DOWNY MILDEW OF GRAPES

Division : Mycota
Subdivision : Eumycotina (True Fungi)
Class : Phycomycetes
Sub Class : Oomycetes
Order : Perenosporales
Family : Perenosporaceae
Causal Organism : Plasmopara viticola

• It is an obligate parasite of vascular plants.

• It parasitise the economically valuable plant is grape vine (Vitis vinifera).
Symptoms:
• mildews are plant diseases in which pathogen (fungus) is grown on the lower surface of the
leaf of the host.
• they appear whitish green, or grey brown patches of different sizes on herbaceous stem or
roots. the fungal growth is superficial
the disease appear on all aerial parts of the grape vine.
• they are more prominent on leaves, young shoots, immature berries.
• the first apperance of disease is the sign of small greenyellow spots on tne upper surface of
leaves on the opposite sides below the spots.
• downy growth is present which is whitish, later on dark brown spots are produced on leaves.
• the growth on lower surface becomes dirty grey finally the leaves dry up and fall off.
• Diseased roots remain stunted in growth, and due to hypertrophy may become swollen. the
cells divide and redivide and becomes swollen.
• Infected leaves, shoots, tendrils become covered with whitish growth of fungus. infected parts
have water soaked spongy apperance.
• The older part may rot and crack. after the growth of fungus, entire branch of berries is
destroyed.
• When infection is in early stage, fungal growth is visible on surface of berries.
• When fruits are half grown and at this stage infection occurs, the fungus is confined to inside
portion of the berries.
DISEASE CYCLE :
• the vegetative mycelium is coenocytic, develops intercellular in the hosttissue.
• it sends its haustoria into the host cells to absorb nutrients.
• the hyphae are hyaline, thin, with granular protoplasma they secret enzymes with the help of
which they absorb food from the cell.
• the mycelium collects in the substomatal cavity.
• agroup of hyphae grow upright from the hypal pad and emerges out of stomata and functions
as sporangiophore. it may have 1 to 10 branches.
• each sporangiophore is monopodially branched.
• each branch bears branchlets. the branches and branchlets lie at right angle to main axis.
• the growth of sporangiophore is determinate (definite). it bears sporangia at tip.
• sporangia develop at the alternate branchlet called sterigmata.
• sporangia are small, ovid, uninucleate, they undergo repeated divisions.
• this multinuclate protoplast is then divided into several uninucleate daughter protoplast.
 sporangia are shed and dispersed by wind.if they fall on the suitable moist leaf surface they
germinate.
 a circular cone appears at the papilla. the uninucleate protoplast get metamorphosed into
biflagellated zoospores.
 zoospores are plano-concave. they swim in thin film of water and come to rest in the vicinity
of stomata.
 each zoospore rounds up, come to rest and soon produce a germ tube. this germ tube enters
into the host through stomata.
 the conidia and antheridia are formed in the intercellular spaces of the host cells.
 the oogonium is globose and terminal. the contents of the oogonium are differentiated into
periplasm and central ooplasm. this ooplasm functions as oosphere.
 antheridium is clavate with 12 nuclei. at the point of contact with oogonium the anthredium
sends forth a delicate tube called fertilization tube.
 through this fertilization tube male nucleus pass and unite with egg nucleus.
 fused egg is called zygote which secretes wall around and becomes oospore. oospore
germinates in the spring season.
 before germination two nuclei fuse. this fusion of nucleus undergo repeated divisions to form
5o nuclei.
 first division of nucleus is meiotic which is followed by mitosis.
 at this stage the wall of oospore bursts and small germ tube comes out.
 the end of germ tube swells forming sporangium and carrying 50 nuclei
 these nuclei get metamorphosed into zoospore. these zoospores are uninucleate, reniform.
 they come out from sporangium through apical pore they germinate on host.

Control Measures
 spraying the grapes with fungicides found to be effective measure.
 bordeux mixture, ferban and captan are the best fungicides.
 sanitation is very important. fallen leaves and branches which are infected should be
collected and burnt.
 vines should be planted with proper spacing and should be treated in amanner that leaves
 do not remain near the ground.
 fungicides like bordeux mixture, zeneb 2 % should be sprayed
 resistant varieties should be used.

Grassy shoot of sugarcane

Symptoms:
 Initial symptom appears in the young crop of 3 – 4 months age as thin papery white
young leaves at the top of the cane.
 Later, white or yellow tillers appear in large number below these leaves (profuse
tillering).
 The cane becomes stunted with reduced internodal length with axillary bud sprouting.
 This disease appears in isolated clumps.
Pathogen:
 The disease is caused by Mycoplasma like organisms. Mycoplasma cells are physically
small – less than 1 µm – and they are therefore difficult to detect with a conventional
microscope.

Management strategies
Cultural method:
 Growing resistant varieties viz., Co 86249, CoG 93076 and CoC 22
 Avoid ratooning if Grassy Shoot Disease incidence is more than 15 % in the plant crop
 If disease symptoms are visible within two weeks after planting, such plants can be
replaced by healthy plants.
 Uprooted infected plants need to disposed of by burning them.
Physical method:
  Rogue out infected plants in the secondary and commercial seed nursery.
 Treat the setts with aerated steam at 50°C for 1 hour to control primary infection.
 Treating them with hot air at 540C for 8 hours and spraying twice a month with
aphidicides.
Chemical method
 Spray dimethoate @ 1ml in 1 litre of water to control insect vector
 Apply pesticide methyl-demeton @ 2ml/lit of water for controlling aphids.

Late blight of potato

Causal organism: Phytopthora infestans
Symptom:
 It affects leaves, stems and tubers.
 Water soaked spots appear on leaves, increase in size, turn purple brown& finally black
colour White growth develops on under surface of leaves.
 In tubers, purplish brown spots and spread to the entire surface on cutting, the affected tuber
show rusty brown necrosis spreading from surface to the center.
Pathogen
 The mycelium is endophytic, coenocytic and hyaline which are inter cellular with double
club shaped haustoria type.
 Sporangiophores are hyaline, branched intermediate and thick walled.
 Sporangia are thin walled, hyaline, oval or pear shaped with a definite papilla at the apex.
 The sporangium may act as a conidium and germinate directly to form a germ tube.
 Zoospores are biflagellate possess fine hairs while the other does not.
Mode of spread and survival
 The infected tubers and the infected soil may serve as a source of primary infection.
 The diseased tubers are mainly responsible for persistence of the disease from crop to crop.
 The air borne infection is caused by the sporangia.
 Favourable conditions RH->90% , Temp.-10-25°C and Night temperature:10°C.
 Cloudiness on the next day Rainfall at least 0.1mm, the following day.
Management:
 A regular spraying and dusting during the growing season give effective control.
 First spraying should be given before the commencement of the disease and subsequent
should follow at regular interval of 10 -15 days.
 Protective spraying with mancozeb or zineb 0.2 % should be done to prevent infection of
tubers.
 Destruction of the foliage few days before harvest is beneficial and this is accomplished
by spraying with suitable herbicide.
 Tuber contamination is minimized if injuries are avoided at harvest time and storing of
visibly infected tubers before storage.
 The resistant varieties recommended for cultivation are Kufri Naveen, Kufri Jeevan,
Kufri Alenkar, Kufri Khasi Garo and Kufri Moti.
 Black stem Rust of Wheat
Systematic position:
Kingdom: Fungi
Phylum: Basidiomycota
Subphylum: Pucciniomycotina
Class: Pucciniomycetes
Order: Pucciniales
Family: Pucciniaceae
Genus: Puccinia
Species: graminis f.
Distribution:
 Disease is present almost everywhere wherever wheat crop is grown.
 Epidemics of stem rust of wheat often occur in different parts of the world.
 More prevalent in North America, Ethiopia, India, China and Australia.
Symptoms:
 Do not produce symptoms until 7-15 days from infection.
 the oval pustules (uredinia) of powdery, brick-red urediniospores break through the
epidermis. Microscopically, these red spores are covered with fine spines.
 The pustules become abundant and are produced on both leaf surfaces and stems of wheat
hosts.
 Later in the season, pustules (telia) of black teliospores begin to appear in infected grass
species.
 Microscopically, teliospores are two celled and thick walled.
 The stem become dry and cracked and most severely attacked.
 The plant produces less or no grains.
 A number of physiological changes occur by rust infection.
 Pycnia appear on barberry plants in the spring, usually in the upper leaf surfaces. They are
often in small clusters and exude pycniospores in a sticky honeydew.
 Five to 10 days later, cup-shaped structures filled with orange-yellow, powdery aeciospores
break through the lower leaf surface.
 The aecial cups are yellow and sometimes elongate to extend up to 5 mm from the leaf
surface. Microscopically, aeciospores have a slightly warty surface.
Causal organism:
Black or Stem rust of wheat is cause by Puccinia graminis tritici.
Pathogen characters:
 The pathogen is an obligate parasite.
 It cannot exist as saprophyte.
 In most rust fungi, only the teliospores survive apart from a living host plant for more than
few months under field conditions.
 Pucciniagraminis is heteroecious and polycyclic fungi which completes its disease cycle in
two hosts.
 Wheat; Primary host, Barberry; alternate host.
 Accordingly, in wheat the mycelium is dikaryotic and in berberry monokaryotic.
Stages in Pathogen:
Fungus gains entrance to host through stomata.
Five spore stages of Pucciniagraminis
• Stage 0: Spermatogonium, produces spermatozoa and receptive hyphae.
• Stage I: Aeciums produce aeciospores.
• Stage II: Uredium produce urediospores.
• Stage III: Telium produce teliospores.
 Stage IV: Basidium produce basidiospores.

mode of spread.
 Stem rust is favored by hot days (25-30°C/ 77 86°F), mild nights (15-20°C/59-68°F), and
wet leaves from rain or dew.
 It appears in the month of March in Northern India. In Southern and Peninsular India it
appears very early in the 4th week of November.
 Both aeciospores and urediniospores require free water for germination like other spore
stages.
 Infections occur through stomata.
 Primary spread - Urediniospores and aeciospores are wind borne.
  Secondary spread - Rain is necessary for effective deposition of uredinospore involved
in regional spore transport.
 Teliospores remain with the straw.
Disease cycle:
 Urediniospores and teliospores occur on Wheat.
 Fungus gains entrance to host through stomata.
 Early spring, aeciospore infects Wheat to start infection.
 Spore stage gives plant its characteristic rusty color.
 Uredio spore stage is "repeater stage". Continually re infects wheat into late summer.
 Late summer, uredium converts to telium and produce telio spores.
 Telio spore are thick-walled, with two cells and black.
 Teliospore over winters.
 Following spring, germinates to produce basidia and basidiospores.
 Basidiospores Convert into sporangium.
 Then sporangium converts into aeciospores and the cycle continues.
Management of Disease:
 Adjustment of sowing dates.
 Growing short and long duration crops.
 Applications of balanced fertilizers to the crop.
 Eradication of barberry trees around the wheat field.
 Cultivation of Rust Resistant Varieties: NP 718, NP 710 and NP 770.
 Lerma Rojo, Safed Lerma, Choti Lerma and Sonalika are highly resistant to all three
rusts in the field.
 Use of Fungicides Including Antibiotics:
 Wilt of Tur
Causal organism Pathogen: Fusarium oxysporum f. udum
Host: Cajanus cajan
Symptoms
Pigeon pea plants are susceptible to infection by the wilt pathogen at all stages of development.
The disease may appear from early stages of plant growth (4-6 week old plant) up to flowering
and podding. The main symptoms of the disease are the wilting of seedlings and adult plants
characterized by gradual, sometimes sudden, yellowing, withering and drying of leaves followed
by drying of entire plant or some of its branches. Such plants exhibit loss of leaf turgidity,
interveinal clearing and chlorosis before death. Sometimes lower branches show die-back with
the purple band extending from the tip downward with intensive xylem blackening. The wilting
is brought about by the plugging of the vascular tissue of the stem and roots of the host plant
by dense masses of mycelial hyphae.
MYCELIUM
The fungus is confined to vascular tissues and is both inter- as well as intracellular. The septate
hyphae run across the cells, growing rapidly along the inside of the walls of larger vessels. This
results in the plugging of such vessels. The mycelium is hyaline, septate, branched and produces
spores of three types inside the host. These spores are – micro-conidia, macro-conidia, and
chlamydospores. Microconidia are generally tiny structures produced in large numbers from the
tips of conidiophores which are indistinguishable from the vegetative hyphae They are small,
hyaline, elliptical or curved, and unicellular or with one or two septa, measure 5-15 x 2-4 µm,
and are produced on hyphal branches.
Disease Cycle
Primary Infection The primary infection occurs mainly through the fine rootlets, which are
penetrated by the hyphae perennating in the soil or the hyphae formed as a result of the
germination of conidia and chlamydospores present in soil.
From infected fine rootlets the pathogen mycelia ultimately pass into the larger roots, which
are not directly penetrated by the hyphae unless they are injured.
Secondary infection in case of this disease is rare as the conidia produced on aerial parts of the
host and causing infection.
Control measures
1. The use of resistant varieties is of foremost importance. Varieties NP 15, NP 38, C11, C28,
C36, F18, T17, NP15, NP38, and NP41 are resistant to wilt of pigeon pea lines ICP4769, 0063,
9168, 10958, 11299 and cultivars C11 (ICP7118) and BDN 1 (ICP 7182) have been found showing
medium to long duration resistance in all the 5 years of multi-locational trials (15 different
locations) in Bihar, U.P., Maharashtra, Bengal, Delhi, and Karnataka.
2. Pigeon pea is generally grown in inter- and mixed-cropping systems in rotation with other
crops.
3. Mixed cropping with Sorghum (Jowar) has been found to be most effective. Two cycles of
sorghum followed by pigeon pea has been found to reduce the disease incidence by 16%.
4. Seed borne infection can be eliminated by seed dressing with a mixture of benomyl and
thiram.

Papaya Mosaic
An outbreak of the papaya mosaic virus disease was first encountered in 1959 in Waimanalo
Valley on the windward side of the island of Oahu (9). By 1961, it had spread rapidly and had
restricted papaya-growing in a number of commercial orchards (fig. 1) . The mosaic disease is
very destructive; losses ranging from 5 to 20 percent are common in many orchards but losses
as high as 75 percent have occurred. In 1962, papaya mosaic was found in the Puna district of
the island of Hawaii.
Symptoms
Leaves.
Initially, the leaves develop a rugose appearance. The underside of the leaves shows thin,
irregular, dark-green lines which appear to etch the borders of cleared areas along the veins.
Younger leaves of the crown are generally stunted and severely chlorotic with vein-banding (fig.
2) or transparent oily areas scattered over the leaf or along the leaf veins. In mature leaves, the
chlorotic pattern frequently is expressed as extensive veinclearing, and numerous small rings
(fig. 3) develop which are transparent and yellow to tan in color. In severely affectedtrees,
defoliation progresses upward until only a small tuft of leaves remains at the crown. Leaf
symptoms for papaya mosaic contrast with the more mild and diffuse mosaic pattern of the
papaya ringspot disease. However, stunting of all parts occurs in trees affected with the papaya
ringspot virus under adverse environmental stress.

Stem and petiole.

On the stems of infected plants are found pinpoint-size spots. As the infection progresses, these
spots may develop into linear or, in some instances, distinct concentric ring patterns (fig. 4)
which become more intense in color and larger in size. On the petioles, the sPOts are more
irregular in distribution, linear in shape, and at times more elliptical than on the stems. They are
also generally lighter in color than those of the stem. In severe infections, petioles are stunted
and may bend downward.
Fruit.
On the fruit, symptoms may be manifested in all stages of maturity. Small, dark-green ringspots,
ls inch in diameter, have been observed on fruits as young as 2 weeks old. Typically, rings
initially show either on the stem end or blossom end. The rings at first may be incompletely
closed and irregular, but as the fruit develops, targetlike spots will increase in diameter from ls
inch, consisting of only 1 ring, to about 1 inch with approximately 8 distinct, slightly raised,
concentric, brownish rings with a green outside ring (fig. 5) . On ripe fruit, there is no mottling
of colors as found in papaya ringspot disease (fig. 6).
Transmission
The papaya mosaic disease is readily transmitted either mechanically or by several aphid
species, including the green peach aphid, Myzus pfIrsicae. Attempts to transmit the virus to 56
species of plants representing 15 plant families have been unsuccessful, except for papaya and
species in the family Cucurbitaceae (16). Although squash, pumpkin, and cantaloupe are
susceptible to the virus, watermelon is the best source-plant, followed by cucumber, then
papaya. Only one aphid is required to infect a plant. An aphid is able to acquire the virus from a
diseased plant during a IO-second feeding period and to infect a healthy plant in a feeding
period of the same duration. After acquisition of the virus, the aphid rapidly loses its ability to
transmit and within an hour little or no transmission occurs. Symptoms normally appear 18 to
24 days after inoculation.
Control
At present, the only satisfactory way of controlling mosaic is by destroying the source of the
virus. Once infected, a tree will always remain infected. Complete recovery from the disease
does not occur. Partial recovery is only apparent and temporary. A roguing program with the
following specific steps is necessary for control of this disease: 1) Spray all infected trees with
an insecticide so that aphid carriers are destroyed. 2) Cut and remove from the growing area of
papaya and cucurbitaceous plants all infected trees, so that the disease cannot spread and all
infected plant parts will dry out and die. 10 3) Avoid nearby cultivation of all cucurbitaceous
plants, as the virus is found naturally in several species in this plant family. 4) Control aphids
with pesticides, since they are the disease carriers.