MANGO

Anthracnose

Disease symptoms

• The disease causes serious losses to young shoots, flowers and fruits It is also affects fruits during
storage.
• The disease produces leaf spot, blossom blight, wither tip, twig blight and fruit rot symptoms.
Tender shoots and foliage are easily affected which ultimately cause „die back‟ of young branches.
Older twigs may also be infected through wounds which in severe cases may be fatal.
• Depending on the prevailing weather conditions blossom blight may vary in severity from slight to a
heavy infection of the panicles. Black spots develop on panicles as well as on fruits. Severe
infection destroys the entire inflorescence resulting in no setting of fruits. Young infected fruits
develop black spots, shrivel and drop off.
• Fruits infected at mature stage carry the fungus into storage and cause considerable loss during
storage, transit and marketing.

Survival and spread

• Fungus survives in dead twig and other host for long time which is the source of primary infection.

Favourable conditions

• High humidity, frequent rains and a temperature of 24-32oC fabours the development of disease.
Mango malformation

Disease symptoms

• Vegetative malformation: Vegetative malformation is pronounced in young seedlings. The affected

seedlings develop vegetative growths which are abnormal growth, swollen and have very short
internodes.
• Floral malformation: The flower buds are transformed into vegetative buds and a large number of
small leaves and stems, which are characterized by appreciably reduced internodes and give an
appearance of witches‟ broom. The flower buds seldom open and remain dull green.

Survival and spread

• The disease is mainly spread via infected plant material. Mango malformation disease spreads
slowly within affected orchards.
• The mango bud mite, Aceria mangiferae, has been associated with mango malformation disease as
wounds from the mites‟ feeding activity are thought to facilitate fungal infection.

Favourable conditions

• Moist weather favours the development of disease.

Powdery mildew

Disease symptoms

• The characteristic symptom of the disease is the white superficial powdery fungal growth on leaves,
stalks of panicles, flowers and young fruits.
• The affected flowers and fruits drop pre-maturely reducing the crop load considerably or might
even prevent the fruit set.
• The fungus parasitizes young tissues of all parts of the inflorescence, leaves and fruits.
• Young leaves are attacked on both the sides but it is more conspicuous on the grower surface.
Often these patches coalesce and occupy larger areas turning into purplish brown in colour

Survival and spread

• The powdery mildew fungus overwinters in dormant buds. When conditions are favorable for
growth of the fungus in spring, spores are produced, released, and cause new infections. Secondary
spread of the disease can occur if spores are produced in these new infections

Favourable conditions

• Rains or mists accompanied by cooler nights during flowering are congenial for the disease spread.
Citrus canker

Disease symptoms:

• Initially, disease appears as minute water soaked round, yellow spots which enlarge slightly and turn
brown, eruptive and corky.
 • These pustules are surrounded by a characteristic yellow halo.
• Canker lesions on the fruit do not possess the yellow halo as on leaves. Several lesions on fruit may
coalesce to form larger canker.
• Due to severe infections the there may be defoliation, and twig and stem may show die-back
symptoms.

Survival and spread:

• In lesions on Citrus, and can also survive for long periods in diseased plant tissues
• Citrus leaf miners (Phyllocnistis citrella) help in the dissemination of the pathogen.

Favourable conditions:

• Spring seasion is favourable for the development of disease.

Gummosis

Disease symptoms:

• Disease starts as water soaked large patches on the basal portions of the stem near the ground
level.
• Bark in such parts dries, shrinks and cracks and shreds in lengthwise vertical strips.
• Later profuse exudation of gum from the bark of the trunk occurs.
• Considerable amount of gum formation in sweet oranges may be observed, but relatively little in
grapefruit.

Survival and spread:

• The fungus survives in the form of dormant mycelium and under moist conditions. The fungi
produces large numbers of motile zoospores, which are splashed onto the tree trunks.
• Secondary infections often occur through lesions created by Phytophthora

Favourable conditions:

• The Phytophthora species causing gummosis develop rapidly under moist and cool conditions.
Black scurf/ canker

Disease symptoms:

Black scurf is easily recognised:

• Raised, hard, black patches, irregular in size or shape, on the surface of the tuber. These are readily
rubbed or scraped off
• Brown strands of fungal material called mycelium can sometimes be seen around the black scurf with
the aid of a magnifying glass
• The scurfs themselves are in fact compact masses of fungal mycelium

The fungus can also cause a symptom known as stem canker on potato sprouts (new shoots) and stems:

• Sunken, brown lesions develop on the sprouts before they emerge from the soil
• In severe cases the tip of the sprout is killed. It often shoots again from lower down, but emergence is
delayed
• Rough, brown, sunken patches develop on the stem, below soil level
• If these girdle the stem then stunting and wilting often results, sometimes with the production of small,
green, aerial tubers in the junction between the stem and leaf stalk
Survival and spread:

• Pathogen is soil and seed borne, remain in soil and plant debris including infected tubers

Favourable conditions:

• High temperature and moisture is the favourable for disease development

POTATO LEAF ROLL DISEASE

1. Introduction:
• Potato Leafroll Virus (PLRV) belongs to the Polerovirus genus and
Solemoviridae family.
• It primarily infects potatoes and other Solanaceae family members.
• First described in 1916 by Quanjer et al.
2. Hosts and Symptoms:
• Primary host: Potato (Solanum tuberosum spp.).
• Symptoms:
Leaf Necrosis and Curling:
• Necrosis (death) of leaf margins, which turn brown and purplish.
• Curling of affected leaves towards the center.
Chlorosis and Rolling:
• Chlorosis (yellowing) of leaves, particularly in secondary infections.
• More pronounced rolling of leaves, with entire leaf becoming chlorotic.
Stunted Growth and Reduced Yield:
• Infected plants exhibit stunted growth.
• Smaller tubers are produced, resulting in reduced yield.
Vascular Tissue Necrosis:
 • Necrosis of phloem tissue, especially noticeable in haulm (above-
ground stems).
• Necrosis of vascular tissue in tubers, leading to net necrosis.
Tuber Symptoms:
• Infected tubers retain normal shape but may exhibit necrosis of
vascular tissue.
• Necrotic spots may develop throughout the tissue, especially in
storage.

3. Virus Characteristics and Transmission:

• Extremely small, nearly spherical particle (25 nanometers).
• Transmission primarily by green peach aphid (Myzus persicae).
• Virus acquisition by aphids through feeding on infected plants.
• Complex transmission process involving gut and salivary glands.
• Mechanical transmission not observed.
4. Disease Cycle:
• Introduction via infected seeds or aphid vectors.
• Persistent transmission by aphids.
• Aphids overwinter in woody species, migrate to herbaceous hosts in
summer.
• Spread to potatoes and other crops during aphid feeding.
• Spread also possible through infected tubers in storage.
5. Environmental Factors:
• Prevalent in environments conducive to aphid development.
• Thrives in warm, humid conditions.
• Optimal temperatures for green peach aphid: 13-19°C.
6. Importance:
• Causes significant yield loss in potatoes.
• Economic impact due to reduced tuber quality and quantity.
• Particularly problematic in seed potato production.
7. Management:
• Control aphid populations to reduce transmission.
• Use systemic and foliar insecticides for aphid control.
• Sanitation practices to reduce reservoirs.
• Seed certification programs for virus detection and rejection of infected
seed lots.
8. Diagnostic Methods:
• Diagnosis based on symptoms in infected species.
• On-site detection using PLRV AgriStrip-magnetic, capable of detecting
low titers.
9. Economic Impact:
 • Annual potato loss in the U.S. estimated at $100 million due to PLRV
and other aphid-vectored viruses.

Causal organism: Fusarium oxysporium f. sp. Capsici

✓ Symptoms

✓ The leaves turn yellow and wilt.

✓ The chlorotic symptoms being to appear on one side of the leaf

✓ Dropping of leaves which led to drying of leaves and branches.

✓ Browing of the vascular system can be seen in a cross section of the lower stem or by
removing lower stem and roots.

✓ At last it cause the death of plant.

Management:

• Use disease free seeds

• seed treatment - thiram 2 kg/ha or zineb 2.5 kg/ha
• Three sprayings with captan 0.2 %- 1st spraying - just before flowering, 2nd at the time of fruit
formation and 3rd - fortnight interval after second spraying

Biocontrol

• P. fluorescens, Bacillus subtilis -effective (Rajavel, 2000)

• P. fluorescens and T. viride (Muthuraj, 1998)
• Saccharomyces cerevisiae & P. fluorescens (Jayalakshmi et al., 1998)
• Essential oil - Nigella sativa - antimicrobial activity

urple blotch/scald disease: Alternaria porri

Symptom:

• Leaves - whitish minute dots on leaves with irregular chlorotic areas on tip portion
• Circular to oblong concentric black velvety rings appear in chlorotic area
• Lesions develop towards the base of the leaves
• Leaves die from the tip downwards, break at the point of infection and hang down
• Bulbs – semi watery rot, shrinkage of the fleshy bulb scales and desiccation followed by these
scales becoming dry and papery

Identification of pathogen:

• Mycelium - branched, coloured and septate

• Conidiophores - singly or in groups, septate, pale to mid brown
• Conidia - solitary, straight or curved

Mode of spread and survival:

• Carried through seed bulbs collected from infected field

• Spreads mainly through air borne spores
• Pathogen enters through stomata or wounds
• Survives in plant debris for 8 months

Epidemiology:

• Temp - 21 to 30oc
• RH - 90 %

Management:

• Seed treatment - thiram @ 2.5g/kg of seed

• Three sprays of Copper oxychloride - 0.25%, Chlorothalanil - 0.2% and Zineb -
0.2%
• Mancozeb - 0.2%
• Varieties - New Selection, Red Creole - resistant

STEMPHYLIUM LEAF BLIGHT

Symptom

• Initial infections on the leaves and leaf sheaths are small, light yellow to brown, and water-
soaked.

• As the lesions expand, they coalesce, causing extensive blighting of the leaves.

• Typically, lesions are found in higher numbers on the side of leaves facing the prevailing
wind.

• The centers of lesions turn brown to tan, then dark olive brown, and finally black as the
fungus sporulates
 • Sometimes fruiting bodies called perithecia may appear in infected tissue as small, black,
pinhead-like raised bodies. Causal organism: Stemphylium vesicarium (Teleomorph:
Pleospora allii) Sub-division: Deuteromycotina

Disease cycle:

• Primary infection: Plant debris and seed bulb

• Secondary infection: Air-borne conidia

Favourable condition: Warm humid weather with rains or heavy dew

Management • Spray with Carbendazim + Mancozeb @ 0.25

• Bacterial wilt can cause severe losses in cucumbers and muskmelons.

It is less common and less severe in pumpkins and squash.
• Plants wilt in the field. They often recover overnight but continue to
wilt each day.
• Wilt is often isolated to a small area or individual plants.
• Wilt progresses down the vine until the entire vine wilts or dies.
• Leaves eventually yellow and brown at the margins, then completely
wither and die.
• The bacteria overwinter in the gut of striped and spotted cucumber
beetles. It cannot overwinter in Minnesota in plant debris.
• Managing cucumber beetles provides the most effective control of
bacterial wilt.
• Pesticides will not cure a cucurbit plant infected with bacterial
disease.
Life Cycle:
E. tracheiphila is dispersed within and among fields by the striped cucumber
beetle. The bacterium is transmitted mechanically by contact with contaminated
mouthparts and does not reproduce within the beetle. The beetles feed on
leaves and stems, E. tracheiphila multiplies in the wound, enters the xylem
vessels (water conducting tissues), and moves through the petioles to the stems.
Masses of bacteria, gums, and resin plug the vascular system, resulting in wilt.
Bacteria spread throughout the plant through adjacent xylem vessels. Infected
plants serve as a reservoir of bacteria for subsequent infections. Cucumber and
muskmelons are more susceptible to bacterial wilt than winter squashes and
watermelon.

Mode of spread and survival

The bacteria apparently overwinter in cucumber beetles and they appear to multiply in the beetle.
The bacterium is not seed borne or soil borne. Bacteria in stems can survive for one month. Beetles
prefer to feed on plants with bacterial symptoms than on healthy plants. Beetle can remain infective
for atleast three weeks. Striped cucumber beetle and the 12- spotted cucumber beetle help in the
spread of the bacterium.

Management

• In general, more bacterial wilt is seen on the edges of fields where beetles first encounter
plants. Larger plantings must be protected by insecticides.
• Carbaryl, Malathion, or rotenone insecticides or combination products are registered to treat
cucumber beetles.
• They will provide control of the beetles if applied when beetles first appear in the spring.
• Early control, beginning as soon as the plants emerge, is most important as a single beetle
can introduce the bacteria. One to four generations of the beetle may occur on unprotected
plants and applications of these insecticides at weekly intervals may become necessary.
• Apply a light even coating of the insecticide over the entire plant, especially where the stem
emerges from the soil (where the beetles often congregate).

DOWNY MILDEW OF GRAPEVINE

CAUSAL ORGANISIM: Plasmopara viticola

Economic importance • Since 1875, this disease caused heavy losses in France to wine
industry. • It led to discovery of Bordeaux mixture by Prof. Millardet in 1885. • When all the
condition favourable losses vary to 50- 100%.

SYMPTOMS • Symptoms appear on all aerial and tender parts of the vine. Symptoms are
more pronounced on leaves, young shoots and immature beries. • Irregular, yellowish,
translucent spots on the upper surface of the leaves. • Correspondingly on the lower surface,
dirty white, powdery growth of fungus appears. • Affected leaves become, yellow and brown
and gets dried due to necrosis • Premature defoliation. Dwarfing of tender shoots. • Infected
leaves, shoots and tendrils are covered by whitish growth of the fungus. • White growth of
fungus on berries which subsequently becomes leathery and shrivels. Infected berries turn
hard, bluish green and then brown. • Later infection of berries results in soft rot symptoms.
 Normally, the fully grown or maturing berries do not contact fresh infection as stomata turn
nonfunctional. • No cracking of the skin of the berries.

PATHOGEN • P. viticola is a biotroph. The intercellular mycelium of the fungus is coenocytic,

thin-walled, hyaline, and produce spherical or pear shaped haustoria. • Sporangiophores
arise from hyphae under high humid conditions. The branching of the sporangiophores is at
right angles to the main axis and at regular intervals. • From the apex of each branch 2-3
sterigmata arise and bear lemon shaped, papillate sporangia. Sporangial germination may be
through zoospores or by germ tube based on humidity and temperature.

SPREAD AND SURVIVAL • Sporangia or zoospores by wind, rain etc. • Oospores present in the
infected leaves, shoots and berries. Also as dormant mycelium in infected twigs.

FAVOURABLE CONDITIONS • Optimum temperature : 20-22°C. • Relative humidity : 80-100 %

MANAGEMENT

• Collect and burn fallen leaves and twigs. • Sanitation of the orchard. • Vine should be kept high
above ground to allow circulation of air by proper spacing • Pruning (April- may & September and
October) and burning of infected twigs • Grow resistant varieties like Amber Queen, Cardinal,
Champa, Champion, Dogridge and Red Sultana. • The disease can be effectively managed by giving 3-
5 prophylactic sprays with 1% Bordeaux mixtureor Fosetyl -Al (Aliette) 0.2% or metalaxyl + mancozeb
0.3 to 0.4% or Azoxystrobin or Dimethomorph.  Chemical -5 sprays with 1% Bordeaux mixture • 1 –
Immediately after pruning of vines • 2 - When new flush formed (3-4 weeks after pruning) • 3 –
Before buds open • 4 - When bunches or berries have formed

POWDERY MILDEW OF GRAPEVINE

• CAUSAL ORGANISIM: Uncinula necator (I.S: Oidium tuckeri)

ECONOMIC IMPORTANCE • Losses in yield of fruits may be upto 40-60%. • In addition to loss of yield,
infected berries tend to be higher in acid content than healthy fruits and are unsuitable for wine
making

SYMPTOMS

• The disease attacks the vines at any stage of their growth. All the aerial parts of the plant are
attacked. Cluster and berry infections usually appear first. • Small whitish patches appear on both
the surface of the young leaves. These patches enlarge covering the leaf surface with a characteristic,
whitish powdery coating. • In advanced stage affected leaf turn greyish white and become dwarf
,twisted and malformed. • Discolouration of stem to dark brown. • Floral infection results in
shedding of flowers,discolouration of flower and poor fruit set. • Early berry infection results in
shedding of affected berries . • Powdery growth is visible on older berries and the infection results in
the cracking of skin of the berries. Often infected berries develop a net-like pattern of scar tissues.

PATHOGEN

• The mycelium is ectophytic and produces bilobate or multilobate appressoria. • The conidiophores
are simple, multiseptate and erect bearing a chain of 3-4 conidia. • Under Indian conditions, perfect
stage of the fungus is not found. • When the mating types are present cleistothecia can form on all
infected tissues during later part of the growing season. • The cleistothecium,which is characterized
by the presence of long appendages ending in spirals, carries inside the closed sac the asci and
ascospores.

MODE OF SPREAD AND SURVIVAL

• Through dormant mycelium and conidia present in the infected shoots and buds. • Through air-
borne conidia.

FAVOURABLE CONDITIONS • Warm and dry weather with sufficient humidity 57% above. •
Temperature in the range of 21-300C fav. For disease development.
MANAGEMENT 

Clean cultivation of vines or removal and destruction of all diseased parts.  Dustings of vines with
300 mesh Sulphur (1st when new shoots are 2 weeks old, 2 nd prior to blossoming, 3rd when the
fruits are half ripe).  Prophylactic spray with Bordeaux mixture 1% or Lime sulphur at dormant stage
delays development of disease by decreasing initial inoculum.  Spray wettable sulphur @0.3% or
karathane or calixin @0.1%  Morestan @0.03% sprayed at 4 days interval starting from last week of
December to 1st week of March  Grow resistant varieties like Red sultana, Skibba White, St.George
etc.

ANTHRACNOSE / BIRDS EYE DISEASE OF GRAPEVINE

CAUSAL ORGANISIM: Elsinoe ampelina (I.S: Gloeosporium ampelophagum or Sphaceloma

ampelinum)

• It is especially serious on new sprouts during rainy season. • Among various foliar diseases of
grapevine in India, anthracnose has longest spell spread over the period from June to October.

SYMPTOMS • Visible on leaves, stem, tendrils and berries. • Young shoots and fruits are more
susceptible than leaves. • Circular, greyish black spots with yellow halo appear on leaves. • Later the
centre of the spot becomes grey, sunken and fall off resulting in a symptom called ‘shot hole’. • Black,
sunken lesions appear on young shoots. • Cankerous lesions on older shoots. Girdling and death of
shoots occur. • Infection on the stalk of bunches and berries result in the shedding of bunches and
berries respectively. • Sunken spots with ashy grey centre and dark margin on fruits (Birds eye
symptom). In warm and wet weather pinkish spore mass develop in the centre ofthe spots. •
Mummification and shedding of berries.

ETIOLOGY

• Anamorph – Gloeorporium ampelophagum, produce hyaline, single celled conidia. • Teleomorph -

Elsinoe ampelina, Produces hyaline 4 celled ascospores. Mode of spread and survival • Survives as
dormant mycelium in the infected stem-cankers. • Secondary spread is by means of conidia formed
in the leaf and other plant parts which are easily disseminated by wind and splashed rain. •
Continuous drizzle of rain for 2-3 days encourages the disease. No infection can take place in the
absence of rain. Wind associated with warm atmosphere (temp.) and heavy rains favour the disease
spread.

Disease cycle

Elsinoe ampelina overwinters in the vineyards as sclerotia (fungus survival structures) on infected
shoots (Figure 4). In spring, sclerotia on infected shoots germinate to produce abundant spores
(conidia) when they are wet for 24 hours or more at temperatures above 36℉. Thereafter, 2 mm or
more of rain disseminates conidia to green tissue, where they germinate to cause primary infection
when free water is present for at least 12 hours. Conidia can germinate and infect at 36-90℉. The
subsequent incubation period varies from 13 days at 36℉ to four days at 90℉. The optimal
temperatures for disease development are 75-79℉. Another type of spore, called an ascospore, is
produced within sexual fruiting bodies may also form on infected canes and berries left on the
ground or in the trellis from the previous year (Figure 4). Temperature and moisture are the main
environmental factors influencing disease development.
Disease Management.

Cultivar Selection Particularly susceptible cultivars are Marquis, Concord Seedless, Mars, Niagara, and
Vidal.

Sanitation and Canopy Management Inoculum can be reduced by removal of all infected woody
tissue in the early spring as part of normal pruning.

Fungicide Application An early application of lime-sulfur to the vines before bud swell has been
shown to reduce the initial spread of grape anthracnose. Fungicide sprays over the course of the
season can prevent the rapid defoliation from outbreaks of this disease. Fungicides 1. Mancozeb 2.
Chlorothalonil 3. Thiophanate-methyl 4. Captan