1.

 Early Blight of Potato:

Pathogen Alternaria Solani:
The disease is quite common in India, and occurs on about three week old plants. Since this
blight occurs earlier than the ‘late blight’ of potato (caused by Phytophthora infestans), it is
called ‘early blight.’
Symptoms:
Well-defined leaf spots appear on the leaves which grow and cover bigger portions or the
entire leaves.
This is called blight. The pale-brown leaf spots show concentric rings, called target board
symptom. In humid weather the disease spreads faster. The infected tissues die, dry and fall
off. This greatly reduces the photosynthetic area of the leaves.
The Disease Cycle (= Life Cycle of the Fungus):
Conidia or mycelia lie in the soil or on plant debris and perennate the fungus in absence of
the crop. When the potato crop is sown and the leaves are formed, the conidia reach the
leaves through wind and germinate. The germ tubes enter the leaves through stomata or by
direct penetration of the epidermis, and form inter-, or intracellular mycelium.
The mycelium secretes enzymes and toxins which kill the cells. The fungus derives nutrition
from these dead cells. When the cells die, the leaf-spot symptoms appear. Clavate conidia
having, both transverse and longitudinal septa are formed on the hyphae.
The conidiophores show ‘knee’-like swellings which indicate the position of the detached
conidia. The conidia are wind-disseminated, and in this way the disease spreads to more
plants throughout the season. In the absence of the host plant, the hyphae or conidia remain in
the fallen leaf tissues or in the soil.
Control Measures:
1. Field sanitation and rotation of crops can minimize the disease.
2. Regular spray of fungicides like Dithane Z-78 controls the disease.
2. Blast Disease of Rice:
Pathogen-Pyricularia Oryzae:
This is the enemy number one of rice crop and occurs in India frequently.
Symptoms:
Spindle-shaped spots, ash-coloured in centre with brown margins, appear on the leaves,
culms, glumes, and the stalk (neck) of the panicle. The ears are also infected and bend
downward due to rotting of the stalk.
The Disease Cycle (= Life Cycle of the Pathogen):
The conidia survive in plant debris, in soil, or on the collateral hosts. When the rice crop is
available, the wind-blown conidia land on the leaves. On germination, the germ tubes enter
the leaves to establish an intra-cellular mycelium. The fungus grows inside the host tissues
and forms conidiophores which emerge through the stomata and bear conidia. The conidia
spread the infection throughout the season. When the crop is harvested, they remain in the
debris, left behind in the fields. Alternatively, the conidia may infect and live on other
collateral hosts, until the next rice crop is available.
3. Grey Blight Disease of Tea:
Genus Pestalotiopsis:
The conidia are spindle-shaped or clavate, five-celled, the three middle cells are coloured
while the terminal cells are hyaline. The upper terminal cell, called the apical hyaline cell,
bears 2-3 setae. The posterior hyaline cell is called the lower hyaline cell. It bears a short
pedicel, with which the conidia are attached to the conidiophore in the acervulus.
Pestalotiopsis causes many important diseases, viz., grey blight of tea (P. theae), leaf spot of
litchi (P. paucista), and leaf spot of mango (P. mangiferae).
Grey Blight of Tea (Thea Sinensis):
Pathogen-Pestalotiopsis Theae (=Pestalotia Theae):
Symptoms:
This is the most common blight disease of tea leaves and does considerable damage to the
crop. First, small brown spots appear which later spread and cover the entire leaf blade. The
old lesions turn grey and masses of conidia appear as black dots on the grey background. The
infected portions turn brittle and fall off, leaving irregular cuts on the leaves.
Life Cycle:
The hyphae are hyaline, septate, branched and grow inter-, and intracellularly inside the host.
Acervuli are formed below the epidermis, which have a distinct basal wall, from which
conidiophores arise and bear conidia. The epidermis later breaks and the conidia lie on the
surface of the leaves.
The conidia are spindle-shaped, 5-celled; the 3 central cells are dark while the terminal cells
are hyaline. The apical hyaline cell bears 2-3 setae, and the lower hyaline cell bears a pedicel.
The conidia germinate mostly by the central cells and infect more leaves. In absence of the
host, the mycelium persists in dead host tissues.
ADVERTISEMENTS:
Control:
1. The blighted leaves should be collected and burnt to prevent infection next year.
2. Spraying of the crop should be done frequently by Bordeaux mixture.
3. Water-logging favours the disease and, therefore, should be avoided.
4. Loose Smut of Wheat:
Pathogen – U. Tritici:
Symptoms:
Plants, produced by internally-infected seeds, contain the hyphae in every nook and corner of
their body. But marked symptoms appear only when ‘ears’ come out. Sometimes, the infected
plants are stunted in growth. The ears instead of containing grains contain black mass of
spores. The sori in the early stages are covered by a thin membrane derived from host tissue
but later the membrane ruptures and the spores become a loose mass; hence the name ‘loose’
smut.
Life History:
The disease is internally seed-borne, i.e., the fungus lives in a dormant stage in the embryo of
the seed. Such seeds look perfectly normal and there is no method to detect the infection
unless they are grown and watched till the ‘ear’ formation.
The seedlings, and later the whole plant are infected by its extensive dikaryotic mycelium,
which grows intercellularly and derives food through haustoria. The plants are said to be
systemically infected. The hyphae collect in the ovaries and the hyphal cells round off,
develop thick walls and become teliospores.
The farmer is taken by surprise when smutted ‘ears’ appear from healthy- looking plants. The
teliospores, after the rupture of the covering membrane, are blown by the wind. When the
teliospores are blown off, only the rachis is left behind. The teliospores land on the feathery
style or ovary of wheat flowers, germinate to form a promycelium.
Karyogamy, followed by meiosis, results in the formation of 4 haploid nuclei, 2 of each
mating type. Septa are laid down in the promycelium so as to form four cells, each containing
a single haploid nucleus. From each cell a thin hypha-like outgrowth emerges.
These are called the infection threads, the counterpart of basidiospores, formed in other
species of Ustilago. The typical basidiospores are not formed in this species, but their
function is performed by the infection threads. These infection hyphae individually are
unable to grow and parasitize the ovary unless two infection threads of opposite mating types
fuse and form a dikaryotic hypha.
Thus, what the single nucleus fails to do is done by the joint action of two nuclei. The
dikaryotic hypha grows through the ovary wall and reaches the ovule. It crosses the testa,
endosperm and ultimately infects the embryo. The mycelium becomes established in the seed
formed by the infected ovule and becomes an inseparable part of it.
The hyphae lie dormant in the seed and spring to life again when the seed is sown in the field
and a seedling is formed. Such internally infected seeds give rise to systematically infected
plants. The fungus lives its somatic life and at the end of the wheat season forms sori
transforming the entire inflorescence, except the rachis, into a black mass of spores.
Control Measures:
1. Seeds for sowing should be obtained from reliable places where the disease does not occur.
2. If there is any doubt, the seeds may be treated by ‘hot water method’. The method was
discovered by Jensen in 1889. Seeds are soaked in shallow warm water contained in pots and
then spread out in the scorching sun during the day. The hyphae die due to the heat of the
sun, much quicker than the embryo. The safety line is very thin and there is every chance of
killing the seeds. But the risk is worth taking.
3. Use of resistant varieties is the best method of avoiding the disease.
5. Wheat Rust:
Three types of wheat rusts are known and all of them occur frequently in India.
These are:
1. Black or stem rust caused by P. graminis tritici.
2. Orange or brown rust caused by P. recondita (= syn. P. triticina).
3. Yellow or stripe rust caused by P. striiformis (= syn. P. glumarum).
Black Stem Rust of Wheat:
Pathogen – Puccinia graminis tritici.
It is a macrocyclic, heteroecious rust as it produces all the five known types of spores
(basidiospores, spermatia, aeciospores, uredospores and teliospores) and needs two hosts –
wheat and barberry, to complete the life cycle. Uredo-and teliospores are produced on wheat
while spermatia and aeciospores are produced on barberry. Basidiospores are produced on
promycelium formed by teliospores on germination.
Control of Wheat Rust:
Use of Resistant Varieties:
Rust-resistant varieties of wheat are available and their use is the safest and cheapest method
of control.
Barbery Eradication:
For a heteroecious rust, like the black rust of wheat, it might be expected that eradication of
one host – the economically unimportant host, barberry, may control the disease by cutting
down the life cycle of the fungus. It proved effective in the U.S.A. But if infection occurs by
uredospores brought by winds, barberry eradication may not be of any use.
In the plains of India, for example, the source of primary infection lies in the hills.
Nevertheless, barberry eradication will be helpful in one way, that its absence will exclude
the chances of dikaryotization and development of new genetic varieties of the fungus.
Brown and Yellow Rusts of Wheat:
The uredial and telial stages of brown and yellow rusts of wheat are depicted in.
6. Smut of Maize:
Pathogen-Ustilago Maydis:
The pathogen is much different from the other smut fungi.
The important differences are the following:
1. In addition to parasitic life, it grows well saprobically in the soil.
2. It grows intracellularly and does not form haustoria.
3. Does not grow systemically in the host but remains localized to several independently
infected parts.
4. Smut sori are formed on almost all the above-ground parts of the plant-the cob, the leaf,
and the stem.
5. The fungus induces tumor formation. The outgrowths, as big as a child’s head are
frequently formed. These are filled with teliospores.
6. The primary mycelium, which in other species is incapable of growth in the host tissue,
grows sufficiently well in the host tissue. However, the dikaryotic secondary mycelium grows
more vigorously than the primary mycelium.
Symptoms:
Sori (galls) containing teliospores are formed on all above-ground parts. Galls of different
sizes appear; the biggest galls are formed on the cobs.
Life History:
The fungus lives saprobically in the soil. When the maize crop is available in the field, the
basidiospores, blown by wind, reach the plants and germinate to form a monokaryotic
primary mycelium.
The primary mycelium makes some growth in the host tissue, but the vigorous growth starts
only when the dikaryotic secondary mycelium is established by anastomosis and fusion of
hyphae of opposite mating types. Dikaryotization is necessary for gall formation. The fungus
does not spread in the host tissue but remains confined to the vicinity of the place of infection
and form a sorus of teliospores.
Big masses of sori appear in the, form of galls or tumors. Each gall is the product of a
separate infection. The teliospores are formed by rounding up of the binucleate cells. In the
beginning, the telia are covered by the host tissues but later, the covering ruptures and the
teliospores become free.
The spores are disseminated by the wind. They germinate to form a club- shaped
promycelium in which karyogamy and meiosis occur, resulting in the formation of four
haploid nuclei. Segregation of sex occurs during meiosis and out of the four nuclei formed;
two are of one mating type and two of the other mating type.
Four septa are laid down which divide the promycelium into four cells, each containing one
haploid nucleus. A bud develops on each cell into which passes the nucleus. The bud later
develops into a basidiospore. The basidiospores are passively discharged, and blown by the
wind to cause more infection. These form secondary sporidia by budding.
Control Measures:
1. Use of resistant varieties is the safest and cheapest method of control.
2. Soil sanitation- The soil should be sprayed with fungicides to kill the fungus present in the
soil.
7. Late Blight of Potato:
Pathogen- Phytophthora infestans
The disease is worldwide in occurrence and is also reported from all parts of India.
Epiphytotics never occur in the plains, but are frequent in the hills. The non-availability of
high relative humidity during the crop season (October-December) prevents the disease
occurrence. The fungus, present in potato tubers, fails to survive the high summer
temperature in the plains. The disease recurrence occurs through ‘seeds’ (tubers) stored in
cold-storages.
The name late blight, is given to this disease because, compared to another disease-early
blight (caused by Alternaria solani), it occurs late in the season. The brown spots appear on
leaves only at the time of flowering; grow very fast and soon cover the entire foliage.
Ultimately, the infection reaches the underground portions of the plant and infects the tubers.
Independent infection of tubers also takes place by zoospores present in the soil.
8. Colocacia Blight:
Pathogen- P. colocasiae
The disease occurs during the rainy season (August-September). Circular to irregular brown
patches appear on the leaves which show distinct zonations. Drops of a yellow liquid appear
on the brown areas. The affected tissues dry and fall off, leaving holes and cuts on the surface
of the leaves. The corm also gets infected and starts rotting. The disease perpetuates from
season to season through infected corms which are used as seeds.