. During severe attack the affected leaves may fall down. The fungus
produces long, slender, colourless to dark, curved multicellular conidia on conidiophores.
The conidia developed on tips of conidiophore and can be easily blown off by wind and cause
infection to healthy plants. Most cercospora species produce mycotoxin, cercosporin which
kills cells in light. The pathogen overwinters on or inside seed and also on affected leaf
tissues as mycelium or spores. The disease is retarted by dry weather. Most of the
Cercospora species have teleomorph as cochliobolus but teleomorph of grey leafspot fungus
is not known. The control strategies are applicable as with zonate leaf spot.

26

6. Brown Spot
The brown water soaked lesions appear on leaves. The spots may coalesce and form larger,
brown patches. The lesions are mostly found on basal portion of leaves but may also appear
on leaf sheaths and stem. The causal fungus, Physoderma maydis belongs to family
Physodermaceae, order Chytridiales of the sub-division Mastigomycotina. The sporangia are
brown in colour and are air born and release zoospores. Zoospores attach to leaf and cause
infection. The fungus is an obligate parasite. Field sanitation can control the disease.

7. Helminthosporium Leaf Spots
These leafspots are caused by five species of Helminthosporium; H. turcicum; H. maydis; H.
carbonum; H. rostratum and H. sativum and all these species are found in India. The first
three species cause severe diseases. The genus Helminthosporium was converted to
Drechslera and finally has been placed to genus Bipolaris. These diseases are also called as
leaf blights and Northern leaf blight in America.

Fig15. Maydis leaf
blight of maize
Fig.16. Turcicum
Leaf Blight of maize
Fig.14. Stalk rot of maize
caused by Rhizoctonia
solani f sp.sasakii

















8. Maydis Leaf Spot
The disease is caused by Drechslera (= Bipolaris) maydis (Nisik) Subram. & J ain) and the
perfect stage or teliomorph is Cochliobolus heterostrophus (Drechsler) Drechsler. The
symptoms appear as large number of minute to large spots of 3.75 cm long and 1.75 cm in
width on leaves (Fig.15). The lesions are oval and zonated. These lesions coalesce and leaves
may show brown coloured stripes. The growth of affected plants is stopped and devoid of cob
formation. The infection takes place by the inoculum which survives as mycelium or conidia
on leaf debris in soil. The conidia develop on conidiophores under favourable conditions of
temperature over 35 C and high humidity. The control measures as applicable with turcica
leafspots are also applicable with maydis leaf spot disease. The resistant hybrid such as
Ganga white-2 and composite maize like Vijay etc. have been developed in India.

9. Turcica Leaf Spot or Leaf Blight
The disease symptoms appear as boat shaped, light grey or brown lesions on lower leaves and
also on the upper leaves. In severe infections, all the leaves are affected and infected plants
look like cold injury (Fig 16). The cobs are small and poorly filled. The disease predisposes
the plants for bacterial stolk rot. The perfect stage of the pathogen Bipolaris turcicum is
Trichometasphaeria turcica (Pass.) Luttrell. The fungus develops conidia on the
27

conidiophores which are geniculated and each conidium has 3 8 septa and is slightly
curved. The conidia reach to the host through wind and cause infection through bipolar
germination on free water on leaf and at a temperatue from 18 -27 C. They can cause leafspot
symptoms within 7 12 days. The perfect stage, T. turcica forms the perithecia in which Asci
and ascospores are enclosed. The control measures are use of certified disease free seeds,
crop rotation and use of resistant cultivars.

Diseases of Sorghum
1. Sorghum Smuts
There are seven smut diseases but only four are found in India. The causal fungi belong to the
family Ustilaginaceae, order Ustilaginales and sub-division Basidiomycotina. The damage is
confined mostly to the heads or penicles, reducing both the grain yield and forage value.

(i)Covered Smut or Grain Smut of Sorghum
This smut is caused by Sporisorium sorghi (Link) Clint (syn: Sphacelotheca sorghi). The
smut is more common where farmers use untreated seed. Seeds in a smutted head are
converted into dark brown powdery masses of teliospores or chlamydospores. The smut
spores are covered with a tough grayish white or brown membrane. This membrane is
ruptured during harvesting and threshing and the spores are attached to the healthy grains
where they remain attached till the seed is sown next year. The smut sori are smooth, oval or
cylindrical or may be white, gray or brown.
When the infested seeds are sown, the teliospores which are 4-7 in diameter germinate
alongwith the seed and a four celled promycelium bearing lateral sporidia is formed. The
sporidia germinate and infect the developing seedling. Sometimes the teliospores germinate
directly by producing germ tubes. The fungal mycelium grows systemically along with the
plant but does not show any disease symptom until heading. While heading, the teliospores
are formed and the whole seed is converted into smut sori covered with a membrane. During
threshing time the membrane ruptured and the teliospores are fallen down on soil and also
adhere to healthy seeds. The teliospores on soil normally do not cause any infection to
seedlings. The optimum temperature for disease development is 25 C and the infection
decreases at temperatures between 35-40 C. Several physiologic races of covered smut are
known worldwide.
(ii)Loose Smut of Sorghum
This disease is caused by the fungus Sporisorium cruenta (syno: Sphacelotheca cruenta
(Kuhn) Potter.). All seeds in an infected panicle are smutted. Some kernels are transformed
into leafy structures and are escaped of infectiom. The seeds are converted into 2.5 cm long,
pointed smut sori which are surrounded by thin gray membrane. This membrane is usually
ruptured at the time when panicle emerges from the boot. Infected panicles emerge earlier
than healthy ones. The smut sori contain dark brown to black teliospores which are blown
away by wind leaving a long, black pointed conical and curved structure (columella) in the
centre. Some of the teliospores (6-10 in diameter) adhere to the surface of healthy kernels
on near by plants and carry with the seed. The affected plants are stunted with unusual
excessive tillering and have thin stalks as compared to healthy plants.

When infested seeds are sown, the teliospores germinate along with the seed through a thick
four celled promycelium bearing lateral sporidia. The sporidia germinate and infect the
seedling. The infection occurs at a temperature 20-25 C with a wide range of humidity. The
28

fungus grows systemically with the plant without showing any visible symptoms. The
symptoms appear only when the head emerges. The normal seeds are replaced by long, black
and pointed smut galls or sori. Teliospores in soil are not important for infection.
The major difference between covered and loose smuts is that the plants affected by loose
smut are stunted, have thin stalks and heads emerge earlier than healthy plants and also
abundant tillering was observed with loose smut infection.

(iii)Head Smut of Sorghum
Head smut is caused by Sporisorium holci-sorghi (syn: Sphacelotheca reiliana (Kuhn)
Clinton). This fungus attacks both sorghum and corn but both the hosts are attacked by
different physiological races. Smutted plants have week root systems and are more
susceptible to stalk rot and root rot fungi.

Infection first appears even when the heads are still in boot. The heads are completely
converted into a large smut galls covered by a thick whitish membrane. The membrane
ruptured before the heads are emerged and dark brown to black teliospores are exposed. The
teliospores are intermingled with a network of long, thin, dark broom like filaments of
vascular tissue. The heads are totally smutted with characteristic witches broom (many
small, rolled leaves coming out from heads of suckers at the nodes). The affected plants
remain dwarfed or stunted. The teliospores are blown off by wind or rain to the soil and plant
debris and survive there till the next crop is sown. The parts of the panicle left out from
infection show sterility and proliferation of individual florets. Occasionally smut galls may
develop on leaves and stem of sweet sorghum.

When sorghum seeds are sown the teliospores (9-14 in diameter) which are already in the
soil germinate along with the seed producing a four celled branched promycelium that bears
sporidia terminally near the septa. The poridia sprout by producing yeast-like secondary
sporidia or may germinate directly by producing a germtube that penetrates meristematic
tissue of seedlings. The sporidia germinate faster at a temperature of 27-31 C in moist soil.
The infection of seedlings can also takes place by teliospores already adhere to seed during
the last season. The healthy soil thus can be infected through seed infection. Apparently, seed
infection is not important in causing infection.

(iv) Long Smut of Sorghum
The disease is caused by Tolyposporium ehrenbergii (Kuhn) Pat. The spores are covered into
a solid ball. The surface of spores is echinulated. The spores germinate by the formation of
promycelium. Numerous sporidia are formed singly or in chains. The spores are soil borne.
The sporidia produced by soil borne spores are wind borne and reach to buds and initiate a
systemic mycelium which later expresses in the head. The ovary is converted into smut sorus.
The primary inoculum may be introduced from alternate hosts. Since the infection is air-
borne, control is difficult.

Control of Sorghum Smuts
Covered and loose smuts are easily controlled by seed treatment with a protectant fungicide.
Since physiological races of the three smuts can hybridize with one another, it is extremely
difficult to develop highly resistant or immune hybrids, varieties or cultivars. However,
resistant varieties have been developed for example in India SPV 104, 115, 102, 245 etc have
been found resistant against covered smut in Maharashtra. Some sweet sorghum varieties are
resistant to Head smut. Other seed treatments like soaking seed in Formalin (0.5%) or copper
29

sulphate 0.5-3.0 % solution for 10-15 minutes, seed dressing with mercurial fungicides like
Agrosan GN (1:500) are effective to control smuts.

Other measures like collection and burning of smutted heads before the spores are scattered,
crop rotation and deep ploughing during summer months are useful to avoid damage by
sorghum smuts. Solar heat treatment was recommended in India by Asthana, 1946. During
summer months seeds are kept in ordinary water for 4 -10 hours during night and then dry
them for 10-12 hours in the sun. The method was found effective in Uttar Pradesh.

2. Grain Mold of Sorghum
About 40 genera of fungi are detected in moldy sorghum grains and some of them produce
mycotoxins. Fusarium species are more prevalent in mold affected sorghum. Fusarium
thapsimum appears to be the most prevalent fungus associated with sorghum grain mold.
However, the disease varies from region to region and depends on sowing dates, relative
humidity and temperature. Earlier sowings had the highest incidence of the grain mold when
temperarure ranges from 20 to 24 C.

The grain mold can be controlled with proper storage to avoid fungal growth. The moisture
contents below 14 % or more and a temperature of 5-8 C are ideal for storage. The storage
should be kept free from insects and mites. Quick drying of seeds and keep them in storage
bins with good aeration systems also useful for protection against grain mold. It has been
recently shown that agents like hydrated sodium calcium aluminosilicate bind the
mycotoxins, making the grains safe for consumption.

3. Anthracnose of Sorghum
The disease is caused by the fungus Colletotrichum graminicola (Cess) Wilson. It causes
damage to foliage and stems of sorghum. On susceptible hybrids stem holding the head
(peduncle) shows sunken areas with distinct margins. If infected stem is cut lengthwise
invasion of soft pith tissue visible as brick red discoloration would be seen. The peduncle
infection inhibits the flow of water and nutrients to the grains resulting poor grain
development. The fungus also invades individual grain and small branches of the panicle
causing severe losses to the yield.

The lesions also develop on leaves as small, elliptical to circular usually less than 3/8 inch in
diameter. The spots have circular straw coloured centre with wide margins which may be
reddish to black purple. The spots may coalesce to form larger areas of infected tissue. The
pathogen lives saprophytically on crop residue. Towards maturity of the plants black acervuli
appear on the stems, leaves and sometimes on spikes of infected heads. The fungus survives
as mycelium on crop residue and is a major problem where reduced tillage is practiced for
minimizing loss of soil or water.

The fungus produces one celled, ovoid, cylindrical and sometimes curved colorless conidia in
acervuli. The conidia are pink in colour. The acervuli are subepidermal and break out through
the surface of plant tissue. The infection is favoured by high temperature and humidity. The
conidia are spread by splashing rain, insect and tools etc. The sporidia germinate directly in
the presence of water and invade host tissues. The mycelium spread within the plant inter and
intracellularly and cause disease symptoms on stem and leaves.

The use of resistant hybrids and good management of crop residue are effective control
measures.
30

Diseases of Bajra (Pearl Millet)
1. Downy Mildew or Green Ear Disease of Bajra
This is one of the serious diseases of bajra (Pennisetum typhoides) and found in all bajra
growing countries. The disease is known to occur in all bajra growing states of India
especially in water stagnated areas. The yield loss in bajra hybrids has been reported upto 30
per cent.

Symptoms: The disease symptoms begin as chlorosis of basal leaves. Older leaves show
more chlorosis than younger leaves. Infected plants look weak, stunted and light yellow in
colour. As the disease advances, the leaves show chlorotic stripes parallel to leaf veins. The
chlorotic areas develop abundant white asexual sporangia on the lower leaf surface and can
be observed as whitish growth in the morning. The floral parts are transformed into leafy
structure and the whole ear looks like a bunch of leaves and this stage is normally called as
green ear (Fig.17). There is either no grain formation in infected ears or lower half of the ear
transformed into leafy structures and upper half develops normal grain. Although the ear size
remains as that of healthy ears but in some cultivars the ear size is reduced and the complete
ear is turned into leafy structures (Fig 17). The affected plants may develop excessive tillers
and give bushy appearance as the internodes become short.






Fig.17. Symptoms of Green ear disease of Bajra on Plant and inflorescence

Pathogen: The causal pathogen is Sclerospora graminicola (Sacc.) Schroet which belongs to
family Peronosporaceae, order peronospores and class Oomycetes of Eumycota. The
pathogen produces asexual sporangia on sporangiophores during the night under moderate
temperature of 20C and high humidity. There is no sporulation below 70% relative humidity.
Sporangia are broadly elliptical and papillate. The sporangia germinate in the presence of free
water and liberate 1-12 zoospores on the leaves. Sporangia generally do not remain viable
after the day break. Zoospores encyst and germinate through germtube. The oospores are
formed as sexual spores when the crop is near maturity. They are thick walled, spherical,
brownish yallow and 22-25m in diameter. The oospores can survive from 8 months to 13
years under laboratory condition.

Disease Cycle: The disease is principally soil-borne but evidence of its seed-borne nature is
also available. The oospores which remain viable in soil or on infected debris germinate
when the crop is sown and are the source of primary infection. The spores germinate through
the germtube and cause infection by penetrating root hairs of the developing seedlings. The
mycelium of the fungus become systemic and grow along with the plants and cause
symptoms on leaves and ears and also develop asexual spores (sporangiospores) on the lower
surface of the leaves. The spores are spread through rain, wind or insects to the near by
healthy plants causing the secondary spread of the disease.
31

Control: The use of certified seed, eradication of infected plants, crop rotation for at least
five years and seed treatment with fungicides like metalaxil and spray with fungicides (0.05
0.01% ridomil) are effective to manage the disease. However, the best control is to grow
resistant hybrids, variety or cultivars which are now available for different regions in India.
For example, variety HB-1 is highly resistant to the disease.

2. Ergot Disease of Bajra
This is the most important disease of bajra hybrids. The form in which the pathogen
overwinters is called a sclerotium and this small structure is normally referred as ergot.

Symptoms: The disease occurs at the time of flowering. Small droplets of cream to pink
mucilage droplets of honey dew ooze out from ergot infected florets on bajra panicles. A
few to many such spikelets may be found in a group, which darken with age, and after 12-15
days , these droplets dry and harden , and dark brown to black sclerotia develop in place of
seeds on the panicles (Fig 18). The sclerotia are larger than seeds and are irregular in shape
measuring about 0.5 to 1 cm in length and 1 to 2 mm in diameter.

Pathogen: The causal pathogen is Claviceps fusiformis Loveless =Clavicep microciphala
(Walter) Tul. in the family Erysiphaceae, order Clavicipitales of the sub-division
Ascomycotina. The pathogen attacks the ovary and grows profusely producing hyphal mass
which forms the sclerotium. These hyphae develop small conidiophores on which conidia are
produced. The conidia are hyaline, one celled, lunate and measure 13-25 X 3-6 micron. The
honey dew droplets in the affected ears are full on conidia. Conidia may also produce
secondary conidia after germination. When the sclerotium bodies are cut open, the central
portion will show the white hyphal strands. The Sclerotia germinate following rain and form
1-16 fleshy stipes which are 6-20mm long. The asci develop on these stripes. Each ascus is
apical, globular, capitulate, light to dark brown with numerous perithecial projections. Asci
are interspersed with paraphyses. Ascospores emerge through ostioles. Thread-like
ascospores are hyaline, septate and measure 100-1700 X 0.5-0.7m. The Ascospores infect
the emerged stigmas before pollination. The infection is favoured with a relative humidity of
more than 80% and temperature 20 30C. The sclerotia contain ergotoxin, which when
consumed in excessive quantities is toxic to animal life.











Fig .18: Symptoms of Ergot disease of Bajar on panicles

Disease Cycle: The fungus spreads from plant to plant through conidia. The honey dew
having conidia attracts insects, which help in the the spread of the pathogen. The sclerotia
help the pathogen to perpetuate from season to season.. They remain in soil or plant debris
and germinate during the crop season. After germination they produce Asci. The ascospores
from ascus can cause infection of spike and produce the conidial stage. The honey dew
32

contains millions of asexual conidia which are dispersed by insects. Alkaloids and lipids
accumulate in the sclerotium. When the mature sclerotium drops to the ground, it remains
dormant until proper conditions trigger its germination.

Control: Since the pathogen is air borne, affecting the spike only at the time of flowering, it
is difficult to control. Early sowing of crop, crop rotation, use of certified seed or seed
treatment with fungicides and sanitation are the methods for management of ergot disease.
For small quantity of seed, the ergot can be removed by a putting seeds in 10% salted water
and collect the sclerotia which will float over the water. Resistant hybrids are available and
should be used for effective control of the disease.

Diseases of Sugarcane
1. Red Rot of Sugarcane
Red rot of sugarcane was first recorded from java in 1883 and in Indian subcontinent by
Barber and later by Butler in 1906.

Symptoms: The symptoms of red rot first appear on the midrib of leaves as red bright lesions
with ash grey centre. Near harvesting of the crop (September-October onwards) the leaves
show drooping and colour change of upper leaves. Initially, third or fourth leaf from the top
show withering and finally the whole crown droop and withers.The withering of leaves
progresses downwards as the disease advances. In severe cases, pith of canes dries up and
canes shriveled loosing their weight. If such canes are split open, reddish colour areas can be
seen giving an alcoholic smell which develops due to fermentation of sugar. The size of
lesions and reddish areas depend on the variety.

Pathogen: The disease is caused by the pathogen Colletotrichum falcatum Went. which
belong to the order Melanconiales of Deuteromycotina. The perfect stage is Physalossora
tucumanensis Speg. =Glomerella tucumanensis Van Arx and muller.

Disease Cycle: The pathogen develops fruiting bodies on rind, usually just below or above
nodes. The spores can survive in soil for a long time. The pathogen produces conidia in
acervuli which are colorless, one celled, ovoid, cylindrical and sometimes falcate or sickle
shaped, granular and guttulate measuring 16-48 X 4-8m. The acervulus is ovoid, sub-
epidermal measuring 70- 300 m long and has bristle-like structure on it. The acervuli break
out trough, the surface of plant tissues and the conidia are exposed and spread through
splashing rain, insects or tool etc. The conidia germinate in presence of water on leaves and
penetrate the host directly and form chlamydospores inside the host tissues. The
chlamydospores survive in soil and infect sugarcane plants when conditions are favourable.
The disease perpetuates from year to year through soil, decaying leaves and planting the
diseased setts or through the diseased canes lying in the field. The ratoon crop helps in
multiplication and penetration of fungus.

Control: The cultivation of disease resistant varieties is the best control of the disease. In
India, several genotypes such as COLK 8102, COLK 7810 etc. and clones such as CO 86249,
CO 81011 etc. are resistant to red rot of sugarcane. Other measures like crop rotation, use of
disease free seed setts or treating them with fungicides and collection and burning of affected
parts after harvesting are also useful for managing the disease. Ratoon crop should not be
taken if first crop is found infected. The common control in practice is hot air treatment with
33

54C temperature for 10 hours and hot water treatment at 50C for two hous. This facility has
been created for farmers at the site of sugar Factories in India.

2. Smut of Sugacane
The smut of sugarcane commonly known as whip smut is found in many sugarcane growing
countries including India. The disease appears to move from wild canes to improved
varieties.

Symptoms: The disease show a whip-like black shoot at the apex of diseased plants which
may be several feet in length and curved. The smut powder covered with a thin silvery
membrane is attached to the whip. The membrane is ruptured and a thick mass of millions of
smut spores is scattered by wind. In case of systemic infection, the nodes or eyes produce
lateral shoots on affected plants which may also develop whip but if the infection is localized,
main shoot may not develop the whip. The smut masses are present in several layers on
whips.

Pathogen: The causal pathogen is Ustilago scitaminea Syd. Which belongs to family
Ustilaginaceae, order Uatilaginales of the sub-division of Basidiomycotina. The smut spores
are spherical, punctuate walled, light brown in colour about 5-10 in diameter. Under moist
condition, the spores germinate and form a septate promycelium. The sporidia develop from
each cell of the septa which are elongated and develop infection threads after their
germination. Sometimes the sporidia form more sporidia in chain. The spore germinates at a
temperature of 25-40 C with a relative humidity of 100%.

Disease Cycle: The sugarcane crop is available in the field throughout the year. The spores
from the whip blown by wind are deposited on the junction of leaves and leaf sheaths of
healthy plants and create infection at the nodal region. The infection occurs through
germinating shoot on the host tissue or through the injuries made by insects. The disease
perpetuates by planting diseased seed setts or through spores brought by wind on to the buds
or through ratoon crops

Control: To remove smutted whips, avoid ratoon crop, disinfection of seed setts such as
dipping in 1% formalin solution for 5 minutes covering with moist cloth for two hours,
avoiding use of susceptible varieties and hot water treatment at 55-60C for 10 minutes before
planting are suitable methods for control of sugarcane smut. However, use of resistant
varieties already known in CO series like CO 1148, CO 7108 etc. developed in India is the
best control of the disease.

3. Wilt Disease of Sugarcane
Wilt is a destructive disease of sugarcane in India. It is also reported from the Philippines,
South Africa and West Indies.

Symptoms: The symptoms appear as yellowing and withering of the top when sugarcane
crop is near harvesting. The affected canes rapidly dry and become light and hollow. A few
leaf joint may show reddening when split open. The pith becomes hollow. The main and
adventitious roots may show red colouration and die. Gum may appear in lumen of the
vessels, intercellular spaces and in the cells near vessels.

Pathogen: The disease is caused by Cephalosporium sacchari Butler of Deuteromycotina.
The conidiophores are septate, vertically branched and with pointed tips measuring 6-30x3-
34

4 Conidia develop in succession at the tips and are hyaline, ovoid, oblong ellipsoid and
measure 4-12 X 1-3. The fungus has three strains based on the difference in mycelium
colour and size of conidia. However, it has now been found that fungi, Acremonium fulcatum
and Fusarium moniliforme are also associated with sugarcane wilt.

Disease Cycle: The pathogen survives in vascular tissues of apparently healthy canes for
longer periods. If such canes are used for seed setts they function as the source of inoculum.
The healthy plants are infected through injuries from this inoculum. More wilt was observed
when canes are infected with red rot disease. The fungus causes disease symptoms when the
crop is near harvesting.
Control: Use of disease free setts, destruction of diseased plants and use of resistant varieties
like CO 356, CO 1158 etc are the methods for wilt control in sugarcane

Diseases of Groundnut
1. Early and Late Leaf Spots of Groundnut
The disease is commonly called as tikka disease. It is caused by two fungi, Cercosporidium
personatum (Cercospora personata) and Cercospora arachidicola. Both the pathogen can
occur on the same leaf. C. personatum appears first about 30 days earlier than C.
arachidicola when the plants are one or two months old and causes early spots. The C.
arachidicola appears late in the season and causes late leaf spots. C. personatum is more
damaging than the other as its rate of development is fast and may cause severe epidemics.

Symptoms: The lesions developed by the two pathogens differ in shape, size, and colour.
Both leaves and stems may show the lesions caused by the two fungi. The disease symptoms
first appear on the upper surface of leaves as pale areas.The spots caused by C. personata are
small, circular 1-6 mm in diameter and dark brown to black in colour. The spots are not
surrounded by a yellow halo, a characteristic of the spots caused by C. arachidicola. The
lower surface of the halo is dark black. The spots caused by C. arachidicola are circular to
irregular in shape measuring 1-10 mm in diameter. The spots may coalesce at later stages
covering more leaf surface. They are surrounded by a yellow halo. The necrotic areas on the
upper surface of leaf are reddish brown to black and light brown on the lower surface.

Pathogens: Cercosporidium personatum (Berk. & Curt) Deighton (prfect stage:
Mycosphaerella berkeleyii W.A. J ankins) and Cercospora arachidicola Hori (perfect stage:
M. arachidicola W.A. J ankins =C. arachidis Deighton). Both the pathogens belong to the
order Hyphomycetales in the division Eumycota.
Cercosporidium personatum: The mycelium is septste and intercellular. The haustoria are
found in pellisade and mesophyll cells.The conidiophores develop on dense, oval, brown to
black stroma measuring 20-30m.They emerge rupturing the epidermis and are olive brown,
unbranched and geniculate measuring 24-54 X 5-8m. Conidia develop on conidiophores are
cylindrical, light coloured and measure 18-60 X 6-11m with 1-7 septa. The perfect stage M.
berkeleyii belongs to Ascomycotina in which perithesia are ascostromata which develop
asci.The asci contain two celled eight ascospores of 15-35m in size.
Cercospora arachidicola: The mycelium first intercellular but later become intracellular. No
haustoria are found. Conidiophores are similar to C. personatum but differ in size, 15-45 X 3-
5m.Stromata are light to dark brown measuring 25-100m in diameter. Sporidia are hyaline
35

or pale yellow, septate with truncate base and subacute tips. The ascospores of M.
arachidicola are slightly curved, hyaline and two celled measuring 11 X 3.6m.
The two fungi can be differentiated at the time of conidia formation. In C. arachidicola
conidia usually develop on the upper surface of the leaf but rarely on the lower surface. They
are not formed in concentric rings but the conidia of C. personatum are restricted to the lower
surface and the conidiophores develop in cocentric spots.

Disease Cycle: The healthy plants initially infected by the the conidia lying in soil or in plant
debris or in contaminated seed or shells. A period of high humidity for three days is essential
for maximum infection by both the pathogens. Secondary spread occurs through the conidia
brought by wind or insects from the lesions formed on leaves of infected plants. The affected
leaves fall down on the soil and cause infection in the next season.

Control: To remove plant debris, self sown plants of groundnut, crop rotation, mixed
cropping with arhar, early sowing and use of early maturing varieties, seed treatment and
spray with suitable fungicides like Benlate are useful to avoid infection to the crop. Resistant
varieties should always be sown like VIR-3, ICGS -10 etc.

2. Sclerotium Stem Rot of Groundnut
The disorder is caused by the pathogen, Sclerotium (Corticium) rolfsii Sacc. The pathogen
causes disease to numerous crops worldwide including groundnut.

Symptoms: The symptoms of the disease appear as sudden wilting of a branch which is
completely or partially in contact with the soil. The leaves turn brown and wilt. White coating
of mycelium is formed near the soil level. A white mycelium web spreads over the soil and
the basal canopy of the plant. Infection of pegs takes place independent of stem or together
with it. Lesions on developing pegs can retard pod development. Infected pods are usually
rotted. Entire plant may be killed later.

Pathogen: The pathogen, Sclerotium rolfsii Sacc. produces sclerotia of mustard seed size
which appear on the infected areas. The sclerotia fell dawn in soil where they remain
overseason and act as inoculum to cause disease the following season.

Disease Cycle: The pathogen is soil-borne and attacks the basal portion of stem and roots,
causing sudden wilting and/or rotting of the stem tissues

Control: The cultivation in an infected field with an inversion plough significantly reduce
infection of groundnuts by this fungus and also improve the quality of the produce. Lower
plant density increase the incidence of the disease in an infected field, and is therefore not
considered to be a viable form of cultural control. Difenoconazole with biological antagonist,
Trichoderma harzianum has been identified to reduce the inoculum in the soil. Crop rotation
and use of resistant varieties should be adopted.

3. Seedling Rot of Groundnut
This disease is caused by Rhizopus species and highly damaging to crop at early stages of
plant growth.
Symptoms: The disease causes decay of pre-emerged seedlings. Seedlings are reduced to
dark brown or black spongy mass of rotten tissues covered with a mat of mycelium. The grey
black spores are produced on the mycelium.
36

Pathogen: The pathogens causing disease are Rhizopus arrhizus and R. oryzae and R.
stolonifer.These fungi belong to the family Mucoraceae of class zygomycetes of sub- division
Zygomycotina. The pathogens produce two morphologically similar gametes which come in
contact and the point of contact dissolve resulting to plasmogamy.
Control: Removal of crop debris, deep ploughing, harvesting at normal maturity, and to
avoid deep sowing and use of damaged seeds are useful to avoid infection to the crop. Seed
treatment with fungicides like thiram, captan etc. is important for the control of disease.
4. Seedling Blight of Groundnut
Symptoms: Rolling of the hypocotyle and seedling blight are the major symptoms. The
tissues of the cotyledonary nodes are rotted. Whole collar region becomes shredded and dark
brown. Lesions may develop on stem below soil in severe cases. Dead and dry branches can
be easily detached from the disintegrated collar region.
Pathogen and Disease Cycle: The disease is caused by Aspergillus niger and A.
pulverulentus which belong to family Eurotiaceae in subdivision Ascomycotina. The
mycelium of the fungi is septate. Both sexual and asexual reproduction is found. The asexual
spores are the conidia. The conidia are globose and unicellular and spread by wind and cause
infection to healthy plants. The female and male gametes are formed on the mycelium and
form ascus which contains ascospores. The cleistothecium develops at a later stage and the
ascospores are lying within it. The ascospores are released by rupturing the wall of the
cleistothecium and spread by wind to healthy plants where they germinate and cause
infection.
Control: A variety J -11 has been found resistant to the disease which should be used. Deep
planting of seed must be discouraged. Other methods like destruction of plant debris, deep
ploughing, to avoid mechanical damage and crop rotation with gram or wheat are useful to
avoid infection. Seed treatment with fungicides like captan @ 3g/kg or spray with mancozeb
@ 3g/litre of water when the disease is first noticed are helpful to avoid damage by the
disease.

Diseases of Sunflower
1. Sclerotinia Stalk Rot
Sclerotinia has an extremely wide host range infecting about 370 species of plants. Sunflower
crop is more commonly damaged by stalk rot. Sclerotinia is also a pathogen of common
home garden vegetables and flowers.
Symptoms: The symptoms appear on the stalk as a brownish to grey water socked lesion,
most commonly at or near the leaf node. A canker develops around the stalk, and the decayed
tissues have a wet pulpy appearance. The stalk falls at the point of decay and tissue above
canker die. The dense mycelium and sclerotia develop in and outside the stalk when the
weather is wet. Finally affected tissues become bleached and have a shredded appearance.
Stalk decay may move both to upper and lower portion of the stalk upto the base and head.
Sometimes the fungus decays the petiole, reaches to stem and causes rot.
Pathogen: The causal organism is Sclerotinia sclerotiorum (Lib.) de bary. The pathogen
belongs to family Aganomycetaceae, order Aganomycetales and sub-division
Deuteromycotina.
The pathogen produces hard, black coloured sclerotia which are of different shapes and size.
The sclerotia survive in the soil for several years. They germinate and produce either a white
mycelium or a mushroom like structure called as apothecia. The apothecia are tan to brown
37

measuring about 1/8 to inch in diameter. They produce ascospores which can infect the
plants. The ascospores are spread by wind from one sunflower field to another. During dry
periods the ascospores can survive for two to three weeks only.
Disease Cycle: During high soil moisture for at least two weeks the sclerotia germinate to
form apothecia. The apothecia produce ascospores continuously for a week or more
depending on moisture. The ascospores are carried to sunflower plants by wind. Apothecia
are produced abundantly in crop of dense canopies and which are frequently irrigated.
Ascospores germinate on a film of water on senescing plant tissue in the soil before infecting
the plant. They may also infect the host through wound caused by insect etc. The pathogen
can infect the seed and remains on the seed coat in the form of mycelium. However, the
spread of the fungus through seed is not important. The leaf infection can lead to stalk rot.
Control: The control measures of Sclerotinia stalk rot of sunflower are not to plant on
infested soil and to prevent the build up of sclerotia in soils either by monitoring of crop for
disease incidence or through crop rotation. At present, no resistance is apparently available
but some hybrids show difference in susceptibility. Chemical control is not satisfactory.

2. Alternaria Blight of Sunflower
Alternaria blight is a major disease of sunflower in humid areas of India and many other
countries where sunflower is grown as oil seed crop. The yield loss may be from 15-90% and
oil loss from 20-30 %.
Symptoms: The symptoms of the disease appear as dark brown spots on the leaves. These
spots are irregular in shape and size with dark border and grey centre.The spots on young
plants have a yellow halo. The spots may coalesce and the leaf withers. On stem, the lesions
appear as dark flecks which enlarge to form long and narrow lesions. The stem lesions are
randomly distributed and often coalesce to form large black areas resulting breakage of the
stem.
Pathogen: The disease is caused by Alternaria helianthi (Hansf.) Tubaki and Nishihara. The
pathogen belongs to family Dematiaceae, order Moniliales and sub-division
Deuteromycotina. The conidiophores are cylindrical, scattered, gemiculate and septate. The
conidia are ellipsoid, slightly curved with transverse and longitudinal septa and 40-110 x 13-
28 in size. The conidia are not produced in chain.
Disease Cycle: The pathogen overwinters on diseased stalk and can be seed borne but rarely.
Seedling blight caused by Alternaria may develop when sunflower plants emerge in humid
condition in infested soil. Plants at maturing stage are more susceptible than the young plants.
Safflower and cocklebur serve as alternate host of A. helianthi. The disease development is
favoured by 25 27 C temperature and atleat of 12 hours wet foliage. Moisture for longer
periods can cause severe disease.
Control: Satisfactory control measures include crop rotation and chopping and burying of
infected plants. Fungicidal sprays and seed treatment with captan significantly reduce the
infection. The disease is controlled by spraying 0.2% Dithane M-45 any other copper
fungicide on the 30
th
, 40
th
and 50
th
days.




38

Diseases of Mustard
1. Alternaria Blight of Mustard
Alternaria species attack several plant species in cruciferae family and two species, A.
brassicae and A. brassicicola attack to them. Loss to mustard yield has been estimated upto
35 per cent.
Symptoms: The symptoms caused by A. brassicicola appear as dark coloured circular lesions
on the leaf. Concentric rings may also form in the lesions. The spots may be linear on stem,
petioles and pods. Similar spots are also caused by A. brassicae except that these spots are
smaller and lighter in colour. When too many spots are formed on leaves, they die
prematurely indirectly affecting the yield.
Pathogen: Alternaria brassicicola (Schw.) Wiltshire and Alternaria brassicae (Berk.) Sacc.
are the causal pathogens. The conidiophores of A. brassicicola are septate, olive green and
branched measuring 5 7.5 X 35 45. Conidia are linear; develop in chains of 8 10 and
measure 11 17 X 50 75 on maturity. In A. brassicae, the conidiophores arise in fascicles.
The conidia borne singly or in short chains and are dark, obclavate, muriform and measure
125 225 X 16 18. .
Disease Cycle: In temperate regions, these pathogens are seed borne but in tropical regions
seed borne inoculum does not play any role. Spores and mycelium in plant debris serve as
major means of perpetuation especially in tropical regions. Conidia are abundantly formed in
humid weather and disseminated by wind and cause infection to mustard even from other
cruciferous plants. After infection, the fungi become subcuticular in leaves and subsequently
develop conidia which are dispersed and cause infection to healthy crop plants.
Control: Seed treatment is required in temperate regions only but not in tropics. Foliar sprays
with chemicals like Dithane M-45 and other copper fungicides have been found very
effective to control the disease.
2. White Rust of Mustard (Crucifers)
White rust infects a large number of cruciferous plants both wild and cultivated species. In
India, mustard and other Brassica species, turnip, radish, Eruca sativa and several weeds are
found infected with white rust fungus. Seed crop suffers heavily due to infection of the
fungus to floral parts causing deformity.
Symptoms: The pathogen causes both local and systemic infection and symptoms may
appear to all plant parts except roots. In case of local infection, white pustules are irregularly
formed on leaves and stems (Fig.19). These pustules may merge together to form larger
pustules. The host epidermis is ruptured showing white powder of spores. When fungus
becomes systemic it causes deformities to stem and floral parts. Due to hyperplasia and
hypertrophy of tissues, the axis of the inflorescence and flower stalk become thickened, floral
parts become swollen and green to violet in colour (Fig.20). The petals look like sepals and
stamens become leafy. The carpels may be open and ovules and pollen grains atrophied
causing sterility to ovary. The swollen parts carry the oospores of the fungus. In case of early
infection whole plant may remain dwarfed and only small leaves will develop. Swelling on
stem may be restricted to some portion or may spread to whole stem. The stem and floral axis
may twist showing a zigzag appearance and lateral shoots may appear on the stem.
Pathogen: The causal pathogen is Albugo candida (Lev.) Kuntze also known as Cystopus
candidus Lev. The pathogen belongs to family Albuginaceae, order Peronosporales and sub-
division Mastigomycotina of Eumycota. The pathogen is an obligate parasite. The mycelium
develops intercellularly with knob shaped haustoria. The sporangiophores develop from the
39







Fig.19: Symptoms of white rust on leaf and stem of Fig. 20:Influorescence symptoms
Mustard caused by white rust of crucifers

mycelium and produce sporangia in basipetal succession in chains. A gelatinous pad is
formed between the sporangia which swell during the presence of moisture thus helps in
disintegration and freeing the sporangia. The sporangia germinate and produce zoospores in
water. The zoospores swim in water with the help of flagella and later become round and
encysted and go for hibernation. Under favourable conditions (optimum temperature 10 C
and maximum 25 C) the encysted zoospores germinate by producing germtube and infect the
host through stomata and form new mycelium.
Sexual organs are formed from the mycelium within intercellular spaces of systemically
invaded tissues.The oogonium is globose, terminal or intercalary and is clearly defined into a
periplasm and a single central oospere. The antheridium also develops near the oogonium and
at the point of their contact, the wall become thin and a papilla of the oogonium protrudes
into the anthridium but disappears soon. The fertilization tube from the antheridium enters
into the oosphere passing through the thin wall. The nuclei of both antheridium and oosphere
undergo two mitotic divisions and form a granular body known as coenocentrum in the
oosphere. A single female functional nucleus is attached at a point near it. The fertilization
tube penetrates the coenocentrum and finally discharge a single male nucleus which fuges
with the female nucleus and thus fertilization takes place resulting the formation of oospore.
The oospore is formed by the development of a thick and tuberculate wall around the
oosphere. The fuged nucleus of oospores undergoes several mitotic and one meotic division
and thus forms about 30 nuclei. These oospores germinate and produce zoospores for further
infection to the healthy plants.
Disease Cycle: The pathogen perpetuates through oospores lying in the soil or on plant
debris. Weed hosts also serve as a source of primary inoculum. Secondary spread takes place
by means of sporangia and zoospores. Moist and cool weathers favour the development of the
disease.
Control: Early sowing is useful to avoid floral malformation. Other measures like clean
cultivation, destruction of plant residue and crop rotation are also useful to avoid disease in
the crop. If required, fungicides such as Dithane M -45 @ 0.2% etc. should be sprayed.
Resistant varieties like Kranti, TM-20, RN-510, MDYR-2029, NPJ -81, PAB-2001 and PAB-
2002 etc. should be sown.
3. Downy Mildew of Mustard
The disease is commonly found on mustard and damage plants at early stages of growth and
also to inflorescence at later stages. The disease can cause a loss upto 37-47 % with a mixed
infection with white rust in pod yield and upto 17-32 % in seed yield of Brassica juncea.

Symptoms: Pulpish brown spots are formed underside the leaf. The upper surface above the
lesions show tan to yellow colouration. The cottony growth of the fungus appears on the
40

undersurface of the lesions. In systemically infected plants symptoms appear similar to white
rust except that the deformities are more on stem but flower parts donot show deformities
except enlargement and twisting of ovary. The stalks are abruptly bent and flower buds are
atrophied.

Pathogen: The causal pathogen is Peronospora parasitica (Pers.) ex Fr. and belongs to
family Peronosporaceae, order Peronosporales and sub-division Mastigomycotina. The
pathogen is an obligate parasite and the mycelium is intercellular with branched haustoria.
The numerous branched conidiophores emerge through the stomata on the lower surface of
leaves. The conidiophores are dichotomously branched 6-8 times at the tip. A single
conidium is formed on each tip of the branch and is oval, ellipsoidal and hyaline, and
measure 24-27 X 15-20.The conidia fall of and germinate through a lateral germtube.
Sexual organs develop late in the season. The oogonium is spherical and fertilized by a single
antheridium. The oospores are globose measuring 26-43 in diameter and are enclosed in a
crest-like fold and appear pale yellow in colour and germinate by a germ tube. More conidia
develop at 13 C than 18 C.
Disease Cycle: The pathogen perpetuates in soil through oospores. The seeds may also carry
the infection of oospores as a contamination. Wild hosts also serve the source of primary
inoculum. Secondary spread is through conidia.

Control: Cultural practices like crop rotation avoiding cruciferous plants, eradication of
weed hosts, deep summer ploughing and destruction of crop residue are important. Spraying
with fungicides like Dithan Z-78 (0.3%), Blitox-50 (0.3%) etc. is useful to control the
disease. In India at Pantnagar mustard varieties YRT-3 and TMV-2 were found resistant to
downy mildew pathogen.

4. Sclerotinia Stem Rot of Mustard
Indian mustard (B. juncea) is the major oil seed crop in India. The losses caused by the
disease in seed depend on the time of disease appearance. Maximum losses upto 92.32 %
were recorded in seed yield when the plants were infected at the age of 70 days.
Symptoms: First symptoms of stem rot appear in the field 65-70 days after sowing. Diseased
plants can be identified by sudden drooping of leaves and finally drying of plants. Lodged
stems come in contact of soil and develop watery lesions with snowy white mycelium and
black, irregularly shaped sclerotia.
Pathogen: The causal pathogen is Sclerotinia sclerotiorum (Lib.) de Bary and belongs to
family Aganomycetaceae, order aganomycetales and sub-division Deuteromycotina. The
pathogen infects about 400 other plant species.
Disease Cycle: The primary survival structure of the fungus is sclerotium. A sclerotium is a
hard resting structure consisting of a light coloured interior portion called as medulla and an
exterior black protective covering called the rind. The rind contains melanin which is highly
resistant to degradation. The medulla consists of fungal cells rich in glucans and proteins. The
sclerotia can come to the fresh crop by wind from infected fields, remains in plant debris,
through contamination or irrigation. The sclerotia are also carried by seed or contaminated
soil. The disease cycle starts from sclerotia in the soil. They germinate by carpogenic
germination which results in the production of a small mushroom-like structure called as
apothecium. The apothecium produces ascospores which are wind transported to healthy
plants. The sclerotia may also germinated directly producing mycelium on certain hosts.
41

Control: The pathogen is soil borne and the sclerotia can survive in soil for several years,
crop rotation of non-host crops of atleast 4-5 years may be helpful. Use of certified seeds,
avoid excessive irrigation, sowing in rows with wider row spacing and destruction and
burning of crop debris are important to avoid stem rot disease. Chemical controls are most
effective when combined with cultural control strategies and are usually not necessary if
sound cultural practices are followed. In India, genotypes ZYR-6, PCR-10, cutlass etc. were
found resistant.

5. Bacterial Rot of Mustard
Little is known about the disease and its life cycle, but presumably the pathogen gets entry
into the plant through natural openings or wounds.
Symptoms: The disease can be easily recognized by its foul odor. Affected plants are soft
and mushy. The water soaked lesions develop on pods that become necrotic and dry with
time. The disease appears in high humidity and when high doses of fertilizer (nitrogen) is
applied to the crop.
Pathogen: The disease is caused by a bacterium, Pseudomonas syringae pv maculicola. The
bacterium belongs to family Pseudomonadaceae, class Proreobacteria and division
Gracilicute of Prokaryotae.
Disease Cycle: The pathogen enters the host through injuries caused by insects etc. or
through the natural openings. Splashing water, equipments and aerosols disseminate the
bacterium.
Control: Management strategies like crop rotation by non-hosts, removal of plant debris,
weed control in and around fields and furrow irrigation with pathogen free sources of water
such as tube wells, avoiding excessive irrigation and high fertilizer doses are useful to
manage the disease. Copper bactericides may provide suppression of the disease if applied
preventively and regularly.

Diseases of Pigeonpea
1. Wilt of Pigeonpea
The disease is most destructive to pigeonpea throughout India and several African countries.
The plant mortality upto 50% has been observed with severe infection of wilt.
Symptoms: The main symptoms are wilting of seedlings and adult plants. The wilting starts
gradually showing yellowing and dying of leaves following by wilting of whole infected
plant (Fig 21). However, sometimes wilting is sudden. The affected plants can be seen in
patches in the field and can be easily recognized. The tissues of root and stem at the base
show black streaks, which can be easily observed by removing the bark. The branches arising
from discoloured parts show the wilting symptoms first. The wilting may be partial as the
branches on one side will show wilting while on the other side they remain healthy. The
wilting is due to blockage of water conducting tissues by fungal mycelium and by the
production of toxins by the fungus within host and also around the roots in the soil.
Pathogen: The causal pathogen is Fusarium udum Butler.The perfect stage of the fungus has
been reported as Gibberella indica. The pathogen is restricted to vascular tissues. The
mycelium is septate, hyaline, and both inter and intracellular. The fungal hyphae produces
three types of spores within the host tissues; microconidia, macroconidia and
chlamydospores. The micoconidia are minute, elliptical, curved, and unicellular with one or
two septa and measure 5-15 X 2-4 . The macroconidia are long, curved, pointed at the tips
42

with 3-4 septa and measure 15-50 X 3-5 . Chlamydospores are oval, single or in chains,
terminal or intercalary and remain in the soil for long time.
Disease Cycle: The wilt pathogen is soil borne. The pathogen survives in soil as a saprophyte
on dead host roots and other plant parts. The pathogen spores can also survive for long time.
Under favourable conditions, the spores germinate with a germ tube which penetrates the fine
rootlets. The fungus may move to larger roots if they got injury. The affected roots become
black and shriveled. The disease is favoured at a temperature of 17-29 C. The main infection
is through soil only and secondary infection by conidia on above ground parts is rare. The
infected plants develop spores which fell down on the soil and function as inoculum for the
next crop.
Control: The disease is manageable by cultural practices like crop rotation, field sanitation,
deep ploughing during summer, mixed cropping with sorghum, amendment of soil with oil
cakes, trace elements such as zinc and manganese, growing green manure crops in the
rotation. Growing of resistant varieties is the best control. Varieties like Pusa 992, AL 1430,
METH 121, BSMR 853 etc. have been found resistant to wilt of pigeonpea in India.











Fig.21: Symptoms of wilt of Arahar Fig.22: Symptoms of Phytophthora blight of Arahar

2. Phytophthora Blight of Pigeonpea
The disease was first reported from the fields at Indian Agricultural Research Institute by
Williams et al, 1968. The disease commonly occurs in fields having heavy soil and poor
drainage.
Symptoms: Affected plants show as water soaked brown to dark lesions on the leaves which
become necrotic afterward. The lesions on stem and petiole are somewhat brown and sunken.
The lesions enlarge in size and girdle the stem resulting drying of branches and foliage. The
seedlings die suddenly due to infection (Fig 22). No symptoms are found on root system.
Branches and petioles lead to desiccation. In severe cases, the whole foliage becomes
blighted. Infected stem can easily break by the wind. In advanced stages, the stem is
commonly swollen into cankerous structures near the lesions. The seedlings are highly prone
to this infection and dry plants are common during rainy season. The disease is serious when
continuous rains occur or there is water logging in the field. Such conditions can create
epidemic of the disease.
Pathogen: The disease is caused by Phytophthora drechsleri Tucker f. sp. cajani
Disease Cycle: The pathogen survives in soil and on infected plant debris. Cloudy weather
and drizzling rain with temperature of 25 C favour infection. Low lying area where water
stagnates and close spacing encourage blight build up. Warm and humid weathers after
infection result in rapid development of disease.
43

Control: The disease can be managed by avoiding the sowing in fields with heavy soil with
poor drainage system, selection of disease-free fields, soil solarization or summer ploughing
and wide row interspacing are good cultural practices for disease control. Other measures are
to treat the seed with ridomil or metalaxyl (0.3 g per kg of seeds) and two sprays of metalaxil
at 15 days interval starting from 15 days after germination and use of resistant varieties and
cultivation of pigeonpea on ridges.

3. Sterility Mosaic Disease of Pigeonpea
Sterility mosaic is the most damaging disease of pigeonpea endemic in Indian subcontinent.
About 90% of pigeonpea is grown in India and Nepal. The losses caused by the disease in
India and Nepal are more than USD 300 million per annum.
Symptoms: The plants infected with sterility mosaic remain stunted. The leaves show mosaic
symptoms and the symptoms may develop on all the leaves of infected plants. The flowering
is partially or completely stopped and a few flowers which develop are sterile. Infection by
the pathogen in plants when they are less than 45 days old results in 95-100 % losses, while
older plants suffer 26-97 % losses.
Pathogen: A previously undescribed virus, pigeonpea sterility mosaic (PPSMV), shows
properties similar to viruses in the genus Tenuivirus. However, all tenuiviruses are phloem
limited, are transmitted by planthoppers and infects plants only in family Poaceae, thus ruling
out PPSMV as a tenuivirus. In ultrastructural studies of PPSMV infected tissues showed 100
150 nm quasispherical-membrane bound bodies (MBBs) and fibrous inclusions. The
filamentous virus-like particles (VLPs) of PPSMV resemble the nucleoprotein particles of
tomato spotted wilt virus (TSWV), but PPSMV VLPs are slightly larger than those of TSWV
and is not serologically related to maize stripe tenuivirus and peanut bud necrosis tospovirus.
The sterility mosaic causal agent is transmitted by the arthropod mite vector Aceria cajani
an eriophyid mite.
PPSMV and High plains virus share some common properties: transmission by eriophyid
mite A. cajani, 4-7 similar sized MBBs and similar morphology. Similar MBBs have been
detected in plants infected with fig mosaic, wheat spot moaic etc. which are also infected by
eriophyid mite, suggesting that these viruses may constitute a new virus genus.
Disease Cycle: The sterility mosaic thrives readily in crops under irrigation or near irrigated
fields. Such crops remain at risk of early infection. The virus and the vector mite both
survives on self sown plants during off season and when the crop is sown the virus infection
takes place through the vector. The secondary infection takes place from primarily infected
plants in the crop by the mite vector.
Management: Cultivation of disease resistant varieties is the most viable way to manage this
virus disease of pigeonpea. The broad based resistant genotypes are rare in the pigeonpea
gene pool but a related wild species, Cajanus scarabaeoides (synonym C. indicus ) has high
level of resistance. Eradication of self sown plants in and around pigeon pea fields is very
helpful to manage sterility mosaic.

Diseases of Soybean
1. Rhizoctinia Blight of Soybean
This disease is distributed throughout India but more severe in Madhya Pradesh and
Uttranchal. The disease may cause yield loss upto 35 %. The causal fungus infects all plant
parts, root, lower stem of seedlings as well as mature plant, stem, leaves, petioles and pods.
44

Symptoms: Initially the disease appears on lower leaves as water soaked lesions which are
later turned as greyish brown to reddish brown and finally turn dark brown. Subsequently, the
affected leaves get blighted and in severe cases the whole crop looks blighted. During
flowering time the root of affected plants show brown to dark brown discoloration of cortical
region. The root tissues may also be lignified. A reddish brown canker may encircle the stem
at the base and drooping of leaves is also common. Under high humidity the fungal mycelium
can be observed on leaves and in between closely spaced plants. Oval to elongated spots
appear on stem, petiole and pods. Dark brown sclerotia are formed on leaves and petioles.
The disease also affects the seedlings causing stunting and also pre emergence mortility.
Seeds on infected plants may show irregularly shaped tan or light brown sunken lesions.
Pathogen: The disease is caused by Rhizoctinia solani Kuhn. The perfect stage of the
pathogen is Thanatephorus cucumeris. The myceliumof the causal fungus produces branches
at right angle of the main hypha, slightly constricted at the main junction and have a cross
wall near the junction. The pathogen produces sclerotia like tufts of short, broad cells that
function as chlamydospores, or the tufts develop into sclerotia. The basidia of the perfect
stage develop on a membranous layer of mycelium and have four strigmata, each bearing one
basidiospore.
Disease Cycle: The pathogen is seed, soil and air borne. Inoculum in the seed or soil causes
infection and is responsible for pre and post emergence mortality. Inoculum may be splashed
out and infects the stem and leaves of the older plants and spread from leaf to leaf and plant
to plant by contact. The parts detached from infected plants serve as secondary inoculum.
Rain or free moisture on plant surface with warm (24-32 C) and humid weather will cause
severe infection.
Control: Control of Rhizoctinia diseases is difficult but measures like avoiding thick
population, seed treatment with fungicides like captan @ 3-4g/kg, spray of carbendazim etc.
and use of moderately resistant / tolerant varieties like PK 262, 416, SL-295 etc. and
mulching are helpful to avoid losses due to this disease.

2. Pod Blight and Seed Rot of Soybean
It is commonly found in India in the states of Madhya Pradesh, Uttaranchal, Punjab,
Himachal Pradesh and Rajasthan.
Symptoms: The disease symptoms may be observed on any part of infected plant. The
infected seeds are cracked badly, shrivel and remain covered with dirty white mycelium.
Bright red to brown lesions are also produced on cotyledons which may result in seedling
blight. Seedlings emerging from infected seeds have seed coat attached to cotyledons which
may also result to seedling blight. Later in the season, adult plants develop black speck sized
pycnidia which are linearly arranged on infected petiole or abscised leaves, broken branches,
stem and pods. Under favourable conditions such as warm and humid climate, premature
death of branches, shedding of leaves, and undeveloped podes are the common symptoms.
Pod blight results in mouldy and light seeds. Leaf infection is rare and latent infection is
common.
Pathogen: Diaporthe phaseolorum (Cke, and Ell.) Sacc. var. sojae (Lehman) and Phomosis
longicolla are two major pathogens involved with pod blight disease while other species, D.
phaseolorum var. caulivora is commonly associated with seed rot. In India, only D.
phaeolorum var sojae is known to occur.
Disease Cycle: The pathogens are seed and soil borne. The fungus overseasons as mycelium
in host debris and in infected seed. Pycnidia and/or perithecia are produced on plant debris.
45

The dormant mycelium, conidia from pycnidia and ascospores from perithecia cause the
primary infection and develop the lesions. The conidia produced by pycnidia in these lesions
are spread by splashed rains and cause secondary infection. Infection in the pods leads to seed
infection and decay.
Control: The infection can be minimized by ploughing down crop residue, use of healthy
seeds, crop rotation, seed treatment with fungicides like thiram +carbendazim (2:1) @ 3g/kg,
spray with benomyl @ 0.1%, adequate potash in the field and to grow moderately resistant
vars. Like Bragg, HIMSO 1563, NRC 37 PK 262, J S 80-21 etc.

3. Seedling Blight in Soybean
Seedling blight in soybean is caused by several pathogens such as Phytophthora sojae,
Rhizoctonia solani, Fusarium oxysporum or F. solani. These fungal pathogens are soil borne.
R. solani infection has already been covered under Rhizoctinia blight.

(i). Phytophthora Seedling Blight
Symptoms: If the plants are killed at seedling stage, the disease is called seedling blight.
Diseased plants may stand alone or in small circular groups particularly at low spots in the
field or may be seen throughout the plantings. Dead seedlings are visible on the ground.
Infected plants that die before true leaf stage will have a rotted appearance. Infected seedlings
have a grey green colour which later turns to brown. A few days later the infected plants die.
The roots are rotted. Infected plants have a brown discoloration extending from root tips to
the stem. Warm condition is favourable for Phytophthora infection whereas, soybean planted
in cold wet soil infection by Pythium spp. is more common. The symptoms caused by both
the fungi are very similar.
Pathogen: Over 39 races of the pathogen Phytophthora sojae cause seedling blight. The
pathogen produces structures called oospores which enable the pathogen to survive in soil or
on crop residue.
Disease Cycle: The oospores present on crop debris or in soil germinate and produce
sporangia. The sporangia release zoospores which enter in soybean root tips and cause
infection. The oospore may survive in the soil for several years and thus the inoculum is
always there in a contaminated field.
Control: The measures like application of less manure and fertilizer before planting, crop
rotation, seed treatment use of fungicides and to grow resistant varieties are useful to avoid
seedling blight.

(ii) Fusarium Seedling Blight
Symptoms: The disease is most common on seedlings and young plants. Fusarium seedling
blight is frequently found in combination with Rhyzoctiniablight or soybean cyst nematode.
Damage from the Fusarium may be more severe when it occurs in combination with other
diseases or stresses.
Pathogen: The disease is caused by either Fusarium oxysporum or F. solani.
Disease Cycle: These two pathogens can persist in the soil and colonize on various plant
residues and survive as chlamydospores or mycelium. The infection is favoured by herbicide
injury, deep planting, poor seed quality, hail damage, mechanical injuries, poor fertility and
other factors that delay germination and emergence favour the development of Fusarium
seedling blight. The infection initially comes from the soil inoculum.
46

Control: Measures like use of good quality seeds minimize or avoid stress which delay
germination and seed treatment with fungicides are useful to manage the disease.
4. Bacterial Pustule
Pustule has been reported in most soybean growing areas of the world where warm and
humid weather prevails during crop season. The disease may cause premature defoliation,
which may decrease yield by reducing seed size and number of grains.

Symptoms: Early symptoms are minute, pale green spots with elevated centres on both
surfaces of leaves. Later, a small raised, light coloured pustule develops in the centre of
lesions on the lower surface of leaves. Lesions are often associated with main leaf veins. The
spots vary in size from specks to large, irregular mottled brown areas. Leaves become ragged
when dead areas are torn away by wind. Severe disease often results in defoliation.
Pathogen: The bacterium, Xanthomonas axonopodis pv. Glycines is the causal pathogen.
Colonies on beaf infusion agar are pale yellow, become deep yellow with age and are small,
circular, and smooth, with an entire margin.
Disease Cycle: The pathogen overseasons in seeds, in crop residue, and in the rhizosphere of
roots. Strains can infect common bean and cowpea. The pathogen spreads through splashing
water or wind blown rain and during operation when foliage is wet. The pathogen can enter
the plant through natural openings and wounds. Warm weather and frequent showers promote
the development of this disease.
Control: Use of resistant cultivars, crop rotation, tillage, limit cultivation to times when the
foliage is dry and use of copper fungicides are the effective control measures.
5. Soybean Mosaic Disease
The disease is occurring all over the soybean growing areas of the world including India. The
disease can reduce the yield from 50-90% depending on age of plant and time of infection
and affects seed germination, nitrogen fixation and oil contents.
Symptoms: The affected soybean plants show rugocity, dark vein banding and light green
interveinal areas, stunting, leaf curling, and seed coat mottling, male sterility, frower
deformation, less pubescent, necrosis some times necrotic lesions, systemic necrosis and bud
blight
Pathogen: Soybean mosaic virus (SMV) is the causal pathogen. SMV is filamentous;
flexuous rod shaped with a clear modal length of 650-700 nm or 760 nm , 15-18 nm wide.
The pathogen belongs to potyvirrus group in family potyviridae. Virions contain 5.3%
nucleic acid and 94.7% protein. The genome consists of single stranded RNA of the size of
10.4 kb. The genome is unipartite. The SMV is mechanically transmissible by sap inoculation
to hosts, like Chenopodium album, C. quinoa, Cyamopsis tetragonoloba where SMV
produces local lesions and systemic symptoms on hosts like Phaseolus vulgaris, Glycine max
etc. SMV can also be detected in ELISA and PCR systems of diagnosis. Sixteen species of
aphids such as Acyrthosiphon pisuii, Ahis fabae and Myzus persicae are the vectos which
transmit the virus nonpersistently.
Disease Cycle: The pathogen is internally seed borne and initial infection comes from
infected seeds and secondary spread occurs through aphid vectors at a faster rate. Seeds are
means of long distance transport and survival from one season to another. The virus is also
pollen transmitted. Several plant species in families, Chenopodiaceae, Leguminosae,
Scrofulariaceae and Solanaceae are susceptible to the soybean mosaic virus (SMV) and may
serve the source of inoculum for transmission by aphids to soybean crop.
47

Management: Presowing soil application of phorate @ 10kg/ha, avoid monoculture of
varieties, clean cultivation, and foliar sprays of insecticides for aphid control and use of
moderately resistant varieties like J S71-05, Punjab-1, MACS 58 and PK 416 etc. are the
methods for SMV management.

Diseases of Gram
1. Wilt Disease
The disease has been reported from India and Burma and is widely distributed in Indo-
gangetic plains of India.
Symptoms: The affected plants show drooping and their sudden death is very common. The
leaves of affected plants turn yellow and fall off prematurely. Collar region of affected plants
show necrosis and discolouration. Wilting can occur in seedlings and adult plants as well.
Initially petioles and rachis alongwith leaflets show drooping and within 2-3 days drooping of
entire plant takes place (Fig. 23).The affected plants can be pulled out more easily than
healthy plants as most of the lateral roots of infected plants become weak.Transverse sections
of basal region show discolouration of vascular tissues and the fungal hyphae.









Fig .23: A Wilted plant of Gram
Pathogen: The disease is caused by Fusarium oxysporum Schlecht, emend.Snyd. & Hans. f.
sp. ciceri (Padwick) Snyd. & Hans. The pathogen belongs to family Tuberculariaceae, order
Moniliales and sub-division Deuteromycotina. The mycelium is inter and intracellular and
found abundantly in vascular tissues. The pathogen produces micro and macroconidia.
Macroconidia are sickle shaped, septate and hyaline and measure 25-40 x 3-4, while
microconidia are elliptical, have one or two septa and measure 4-6 x 2-4.
Disease Cycle: The pathogen is a facultative parasite and survives for a long time on plant
debris in soil especially on host roots which are left in the soil after harvesting. The pathogen
may produce resting spores known as chlamydospores that can survive under adverse
conditions. As soon as next crop is sown the chlamydospores become active and infect plants.
The disease may also be carried to new areas by contamination of seeds by chlamydospores
in the hylum region of the seed. Pigeonpea, pea and lentil are symptomless carriers of the
pathogen.
Control: The control is difficult as the pathogen survives in soil for long period. However,
cultural practices like date of sowing (crop period from November to February) and
supplement of high organic matter will reduce the disease. Seed-borne inoculum can be
eradicated by treated seed with a mixture of 30% benomyl and 30 % thiram.
48


2. Ascochyta Blight of Gram
The disease occurs in North-western part of Uttar Pradesh, Punjab and Hariyana in severe
form. The disease is also found in Pakistan, countries bordering Mediterranean sea and parts
of eastern Europe.
Symptoms: Brown, circular spots with brownish red margin appear on leaves and pods of
affected plants (Fig 24). On petioles and stem the spots are elongated in shape. The spots on
leaves coalesce turning the leaf completely brown. On green pods, the circular lesions have
dark margin where black dot like bodies appear known as pycnidia. The pycnidia are
arranged in concentric circles. The elongated lesions on stem and petioles also bear black
dots and may girdle the stem. The parts above the lesions droop and wilt. If the stem is
girdled at the base the whole plant will show wilting. During wet weather the disease spread
very fast and may cover the whole field.

Fig.24. Symptoms of Ascochyta







Pathogen: Ascochyta rabiei (Pass.) Labrousse is the causal pathogen. The pathogen belongs
to family Sphaeropsidaceae in Deuteromycotina. The perfect stage of the fungus is Didymella
rabiei (Kov.) Von Arx. The mycelium of the pathogen is septate. The pycnidia develop on
stem, leaves and seed pods are dark brown, globose and measure 140-200. Conidia are
formed within pycnidium and remain viable for long period of time. The pycnidia absorb
water, swell and release conidia. Several strains of the pathogen are known.
Disease Cycle: The pathogen survives on plant debris left in the field and also on seeds
which serve the source of primary inoculum. Further spread of the pathogen is through
conidia which are disseminated by splashing rain, by insects, contact of healthy and diseased
leaves and by the movement of man and animals. The disease spread fast at a temperature of
22-26 C and wet weather.
Control: The disease can be managed by sound cultural practices like removal of plant debris
from the field, crop rotation, deep sowing, mixed cropping with wheat and deep ploughing
during summer and seed treatment with organomercuriales (Agallol, Agrosan etc.). Spraying
fungicides like Zineb, captan etc.ia also helpful. Use of resistant varieties is the best control.

3. Grey Mould of Gram
Grey mould is a major yield reducer of gram in India, Nepal , Bangladesh and Australia.
Symptoms: The disease attacks the base of the stem and collar region of young plants, where
a soft rot develops and then becomes covered with a fluffy grey mould. Infected plants wither
and dye. Leaf infection causes comparatively less yield loss. When disease appears in severe
form the crop is totally lost. Seeds are also infected and they become white due to infection
decreasing the market value of the produce. Crop losses are very high during wet season.
49

Pathogen: The disease is caused by the pathogen, Botrytis cinerea Pers. Ex. Fr. Which
belongs to Deuteromycotina.
Disease Cycle: The pathogen survives in seed and crop residue and in soil. The plants can be
infected at any stage of their growth. Infected seeds are the primary source of inoculum.
Infected plants develop masses of spores which are air borne and spread the pathogen rapidly.
Once the infection is established, conditions under the canopy are ideal for spreading the
disease.
Control: The control options include use of less susceptible varieties, lower seed rate, plant
thinning and delayed sowing and need based foliar sprays with fungicides, crop rotation and
seed treatment with fungicides.

Diseases of Lentil
1. Rust of Lentil
The rust is a common disease of lentil in North India and cause heavy damage to the crop.
Symptoms: The disease symptoms are necrosis and deformity of stem and affected plants
often die. Yellowish powdery pustules are developed on leaves, stem and petioles and even
on pods. These yellow spots have aecia in round and elongated clusters. Uredopustules
develop on both side of leaves, petiole and stem as powdery light brown pustules. Dark
brown or black teliospores also develop in the same sorus at later stages.They mostly develop
on stem and petioles. Later the aecidia and pycnidia develop. It is autoceous rust.
Pathogen: The causal pathogen is Uromyces fabae (Pers.) de Bary. The pathogen belongs to
Basidiomycotina. Aeciospores developed in aecia are round to elliptical, yellowish in colour
and measure 14-22 micron. Uredospores are round to ovate, light brown and measure 20-30 x
18-26 in size. Teliospores are subglobose to ovate, brown in colour and measure 25-38 x
18-27.
Disease Cycle: The dissemination of lentil rust pathogen takes place by aeciospores which
form secondary aecia after infection of leaves. The secondary aecia are formed at a
temperature of 17-22 C but at 25 C the infection causes development of uredia. The
aeciospores and probably the uredospores do not survive during off season. The teliospores
can withstand the summer heat and hence the lentil rust perpetuates in its telial stage in the
left over diseased plants trash or on seed as external contaminant and infects the new crop in
the next season. Aeciospores from lentil have also been found to infect pea and Vicia faba
and Lathyrus.
However, another species of Uromyces, U. pisi (Pers) Wint. is a heteroceous rust and
commonly occur on cultivated pea. The aecial stage of this pathogen develops on Euphorbia
cyparissias L. This rust is not common in India.
Control: Destruction of diseased plant trash after harvest, crop rotation, and seed treatment
with fungicides are the effective control measures.
2. Wilt of Lentil
The disease is common in India on lentil crop.
Symtoms: Like other Fusarium wilts, the infected plants may wither and die. Leaves may
show yellow to brown discoloration and finally drop off. Necrosis and discoloration on collar
region is visible and most of the lateral roots are destroyed due to infection.
50

Pathogen: The disease is caused by the pathogen, Fusarium oxysporum Orthoceros var.
lentidis. It belongs to family Tuberculariaceae, order Moniliales and sub-division
Deuteromycotina. The pathogen is present both inter and intracellularly in vascular bundles
of the host and produces macro and microconidia overthere.
Disease Cycle: The pathogen is a facultative parasite and lives saprophytically on organic
matter in the soil. When the crop is harvested, the roots remain in soil and pathogen survives
on these roots for several years. The pathogen may produce chlamydospores which may face
adverse soil conditions and become active and infect plants when next crop is sown.
Control: The pathogen is soil borne. Crop rotation with resistant crops and soil amendments
with organic matter can reduce the chances of infection. Growing resistant varieties is the
best control.

Diseases of Cotton
1. Anthracnose of Cotton
The disease is found in most of the cotton growing areas of the world.
Symptoms: All the aboveground parts of the plant are infected and plants can be infected at
any stage of their growth.The cotyledons and primary leaves show small reddish circular
spots. The lesions at the collar region girdle the stem resulting death of young seedlings. The
stem of the mature plants can also be attacked resulting split and shredding of bark. On bolls,
water soaked, circular, sunken and reddish brown lesions develop which may cover most of
the bolls including the bracts. The lesions later turn to black with red margins. The lint
become yellow to brown, rot and transformed into brittle fibres. Seeds are also infected and
shrevelled discolored and brown in colour. Affected bolls are smaller in size.
Pathogen: The causal pathogens are: Colletotrichum capsici (Syd.) Butl. & Bisby ( C.
indicum Dast) and C. gossypii Southw. The pathogens belong to family Melanconiaceae,
order Melanconiales and sub-division Deuteromycotina. Perfect stage of C. gossypii is
Glomerella gossypii (Southw.) of the Ascomycotina.
In most of the Indian parts the disease is caused by C. capsici but in Maharashtra it is caused
by C. gossypii. Numerous acervuli are produced on affected parts. The conidia are falcate,
hyaline, thin walled and single celled produced on conidiophores arising out from the
mycelium. The conidia of C. gossypii measure 18-25 x 3.5-5 where as conidia of C. gossypii
are 11-20 x 4-9 in size.
Disease Cycle: The pathogens are seed borne and survive in seed for about a year and are the
primary source of inoculum.Two common weeds namely Aristolochia bractiata and Hibiscus
diversifolius are also susceptible to C. capsici and can also be a source of primary
inoculum.Secondary spread takes place by air and soil borne conidia. The disease spread
rapidly during wet weather.
Control: Seed treatment with conc. Sulfuric acid or fungicides and to use seeds of over one
year old for sowings are important for eliminating seed infection. Boll infection can be
checked by spraying calcium cyanamide @ 30kg/ha to reduce humidity. Removal of
collateral hosts and spraying of plants with 1% Bordeaux mixture or other fungicides can
check the infection.



51

2. Vascular Wilt of Cotton
The disease is common in cotton fields in heavy soil with a soil temperature between 20-30 C
during crop season. Due to unfavourable soil temperature the disease is not found in loamy
and sandy loam soils.
Symptoms: Yellowing and browning of cotyledons and formation of a brown ring on the
petiole are the first symptoms of the disease. The affected seedlings are collapsed due to
infection. In mature plants, symptoms appear as turgidity of leaves followed by wilting and
drooping starting from older leaves upwards and finally involving of branches and whole
plant. The stem of seedlings becomes dark as against partial discoloration of stem of mature
plants. The discoloration confined only one side of the stem. The black streaks can be
observed on stem upto roots after peeling the bark. The plants with minor infection may
recover but remain stunted and unproductive. A discolored ring can be seen in transverse
sections of infected stem and roots. Vascular tissues are filled up with a gummy substance
which contains the fungal hyphae.
Pathogen: The causal pathogen is Fusarium Oxysporum f. vasinfectum (Atk.) Synder &
Hansen. The pathogen belongs to family Tuberculariaceae, ordes Moniliales and sub-division
Deuteromycotina. The mycelium is inter or intracellular and plug the xylem partially or
wholly. Both micro and macroconidia are formed which produce mycelium after
germination. The pathogen also produces chlamydospores.
Disease Cycle: The pathogen can survive in soil for many years. It is also seed borne. The
primary infection takes place by hyphae or chlamydospores available in soil or through seed.
After infection the fungus reaches to xylem and multiplies fast. The vessels are plugged
causing wilting of plants due to non-availability of nutrients. Secondary spread takes place
through conidia which are disseminated by wind, water and insects.
Control: Cultural practices like deep ploughing during summer, application of high doses of
farm yard manure, increased doses of potash and soil amendment with zinc and treatment of
seeds with fungicides can reduce the infection. The indigenous cotton, Gossypium arboretum
and G. herbaceum are susceptible but some varieties of G. hirsutum and G. barbadence
introduced from America and Egypt are immune. Varieties like J ayadhar, J arila, Vijay,
Pratap, Varun and B.D.S. are wilt resistant.

3. Bacterial Blight, Angular Leaf Spot or Black Arm Disease
This is the most serious disorder of cotton crop and is found in most of the cotton growing
countries. The disease is widely distributed in India.

Symptoms: Minute water soaked areas develop on the under surface of cotyledons of
germinating seed. The lesions increase in size, and form black to brown patches causing the
cotyledons to dry and wither. If the disease appears on seedlings they also wither and die. The
water soaked lesions are also developed on both sides of leaves, increase in size and turn dark
brown to black anular spots alongwith veinlets (Fig. 25). The lesions increase in size and
cover larger areas of leaf resulting death of leaf. The infection can spread upto petioles
causing them to collapse.
Lesions on stem, petiole and fruiting branches are elongated, sunken and dark brown to sooty
black in colour. The affected stems show cracking and girdling and can be easily broken by
wind. Similar symptoms appear on bolls which can fall down prematurely.The bacterium
passes through fibres and infects the seed externally or may reach the interior of seed.
52

Pathogen: The bacterium Xanthomonas campestris pv. Malvacearum (Smith) Dye. is the
causal organism of the disease. The pathogen is rod shaped 0.3-o.6 x 1.3-2.7 in size. It is
non-spore forming, encapsulated, gram-negative and motile by a polar flagellum. Several
races of the bacterium are known to occur but race-10 is widely distributed in India.
Disease Cycle: The pathogen may survive in dead leaves for 17 years and in dry or wet soil
for 8 days at 21-30 C. The main source of primary inoculum is contaminated seeds. On
germination of seeds the pathogen infects cotyledons where it maintains the resident
population on first and second leaf but not on third leaf. Under favourable conditions (high
humidity and a temperature of 28-30 C) the inoculum from this source spread to new leaves
and further spread continues. The infection may also come from infected bolls, leaves and
twigs lying on soil. Secondary spread is through splashing rains and dew and spread very fast
at 35 C and high humidity.







Fig.25. Seedling of Cotton showing symptoms of bacterila blight
Control:Removal and destruction of plant debris, deep ploughing, pre-sowing irrigation,
crop rotation, late sowing, early thinning, good tillage, and addition of potash are
recommended to reduce initial infection. Seed treatment with conc. Sulfuric acid can
eliminate external inoculum from seed. For iternal inoculum, treatment with antibiotics like
streptomycin is essential. Hot water treatment at 56 C for 10 minutes is also recommended.
Secondary spread can be checked by spraying copper fungicides (0.2-0.3 %). Five to six
fortnightly sprays starting from the time when crop is 5-6 weeks old depending on severity of
the disease.
Resistant varieties have been developed such as HC-9, BJ A-592, P-14, T-12, 102 B and Riba
B-50 etc. which should be sown. In Hirsutum group resistant cultivars, 70 IH 480/2, 70IH-
480/3, 70 IH-280/9, K 4005, Badnawar-13-1007, Khandwa-2, DHY-286, M-937-CTO-421
have been reported.

Diseases of Potato
1. Early Blight of Potato
The disease is world-wide in distribution wherever potato is cultivated. The disease affects
young crop and may cause yield loss upto 40% if not contained.The disease appears both in
tropical and temperate regions.
Symptoms: Small pale brown spots first appear on leaves. Lowest leaves are attacked first
followed to upper parts of the plant. Concentric rings on leaves surrounded by chlorotic areas
are the characteristic symptom of the disease. In dry weather spots become hard and leaves
are curled but in humid weather big rotted patches are formed and leaves may fall down.
53

Similar patches are developed on stem resulting in the whole plant to collapse. The rotting
may reach upto the tuber. Affected plants develop less and smaller size tubers.
Pathogen: Fungus Alternaria solani (Ell. & Martin) J ones and Grout is the causal pathogen.
The pathogen belongs to family Dematiaceae, order Hyphomycetales and sub-division
Deuteromycotina. The conidiophores of the pathogen emerge through stomata from the spots
and bear conidia. The conidia are beaked, muriform with 5-10 transverse septa alongwith a
few longitudinal septa. Conidia germinate within 35-45 minutes at 28-30C. Other hosts of
pathogen are tomato, chillies, Atropha belladonna, Cymphomandra betacea, Hyascymus
albus, H. niger and Nicotiana alata.
Disease Cycle: The mycelium of the pathogen remains viable on dry infected leaves for 10-
12 months. Conidia are also viable upto 17 months at room temperature. Initial infection
therefore takes places either by mycelium or conidia surviving in soil on dead plant debris.
Contamination of seed tubers with conidia or mycelium may be another source of primary
inoculum. The infection starts from lower most leaves and further spread of the disease takes
place from the conidia formed on these leaves. The conidia are disseminated by water, wind
and insects. Under favourable conditions of rains followed by warm and dry weather the
disease spreads very rapidly.
Control: Destruction of plant debris after harvest and use of certified seed are important
measures to avoid infection. Regular sprays with fungicides at an interval of 10-21 days
depending on severity of the disease should be done. Fungicide Dithane Z-78 @ 2lb/100
gallons of water gives best result. Other fungicides like Dithane M-45 (0.2%), Blitox-50
(0.25%), Captan (0.2%) etc.have also been recommended for disease control. Resistant
varieties like Kufri Navin (for hills), Kufri Sinduri and Kufri J ivan (for planes) should be
used.

2. Late Blight of Potato
The famous Irish famine of 1845-46 was due to failure of potato crop by a disease which was
later identified as late blight of potato. In this famine, millions of people died due to
starvation as potato was staple food of Irish people. Several epiphytotics have been reported
due to late blight in different parts of the world. In India, the disease is found in all the potato
growing areas. The disease also occurs on tomato.
Symptoms: The disease usually appear late in the season than early blight. Brownish black
areas develop on leaves which can cover the whole leaf surface. The disease spreads very fast
when high humidity is there and cover the whole leaf within 1-4 days. The disease can cover
all the leaves and stem of the infected plant and sometimes the whole crop is blighted. The
tubers can also be infected while in soil or during harvesting or in storage.Most of the tubers
of infected plants are rotted showing brown to purple discoloration on the skin of tubers.
Moist atmosphere is suitable for wet rot and dry weather causes dry rot.
Pathogen: The pathogen, Phytophthora infestans (Mont) de Bary is the causal pathogen of
the disease. The pathogen belongs to family Pythiaceae, order Peronosporales and sub-
division Mastigomycotina. The mycelium is endophytic and intercellular. Sporangiophores
develop from the mycelium and come out through stomata or lenticels of tubers. Sporangia
are pear shaped and papillate and develop at the tips of sporangiophores.The sporangia
germinate and form secondary sporangia which produce zoospores upon germination. The
zoospores are biflagellate and cause infection to the host. Sexual reproduction is not known.
Several physiologic races are known in the pathogen.
54

Disease Cycle: Four factors have been suggested for development of epiphytotics by the
disease: (i) night temperature below dew point for at least four hours (ii) minimum
temperature of around 10C (iii) Clouds on the next day and (iv) Rain fall during the next 24 h
at least 0.1mm. Primary infection most likely comes through seed tubers particularly under
Indian conditions. The mycelium from contaminated tubers grows upward in the stem and
cause sporulationon small dwarfed shoots. Infection of foliage takes place from the spores
produced in primary lesions. The sporangia are spread through wind, water and leaf eating
insects to the healthy crops in the region. The spores are washed out to the soil from affected
leaves and infect tubers. The tubers also got contaminated when come in contact of infected
leaves during harvesting or in contact with infected tubers in the storage.
Control: Use of certified seeds, sanitation, delayed harvesting, storage in cool, dry and well
aerated stores are the major precautions to avoid infection.Spraying of crops with fungicides
starting well ahead of disease appearance time can provide good control. Dithiocabamates
(Zineb, Maneb etc) are more widely used to control the disease. Spray with Dithane Z-78 and
Dithane M-45 @ 2-2.5 kg/ 1000 litre of water / ha have been recommended. Early sprays of
Bordeaux mixture (4:4:50) and late spays at an interval of 15-21 days with Bordeaux mixture
(6:6:50) should be given. Late blight resistant varieties have been developed by Central
Potato Research Institute, Shimla for different regions of India as given below:
North-western plains: Kufri J eevan, Kufri Alankar, Kufri Navtal, Kufri Badshah and Kufri
Swarna.
North-eastern region: Kufri Naveen, Kufri Khasigaro, Kufri Himalini, and Kufri Sherpa
Shimla hills: Kufri J eevan, Kufri J yoti and Kufri Muthu
Nilgiri hills: Kufri Naveen and Kufri Moti.
Some high yielding hybrids were also found resistant to late blight of potato.

3. Black Scurf or Rhizoctonia Stem Canker
The disease is found world-wide and causes qualitative damage as it affects the maket value
of infected tubers both for table and seed purposes.
Symptoms: The main phases of the disease are the stem canker and blight phase and the
black scurf phase. The emerging tips of sprouting tubers are affected by the fungus which
may be killed before emergence. Most of the emerging seedlings from the buds are killed in
this way. The plants coming out from left over buds are stunted with yellowish hills. On
growing plants, cankers are developed which inhibit flow of carbohydrates resulting their
accumulation in the tips causing stunting, rosetting and purple colouration of affected plants.
Aerial tubers develop in the axis of branches and petioles. In the black scurf phase, a
superficial black crust on the skin of tubers can be seen. This crust is due to formation of
sclerotia of the fungus. In India, black scurf is more common than stem canker.
Pathogen: The causal pathogen is Rhizoctonia solani Kuhn. of Deuteromycotina. The
basidial stage is Thanatephorus cucumeris (Frank.) Donk.
The mycelium develops superficial scab-like and black sclerotia. Each sclerotium is
accompanied by a superficial, dark coloured, short celled, abundantly branched stout
mycelium. No other spores are produced in asexual stage of the fungus. Basidial stage is
mostly saprophytic. The basidia are formed on dead leaves or stem parts lying near the
ground. The basidia produce thin walled basidiospores; in turn they can produce secondary
basidiospores by repetition on germination. Several srains of the pathogen are known to
occur.
55

Disease Cycle: The pathogen survives in soil or on seed tubers as sclerotia. Sclerotia
germinate at an optimum temperature of 23C. The basidiospores germinate at optimum
temperature of 21-25C. The optimum temperature for infection is 18C. Soil moisture is
secondary to soil temperature for development of soil canker. Disease develops more in
sandy soil. The primary inoculum comes from soil or infected tubers and further spread is
through newly developed sclerotia.
Control: This is a polyphagus pathogen with a large host range. The pathogen can survive in
soil or on tubers for long time.The sanitation and seed treatment are therefore important to
control the pathogen. Soil treatment with PCNB 20-30 kg/ha or soil amendment with neem or
margose cake 25 quantal/ha or with saw dust at the same rate followed by the application of
120 kg nitrogen / ha at the time of planting are effective measures for black scurf control.
Resistant varieties should be grown.

4. Common Scab of Potato
The disease is widely distributed in cool and hilly places. The disease decreases the maket
value of tubers due to rough skin.
Symptoms: Superficial or deep seated lesions are formed on the skin of tubers. The areas of
lesions become rough and are raised over the skin. The lesions have darker corky tissues of
different shape and size. Sometimes the lesions join together covering the complete surface of
the skin.
Pathogen: The causal pathogen of the disease is a bacterium, Streptomyces scabies (Thaxter)
Waksman and Henrici. The spores are smooth walled and cylindrical measuring 0.8-1.0 x
1.2-1.5 in size.
Disease Cycle: The pathogen survives in soil and get distributed through movement of soil
by wind and cultural operations but main distribution is through contaminated seed tubers.
Infection occurs through newly formed unsuberized lenticels, stomata, wounds and may be
directly through the cuticle when skin is thin. The pathogen develops in dead cells and causes
the development of lesions. The pathogen is most active in dry soil, and hence the disease can
be suppressed by irrigation. Optimum infection takes place at 20-22
0
C.
Control: Use of healthy seed tubers, seed treatment with mercurial fungicides like agalol-6
and aretan etc. by dipping for 5 min in 0.25% solution are useful for elimination of disease.
Crop rotation, growing of legume crops before potato planting and application of 20-30 kg /
ha of PCNB (Brassicol) will reduce common scab.

5. Bacterial Brown Rot or Wilt Disease of Potato
The disease commonly occurs in tropical and sub-tropical regions. The disease is known to
occur in India for a long time and locally known as bangle or bangdi due to a brown ring
formation in infected tubers. The wilt disease pathogen also affects chilli, tomato, egg plant
and several wild hosts. It also affects other cultivated plants like caster, groundnut, banana
and ginger.
Symptoms: Diagnostic symptoms are wilting, stunting and yellowing of plants and browning
of xylem. A brown ring is formed within tuber due to discoloration of vascular bundles. In
severe cases, eye buds become black and if infected tubers are cut, grayish white bacterial
ooze comes out of the vascular bundles.
Pathogen: The disease is caused by a bacterium, Pseudomonas solanacearum (Smith) Smith.
The bacterium is rod- shaped, motile and gram-negative type.
56

Disease Cycle: The pathogen survives in soil, infected tubers and alternate cultivated and
wild hosts. Soil is a potential source of primary inoculum. Infected and surface contaminated
potato tubers also serve the source of primary inoculum. The pathogen invades the potato by
way of stolons and also spread by contaminated knife while cutting tubers for sowing. In
Nilgiri hills the bacterium may survive on potato crop grown throughout the year.
Control: Use of healthy seed tubers, treatment of seed tubers with streptocycline (0.02%) for
30 min after giving 5mm deep cut, sanitation and crop rotation are the general precautions
recommended against the disease.
6. Virus Diseases of Potato
Potato is host of several groups of viruses viz; tobamoviruses, potyviruses, tymoviruses,
potexvirus, nepoviruses, luteoviruses, carlaviruses, mop top furovirsuses, potato-T virus,
potato yellow dwarf, nucleorhabdoviruses, potato yellow mosaic bigeminivirus and several
others. In India, two diseases, potato virus Y and leaf roll are of common occurrence and
damaging in potato crop. Recently, a geminivirus which appears to be a strain of tomato leaf
curl geminivirus has been found in an alarming proportion in potato varieties.

7. Potato Y Virus (PVY)
The disease caused by PVY show mild to severe mottling, or streaks with veinal necrosis on
leaves of infected potato plants. However, severity of the disease depends on the cultivar and
the strain of the virus. PVY infects large number of plant species naturally such as tomato
and Nicotiana spp. Plant species in nine families were found susceptible under experimental
conditions.
Pathogen: The potatovirus Y pathogen belongs to family potyviridae. The virus particles
(virions) are filamentous and flexuous with a modal length of 684-730 nm and 11 nm wide.
Virions contain 5.4-6.4 % nucleic acid. The genome is single stranded (ssRNA), linear and
unipartite. The virus is transmitted by several aphid vectors and Myzus persicae is the most
efficient vector which transmits the virus in a non-persistent way. The virus is also
transmitted by mechnical inoculations and also by grafting.
Disease Cycle: Potato plants as ground keepers are reservoir host of PVY. The pathogen
also survives on several solanaceous hosts, thus the inoculum remains throughout the year on
one crop or the other and also on weed hosts. The pathogen from the reservoirs reaches to
potato crop by aphid vectors.
Control: Growing potato crop in aphid free period which is from October to mid-J anuary in
Northern plains of India Destroying haulms of seed potato crop in J anuary when aphid
population starts to build in. A technique known as seed plot technique should be strictly
followed for raising seed potato. Use of certified seed and growing of resistant varieties are
very important to manage the virus.

8. Potato Leaf Roll Virus (PLRV)
Symptoms: Reddening of leaf margins and tips of leaves, leaf rolling, usually leaflets rolled
upwards and starts from lower and oldest leaves are the major symptoms of the disease on
leaves of potato caused by PLRV (Fig.26). Affected plants remain stunted and yield of tubers
is greatly reduced. Tomato and some solanaceous plants are natural hosts of PLRV.
Experimental host range is wide.
Pathogen: Potato leaf roll virus is the causal pathogen and belongs to luteovirus group. The
virions are isometric, 24 nm in diameter and have 30 % nucleic acid and 70 % proteins. The
57

genome is ssRNA, linear and unipartite. The most efficient and impotant vector of PLRV is
Myzus persicae which transmits the virus in persistent manner. The virus is also transmitted
by grafting.








Fig.26. Potato leaf roll disease
Disease Cycle: The primary inoculum comes through infected tubers used as seed and also
from natural hosts. Further spread of the PLRV takes place by insect vector.
Control: The control measures are same as mentioned for potato virus Y. Since the virus is
transmitted in persistent manner, use of insecticides to control the vector population may be
effective especially in seed crop.

Diseases of Tomato
1. Early Blight of Tomato
This is common disease of tomato occurring all over India and other tomato growing
countries. The disease is caused by the fungus Alternaria solani ( Ell.& Mart.) J ones &Grout.
The pathogen attacks the foliage causing characteristic leaf spots and blight. The disease
symptoms, life cycle and control measures are given under early blight of potato.

2. Wilt of Tomato
The disease is found throughout the world and is serious where tomato crop is grown in the
same field continuously.
Symptoms: Clearing of the leaf veins and chlorosis are the initial symptoms of the disease.
Petioles and leaves of affected plants droop and wilt (Fig. 27). In severe cases black
discoloration of vascular tissues can be seen if the roots and stem are split open.
Pathogen: Fusarium oxysporum f. lycopersici (Sacc.) Snyder & Hansen is the causal
pathogen of the disease.The pathogen belongs to family Tuberculariaceae, order Moniliales
and sub-division Deuteromycotina. The pathogen hyphae are found in the vascular tissues
and are inter and intracellular. The pathogen produces both macro and microconidia.
Disease Cycle: The pathogen remains saprophytically in soil and attack the root region when
crop is planted in field or plants are raised in nurseries. After the infection the pathogen
moves upwards and multiply rapidly in vascular bundles causing interference with upward
movement of the nutrients which causes wilting of plants. Probably factors like plugging of
vascular tissues, action of phytotoxins and pectic and cellulotic enzymes acting together
cause the wilting of plants.

58









Fig.27. Wilt of Tomato caused by Fig .28. Late blight of Tomato
Fusarium oxysporum F.lycopersici
Control: Since the pathogen is soil borne, control is difficult. The best control of the disease
is to grow exotic varieties such as Rutgers, Kanora and Roma etc. which have been reported
to have resistance.
3. Late Blight of Tomato
The disease is caused by Phytophthora infestance (Mont.) de Bary. The disease occurs in
some parts of North India particularly in hills and also in Karnataka state. The symptoms are
same as has been described under late blight of potato (Fig. 28). Some species of Solanum
and Lycopersicon are the collateral host of the pathogen. Certain species and varieties of
tomato are resistant to late blight. The disease is controlled by timely spraying of fungicides
such as zineb, nabam, maneb etc.

4. Root Knot Disease of Tomato and Brinjal
Root knot disease is found in most of the countries on various vegetable crops such as potato,
tomato, brinjal, chili, okra, bhendi, cucurbit etc. The losses caused by this disease are from
20-75 % in tomato and 17-81 % in brinjal.
Symptoms: The affected tomato and brinjal plants show unthrifty development and stunted
growth if the infection occurs during early stages of plant growth. Leaves become yellowish
green to yellow and sometimes show scorching along the margins. The roots show galls of
various sizes and shapes (Fig.29). Presence of root galls is the most characteristic symptom of
the disease.
Pathogen: The disease is caused by the nematode pathogens of the genus Meloidogyne. The
common species are M. incognita, M. javanica, M. arenaria which commonly attack tomato
and other vegetables. The male nematodes are vermiform and 1.2 to 1.5 mm x 30-36m in
size. The females are pear shaped and measure 0.15 0.25 mm wide at the base. Upto 600
eggs are laid by each female.
Disease Cycle: A large number of females are found in the root galls which survive in the
soil on plant debris. The second stage larvae are liberated in the soil. Sandy light soil is best
for their movement. These larvae can be killed at higher temperature of 40-50 C and excess
of soil moisture. The larvae are attracted by root exudates and thus come in contact of the
roots. They gathered in a mass around roots and cause infection by penetrating roots of
healthy plants. The male and female nematodes develop depending on the number of larvae
per unit area of the host tissues. If they are more crowded mostly male develops but if only
few larvae are there then females will develop. The reproduction is mostly parthenogenetic.
A temperature of 25-28 C is best for infection and gall formation by nematodes.
59








Fig.29. Root galls caused by root-knot nematode (Meloidogyne spp.)
Control: Cultural practices such as crop rotation, fallow soil, sanitation, deep ploughing
during summer, soil solarization and flooding of soil are important to avoid infection by the
nematodes. The organic soil amendment such as addition of neem cake, karanje cake @ 25
quantals / ha reduced the root knot incidence. The use of soil fumigation with nematocides is
the best method of control but these chemicals are highly toxic and expensive. Resistant
varieties such as SL-120, Nimetex, Y-220, PAU-1(7-3-1-4), Hissar Lalit etc. for tomato and
Vijay, black beauty, T-3, S-149 etc. for brinjal should be used. Transgenic plants and
biological control are promising and may be exploited for nematode control in future.

5. Damping Off of Tomato, Tobacco and Crucifer Vegetables
Damping off is a common disease of nurseries of tomato, tobacco and vegetables. The
disease is found world wide.
Symptoms: The young seedlings are killed before they emerge or the seeds failed to
germinate. Young seedlings can be attacked at any time during germination. The infection
spreads very fast killing the invaded tissues resulting death of seedlings. This is known as
pre-emergence damping off. Next is the post emergence phase in which seedling can be
killed at any time of their growth till the stem becomes hard enough to resist invasion.
Usually roots or stem at or below ground level are attacked. Infected tissues become water
soaked. The infection spreads and basal part of the stem become thinner than rest of the stem
and fall down on the ground. The infection in seedlings continues till they are completely
dead. The disease usually radiates from the point of infection to nearby plants and dead
seedlings can be seen in large areas of nursery beds.
Pathogen: The damping off is caused by several fungal pathogens but most common are
Pythium spp.such as P. debaryanum Hesse, P. aphanidermatum (Eds.) Fitz., P. ultimum Trow
and P. arrhenomanes Drechsler. Several othe fungi and bacteria can also cause similar
symptoms such Phytophthora, Sclerotinia, Fusarium, Rhizoctonia etc.
Pythium produces white mycelium on which sporangia are developed. The sporangia either
germinate directly by germ tube or by producing a balloon like secondary sporangium known
as vesicle. In this vesicle over 100 zoospores are formed and they swim after their release and
then rounded off to form a cyst. The zoospores create new infection after germination. The
sexual stage develops as oogonia and antheridia. The oogonium after fertilization develops
thick wall and known as oospore. The oospores can survive in adverse conditions and this is
the resting stage. The oospores germinate in the same way as sporangia.
Disease Cycle: The pathogen is soil borne. Spore germ tube directly penetrates the seed or
young seedlings when comes in contact. Proteolytic enzymes break the protoplast and in
some cases the cell wall is disintegrated by cellulolytic enzymes causing death of seeds or
60

young seedlings. The disease is more serious in poorly aerated and poorly drained soil. As the
infection progresses the sporangia begin to appear, followed by sexual spores inside or
outside of host tissues. The movement of infection is very fast and can quickly rot even the
fleshy vegetables or fruits in the field, in storage, in transit and even in market when healthy
and infected fruits come in contact.
Control: Sterilization of soil by steam or dry heat will control damping off in nurseries. Use
of seed protectants such as blitox-50 (soaking seeds in 0.20 % solution) for tobacco seeds,
Agrosan-GN or agrosan (seed dressing @ 0.3% by seed weight) for tomato seeds and
mercuric chloride (1: 1000 solution dipping for 5 min.) for cucumber seeds is important for
disease control. Soil treatment of nurseries by formalin ( 1 : 50) drenching or spraying several
days before nursery planting is important. Nursery beds should be raised with light soil
having good proportion of sand with high nitrogen dose. The seeds should be sown thin and
only light irrigation at frequent intervals shoud be given. Spraying of seedlings with
fungicides like metalaxil, captan etc. would be required if soil is heavily infested with the
fungus and was wet for long time.
6. Virus Diseases of Tomato
Tomato plants are susceptible by large number of virus diseases such as leaf curl, black ring,
bushy stunt, golden mosaic, mild mottle, mosaics, yellow leaf curl etc. Tomato spotted wilt,
mosaic, leaf curl and a cucumovirus are important for India.
(i)Tomato Yellow Leaf Curl
Symptoms: The affected tomato plants remain stunted with chlorotic and puckered leaves.
Curling of leaves with bright yellow colour is the characteristic symptoms of the disease.
Pathogen: The causal virus is a geminivirus and belongs to family geminiviridae. The virons
are geminate, 20 nm in diameter and 30 nm. In length.The genome is single stranded DNA,
circular and distributed in both the particles. Virions are found in phloem. The virus is
transmitted by an insect vector, Bemisia tabaci, a whitefly in a persistent manner. The virus is
also transmitted mechanically and by grafting. Several plant species in family solanaceae,
leguminoceae and malvaceae are susceptible to virus infection.
Disease Cycle: The disease spreads through white fly vector when the crops are overlapping
or from symptomless plants like Malva parviflora.
Control: Control of white fly vector by safe chemicals or to grow crop in vector-free period
are the only preventive measures at present.
(ii)Tomato Indian Leaf Curl
The disease is present in tomato throughout India and is a major threat to tomato production.
Symptoms: Affected plants remain stunted, with small chlorotic puckered leaves (Fig.30).
Affected plants look bushy in the field and hardly bear any fruit. The mild or severe
symptoms of the disease depend on the variety and strainof the causal virus.
Pathogen: The causal virus is a geminivirus and belongs to family geminiviridae. The virus
has large number of hosts in several plant families. The virions are geminate (Fig 30), 20 x 30
nm in size. The particles are found in phloem parenchyma and in nuclei. The genome of the
virus is single stranded DNA, circular and in two parts known as DNA-A and DNA-B. The
virus is transmitted by white fly, Bemisia tabaci in a persistent manner.
Disease Cycle: Both virus and its vector have very wide host range. The inoculum is present
throughout the year either on cultivated crops or on weeds. The virus is not seed borne. The
inoculum already present on other hosts is brought to the new crop by insect vector
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Control: Control of vector by insecticides, trap plants and yellow mulches and use of less
susceptible varieties are the only management practices at present.







Fig.30. Tomato leaf curl and Gemini virus particles associated with the disease
(iii) Tomato Spotted Wilt
Tomato spotted wilt virus has been reported from most of the countries infecting one crop or
another. The virus has been reported on potato, sunflower, groundnut, tobacco etc. In India,
the virus is known to infect sunflower, groundnut and several plants of family leguminoceae.
However, there is no authentic report on tomato.
Symptoms: Necrotic or chlorotic local lesions, systemic wilting, necrotic spotting, streaking,
mosaic, mottling, malformation of leaves, vein yellowing, ringspots, line patterns and colour
breaking of flowers are the variety of symptoms found on various hosts.
Pathogen: The causal virus is tomato spotted wilt virus which belongs to Tospovirus group
in family Bunyaviridae. The virus is transmitted by several species of Thrips and
Frankliniella. T. tabaci is the major vector and the virus is transmitted in a persistent manner.
The virus multiplies in vector and has a transovarial transmission. It is also transmitted
mechanically and by grafting.
The virus particles are isometric, enveloped, 85 nm in diameter. Virions contain 5% nucleic
acid, 70% protein and 20% lipid and 5% carbohydrate. The genome of the virus is ssRNA.
The virions are distributed in all parts of infected plants.
Disease Cycle: The inoculum survives throughout the year on one host or the other from
where it reaches the healthy plants by thrip vector. The inoculum is also present in thrips and
they can infect the plant without fresh acquisition on infected plants.
Control: Control of insect vectors and development of virus resistant transgenics are the
main methods to control tomato spotted wilt virus.
(iv)Tomato Mosaic
The disease has a very wide host range and is found throughout the world.
Symptoms: Systemic leaf mosaic with leaf narrowing are the main symptoms of the mosaic
disease.
Pathogen: The causal virus is tomato mosaic virus which belongs to tobamovirus group.The
virus particle are rod shaped, usually straight with a modal length of 300 nm and width 18
nm. Virions contain 5% nucleic acid and 95% protein. The genome is unipartite and is
ssRNA. The virus does not have a vector but is transmitted by mechanical inoculations,
grafting, and by contact of diseased and healthy plants. It is transmitted externally seed
infection.
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Disease Cycle: The primary inoculum comes via seed and then spread by contact. Infection
normally occurs during transplanting.
Control: Seed treatment with sodium hypochloride or any other chemical to remove external
inoculum from seed and use of resistant cultivars are the only measures to manage the
disease.
(v)Cucumovirus Infecting Tomato
Symptoms: Severe leaf malformation, leaf mottling, leaf reduction sometimes showing shoe
sting symptoms (Fig.31),dwarfing and malformed fruits are the main symptoms of the virus
on tomato.
Pathogen: The cucumovirus is a member of family Bromoviridae and has a very wide host
range. Virions are isometric (Fig.31), 29nm in diameter. The genome is ssRNA divided in
several parts. There is non-genomic nucleic acid in the virions known as satellite RNA. The
virus is transmitted by several species of aphids including Myzus persicae in a non-persistent
manner. It is also transmitted by mechanical inoculations and in seeds of a weed, Stellaria
media.







Fig. 31: Cucumo virus infected tomato plants
Disease Cycle: The virus spreads in healthy crop by the aphid vectors from the inoculum
present either on crop plants or in weed host.
Control: Control of aphid vectors and use of virus resistant transgenic plants are the options
to manage the disease.

Diseases of Brinjal
1. Phomosis Blight, Leaf Spot and Fruit Rot
The disease was first reported from Gujarat in 1914 and later to other parts of India. The
causal pathogen causes seedling blight, leaf spots and fruit rot.
Symptoms: The nursery plants show damping off when plants are infected at seedling stage.
Infected leaves show circular spots of cinnamon-buff colour with irregular blackish margin.
Lesions may also develop on petioles and stem. The affected portion of the plant is blighted.
On fruits, minute, sunken, dull and dusky spots appear first which coalesce later converting in
rotten areas. Severely affected fruits show rotting of the entire flesh.
Pathogen: The disease is caused by Phomosis vexans. Numerous pycnidia are developed on
the affected portion of the fruit coat. The fungus is specific pathogen of brinjal.

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Disease Cycle: The pathogen survives in soil on affected plant debris and also externally
seed-borne. When the seeds or seedling are planted in infested soil, the organism become
active and infects the plants.

Control: Field sanitation and seed treatment with fungicides are important control measures.
Treating the seeds with 0.1% mercuric chloride or other organomercuric fungicides can
eliminate fungal infection. In nurseries and fields, spraying with 1% Bordeaux mixture helps
in protecting plants from infection.

2. Bacterial Blight of Brinjal
The disease is found only in tropical and sub-tropical regions. In India, the disease has been
reported from West Bengal. The pathogen also attacks several solanaceous crops such as
potato, tomato and chillies and other cultivated plants which include castor, groundnut,
banana, ginger and many wild plants. The disease is often associated with nematode
infestation.
Symptoms: The most characteristic symptoms are wilting and stunting. The stem at the base
becomes dark brown and constrict leading to wilting of plants.Sudden wilting and drooping
of leaves occur when the infection is severe.
Pathogen: The disease is caused by the bacterium, Pseudomonas solanacearum (Smith)
Smith. Three races of the pathogen have been reported and race-1 causes infection to
solanaceous plants. Details of the pathogen have been mentioned under Bacterial wilt of
potato.
Disease Cycle: The pathogen survives in soil or on alternate or cultivated or wild hosts. Soil
is a potential source of primary infection. The disease destroys tomato, brinjal and chilli crops
every year.
Control: Okra-cowpea-maize rotation reduces the infection by the bacterium. Foliar
application of agrimycin-100, chloramphenicol, or streptomycin sulphate are effective at
100ppm but prior to infection.Rain or irrigation water should not be allowed to flow from
diseased to healthy fields.

Diseases of Chilli
1. Anthracnose of Chilli
This is one of the worst diseases of chilli found in several countries including India.
Symptoms: Symptoms of the disease mostly appear on ripened fruits, hence the disease is
also called ripe fruit rot. Usually circular and sunken spots with black margin appear on fruits
(Fig.32). These spots enlarge and form concentric markings with dark fructifications
representing the fungus acervuli. The fruits with many spots drop off prematurely. The
fungus can also attack fruit stalk and stem causing die-back symptoms.
Pathogen: The causal pathogen is Colletotrichum capsici (Syd.) Butl. & Bisby. The
pathogen belongs to family Melanconiaceae, order Melanconiales and sub-division
Deuteromycotina. The pathogen remains localized on fruit surface and produce acervuli. The
acervuli have hymenial layer with short conidiophores which bear conidia. The conidia are
hyaline and falcate and measure 11-24 x 4-5.5 and contain oil globules. The conidia cause
infection upon germination.
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Disease Cycle: The pathogen is externally seed borne which is the potential source of
primary inoculum. Secondary spread is through conidia which are disseminated by splashing
rain.
Control: Seed treatment with organomercuriales and foliar sprays with copper fungicides at
fortnightly intervals starting from the time of first infection are the best control measures to
contain the disease.







Fig .32 Anthracnose disease of Chilli Fig.33 Mosaic disease of Chilli

2. Mosaic Disease of Chilli
Symptoms: The leaves of affected plants show systemic dark green to yellow mosaic or
mottling with or without deformation of leaves, stunting and extremely deformed
(Fig.33).The affected plants developed only a few deformed fruits.
Pathogen: The associated pathogens are two different viruses. The filamentous particles
belong to potato virus Y and the spherical ones to cucumber mosaic virus. The virus (es) are
transmitted mechanically and also by aphid vectors and infect Capsicum annum, C.
fruitescens, Nicotiana tabacum, N. glutinosa, mustard and radish etc. causing variable
symptoms. The details of pathogens have been described under potato virus Y and cucumber
mosaic diseases.
Disease Cycle: The inoculum of pathogens remain throughout the year on overlapping crops
and on various hosts from where the viruses infect new crop plants by insect vectors
Control: Best control is use of resistant cultivars and control of insect vectors. Application of
NPK reduced the incidence of the disease. However, maximum disease reduction was
obtained with the application of DAP +MOP +rogor. Early planting and growing nurseries
under insect free conditions are also helpful.
3. Virus Diseases of Chilli
In India, the most important disease of chilli caused by virus is yellow mosaic disease which
causes a yield loss of 65-75%. It is a complex disease and eight viruses have been identified
to be associated with the disease in Karnataka and four in Punjab. The most common ones are
potato virus Y, pepper vein banding virus, pepper veinal mottle virus, tobacco etch virus,
tobacco mosaic virus, tobacco leaf curl virus and cucumber mosaic virus. Among them potato
virus Y and cucumber mosaic virus are of common occurrence and cause mosaic disease
either in combination or singly. Sometimes leaf curl caused by geminivirus also appears in
severe form. This has been described under tomato leaf curl disease.



65

Diseases of Vegetable Crucufers
1. Black Rot of Crucifers
The disease is found throughout the world and most members of crucifer family are sceptible
to black rot.
Symptoms: Infected young seedlings show dwarfing, one sided growth and their leaves
droop. In the field, leaves of affected plants show V- shaped chlorotic blotches at leaf
margins which move towards the mid-ribs of the leaves turning the veins black within
chlorotic areas. This blackening advances towards the stem from where it moves upwards and
downwards to other leaves and shoots. Infected leaves may fall prematurely one after the
other. In cross sections of stem and petioles, vascular tissues show blackening and slime
deposits having bacterial population. Cauliflower and cabbage heads, fleshy roots of turnip
and radish are also affected and become discoloured. Invaded tissues may be attacked by soft
rot bacteria giving repulsive odor.
Pathogen: The bacterium Xanthomonas campestris pv. Campestris is the causal pathogen.
Disease Cycle: The pathogen survives on plant debris and on or in the seed. When the crop is
sown, the bacteria infect the cotyledons or young leaves through stomata, hydathodes, and
wound. The bacteria then move intercelullularly and finally reach the open ends of vessels.
The pathogen multiplies in the vessels and spread throughout the plant reaching upto the
seed. The xylem disintegrates at places and bacteria spread to neighbouring parenchyma cells
and kill them. The pathogen spread by splashing rains, winds and farm equipments to other
leaves and infect them.
Control: Use of pathogen-free seeds, seed treatment with hot water (50C for 30 min) and
tetracycline or streptomycin will eliminate bacteria from seed. Sprays with copper fungicides
at 10 days intervals help in reducing the disease incidence.
2. Downy Mildew of Crucifers
Downy mildew is common on cruciferous plants when young and cause significant damage.
During late infection, it infects to influorescence and cause sterility.
Symptoms: The symptoms appear as purplish brown spots on the lower side of leaves.
Above these lesions on upper surface of leaf tan to yellow patches can be seen. The cottony
growth of the mycelium can be seen on lower side of leaves. On the stem, deformities as
swellings appear which may be small to several inches long. The young ovary becomes
elongated and twisted. Often, the floral buds show atrophy and sepals, petals and stamens
shrink.
Pathogen: The fungus, Peronospora parasitica (Pers.) ex Fr. is the causal pathogen.
However, the pathogen occurring on Brassica campestris has been named as P. brassicae by
Gaumann. The pathogen is an obligate parasite. Numerous erect and branched conidiophores
are developed from intercellular mycelium and emerge out through the stomata on the
underside of the leaves. The conidiophores have dichotomous branching six to eight times on
their tips. A single conidium is developed at the tip of each branch. The conidia readily fall
off and germinate by germ tube. Oospores are formed in the floral organs late in the season.
Disease Cycle: The pathogen survives in soil as oospores. Seeds also carry oospores through
contaminating trash. Wild hosts can also serve as the source of primary inoculum. Secondary
spread of the disease is through conidia.
Control: Crop rotation avoiding cruciferous plants, deep ploughing during summer, and
eradication of weed hosts are important cultural practices. Spraying fungicides like Dithane
Z- 78 (0.3%), Dithane M-45 (0.1-0.3%) Ridomil (0.1%) etc. are recommended to control the
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disease. Resistant varieties should be grown. Mustard varieties YRT-3 and TMV-2 and
yellow sarson type-6 are resistant to the fungus.

Diseases of Cucurbits
1. Fusarium Wilt of Cucurbits
This is an important disease of cucurbits and found throughout the world and several species
of Fusarium are known to cause the diseases in plants of family cucurbitaceae.
Symptoms: In young seedlings, cotyledons are dropped and weather due to wilt disease.
Older plants wilt suddenly and vascular bundles at the collar region show brown
discoloration.
Pathogen: The fungus, Fusaium oxysporum Schl. is the causal pathogen. The pathogen
belongs to family Tuberculariaceae, order Moniliales and sub-division Deuteromycotina. The
pathogen produces both macro and microconidia. The conidia germinate and produce hyphae
and mycelium.
Disease Cycle: This wilt is a soil borne disease. Inoculum increases more rapidly in sandy
soils than in clay, silty or loam. The inoculum can reach to high level after just two
successive crops. The fungus available in soil penetrates the root system through injury. After
infection the fungus multiplies and moves to xylem vessels which are later plugged by the
pathogen mycelium. The blocking of xylem vessels intrupts the movement of nutrients
resulting wilting of plants.
Control: Crop rotation with resistant crops to fungus is viable methods of overcoming the
disease. Soil drenching with fungicides like carbendazim etc. can reduce the inoculum. Soil
solarization for 2-4 weeks by using impermeable plastics after amending the soil with
ammonium sulphate is a good method to control the disease. Growing resistant varieties is
the best method.
2. Downy Mildew of Cucurbits
This is an important disease of vegetable cucurbits such as sponge gourd, ridge gourd, bottle
gourd, bitter gourd, snake gourd, pumpkin and cucumber etc.
Symptoms: Leaves first show mosaic like mottling. The pale green areas are separated by
dark green islands. Soon the angular yellow coloured spots restricted along veins develop on
the upper surface of leaves. Below the spots on the lower side of leaf purplish downy growth
appears. The affected leaves die quickly. Usually middle leaves are infected first followed by
other leaves. Only a few small fruits with poor taste develop on diseased plants.
Pathogen: The fungus Pseudoperonospora cubensis (Berkeley & Curtis) Tostowzew is the
causal pathogen. The pathogen is an obligate parasite. The sporangiophores in a group of 1-5
arise from the intercellular mycelium. Sporangia develop on the branches of sporangiophores
usually during night and are dispersed during morning hours. The sporangia produce
zoospores upon germination which cause the infection to plants. Oospore formation is not
common in this species of fungus but has been reported from Madhya Pradesh, Punjab and
Rajasthan.
Disease Cycle: The pathogen infects large number of wild hosts from where the primary
inoculum comes to cultivated crops. In areas where oospores are formed, the primary
infection may be through them. The disease in the field spread through sporangia which are
disseminated by splashing rains and beetles.
67

Control: Spraying of fungicides, zineb, mancozeb and tricop-50 has been recommended to
control the disease. Removal of infected vines and eradication of wild cucurbits from near the
vegetable growing areas are economic control measures in view of the cash value of the crop.
3. Powdery Mildew of Cucurbits
This is a serious disease of cucurbits especially on pumpkins and bottle gourd.
Symptoms: White to dirty grey powdery spots appears on leaves and stem. These spots
enlarge in size and can cover the whole surface of the host. Leaves are fall down during
severe infection. Fruits on affected plants are smaller in size. Humid condition favours the
fast development of disease.
Pathogen: Two fungi, Erysiphe cichoracearum D.C. and Sphaerotheca fuliginea (Schlecht.)
Poll. have been reported as pathogens of powdery mildew of cucurbits.
The size of conidia of E. cichoracearum varied according to physiologic races and
Cleistothecia are not common. The number of ascospores is usually two, rarely three in each
ascus.
S. fuliginea is known to cause powdery mildew of cucurbits in India. The perithecia are
formed from September to February and each perithecium has one ascus.
Disease Cycle: Perithecia develop on left over cucurbits in isolated areas may serve as a
source of primary inoculum. The conidia from wild cucurbits may be another source of
primary inoculum. The conidia are dispersed by wind or insects and infect the plant through
epidermal cells of the host.
Control: Field sanitation and dusting with 200-mesh sulphur @ 25-30 kg / ha is quite
effective to control the disease. Sprays with other fungicides like calexin (0.1 or 0.05 %),
copper sulphate and karathane are also effective. Resistant varieties of each crop should be
grown.
4. Cucumber Mosaic
The disease is world-wide in distribution. Naturally the disease occurs in cucumber and many
cucurbits, tomato and spinach.
Symptoms: The leaves of affected plants show mosaic, severe chlorosis, green blisters and
reduction and narrowing of leaves (Fig. 34). The plants remain stunted and bear deformed
fruits.






Fig.34. Cucumber mosaic disease symptoms and virus particles associated with this disease.
Pathogen: The disease is caused by a virus of cucumovirus group in the family
Bromoviridae. The virus particles are isometric, 29 mm in diameter. Genome of the virus is
single stranded RNA and consists of 18% RNA and 82% protein. The virus is transmitted by
large number of aphid species such as Myzus persicae, Aphis craccivora etc. in a
nonpersistent way. It is transmitted through seeds of 19 plant species.
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Disease Cycle: The virus inoculum is present throughout the year on one crop or the other or
on weeds from where it is brought to new crop by insect vectors. Contaminated seed is
another source of primary inoculum.
Control: Control of cucumber mosaic virus is difficult. However, virus resistant cultivars or
transgenic plants can give protection from the virus. Growing cucumber in polyhouses is
advantageous as the crop remain free from virus resulting in more yield and quality of fruits.


Diseases of Pea
1. Powdery Mildew of Peas
The disease is of world-wide occurrence on pea. Usually the disease appear late in the season
during the pods formation.
Symptoms: The disease symptoms appear on leaves as white powdery patches but soon other
parts of the plant such as stem, pods etc. also show the symptoms. At advanced stages all
aerial parts of the plant are covered with white powder. The white powder consists of the
fungus mycelium and spores. Necrosis of epidermal cells is common.
Pathogen: The disease is caused by a pathogen, Erysiphe polygoni D.C. =E. pisi D.C. This
fungal pathogen is an obligate parasite. The fungal mycelium is ectophytic. The
conidiophores develop from the superficial hyphae and each conidiophore bears several
spores in chain. The mature conidia are dispersed by wind. The conidia are elliptical, barrel-
shaped and measure 25-35 x 13-16 in size. Late in the season black coloured sexual spores,
the Cleistothecia are formed. Each cleistothecium contains 2-8 asci and each ascus has 3-8
ascospores. The Cleistothecia are also formed on plant debris left in the soil.
Disease Cycle: The Cleistothecia persist in the soil till next season of the crop. Under
favourable conditions, the cleistothecial wall disintegrates and ascospores are released. The
ascospores first infect the lower most leaves near the soil of the new crop. Once the infection
is established, secondary spread takes place by the conidia. Available information on survival
of the fungus suggests that the fungal mycelium may also survive in the pea seeds.
Control: Field sanitation, early sowing, seed disinfection by hot water treatment or seed
dresser fungicides are precautionary measures to avoid infection. Chemical control using 200
mesh sulphur dust @ 25-30 kg / ha, o.1% bavistin, 0.2-0.25% kerathane etc. is effective. Use
of resistant varieties like T-10, T-56, P-185, P-383, NDVP-4, Arka Ajit, DP-53, DMR-9,
Pusa Panna etc. is the best method of control.
2. Rust of Peas
Two species of Uromyces occur on cultivated pea I. Uromyces pisi (Pers.) Wint. Which are
heteroceous rust having its aecial stage on Euphorbia cyparissias L. II. Uromyces fabae
(Pers.) de Bary is autoceous rust and occurring on pea and lentil in India. U. pisi is not
common in India.
Symptoms: Small, oval and light to brown coloured pustules develop on both sides of leaves.
The pustules slowly cover the whole surface of leaves. Affected leaves wither and fall off
prematurely. The pustules on the leaves contain uredosori. The dark brown teliosori are
developed both on leaves and stem near maturation of the crop. The aecia and pycnidia also
develop on pea. The morphological characters of aecia and pycnia are similar to Puccinia
graminis tritici except in size and colour etc.
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Pathogen: The causal pathogen is a fungus, Uromyces fabae (Pers.) de Bary which belongs
to family Pucciniaceae, order Uredinales and sub-division Basidiomycotina.
The pathogen produces aecia on stem and petioles which are mixed with spermagonia. The
aeciospores are elliptical and yellow brown in colour measuring 14-22 in diameter. The
uredial stage is repeated several times during crop season. Urediospores are spiny, light
brown, elliptical and measure 2030 x 1826. The teliospores are thick walled and measure
25-38 x 18-27. They are single celled, ovate and pedicillate and produce four celled basidia
upon germination.
Disease Cycle: The pathogen completes its life cycle on pea but other hosts such as
broadbean, lentil, sweet pea, and lathyrus also carry infection as uredial and telial stages of
the fungus and can serve as a source of primary inoculum to pea crop. Further spead of the
disease takes place by means of uredospores.
Control: Economic control of this disease is difficult except to use resistant varieties,

Diseases of Beans
1. Bean Blight
The desease is known to occur in several countries including India.
Symptoms: First symptoms appear as small circular spots with dark green centre surrounded
by reddish margin. The spots coalesce and form large necrotic patches and cause blightening.
The fruiting bodies, pycnidia of the fungus appear in large numbers in the form of small, light
brown, pin head-like bodies on the necrotic spots. Both young and old leaves are susceptible
to infection and severely affected plants are completely deformed. The spots also develop on
pods.
Pathogen: The disease was identified to be caused by the fungus, Foma jolyana Priozy and
Morg. The genera Phyllostricta, Phoma and Ascochyta are closely related. The pycnidia are
formed on leaves. Conidia are formed within pycnidia from inner cells. The conidia can
remain viable in pycnidium for long time.
Disease Cycle: The pathogens pycnidia survive in soil on plant debris and also on seed.
Mycelium may also survive on seed coat. The soil borne and seed borne inoculum acts as
primary source of infection. Further spread of the disease occur through conidia which are
disseminated by splash rains, insects or by contact of leaves.
Control: Removal and destruction of plant debris, seed treatment with thiram and captan and
four sprays of topsin-M (0.1%), or mancozeb (0.25%) at 10 days interval starting from the
onset of disease are very effective measures to control the disease. Use of resistant cultivars is
the best control.
2. Anthracnose of Beans
This is the major disease of beans in many parts of the world. In addition to beans, the disease
also affects cowpea and mungbean etc.
Symptoms: On cotyledons, dark brown, sunken spots appear first followed by necrosis of
veins and adjoining tissues of young leaves. Mature leaves show angular and brown coloured
lesions adjacent to veins. Similar spots with purple border develop on stem and pods. Mature
seeds from infected pods also show brown shades and seedlings develop from such seed
show typical lesions on cotyledons.
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Pathogen: The disease is caused by the pathogen, Colletotrichum lindemuthianum ( Sacc. &
Magn.) Scriber. The perfect stage of the pathogen is Glomerella lindemuthianum (Sacc. &
Magn.) Shear.The conidial stage develops on stromata beneath the cuticle. The cuticle is
ruptured and conidia are released. The conidia are formed singly on the stromatoid masses in
acervuli. The conidia form 1-4 germtube during their germination. The perfect stage has only
been reported in cultures.
Disease Cycle: The causal pathogen is soil and seed borne. In soil, it survives on disease
debris. In seeds, the pathogen survives till the seeds are viable.The primary inoculum usually
comes from seeds. The pathogen grows on cotyledons from where it spreads to other parts of
the plant. The spores are embaded in gelatinous mass and water is required for their release.
Usually they are washed down by rains or dew to stem or new leaves. Movement of insect or
wild animals or man also helps in dissemination. Cool and rainy weather is conductive for
epidemic of the disease.
Control: Use of disease-free seed, removal of plant debris, crop rotation, weed control,
enough spacing between plants are good cultural practices for disease control. Fungicides like
captan, zineb @ 2 kg / ha should be sprayed if the disease is severe. Vita vax and agrosan GN
have bben recommended for seed treatment.
3. Virus Diseases of Beans
Beans are affected by several virus diseases which are originally reported on them or they are
the host of viruses infecting other crops. The most damaging virus diseases in India are: bean
common mosaic, southern bean mosaic virus, urdbean leaf crinkle virus and mungbean
yellow mosaic virus.
(i)Bean Common Mosaic
Symptoms: The main symptoms are mosaic with vein banding, the dark green areas along
main leaf veins. Sometimes accompanied by leaf malformation such as curling or blisters on
leaves.
Pathogen: The causal virus has filamentous particles measuring 750 nm in length and
belongs to potyvirus group of viruses. The virus is transmitted non-persistently by several
aphid species but Aphid fabae and Myzus persicae are the major vectors. It is highly
transmitted through seeds of beans or other hosts like urdbean, mungbean etc. The virus
infects several legumes, tobacco and other plant species.
Disease Cycle: Primary inoculum comes through infected seeds or from nearby infected
crops. Further spread is through vectors.
Control: Use of virus-free seed and cultivation of resistant varieties are the effective control
measures.

(ii) Southern Bean Mosaic
Symptoms: Chlorotic spots, systemic vein clearing or vein banding, mosaic, leaf distortion
and stunting of affected plants are the main symptoms of the disease.
Pathogen: The causal virus particles are isometric, 28 nm in diameter and belong to
sobemovirus group. The particles contain 21 % nucleic acid and 79 % protein. The viral
genome is ssRNA. The virus is transmitted by beetles such as Epilachna variestis in
semipersistent manner. It is also transmitted by mechanical inoculation, grafting and by seed
and pollen.
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Disease Cycle: Primary inoculum comes through seeds or from other crops infected by the
virus through vector. Further spread of the pathogen takes place through beetle vector or by
pollen.
Control: Same as with bean common mosaic disease.
(iii)Urdbean Leaf Crincle Disease
Symptoms: Leaf rugocity, crinkling and distortion of leaves are the major symptoms. The
leaves on infected plants are bigger than normal and more vegetative growth was also seen in
some varieties. The disease also attacks mungbean, cowpea, pigeon pea and tepari bean.
Pathogen: The particles of the causal virus are isometric, 25-30 nm in diameter. Genome of
the virus is ssRNA and unipartite. The virus is transmitted by mechnical inoculations, by
beetles and via seeds.
Disease Cycle: Primary inoculum of the pathogen comes through infected seeds and further
spread is by beetle vector, Henosepilachna dodecastigma.
(iv) Mungbean Yellow Mosic
This is the most serious disease and is found on many legumes and weeds. There is almost a
total loss to yield of mung bean crop if it is infected at an early stage.
Symptoms: The symptoms of the disease as yellow spots on the leaves can be seen when the
crop is about one month old. The symptoms of the disease are so conspicuous that infected
plants can be identified from a distance. Severe yellow mosaic and mottling of leaves are the
major symptoms (Fig.35). The virus become systemic and all leaves of infected plants show
yellow mosaic. Number and size of the podes is greatly reduced. Seeds are smaller in size and
shriveled.
Pathogen: The causal virus is a geminivirus recently named as genus Begomovirus. The
virus is transmitted only by whitefly vector, Bemisia tabci and not by sap inoculations. The
Thailand strain of the virus is mechanically transmitted. The geminate particles measure 30
x18 nm and have ssDNA as their genome. The virus has a wide host range which includes
legumes and weeds.

100 nm









Fig.35: Mung bean yellow mosaic disease, its vector and virus particle
Disease Cycle: The primary inoculum comes from other infected legumes or weeds through
whitefly. Once the infection is established in the crop the disease spread very fast by whitefly
vector and cover the complete field within few weeks.
72

Control: The control of the disease is very difficult because both pathogen as well as vector
have wide host range. The only means of control is by the use of resistant cultivars. Urdbean
varieties T-9, UPU-1, Pat-19, 26, 30 and 35 are fairly resistant. In mungbean, Pant 1,2,3, T-1
and T-44 are resistant , In soybean, PK-416, 472, 1024, 1029, 1042, Pusa 37, SL-295, SL-525
etc. are resistant to yellow mosaic infection.

Diseases of Mango
1. Mango Malformation
The disease was recorded in India in 1910 and presently wide spread in North Indian states.
The disease is also found in Pakistan and Egypt.
Symptom: The dease appear in two phases, the vegetative malformation and floral
malformation. The vegetative phase is more common in young trees. The main symptoms are
excessive vegetative branches of limited growth, swollen and with short internodes and give a
look of rosette. In older trees, similar symptoms also develop but the growth of swollen
axillary buds do not impair but persist and crowded at nodes sometimes form girdle. All such
branches develop floral malformation. Malformed flowers are bigger than normal flowers and
only a few of them are hermaphrodite. Malformed panicles have more flowers but do not bear
fruits. Some light type panicles which are compact bear fruits. The bracts of malformed
flowers are larger and give a leafy appearance.
Pathogen: Several biotic and abiotic factors are reported to cause mango malformation such
as physiological disorder, Eryophyid mite and virus. It is now established that the disease is
caused by a fungal pathogen, Fusarium moniliforme var. subglutinans. Probably Eryophyid
mite acts as a vector of the Pathogen.
Disease Cycle: It has not been fully understood. Spread through vegetative propagation and
by unkown means from tree to tree is possible.
Control: Except pruning of twigs having malformed flowers no other control method is
known.

2. Powdery Mildew of Mango
This is one of the worst diseases of mango which affects almost all commercial varieties of
mango. The severity depends on climatic conditions. The low temperature of 18-20C and
relative humidity of 70-80 % favour the fast spread of the disease. The losses upto 70-80 %
may occur on individual trees when infection is severe.
Symptoms: The appearance of whitish to greyish powdery growth on tender leaves and
influorescence are the main symptoms of the disease. Most of the floral axis, tender leaves
and young twigs of a tree are infected as the disease progresses. Infected floral parts may
drop off prematurely. The axis becomes dry showing die-back symptoms. The fruit setting is
very poor and premature fruit drop is very common.
Pathogen: Oidium mangiferae Berth. is the causal pathogen of mango powdery mildew. The
mycelium is hyaline and produces conidiophores on which conidia are formed.
Disease Cycle: The pathogen spreads from tree to tree by conidia. The pathogen survives in
soil as Cleistothecia on infected plant debris and ascospores attack the lower most leaves.
Further spread takes place by conidia.
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Control: The disease is controlled by giving two preventive sprays of wettable sulphur once
before the flowers open and second after the fruit set. Dusting with 200 mesh sulphur powder
can also check the disease. Orchard sanitation is important to avoid infection.
3. Bacterial Blight of Mango
The disease is known to occur in India and a similar disease was reported from South Africa.
Symptoms: Initially small, water soaked lesions develop on leaf blade.The lesions start from
the leaf tip and slowly cover most of the leaf surface, petioles, fruits and tender stem. The
lesions are rough and slightly raised due to heavy exudates of the bacteria. Most of the
infected leaves are drop down. On fruits, the lesions are first water soaked and later turn
black.The fruit skin may be cracked and badly affected fruits are dropped.
Pathogen: The causal bacterium is Xanthomonas campestris pv. Mangiferaeindicae (Patel et.
al., Robbs et al.).The bacterium is rod shaped measuring 0.36 0..54 x 0.45-1.44 in size.
The bacterium is gram-negative and has a single polar flagellum. The bacterial cells are either
single or in chaines and are motile.
Disease Cycle: The blight bacterium is a phyllopane and remains in the orchard throughout
the year. It infects the new trees through injury mostly caused by insect feeding such as
weevils, bugs and leaf Webbers. These insects also carry the bacterial cells on their legs and
mouth parts and thus transmit the pathogen mechanically.
Control: Seedling certification, inspection and orchard sanitation are important measures to
contain the disease. Three sprays of streptocycline (100 ppm) or agrimycin-100 (3000 ppm)
should be sprayed after first visual symptoms at 10 days interval. Monthly sprays of bavistin
(1000 ppm) or copper oxychloride (3000 ppm) were also found effective.

Diseases of Apple
1. Apple Scab
This is the most serious disease of apple throughout the world where apple is grown. The
disease was first reported from Sweden as early as 1819. In India, the disease was first
reported from Kashmir velley in 1935 on a popular variety of apple Ambri. Since then it
has been found in most groves of apple in the country. The losses caused by the disease had
been very heavy and are both types, qualitative and quantitative. The affected fruits have
lower market value.
Symptoms: The symptoms appear during spring on young leaves and flower buds. Then the
infection moves to fruits, parts of flowers and even young shoots. Light or olive green
irregular spots develop on both surfaces of leaves. The spots are mostly circular and tissues
around them are thicker and sometimes raised. On fruits, early spots develop near calyx but
stalk end lesions appear later. The size of spots depends on the variety and time of infection
of fruit development. The spots are initially dull but later turn to black. Splitting of fruit skin
on spot area is common with early infection. Corky layers with deep cracks are often seen on
mature fruits. Affected fruits are malformed. The bark of twigs can split at the point of spots
and give a silvery grey look. The lesions can develop on fruits even in storage.
Pathogen: Apple scab is caused by the fungal pathogen, Venturia inaequalis (Cke.) Wist
which belong to family Venturiaceae, order Pleosporales and the sub-order Ascomycotina.
The imperfect or conidial stage is Spilocaea pomi Fr. Ex Fr.
The mycelial strands develop on leaves and fruits between epidermis and cuticle. In dead
leaves, mycelium is a saprophyte where it grows and form ascostroma. The conidiophores
74

develop from the hyphal strands or from the compact stroma. The conidiophores bear conidia
which are ovate and lanceolate and measure 12-22 x 6-9. Perfect stage of the pathogen
develops on fallen leaves where ascospores are formed.
Disease Cycle: The scab pathogen has two stages in its life cycle, the saprophytic stage
which is found on dead leaves and where the pathogen overwinters. The parasitic stage is the
second stage in which the pathogen completes its parasitic life cycle on living parts of the
plants such as on leaves, flower, twigs and fruits. Ascospores developed on dead leaves are
the primary souerce of infection. They infect young leaves and buds during spring. Secondary
spread of the disease is by conidia developed after the primary infection sets in.
Weather conditions are very important for the development and release of ascospores and
formation of conidial cycle. The optimum temperature for ascospore maturation is about 20C.
Rains favour ejection of ascospores. The ascospores germinate and cause infection at a
temperature of 10-22C and free water or 90% relative humidity.
Control: The forecasting systems to warn possible time of disease appearance have been
developed based on: I. ascospores ready to mature II. Ascospores release is expected III.
Ascospores release has taken place and IV. Infection period has occurred. These informations
are collected from the fungal stages on dead leaves. It is therefore important to collect and
burn the fallen leaves. Spray of 5% urea in the autumn before leaf fall and 2% urea before
bud burst is used. Post harvest spray with 0.4% benlate or other fungicides will reduce
perithecia formation on fallen leaves. Spray schedules have been developed for different
apple growing regions. For example, in Himachal Pradesh following schedule of fungicide
sprays has been developed:
First spray of difolton @ 300g / 100L water or other benzimidazole during March-April.
Second spray of dithane M-45 @200g / 100L water or captan @200g / 100L water during
April-May.
One to three sprays of dithane M-45 @ 250g / 100L water at post blossom stage during
summer at 10-15 days interval.
2. Powdery Mildew of Apple
The disease causes severe losses to apple nurseries and orchard trees throughout the apple
growing regions of the world. Pear and Quince are also susceptible to powdery mildew
disease.
Symptoms: A white powder is seen on leaves and young shoots of plants. Affected leaves
are narrower and longer than healthy leaves.. Later, the leaves curl from margins and become
brown coloured. Infected buds die; fruits are reduced in size, deformed with a rough skin.
Pathogen: Podosphaera leucotricha Ellis & Ever is the causal pathogen of the disease. The
pathogen belongs to family Erysiphaceae of the sub-division Ascomycotina. Aerial
conidiophores arise from the mycelium on leaves and shoots. Each conidiophore develops
conidia in chain which are of 25-30 x 10-12 in size.The Cleistothecia are embaded in the
mycelium. Each cleistothecium contain a single ascus which borns ascus.
Disease Cycle: Cleistothecia play little role in the perennation of the pathogen. The primary
source of inoculum is the resting mycelium or encapsulated haustoria in the buds. When such
buds sprout in next season, large number of conidia are formed which are wind borne and
serve as secondary inoculum. Conidia germinate at a temperature of 19-25 C and penetrate
the leaf at high humidity.
75

Control: Dusting the trees with sulphur can control the disease. Prunning of affected shoots
and spraying with fungicides like bavistin (0.05%) or morocid (0.1%) or kerathane help to
protect from infection.
3. Stem Black of Apple
The disease has been reported from Kumaun hills. The disease affects twigs and stem. The
symptoms are seen as black streaks on stem starting from pruned end. Affected stem shows
cracking followed by engirdling of stem and killing the tissues. The disease is common on
thick mature stem than on young ones. The disease is caused by the fungus Coniothecium
chomatosporum Corda. The disease can be controlled by applying fungicidal paste to pruned
ends.

4. Stem Brown of Apple
Symptoms: The disease usually starts from wounds caused by pruning and then moves
downwards to twigs and stems causing dieback symptoms.The bark becomes loose due to
infection and become papery brown and peels off exposing the dark brown stem. Horizontal
and vertical cracks develop on stem. The infection is more on mature stems than young
branches.
Pathogen: The fungus, Botryosphaeria ribis Cross & Dugg. is the causal pathogen. Pycnidia
and perithecia are formed on dead twigs and stems from where the spores of the pathogen
reach to the cut ends or wounds and get entry to the plant.
Control: Sanitary measures and to apply fungicidal paste to cut wounds may avoid infection.

5. Pink Disease of Apple
The disease is wide spread in many apple growing countries and also known as dieback, pink
canker, or twig blight.
Symptoms: Canker, blight and dieback symptoms are seen on trunk, stem and twigs.
Infection mostly starts from the forks of thick branches proceeding upwards and downwards.
The lesions are sunken, dull brown with cobweb-like growth. The mycelium remains
superficial and transforms into pinkish encrustations during rainy season. Disease causes
wilting of shoots and drying up of branches.
Pathogen: The disease is caused by the fungal pathogen, Corticium salmonicalor Berk. &
Br. ( Synonym : Botryobasidium salmonicolor (Berk. & Br.) Venkatnarayan; Pellicularia
salmonicolor (Berk. & Br.) Dast.). The perfect stage is Necator decretus Mass. The pink
conidia are produced on the surface of infected branches and stem.
Disease Cycle: The pathogen persists season to season through dormant mycelium inside the
bark and the cankerous tissues.
Control: Removal of affected branches and applying fungicide paste to cut ends/wounds is
important preventive measures.

6. Fire Blight of Apple
The disease was first recorded In United states as early as 1780 and often appears in
epiphytotic form. The disease is also known to occur in India but is not of much economic
importance as now.
Symptoms: The blossoms become brown and then black showing a brunt appearance, hence
the disease is called as fire blight. Droplets of amber coloured exudates having masses of
bacterial cells appear on the pedicels. The disease also attack leaves and spur. Late in the
season, cankers develop on branches and twigs.These cankers can engirdle the branches and
76

trunk and may cause collar blight. . A greyish brown liquid exudes from the canker. Early
infection of influorescence can cause complete loss to the crop. But if the infection sets in
after fruit set, brown circular lesions develop on unripe fruits which may drop prematurely.
Pathogen: The bacterium, Erwinia amylovora (Burrill) Bergey et. al., is the causal pathogen
of the disease
Disease Cycle: The sugary exudates having large number of bacterial cells attract flies, bees
and ants which carry the bacteria from place to place from infected to healthy trees. The
disease spread like a wild fire during flowering season. In the off season bacterium survives
in cankers on stem. When inflourescence appear, the ants carry the infection from sugary
exudates coming out from cankers on infected plants. Secondary spread takes place by honey
bees while visiting infected flowers and then to healthy flowers.
Control: Prunning of affected trees during off season and applying 0.1% Bordeaux mixture
can control the disease. Spraying of 100 ppm of streptomycin sulphate in 1% glycerine
during pre-blossoming and blossoming time gives effective control of the disease.

7. Collar Rot of Apples
Collar rot disease is present in all the apple growing region of the world. In India, this disease
was reported in 1960.
Symptoms: Affected trees are typically unthrifty showing poor terminal growth and are
stunted. Foliage is sparse and chlorotic and develops purple discoloration in the autumn.
Fruits tend to be small and colour prematurely. Affected trees declined over the years.
However, trees may decline suddenly in excessive wet autumn and spring. Crown and collar
portion of the plants show brown necrotic areas on the phloem and the cambium. The
necrosis may extend upto 1m above the trunk but not much below the graft union.
Pathogen: Several Phytophthora species have been reported as the cause of the disease from
different regions. In India, major pathogen of the disease is Phytophthora cactorum ( Lebert
and Cohn)Schroter, although other Phytophthora species such as P. cambivora, P. citricola,
P. syringae and Pythium ultimum were also found associated with collar rot symptoms..The
pathogen is semi-auatic, soil borne, homothallic with a complex life cycle consisting of an
asexual phase in which motile zoospores are produced from sporangia and a sexual phase
resulting in the formation of oospores.
Disease Cycle: The pathogen can survive in soil where a soil temperature remains 12-20C
and pH 5-6. It survives as chlamydospores in the plant debris or soil and may colonize fallen
apple fruits on the orchard floor. Mainly infection of stem occurs through mycelium
penetration at the ground line but zoospore infection is also common. Oospores usually serve
as a source of primary inoculum. Secondary spreads takes place through zoospores.
Control:Planting in well drained soil, water management and high graft union are most
important for reducing the incidence of collar rot. Clonal rootstocks, M-2, M-4, MM-110,
MM-114, MM-115 and crab apple are resistant under Indian conditions. Fungicides,
mancozeb and copper oxychloride are usually effective in soil drench. Irrigation mixed with
Ridomil MZ (0.2%) at 1.5 ft radius soil around the tree trunk and outside portion of basin
with Bavistin (0.1%) can eradicate the infection. Fosetyl-aluminium application as foliar
spray completely controlled the disease. Isolates of Trichoderma and Gleocladium species
identified as potential biocontrol agent for the contro of collar rot disease of apple.


77

Diseases of Papaya
1. Stem or Foot Rot of Papaya
This disease is wide spread in papaya plantations of India, Sri Lanka, Hawaii and South
Africa.Under favourable conditions of high rain fall and high temperature, the whole
plantation is wiped out within one season.
Symptoms: Initially, water-soaked patches appear on the stem at ground level. These lesions
enlarge and girdle the entire base of the stem and finally rot it. The terminal leaves wilt and
fall off prematurely. The fruits if there are also fall down. The affected plants died within a
short period due to rotting of stem and roots. The tissues below the bark give a honeycomb
appearance. The plants can die at any stage of their growth.
Pathogen: The disease is caused by Pythium aphanidermatum (Eds.) Fitz. However, in
Hawaii, Phytophthora parasitica is also known to be associated with this disease. The
mycelium is intercellular with branched hyphae. The entire thallus is full of oospores,
oogonia and antheridia both within host tissues and its surface. The sporangia are 500 x 20
in size and upon germination form a bladder-like vesicle having 30-40 zoospores. The
oospores are formed after fertilization of sexual structures. They germinate and cause
infection.
Disease Cycle: The pathogen is soil borne. The oospores are formed on the papaya residue in
soil. The pathogen can survive on dead organic matters as saprophyte and causes infection
when suitable host is grown in such soil. The secondary spread takes place by zoospores.
Control: Planting in well drained soil, uprooted and burnt of infected plants and avoid
planting on the same place are the best cultural practices for disease management. Chemical
control is also possible at early stages of infection by removing infected tissues and applies
the fungicidal paste. Soil drenching and spraying the stem with 6:6:50 Bordeaux mixture or
0.2% Esso fungicide-406 or captan may reduce the incidence of the disease.

2. Papaya Viruses
Papaya is infected by three important viruses viz; papaya mosaic, papaya ringspot and papaya
leaf curl. Papaya mosaic is caused by a potexvirus and has not been found in India. The other
two are commonly found in papaya plantations.
(i)Papaya Ringspot (PRSV)
Synonyms: papaya distortion mosaic, papaya leaf distortion, papaw distortion ringspot and
papaw mosaic.
Symptoms: Mottling and malformation of leaves, ringspot and shoe sting effect of leaves and
streaking or rings on fruits, stem and petioles are the main symptoms of the disease (Fig 36).
Cucurbita pepo, C. melo, Chenopodium amaranticolor, C. quinoa are the experimental host
of the virus.






Fig.36. Papaya mosaic symptoms on plant and fruit and potyvirus particles associated with it
78

Pathogen: The causal virus particles are filamentous with a modal length of 760-800 nm
with a width of 12 nm. The virus belongs to potyvirus (potyviridae) group. The genome of
the virus is ssRNA, unipartite and 12 kb in size. The virus has two strains; PRSV -W that
infects watermelon but not to papaya and PRSV-P strain which infects both papaya and
cucurbits. The virus is transmitted by aphid vectors, Myzus persicae and Aphis gossypii in a
non-persistent manner. A protein, the helper component is required for virus transmission. It
is also transmitted by mechanical inoculations.
Disease Cycle: The virus survives on papaya plants in the field from where it infects healthy
papaya by aphid vectors. The aphids that have fed on infected plants when feed on healthy
plants the virus is transmitted by feeding process.
Control: Avoiding vectors, removing source of inoculum are the measures for management
of the disease. No variety of papaya is resistant and hence growing virus-resistant
transgenics, if available is the best method of disease control.

(iii) Papaya Leaf Curl
The disease is common on papaya in India but the incidence is less as compared to PRSV.
The affected plants do not bear any fruit causing heavy loss to the farmers.
Symptoms: The most characteristic symptoms are severe curling, crinkling and distortion
and rugocity of leaves and reduction of leaf lamina in size (Fig.37). Leaves become leathery
and inverted cup shaped and veins are highly thickened. The petioles are twisted in a zig-zag
manner. The growth of affected plants is reduced and affected leaves appear as a bunch of
leaves at the top. Affected plants do not bear any fruit.








Fig. 37: Papaya leaf curl disease
Pathogen: The causal virus particles are geminate and the virus belongs to family
Geminiviridae. The genome of the virus is single stranded DNA and divides into two parts,
DNA-A and DNA-B. The virus is transmitted by whitefly, Bemisia tabaci and also by graft
inoculations.
Disease Cycle: The virus is not seed borne. The inoculum survives on papaya in nature or
may be on other plants like tobacco, tomato, and several weed hosts. From these sources, the
virus infects papaya by the whitefly vector. Affected plants never recover from the disease
and hence are a perennial source of inoculum.
Control: Affected plants must be uprooted and destroyed. The vector may be kept under
control. No source of resistance is available.


79

Diseases of Citrus
1. Anthrcnose Disease of Citrus
There are three anthracnose diseases of citrus caused by Colletotrichum species: I. post-
bloom fruit drop II. Lime anthracnose and III. Post-harvest anthracnose.

(i)Post-Bloom Fruit Drop (Pfd)
Symptoms: Water soaked lesions developed on petals which eventually become pink and
then orange brown. Petals become dry and hard but remain attached to the flower. The
fruitlets abscis at the base of the ovary. Fruit setting is stopped. Leaves around the affected
flourescence are small, chlorotic, twisted with enlarged veins.
Pathogen: The disease is caused by the fungal pathogen, Colletotrichum acutatum J .H.
Simmonds. The conidia of the pathogen are fusiform and developed in acervuli on the surface
of petals. Conidia germinate and produce appresoria.
Disease Cycle: The pathogen survives on buttons, leaves and twigs. When the first flowers of
the next bloom open the appresoria are stimulated to germinate and form hyphae with a few
conidia. The conidia are dispersed by splashing rains to new flowers, completing the cycle. In
adjacent plantings, fungus moves by bees or other insects when they visit new flowers. Long
distance spread occurs through transportation of infected petals by equipments or vehicles in
harvesting sacks.
Control: Avoid overhead irrigation, removal of declining trees before bloom, wider tree
spacing are important to avoud PDF. Fungicide sprays during bloom such as benomyl or a
combination of benomyl and ferbam and captafol are very effective.

(ii)Lime Anthracnose
Mexican lime or kagzi lime is the only known host of the disease.
Symptoms: The disease affects flowers, young leaves, shoots and fruits. Infected fruitlets are
dropped. In severe cases, leaves become totally blighted and drop causing shoot-tip
dieback.Under favourable conditions, necrotic lesions are formed on leaves and fruits. Fruit
lesions are larger and deeper than leaves.
Pathogen: This disease is caused by the pathogen, Colletotrichum acutatum = Gloeosporium
limetticola Clausen.
Disease Cycle: The acervuli of this strain of pathogen are produced on all infected parts:
leaves, twigs, flowers and fruits. Therefore, the inoculum is more readily available than PDF
strain which makes acervuli only on petals.
Control: The disease is difficult to control because of the constant emergence of new leaves
and frequent flowering and the large amount of inoculum produced on infected tissues.
Fungicides such as mancozeb and captafol are effective but must be applied frequently.

(iii) Post-Harvest Anthracnose of Citrus
The disease appears only on fruits that are injured by pests, chemical injury, or held too long
in storage.
Symptoms: Brown to black lesions are formed on fruit rind. The fruits become soft. As the
decay progresses a soft rot occus.
Pathogen: The disease is caused by Colletotrichumgloeosporoides (Penz.) Penz. Sacc. In
Penz.
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Teleomorph: Glomerella singulata (Stoneman) Spauld & H. Schrenk. The acervuli of the
pathogen are superficial. The conidia are broadly oval and contain one or two oil drops. The
conidia germinate and produce an appresorium which contains distinct collar.
Disease Cycle: The conidia develop abundantly on dead twigs and are spread by rains.
Ascospores are air borne and travel long distances. After the conidia germinate, fungus
remains quieacent as ungerminated appresoria. Further infection takes place when appresoria
germinate on new host.
Control: Good cultural practices and proper handling of fruits to avoid injury and washing
after harvest will reduce the disease. Post-harvest treatment with thiabendazol and storage of
fruits below 10C will help to control the disease.
2. Citrus Canker
There is a distinct form of citrus canker bacterial disease. The disease is found in one or other
form in all the citrus growing countries. Asiatic form of canker is most widely distributed.
The disease is serious where warm temperature and rain fall are frequent during shoot
emergence and development of young fruits. In general, Mexican lime and trifoliate orange
are more susceptible, sour orange, lemons and sweet oranges are moderately susceptible and
mandarins are moderaly resistant.
Symptoms: Circular, pin-point, raised lesions appear on leaves which may increase in size
with time. The leaf minor (Phyllocnistis citrella) can greatly increase the number of lesions.
On fruits, the lesions can vary in size.The lesions can develop on both surfaces of leaves and
become corky with raised margins and sunken centre. Lesions on fruit and stem are upto 1
mm deep and are superficial similar to leaves (Fig.38). A yellow halo with water soaked
margin around the lesions on leaves is the most characteristic symptoms of the disease. The
halo disappears in older lesions.







Fig 38: Citrus cancer symptoms on leaves and fruit
Pathogen: The disease is caused by the bacterium, Xanthomonas campestris pv. citri (Hasse)
Dye (Syn. X. citri (Hasse) Dowson and X. axonopodis pv. citri (Hasse) Vaut. It is a rod
shaped, gram-negative bacterium with a single polar flagellum.
Disease Cycle: The pathogen survives in lesions on leaves, stems and fruits. It can also
survive for several years on woody branches. The bacteria ooze out from the lesions when
free moisture is on them and can be dispersed to infect new growth. Wind driven rains are the
main dispersal agent and bacterium penetrates through stomata or through injuries made by
insects or during tree operations. The bacteria remain alive in lesions on leaves and fruits
until they drop down.
Control: No planting material should be allowed from canker having regions. Nursery and
orchard infections quarantines and on-site burning are important to avoid the spread of
bacterium. Control of leaf minor and frequent sprays of copper are helpful to check the
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canker infection. In sandy areas, vegetable growing between plant rows may be helpful to
avoid wind injury by wind blown sand.
3. Citrus Decline
Citrus decline is common in citrus plantations of India. The disease is most commonly known
as citrus die-back.
Symptoms: Severity of symptoms may vary with season, cultivar, age of tree and nutritional
status of the affected tree. Symptoms first appear on one branch with a chlorotic leaf patterns
similar to zinc or iron deficiency. Irregular blotches or mottling sometimes with yellowing of
leaf veins or of entire leaf are prominent. There is leaf fall of heavily infected branches and
the leaf-less branches start dying from the top downward because they are attacked by several
fungi. The affected trees are stunted and have sparse growth. Such trees bear lopsided fruits
which are bitter in taste and have abortive seeds. Finally such trees are declined. This type of
decline is known as slow decline. However, sometimes the affected tree shows wilting
symptoms for a few weeks and then decline or dead. Such decline is known as sudden decline
(Fig.39)







Fig 39: Decline of citrus trees
Causes: The disease has been reported to be caused by several abiotic factors such as
nutritional deficiency, soil and physiological disorders, poor management of orchards etc. but
the possible cause of the disorder in India has been reported due to greening bacterium
followed by infection by several fungi such as Colletotrichum gloeosporoides, Diplodia
natalensis, Curvularia tuberculata and Fusarium species. However, recent investigations
revealed that a few viruses and virus-like diseases, some of them were not known earlier are
also involved with citrus decline complex. These diseases including citrus greening are
described in this chapter.
4. Citrus Greening Bacterial Disease
The greening disease is now known as Haunglongbing as this disease was first reported by
this name from China. Until 1970, the disease was considered to be of viral origin but now it
is known to be caused by a phloem limited fastidious (uncultured) bacterium Candidus
liberibacter spicies belonging to the alpha-proteobacterial sub-division. It seriously affects
production of citrus in Asia, South East Asia, Indian sub-continent, Peninsula and Africa.
Recently, it has been reported from North and South America.
Symptoms: The symptoms of the disease are somewhat similar to dieback described above.
Leaf mottling is the characteristic symptom of the disease. Fruits on affected trees are poorly
coloured.
Pathogen: Two forms of bacterium causing greening disease are known; the Asiatic form
and the African form. Asian form bacterium is Candidus liberibacter asiaticus and the
African form is Candidus liberibacter africanus. In electron microscopy the bacterium looks
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pleomorphic bodies of various sizes in the sieve tubes of phloem tissues of infected leaves
(midribs). The bacterium in Asian countries is transmitted by a psyllid vector, Diaphorina
citri and African bacterium is transmitted by another psyllid, Trioza erytreae. The disease is
also transmitted by grafting and dodder, Cuscuta campestris from citrus to periwinkle
(Catharanthus roseus). The dodder transmission can be used for disease diagnosis.
African greening show symptoms at cool temperature (20C) but the Asian form can show
symptoms at both cool and warm conditions (35C).
Disease Cycle: The inoculum of the bacterium is available on infected citrus trees from
where the vector can carry the infection to healthy plants.
Control: Control of vector population, reduction of inoculum sources by pruning affected
branches or by eradication of affected trees, use of disease-free budwood for propagation and
if possible use of disease or vector-free areas for nurseries are the important preventive
methods.
5. Citrus Tristeza Virus Disease (CTV)
Citrus tristeza is most devastating disease and citrus industry in several countries was wiped
out due to this virus. The disease probably originated in Asia from where it is spread
throughout the world through movement of infected planting material. The disease is
responsible for quick decline in certain stock-scion combination.
Symptoms: Stunting, stem pitting, chlorosis of leaves and reduced fruit size are common
symptoms (Fig.40). Sweet orange trees grafted on sour orange root stock are commonly
declined. Leaf cupping and vein clearing symptoms are observed on indicator hosts, Kagzi
lime and Citrus excelsa. Symptom severity is highly variable between CTV isolates. CTV
infects most citrus species, cultivars, and intergeneric hybrids. The only non-rutaceous host is
Passiflora species.
Pathogen: Citrus tristeza virus belongs to closterovirus group. CTV has flexuous particles of
2000 nm length. The virus is transmitted by several aphid vectors but Toxoptera citricidus is
the most efficient vector. It is graft and mechanically transmitted by stem slash inoculation.
CTV genome is positive sense single stranded RNA.







Fig. 40: Stem pitting symptoms due to Fig 41. Symptoms of Indian Citrus
Citrus tristeza virus ringspot on Citrus leaves

Disease Cycle: CTV is spread by movement of infected planting material and by aphid
vectors from the inoculum present in orchard trees.
Control: Prevention by quarantine to new areas, and budwood certification are important to
check the losses caused by CTV. CTV tolerant root stocks such as trifoliate orange or its
hybrids should be used. Cross protection using immunization of plants by mild strain is
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important method to control CTV. Shoot-tip grafting and thermotherapy are other methods of
eliminating CTV.
6. Indian Citrus Ringspot Disease
The disease commonly occurs on Kinnow mandarin and sweet oranges in India. This disease
is a major constraint in citrus production in the country and restricted to India so far.
Symptoms: The leaves of affected trees show rings of various sizes. These rings have yellow
border and dark green centre (Fig.41)These rings enlarge in size and may cover the whole
leaf surface. Infected leaves fall off prematurely. Affected trees show die-back symptoms at
later stages of their growth commonly after first or second harvest. On inoculated Mosambi
plants, vein clearing or flecking symptoms develop on young leaves. These symptoms
survive till maturation of leaves. The mature leaves show ringspot symptoms.
Pathogen: The disease is caused by a filamentous virus having a modal length of 650 nm.
The virus belongs to genus Mandrivirus of family Flexiviridae. The virus genome is ssRNA.
The virus is named as Indian citrus ringspot virus (ICRSV). ICRSV is transmitted by grafting
and also by mechanical inoculations from citrus to herbaceous hosts.
Disease Cycle: The virus spreads through vegetative propagation when infected budwood are
used. No vector spread is known.
Control: Use of healthy planting material is the only method of control currently available.
7. Citrus Yellow Mosaic
The disease is found on satgudi and Mosambi sweet oranges in South India and in
Maharashtra. An incidence of the disease upto 70% was observed on Satgudi in Andhra
Pradesh.
Symptoms: The most characteristic symptom of the disease is yellow mosaic on leaves of
infected trees (Fig.42). The trees are systematically infected.The trees over 10 years of age
show decline. Most of the commercial cultivars are susceptible to virus infection.
Temperature does not appear to effect the symptom development.






Fig.42. Symptom and virus particles of Citrus yellow mosaic disease
Pathogen: The causal virus has bacilliform particles measuring 130 x 30 nm in size. The
genome of the virus is double stranded DNA and the virus belongs to Badnavirus group. The
virus is named as citrus yellow mosaic badnavirus (CYMBV). The vector of the virus is a
mealybug, Planococcus citri. The virus is also transmitted by grafted.
Disease Cycle: The primary spread of the virus is through the use of infected budwood for
propagation. Secondary spread may be by the mealybug vector but the spread by the vector is
comparatively low.
Control: Use of healthy planting material and control of mealy bug from citrus and
neighbouring crops such as sugarcane are the methods to control the disease.
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8. Citrus Exocortis Disease
This is the disease of rootstocks used for citrus propagation and found throughout the world.
Symptoms: Bark scaling, tree stunting, and stem blotching of trifoliate orange, sweet lime,
Rangpur lime and some citrons and lemons are the main symptoms of the disease (Fig.43).
The disease is apparently symptomless unless grafted on sensitive rootstocks.







Fig. 43: Bark scaling symptoms on rootstock due to exocortis disease
Pathogen: The disease is caused by a viroid pathogen known as citrus exocortis viroid
(CEVd). It is an infectious, circular, single stranded RNA of about 371 nucleotides which are
highly base pared, forming a stable rod-like structure. CEVd is graft and mechanically
transmitted disease. It is also transmitted through contaminated operational tools. Seed and
vector transmission has not been confirmed. CEVd can be detected most reliably by grafting
on Etrog citron which will show epinasty of leaves.
Disease Cycle: Dissemination of the pathogen occurs through propagation of symptomless,
CEVd infected budwood. Further spread takes place through contaminated tools used for
orchard operation.
Control: Use of CEVd-free budwood and avoiding of spread by treatment of tools with
sterilant like sodium hypochlorite (1%) are the methods to control the disease.

Diseases of Peach and Pear
1. Peach Leaf Curl
The disease is found worldwide and is a serious disease of peach.
Symptoms: Parts of peach and nectarine leaves are swollen, distorted and curl downwards.
Affected leaves first appear reddish, then turn yellow, also flowers, fruits abd current years
twigs may be affected. In plums, the disease first appears as small white blisters on the fruit.
The disease can be very severe in wet humid regions where bud brust can be delayed for 2-7
weeks.
Pathogen: The disease is caused by the pathogen, Taphrina deformans (Berk.) Tul. which
belongs to the sub-division Ascomycotina. The pathogen has a yeast-like phase on host
surfaces and a parasitic phase inside the vegetative growth and fruit. Intercellular growth of
the pathogen causes cell division and cell enlargement (hyperplasia and hypertrophy) that
result in thickened, curl to convoluted or blistered leaves, shoots or fruits.
Disease Cycle: The conidia survive the off-season within the infected host tissues and
become active in the next season to cause infection. The ascospores are formed on freshly
infected tissues and are the chief source of secondary infection. They multiply by budding
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and the resultant conidia germinate to infect the host tissue or remain dormant in the off
season.
Control: One spray of lime sulphur before bud break and second spray in the fall are
effective to eliminate the disease. Spray with 0.3% fytolon or blitox-50 (0.25%) also gives
protection from the disease.
2. Brown Rot of Peach
The disease causes great loss due to decay of fruits in the orchard, in transit, in the market
and prior to consumption. The disease is widely distributed in peach plantations throughout
the world. Infected flowers wilt and turn brown due to brown rot. Infected fruits develop
circular light brown spots that rapidly extend to decay the flesh. Spurs on peach trees may be
blighted near harvest following fungal invasion from infected fruits including shriveled
mummies ones. The fungus forms small cankers on non-bearing shoots. The disease is caused
by the fungus, Sclerotinia fructicola (G. Wint.) Rehm. The teliomorph is Monilinia fructicola
(G. Wint.) Honey. The conidia and ascospores develop on mummified fruits and pedicels.
Conidia are formed in chains on infected tissue. The inoculum remains available on infected
trees from where the infection spreads to healthy plants. No control measures are known.

3. Peach Scab
The disease is economically important in regions of high rain fall, high humidity and warm
temperatures between bloom and harvest usually rare in semi-arid peach producing regions.
Symptoms: Circular, olivaceous to black, velvety spots are produced on fruits and twigs, less
frequently on leaves. Lesions of fruit coalesce followed by cracking of fruits. These lesions
reduce the appearance, quality and market value of fruits. Lesions on shoots and twigs are
slightly raised, circular to oval becoming brown with slightly raised purple margins later in
the season.
Pathogen: The disease is caused by the fungus. Anamorph: Cladosporium carpophilum
Thum = Fusicladium carpophilum (Thum.) Qudem. Teleomorph: Venturia carpophila
(Thum.) Quedem.
Disease Cycle: The pathogen overwinters in lesions on twigs with conidial production which
begins when shucks covering the fruit split.
Control: To develop planting material through tissue culture is the best control of the
disease.

Diseases of Guava
1. Wilt of Guava
Guava wilt is a common disease in India.
Symptoms: The symptoms appear as browning and wilting of leaves, discoloration of the
stem and death of branches on one side. The infection may girdle the entire stem resulting
wilting of the whole plant. The leaves may fall off and trees usually collapsed within a year
or earlier depending on the intensity of infection. When the stem is cut open vascular tissues
will show dark colour extending upto the cambium region. The fungus normally present in
tissues of the stem near ground level.
Pathogens: The disease is caused by fungi, Fusarium oxysporum f. psidii and Cephalosprium
species. Wilt associated with pathogens, F. solani and Macrophomina phaseoli bring about
gradual decline and death of undernourished 1-5 yr old guava trees in West Bengal. A disease
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brought about by the wound parasite, Myxosporium psidii, causes the death of many guava
trees, especially in summer, throughout Taiwan.
Disease Cycle: The pathogens are soil borne. The fungus may invade the trunk and roots
through tunnels bored by the larvae of Coelosterna beetles.
Control: No effective control is known.

2. Stem Canker of Guava
Symptoms: The disease is found in some parts of India. The symptoms appear as cracks and
lesions on the stem. The stem tissues are killed by the pathogen resulting wilting of branches
due to lack of transportation of nutrients.
Pathogen: Canker disease is caused by the fungus, Physalospora psidii Stevens and Pierce.
The perithecia of the pathogen are formed on the infected tissue.
Disease Cycle: The pathogen remains inside the infected tissues beneath the bark and
becomes active whenever weather conditions are favourable. The pathogen spreads from
plant to plant by air-borne spores.
Control: The infected branches should be cut and destroyed. The cut ends should be pasted
with fungicidal paste. Prunned ends should be painted with fungicidal paste such as Bordeaux
paste. Insecticidal sprays after pruning will help in preventing the disease.
3. Guava Anthracnose
Anthracnose disease is caused by the pathogen,Colletotrichum gloeosporioides.The pathogen
attacks the fruits usually during rainy season. The lesions of the disease appear on fruits. In
field conditions, the development of lesions was greater on punctured guavas than on
uninjured or sand injured ones, both in rainy and winter seasons. Disease incidence increased
as inoculum density increased from 101 to 106 conidia/ml. The optimum temperature for
severe infection was 30 C and high humidity is essential for infection. The control of the
disease is the same as with other Anthracnose diseases described earlier.

Disease of Grapes
1. Powdery Mildew
Under favourable conditions, powdery mildew appears in epidemic form in vine plantations
in India.
Symptoms: All stages of plant growth are susceptible to infection. The symptoms appear as
white powdery patches on affected parts. All above ground parts including fruits, leaves,
stem, tendrils and flowers are susceptible to infection. Both surfaces of leaves and other plant
parts show powdery pustules. The pustules subsequently become grey and finally dark
coloured. Affected leaves become malformed and colourless. Affected plants remain dwarfed
and give wilting appearance. The stem turn brown and infected berries become malformed
and rarely ripe. There is no fruiting if the infection occurs early.
Pathogen: The causal pathogen is a fungus, Uncinula necator (Schw.) Bur. The mycelium of
the fungus is superficial and gives rise to conidiophores. Each conidiophore bears 3-4 conidia
in chain measuring 25-30 x 15-17. The conidia are disseminated by wind. In India, perfect
stage is not known but it is formed in other countries. The perfect stage of the pathogen
produces Cleistothecia and each cleistothecium carries asci and ascospores.
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Disease Cycle: In countries where Cleistothecia are formed, inoculum is carried by
cleistothecia from season to season. The pathogen is favoured by warm temperature with
enough humidity and cloudy overcast weather. Conidia are borne by wind and cause infection
from plant to plant.
Control: Cultural practices like pruning after shedding of leaves, thinning out and cutting
back of laterals and removal and destruction of diseased parts are helpful for healthy
grapevine cultivation. The disease can be controlled by sulphur (300-mesh) dusting. The first
dusting needs to be given when new shoots are 3-6 long, second spray before blossoming
and the last at 40-50 days later. New fungicides, bayleton and kerathane are highly effective
against powdery mildew of grapes.
2. Downy Mildew of Grapes
It is a historical disease as it brought several epidemics in France badly affecting the wine
industry. The disease could not be controlled till Professor Millardet of Bordeaux University
made an accidental discovery of Borsdeaux mixture in 1885. The disease is now known to
occur in all wet grapevine growing regions of the world.
Symptoms: The symptoms are more pronounced on leaves, young shoots and immature
fruits than other aerial parts of the plant. Initially, irregular yellow spots are formed on upper
surface of leaves. On the ventral surface, below the spots, downy growth of the fungus can be
seen. Later, the spots become necrotic and the spots become brown and lower surface of the
leaves become dirty grey. Dirty spots coalse and form larger necrotic areas. Shoots become
hypertrophied. The affected bunch of fruits is destroyed.
Pathogen: The fungus, Plasmopara viticola (B. and C.) Berl. & de T. is the causal pathogen
of the disease. The mycelium is intercellular and produces conidiophores during night in high
humidity conditions. Conidiophores emerge directly from the cuticle of leaf and from
lenticels of young berries. The branching of conidiophores is at right angle to the main axis
and at regular intervals.From the tip of each branch 2-3 sterigmata arise and bear lemon-
shaped sporangia. The sporangia produce zoospores after germination. Each zoospore has
two flagella at the apex. Oospores are produced in tissues adjacent to midribs of leaves. The
oospores germinate and produce sporangia.
Disease Cycle: The pathogen is an obligate parasite and survives in active phase on
evergreen grapevine. The main source of survival is oospores which survive on leaves and
shoots lying on the ground. The oospores germinate under favourable conditions and infect
lower leaves of the plant. Then the sporangia are formed which soon detached from leaves by
wind causing infection to new plants. Water is another source of their dispersal. The germ
tube of sporangium forms zoospores which enter the host through stoma and lenticels.
Control: Proper sanitation, suitable spacing, removal of leaves at ground level are important
to avoid infection. Fungicides are effective. Zineb or maneb (0.2%) , captan (0.2-0.5%),
Bordeaux mixture 4:4:50 are commonly used. Among the new fungicides ridomil is very
effective to control downy mildew infection.
The following spray schedule has been developed.
Immediately after pruning.
Three to four weeks after pruning.
Before buds are open.
After setting of berries.
During growth of shoots.
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The resistant varieties are Amber, Queen, Champion, Cardinal, Champa and red Sultana.

Diseases of Sapota (Achras sapota L.)
Sapota commonly known as chiku is a very popular fruit crop in India. Only a few diseases
of sapota are known in the country. A leaf spot disease caused by fungus, Phavophleospora
indica Chinnappa is known to occur on sapota in South India but the sooty mold disease is
economically more important.
Sooty Mold
This ectoparasitic disease is most common on sapota which hampers the tree growth. The
pathogen which causes sooty mould is non-pathogenic and develops as saprophyte on the
honey dewssecreted by the insects on leaves and twigs of host plant. The insects commonly
secret honey dews are scale insects, aphids and whiteflies. The honey dew attracts the fungus,
which multiplies rapidly, covering the leaf surface. The foliage becomes black which affects
the photosynthesis and thereby interfere in the normal growth of the plant. The sooty mold
pathogen can also multiply on fruits making them unfit for market. The disease is caused by
fungus, Capnodium species. The disease may be controlled by spraying of insecticides to
control insects followed by spraying of a starch solution which dries up and comes out in
flakes alongwith the mold. Another spray of insecticide would help in eradicating the insects,
thereby avoiding another onset of sooty mold fungus.

Diseases of Ber (Ziziphus mauritiana Lam., Ziziphus jujube L.)
The tree is most commonly affected by a parasitic vine (Cuscuta spp.). Powdery mildew
(Oidium sp.) causes defoliation and fruit drop. Sooty mold (Cladosporiumzizyphi) casuses
leaves to fall. Leaf spots are caused by Cercospora spp. and Isariopsis indica var. zizyphi.
Leaf rust is caused by Phakospora zizyphivulgaris, ranges from mild to severe on all
commercial cultivars in Punjab. A witches broom disease caused by phytoplasma was
reported from Pune.
Fruits on the tree are attacked by Alternaria chartarum, Aspergillus nanus, A. parasiticus,
Helminthosporium atroolivaceum, Phoma hessarensis and Stemphyliomma valparadisiacum.
Twigs and branches may be affected by Entypella zizyphi, Hyphoxylon hypomiltum, and
Petillaria atrata. In storage, fruits may be attacked by fungi, Alternaria brassicicola, Phoma
spp., Curvularia lunata, Cladosporium herbarum. Fruit rots are caused by Fusarium spp.,
Nigrospora oryzae, Epicoccum nigrum, and Glomerella cingulata.

Diseases of Custard Apple (Anona squamosa L., A. reticulate l )
This common fruit is grown all over India. The trees are affected by a few fungal diseases.
1. Leaf Spot
Symptoms: Water soaked lesions mostly angular in shape are developed on leaves. The
lesions are dark brown to greyish and vary in size. Single leaf may have over 100 lesions.
The lesions dry off and wither resulting in a scorched appearance of the affected leaf. The
fruits may also be infected in severe cases.
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Pathogen: The fungus, Cercospora anonae Muller & Chupp. is the causal organism. The
pathogen belongs to family Dematiaceae, order Moniliales, and sub-division
Deuteromycotina.
Disease Cycle: The pathogen perpetuates only through the conidial stage. The pathogen
survives in the host tissues all the year around and thus inoculum is also available for new
infections.
Control: The fungicidal sprays can be given in advanced cases.
Another leaf spot is caused by Pleosphaeropsis anonae Chona & Munjal
2. Root Rot
The disease is caused by Diplodia natalensis Evans. The pathogen is a soil inhabitant,
attacking the roots and spreading upwards to the basal portion of the stem causing the wilting
of plants. When the disease appears in one or two plants in the plantation, the area of such
trees must be isolated, and plants should be cut and destroyed. Other plants can be replaced
by a protective cover on the trunk with Bordeaux paste and also drenching the soil around the
stem with Bordeaux mixture.

3. Fruit Rot
The pathogen attacks the young leaves, stem, influorescence and fruits. The affected fruits
develop black spots and the skin becomes discoloured.The fruit pulp below the spots
becomes hard and decay at ripening. The affected fruits may drop off prematurely. Severely
spotted fruits have low market value.The disease spreads rapidly during rainy season.
The disease is caused by Glomerella cingulata (Stonem) Spauld & Schrenk which is the
perfect stage of Colletotrichum gloeosporioides Penzing.
The disease can be managed by avoiding overcrowded planting and giving preventive sprays
with Bordeaux mixture. Dipping mature fruits in hot water at 51 C for 15 min saves them
from damage during storage.
4. Pink Disease
Pink disease of custard apple is caused by the fungus, Pellicularia salmonicolor ( BERk. &
Br.) Dastur. A pinkish powdery coating on the stem appears as initial symptom of the disease.
Later, the girdling of stem happens. The pink colour is due to the conidia produce on the stem
surface. Affected shoots show wilting, shredding of leaves and finally the braches dry up. In
some cases, the fungus may produce the pustules which are of orange red colour and are
arranged in rows along the stem.
The pathogen persists from season to season through dormant mycelium inside the bark and
cankerous tissues.
The disease may be checked by cutting and removing the affected branches. Cut wounds may
be protected with fungicidal paste.

Diseases of Coconut Palm
Coconut Cadang-Cadang Disease
The disease causes heavy losses to the coconut palm industry in the Philippines. It is not
found in India so far.
Symptoms: The initial symptoms are the rounding of nut shape; and appearance of fine,
translucent, bright yellow spots on leaves. Influorescence then become necrotic, nut
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production decline, and finally stopped. General chlorosis and death of the crown are the
advanced symptoms. Eight to ten years are taken between the appearance of first symptoms
and death of the palm.
Pathogen: The disease is caused by a viroid pathogen which belongs to potato spindle tuber
viroid group. The viroid has 287-302 nucleotides. No mechanism of its natural spread is
known. A low rate of seed transmission was observed and pollen transmission is suspected.
The pathogen is experimentally transmitted by high pressure injection into the shoot of
germinating nuts.
Disease Cycle: The inoculum remains in infected trees from where it may go by unknown
agents or spreading by contaminated seed or operational tools.
Control: The infection can be avoided by using sterile operational tools. No resistance has
been found.
2. Phytoplasmal Diseases of Coconut Palm
Three important diseases of phytoplasmal origin have been repoted. In India, rootwilt and
tatipaka are commonly found.
(i)Root Wilt or Kerala Wilt
Symptoms: The symptoms of the disease normally appear when the plants are about 30
months old. The most characteristic symptom is bending of leaflets called as flexidity. In
older palms, yellowing and marginal necrosis of the older leaves also develops (Fig. 44).
Parts of affected palms show degeneration of phloem, disorganized tracheal elements and
tylosis in the metaxylem. They eventually rot. The disease is not lethal but productivity is
significantly reduced.






Fig. 44: Coconut root wilt disease.
Pathogen: The disease is now known to be caused by a phytoplasma, a mollecute, formerly
known as Mycoplasma-like Organism (MLO). The pathogen has pleomorphic bodies which
can only be viewed in electron microscope. These organisms are limited to the sieve tubes of
the phloem tissues. The root wilt phytoplasma is transmitted by insect vectors, Stephanitis
typica-a lace-bug but Proutista moesta is the efficient vector.
Disease Cycle: The inoculum is available in the infected plants from where the pathogen
spreads to new plants.
Control: Tetracycline therapy gives temporary remission of disease symptoms but no control
of the pathogen.Movement of planting material from infested areas to new areas should be
avoided.

(ii)Tatipaka Disease
Reduction in number and size of leaves, fasciation, light green leaves and chlorotic spots on
leaves are the main symptoms of the disease. Abnormal bending of fronds, tapering of stem
and production of small sized influorescence bearing atrophied empty nuts can also occur.
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The disease is caused by a phytoplasma but no vector or other means of spread are known.
The disease can be controlled as mentioned under root wilt.
3. Bud Rot and Fruit Rot Fungal Diseases of Coconut
These diseases are prevalent in most of the coconut growing countries.
Symptoms
Bud Rot: The initial symptoms are chlorosis and collapse of the youngest leaves. The buds
rot and spear leaves withers of the infected plants. Successive leaves turn yellow and die
resulting death of central fonds and only outer fringe remains with green fonds. Eventually
the whole palm dies.
Fruit Rot: Two to five months old nuts are attacked. Symptoms begin as water-soaked
lesions near the perienth. The lesions turn brown and become irregular in shape. They spread
into the husk and may reach the endosperm. Premature nuts may fall any time. The pathogen
can also infect the influorescence.
Pathogen: Phytophthora palmivora (Butler) Butler Sensu lato is the causal pathogen of these
diseases but now P.arecae is also regarded to be a part of this complex.The pathogen has a
wide host range in different countries but in India, the additional host is Borassus flabellifer.
The pathogen belongs to family Pythiaceae, order Peronosporales and sub-division
Dueteromycotina. The sexual and asexual stages of Phytophthora spp. have been mentioned
in earlier chapters.
Disease Cycle: The pathogen is most active during wet weather. Spores are dispersed by rain
splash and through air currents. Palms may be predisposed by damage or adverse growing
conditions. Resistant chlamydospores can survive in soil and coconut debris including nut
tissues. Nuts may be infected internally.
Control: When the infection starts to the outer leaves, these leaves alongwith older ones
should be shaved off and remaing central shoots and the entire crown must be sprayed with
one per cent Bordeaux mixture or any other suitable fungicides. In endemic areas, spraying
more than once is essential. Planting material should move in the form of embryo and pollen.
Nuts should be partially de-husked and treated with a fungicide before planting to avoid the
possibility of seed transmission.


Management of Plant Diseases through Host Resistance
Selection and breeding of plants with genetic resistance to parasites is one of the most
effective methods of disease control. Once the plant has been bred, and seed multiplied, no
further measures are required. However, resistance is not always durable owing to the loss of
effective avirulence genes by the parasite. Breeding for durable resistance could become a
reality if we knew the nature of genes that conferred this character. Plant has many
genetically determined components/factors known as resistance and susceptible factors. The
parasite is known to have many genetically determined components which are known as
virulence or pathogenecity factors. If these facors are matched with susceptible factors of the
host, the reaction is known as compatable. But when virulence or pathogenicity factors are
not matched with susceptiblilty factors of the host, the reaction is incompatible. Similarly,
where virulence factors are matched with resistance factors in the host, the reaction is
compatible. But when virulence factors are not matched by resistance factors in the host, the
reaction is incompatible. Currently, it is thought that such genes encode products which
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recognize essential fitness components of the parasite. Consequently, parasites that have lost
their avirulence/fitness genes are unable to cause disease even in susceptible hosts.

To obtain the desired variety through selection we must have:
Resistant lines or biotypes in the population we are working with.
The technique for screening the varieties for resistance must be reliable.
The selected variety should combine other desirable properties, including better
agronomic qualities.
The variety must be tested under optimum conditions for resistance to the disease.

World-wide search for genetic material in different crop plants has been going on and
extensive collections of germplasm are available at many institutions. These include wild and
cultivated plants carrying resistant genes for various plant pathogens. Selection of resistance
sources/lines and mating them with susceptible but commercially good types produces off
springs, some of which possess desirable agronomic qualities as well as resistance to the
disease. The process of developing varieties is time consuming. The offsprings and their
progenies are to be carefully screened and tested in a number of places in different
agroclimatic zones under conditions most favourable for disease development.

During the association of plants with parasites, a basic compatibility evolved which is likely
multigenic on the part of both host and parasite. However, it may easily be upset by single
gene changes either in host or parasite. The pathogens are constantly changing, evolving new
varieties or races of their species of their pathogens. While new races are evolved, many of
which may be more virulent and aggressive pathogens than the parents. While newer crop
varieties are evolved to manage the diseases, newer races of the older pathogens arise to
attack the newer varieties. Hence, it is never ending struggle for scientists to go on evolving
newer crop varieties not only to secure better agronomic qualities and increase production but
to combat new or more virulent pathogens.

Eriksson in 1884 showed that cereal rust pathogen, Puccinia graminis consists of different
races which differ in their pathogenicity but can not be differentiated morphologically. For
example, some of them could attack to wheat but not to other cereals such as oat and rye.
Stakman later showed necrotic or hypersensitive reaction which a pathogen causes to its host.
Biffen in 1905 reported that resistance of two wheat varieties and their progeny was inherited
in a mendelian fashion.. Stakman established that the races can be identified by infecting a set
of host differential varieties. This work helped to determine the presence or appearance of
new physiologic races.

There are two types of generic resistance to pathogens in plants i.e. monogenic and
polygenic. While monogenic characters are stable over a wide range of conditions, polygenic
resistance is highly variable and is influenced by environmental conditions. Polygenic
resistance is also influenced by host nutrition, while monogenic resistance is completely
stable. Repeated selections through breeding or resistance in a crop result in accumulation of
more genes for resistance in new varieties, which is the case in most of the varieties of crop
plants which are widely cultivated over the world. Another finding is that in a crop variety
there may be a gene which may inhibit completely or partially the explanation of resistance to
a disease. Similarly an inhibitor gene may suppress the expression of susceptibility in some
varieties. It has been shown that resistance in some varieties may fluctuate within certain
limits. If the pathogen is capable of producing many races, the monogenic resistance in the
host may break and the host may become susceptible to one or more of the newer races of the
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pathogen. This is what happens in wheat varieties which breakdown for infection by newer
rust races. If large number of genes for resistance is accumulated in one variety, by repeated
breeding or selection, then the possibilities of its continued resistance to most races of rust are
better.

Host resistance may be inherited as a qualitative or quantitative character, and its expression
is influenced by environments. In polygenic avirulent gene combination in the pathogen,
vulnerability of host may endure.

The work on genetics of disease resistance and susceptibility could not progressed till Flor in
1946 while working on flax rust caused by Malampsora lini showed that for each gene for
resistance in the host, there was a corresponding gene for avirulence in the pathogen and for
each gene for virulence in the pathogen there was a gene for susceptibility in the the host
plant. This relationship is popularly known as gene for gene hypothesis. This classical work
made it clear to understand the relationship of plants and their parasites in a generic sence.
Flor also established the inheritance of virulence in M. lini and found that avirulence was
dominant. The generic relationship may be stated as: for each gene determing resistance on
the part of the host there is a comlementary gene determining avirulence on the part of the
pathogen. Gabriel and Rolfe in 1990 pointed out that the virulence is not necessarily a single
gene trait and that where it is oligogenic, the interaction may be gene for gene pathway rather
gene for gene.

Temperature and genetic background can have significant effects on the expression of
resistance gene. For example, the gene Sr6 which is resistant to races of stem rust of wheat
Puccinia graminis tritici that have a corresponding avirulence gene, P6 is temperature
sensitive. At 15 C, Sr6 is effective, developing only a fleck but it is ineffective at 24C giving
a medium sized uredial pustule. Resistance genes generally give protection for a few years
and then fail owing to change in the corresponding avirulence gene in the pathogen. It has
also been shown that a gene which conferred durable resistance interacts with a parasite gene
that contributed significantly to the parasite fitness.

The presence of inhibitor genes interfere with the interaction of the products of resistance and
avirulence genes and thus block the recognition phenomenon which leads to the resistant
reaction. Inhibitor genes may also be temperature dependent.

Advances have also been made in the genetics of pathogenicity and virulence factors. These
have proved the importance of toxins and cell wall degrading enzymes. Studies have
confirmed that the pathogens that are able to avoid or degrade such resistance factors as
saponins and phytoalexins being virulent and those that are unable to do so being avirulent.

Venderplank in 1963 suggested that the resistance is of two types; one known as vertical
resistance which is controlled by a few major resistance genes. This resistance is effective
against one or few races of the pathogen, and the other known as horizontal resistance which
is determined by many minor resistant genes and is weaker but effective against all races of
a pathogen. Some pathogen genes for virulence and even more genes for avirulence have
been isolated and the sequences and products such as enzymes, toxin, inhibitors, growth
regulators etc. of many of the genes have been studied. The resistance in plants may be
cytoplasmic resistance or morphological or mature plant resistance.

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(i)Cytoplasmic Resistance
This type of resistance is more common in improved varieties of wheat. When a resistant
variety is exposed to uredospores or aeciospores, the spores germinate and form appresoria in
the same fashion as on susceptible varieties. In the resistant variety, only a few stomata may
permit entry of the infection hypha while in the susceptible variety many infection hyphae
will succeed. After penetration, a susceptible variety will permit the germ tube to form sub-
stomal vesicle, subsequent mycelia and haustoria which will ultimately enable the pathogen
to develop a pustule. However, in the resistant variety, the protoplasmic contact will inhibit
the pathogen. A small haustorium may be formed but the further development of the
pathogen will cease due to death of the haustorium mother cell. This type of resistance is
based upon the interaction of protoplasts of the host and the pathogen. For every gene in the
rust pathogen that controls its virulence, there is a corresponding gene in the host that control
its resistance. These genes control the production of specific enzymes and other proteins.

Some parasites have evolved several ways to establish physiological contact with their host
plants. At the prepenetration stage they may respond to chemotaxis or the compounds
diffusing from their host. Alternatively, the response may be thigmotropic as in the
development of infection structures by rust fungi. Thereafter, the cuticle and cell wall may be
pentrated by mechanical force, an array of enzymes or a mixture of the two.

The importance of cutinases and pectinases has been established in some host-parasite
interactions both by classical biochemical studies and by molecular techniques. Other
enzymes which may be of importance to the pathogenicity or virulence of plant parasites are
cellulases and proteases. Lignin is often a prominent constituent of plant cell walls and play
significant role to avoid infection.

The toxins are heterogenous group of compounds and are deleterious to the normal
functioning of plants. The primary lesions caused by toxins have been elucidated in a few
cases. The most important role of toxins is to impair the defence responces of the plant. The
hypersensitive reaction is the first response of a plant to an incompatible parasite. Infected
cells die rapidly and in doing so they trigger a range of defence reactions that confers
increased resistance to tissues close to the site of infection. This is known as local acquired
resistance. But if the signal is systemic then it is called systemic acquired resistance (SAR).
Salicylic acid, a relative of aspirin and some other substances have been recognized which
trigger SAR genes. SAR increases the synthesis of pathogenesis related proteins (PR
proteins). Several PR proteins are now known to have chitinase and glucanase activity. The
synthesis of low molecular weight compounds, the phytoalexins are triggered by components
of the parasite as well as the plant and termed as biotic elicitor. They are also triggered by a
range of physical and chemical treatments and they are referred as abiotic elicitor.
Phytoalexins play key role in resistance.

Other defence responses include lignification, suberization, the synthesis of hydroxyproline-
rich glycoproteins, the formation of papillae and the deposition of callose.

Many symptoms caused by plant diseases by biotrophic parasites are considered either by
degradation of enzymes or toxins or by hormonal imbalance due to infection. Enhanced
concentration of auxins and cytokinins can cause symptoms like hypertrophy and local
increase in cytokinin concentration caused by parasites can give rise to green islands resulting
in redirection of nutrients. Stunting of infected plants has been attributed to reduced
concentration of gibberlins or enhanced concentration of ascorbic acid. Ethylene can give
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effect to epinasty, abscission of organs, chlorosis and necrosis as well as the promotion of
certain difence responses.
(ii)Morphological or Mature Plant Resiatance
A given variety may be susceptible to a given set of races but highly resistance to some races
when the plants have matured. The resistance increases with the age of plants. The resistance
based upon the relative amount of the thick walled collenchyma developed in different
varieties at maturity of plants. The collenchyma is not invaded by rust pathogens. The
resiatance of a plant to the disease is greatly influenced by environment including host
nutrition, and by the environment-physiologic race complex.

Acquired resistance can be exploited to give good control of disease. In particular, cross
protection has been used with some virus diseases with encouraging results. More
information would be required in order to build up a complete picture of such defence
mechanisms so that the protection they give may be logically exploited.
During recent years lot of work on the genetics of resistance of wheat rusts has been done
which is summarized below:
Genetics of Resistance to Rusts in India
Identification of sources of resistance in leaf rust (P. recondata)
Seedling Resistance: A series of nearly 45 leaf rust loci with allelic series at some loci for
reaction to P. recondata have been described. Among the leaf rust resistance genes, Lr9, Lr19,
Lr 24, Lr 25, Lr.28, Lr 29, Lr 32, Lr 39, Lr 40, Lr 41, Lr 42, Lr 43 Lr 44 and Lr 45 are
effective against all the pathogenic variability present in the country.
Adult Plant Resistance (APR): Lines carrying known single gene for APR showed field
resistance with Lr 22a and Lr 34. Lr 22a derived from Triticum tauschii. It also showed
excellent resistance under field condition in a line Tc +Lr 22a. Lr 34 showed resistance to
highly virulent and prevalent pathotypes.

Lr 35 from T. speltoides/ T. monococcum and Lr 37 from T. ventricosum were effective in
adult plants. Lr 37 confers slow rusting.
Identification of Novel Resistance: Near isogenic lines for seedling resistance genes Lr 14b,
Lr 14ab and Lr 30 in Thatcher background identified additional plant resistance gene(s).
The wheat rye translocation chromosome (IB/IR) which carries Lr 26 has been the most
widely exploited source of rust resistance in the development of wheat cultivars. Using these
combinations, selection 212 was developed. These genes are effective to all highly virulent
and prevalent pathotypes of leaf and stem rusts. Kundan is slow ruster wheat.
Stem Rust (P. graminis tritici): The stem rust resistance (Sr) genes identified are Sr 24, Sr
25, Sr 26, Sr 27, Sr 31, Sr 32 and a combination of sr 36+9b and Sr 36+9c. In order to exploit
the stem rust resistance genes of significant potential Sr 24, Sr 26, Sr 31, Sr 32, Sr 36+9e and
SrAgi have been introgressed into variety Kalyan sona.
Stripe Rust Resistance: Yellow rust genes Yr 5 and Yr 10 are available in European
population. Yr 5 has been matched by virulent races in India. More details on genetic analysis
of wheat cultivars resistant to wheat rusts in India are given on chapter of wheat rusts.



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Molecular Apptoach to Disease Resistance
Since 1980, great emphasis was given on determining the molecule and the genetic
connection of any substance involved in disease development. Already the number, location,
size, sequence and function of most or all genes of many viruses are known in detail. Many
of these genes have been transferred into the plants and such plants showed resistance.
Similar transfers have been done with a few bacterial and fungal genes coding for certain
pathogenesis-related proteins. In 1941, Beadle showed that one gene codes for one enzyme.
In the following year Flor described the gene for gene concept.

Studies on bacterium Agrobacterium tumefaciens showed that the T-DNA of its Ti plasmid
contains several genes, two of which code for growth regulators and were responsible for
developing tumors by the infected cells.It was later demonstrated that the two genes could be
removed and replaced with one or more genes from other organisms such as plants, other
bacteria, viruses and even animals, genes that could be transferred into and translated by the
plant cells.This discovery made it possible to transfer foreign genes into plants at will and
combind with tissue culture whole plant can be developed from single cell. Now several
methods are available to introduce foreign DNA into plant cells. Some bacterial and fungal
genes, coding for enzymes that breakdown the cell wall of the pathogen, have been
engineered into plants which provided resistance against these pathogens.

A molecule in the cell wall of Phytophthora megasperma found to act as elicitor of the
defence response in its soybean host. The elicitors interact as a receptor molecule on the plant
cells. Almost subsequently the avirulence gene was isolated from Pseudomonas syringae pv.
Glycinea. These discoveries helped in our understanding of pathogen virulence and plant
disease resistance. Hypersensitive response protein (hrp) genes affect the transport of proteins
of pathogenic bacteria into plant cells.

In 1986, Beachy and his team developed virus resistant transgenic tobacco plant by
introducing the coat protein gene of TMV. The resistance in such transformed transgenic
plant is known as pathogen derived resistance. Plants transformed with the genes that code
for chitinase showed resistance to the disease caused by fungi that contain chitin in their cell
wall. Tobacco plants transformed with the gene stilbene synthetase, the enzyme that
synthesizes a phytoalexin showed disease resistance. The first fungal avirulence gene (avr 9)
was isolated from Cladosporium fulvum and first plant resistance gene (Hm-1) was isolated
from corn. Hm-1 operates by producing a protein that detoxifies the host-selective toxin of
the pathogen Cochliobolus carbonum. Later many plant resistance genes were isolated. All
these genes shared leucine-rich repeat in the protein they coded for.

Plant pathogens produce proteins that actively suppress the defence reaction of their host
plants. In addition, the avirulence proteins of some pathogens contain signals that allow these
proteins not only to be introduced into plant cells, most likely through the hrp protein system,
but also to move into and function into plant nucleus.

A new type of defence against pathogens is through RNA-silencing i.e. of regulating genes
based on targeting and degrading sequence specific RNAs. RNA silencing can be induced
experimentally and targeting to a single specific gene or to a family of related genes. This
discovery will play an important role in engineering resistance into plants. The complete
sequence of the genome of organisms will help to locate, identify, compare isolates and
manipulate the genes for pathogenicity in the pathogens and of resistance in their host plants,
97

as well as introduction of them into specific locations of the plant genome where they would
be most effective.

Genomes of the experimental plant, Arabidopsis thaliana, several plant viruses and viroids,
bacteria, Ralstonia solanacearum and Xylella fastidiosa, fungus, Phanerochaete
chrysosporium and nematode, Caenorhabditis elegans and several other pathogenic fungi
like Magnaporthe grisea, Ustilago maydis, Cochliobolus heterostrophus, Botrytis cinarea,
Fusarium graminearum, Phytophthora infestans etc. have been completely sequenced.
Several resistance genes have already been identified, isolated, transferred into susceptible
host plants and such transformed plants showed resistance.

It is hoped that Molecular Plant Pathology will provide cultivars that can resist disease in the
presence of pathogen, without the need to use any pesticide.

Suggested Readings
1. Agrios, G.N. 2005. Plant Pathology Vth edn. Academic Press, New York.
2. Brunt, A.A., Crabtree, K., Dallwitz, M.J ., Gibbs, A.J ., Watson, L. and Zurcher, E.J . (eds) (1996
onward) Plant Viruses on Line: description and lists from the VIDE database.
http://biology.anu.edu.au/groups/mes/vide/
3. Dasgupta, MK. 1998. Phytonematology. Naya Prakash, Naya Udyog, Bidhan Sarai, Kolkata, India.
4. Gupta, VK and Sharma, Satish, K. (eds.) 2000. Diseases of Fruit Crops. Kalyani Publishers, New
Delhi.
5. J ohnson, R. and J ellis, GJ (eds.) 1993. Breeding for Disease Resistance. Kluwer, Hingham,
Massachusetts.
6. J oshi, L.M., Singh, D.V., and Srivastava, K.D. 1986. Problem and progress of wheat pathology in
South Asia. Malhotra Publishing House, New Delhi
7. Mehrotra, RS. 2003. Plant Pathology. Tata McGraw Hill, New Delhi.
8. Rangaswami, G. 1998. Diseases of crop plants in India,3
rd
Edn. Prentice-hall of India, New Delhi.
9. Raychaudhuri, SP, and Verma J eev, P. (eds) 1984-1990. Vol. I. Diseases of Cereals, Vol.II. Diseases of
Fruits, Vol.III. Review of Tropical Plant Pathology (Vegetable Diseases, Vol IV. Diseases of
Plantation Crops and Forest Trees Vol. V. Diseases of Fibre and Oil Seed Crops. Today & Tomorrow
Printers and Publishers, New Delhi.
10. Singh, R.P. et. al. 2006. The wheat rusts.htpp://www.fao.org/docrep/2006/y4011e/y4011eog.htm
11. Singh, R.S. 1998. Plant diseases, 7
th
Edn. Oxford & IBH Pub. Co. Pvt. Ltd. New Delhi
12. Singh, U.S., Mukhopadhyay, A.N., Kumar, J . and Chaube, H.S. 1992. Plant diseases of International
importance, Vol 1-4, Prentice Hall, Eaglewood cliffs, New J ersey.
13. Smith, K.M. 1972. A text book of plant virus diseases. Academic Press, New York.
14. Timmer, L.W., Garnsey, S.M. and Graham, J .H. 2000. Compendium of citrus diseases 2
nd
edn. APS
Press, St. Paul, MN.
15. Vanderplank, J E. 1984. Disease Resistance in Plants. 2
nd
Edn. Academic Press, Orlando, Florida.


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