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Sushovan Bera Associate Professor Jogamaya Devi College

Biotic (transmissible)


Abiotic (not transmissible) ~ 70%

• • •

(freezing,flooding,drought,light, wind, hail etc.)

(mechanical damage, planting problems etc.) (fertilizers, herbicides, pesticides & others)


Physiological Disorders:
(abnormal growth due to genetic and/or environmental interactions)

Low soil moisture – Stunting, pale green / yellow coloration, less flower & fruits death. i) Drought : Reduced growth, scorched leaf, defoliation death. ii) Excessive soil moisture – Tree suffer slowly than field crop, root system poorly develop, fibrous roots get damaged, pale coloration of leaves, lack of vigor, wilt [ CO2 accumulation & anaerobic respiration ] b. Soil texture – Affect water retaining capacity; in both hard & course soil stunted growth due to poor root growth occurs. c. Soil reaction – Around neutral & acidic pH preferable; unfavourable pH alter mineral uptake Symptom expression. [ High acidity:- use lime; High alkalinity:- use sulphur or irrigate to wash]

Soil moisture :

sun scald. freezing temperature form ice crystals. affected tissue become translucent black dry up. Temperature: High : Leaf scorching. premature shedding fruits.   Relative humidity: Low RH Scorching / shriveling of fruits. water soaked appearance etc. . wilting. [ inactivate enzymes adverse biochemical reaction death]  Low : Damage shoot tips. discoloration.

sun scald. Black heart of potato.  Lack of oxygen: Cells die due to suboxidation & anaerobic respiration. brown and reddish brown coloration of leaf. Brownining of apple etc. High light: Water soaked spots. .

   Sulphur dioxide: Water relations of cells disrupted. water soaked spots appear. . Hydrogen fluoride: Rapid plsmolysis and internal cell collapse burnt appearance. water soaked spots. cells collapse. mesophyll damages chlorosis.finally mottling & chlorosis. Ozone : Affect palisade cells.

necrotic interveinal area.Chlorine: Bleached. abnormal development of leaf.  Photoactive pollutants: sunlight NO2 + O2 O3 + NO O3 + (NO + un-burn hydrocarbon) = O3+PAN Peroxy acyl nitrate (PAN) leads to banding effects on leaf. injury around stomata & mesophyll tissue. scorching of leaf margins .  Ethylene: Stunting.  . early senescence of flowers fruits.

usually occurring as a side effect of pharmacological agents. .Iatrogenic disease produced by appropriate therapy for another disease.

Damage symptoms vary with pesticides and the types of plant that has been affected. impurities.i. High temperature can speed up phytotoxicity. fruits. Sometimes. the damage appears as distorted leaves. condition of plant at the time of treatment. solvent in formulations.. flowers or stems. Plant damage can be caused by the a. .     Phytotoxic effects can range from slight burning or browning of leaves to death of the plant.

Deformed cotton leaf Paraquot injury of apple Glyphosate damage to cucumber plant Dimethoate injury Kresoxim injury Glyphosate damage to apple tree .

       Growth Regulator inhibitors Photosynthesis inhibitors Pigment inhibitors Seedling growth inhibitors Root inhibitors Shoot inhibitors Cell membrane disruptors Lipid synthesis inhibitors Amino acid synthesis inhibitors .

crinkled or have a ‘drawstring’ appearance caused by irregular growth of the leaf edges. In broad leaf plants stems curl. . Leaf and stem malformations b. twist and droop. c.a. Leaves are cupped.

spotting and yellowing or bronzing of leaves. yellowing and then browining of leaf margins .  Specking. Yellowing between leaf veins . . in veins. finally death.

New growth is yellow to white with sometimes a hint of purple or pink. c.Leaves turn yellow or white and then often translucent. b.a.These symptoms can be found on cotyledons to the newest leaves of susceptible plants. .

g. especially lateral roots. . Callus tissue formed on the plant stem near the soil surface. Dinitroaniline: Benetin. Stunted growth with purple discoloration because roots can not take up enough phosphorus. b. Oryzalin) a.ROOT INHIBITORS: (e. Root system appear stubby & thick. c.

Improper leaf unfurling. Shoot inhibitors: ( e.g. the midrib may draw in the leaf edge in drawn string effect. Butachlor) a. d. In broad leaf plants. buggy. whipping(tightly rolled leaves). leaf wrinkling. Leaf puckering. c. b. Acetamide : Acetachlor. . Stunting.

Plants rapidly turn yellow or pale and look water soaked.Leaf burn and red stem. c.a. b. . then dry up.Specks of burned tissue on non-target vegetation.

c.Initial injury is seen where the newest leaves are developing.Base of new leaves become mushy. stem sheath. d. b. has a rotted appearance. leaf margins and / or leaf blade. .Reddish blue pigmentation may be observed on stem.Symptoms develop slowly within 14 days.a.

Plants treated with glyphosate or sulphosate turn yellow in 5-7 days.a. yellow tissue and green tissue at the same time. . then turn brown & dies in 10 – 14 days. b. An individual plant may have dead tissue.



.      Nutrient deficiencies: Nitrogen. bluish green/ brown coloration of leaf.Poor growth.Die back. Potassium.Small leaf. Manganese. pale green coloration. light yellowing of leaf etc. stunting. Sulphur. Phosphorus. stunting. drying of flower & fruits. premature senescence. premature senescence.Chlorosis.Poor growth.

Chlorosis progresses from light green to yellow. . Entire plant becomes under prolonged stress.General chlorosis. yellow Growth is immediately restricted and plants soon become spindly and drop older leaves. Drying of flower & fruits.

 Poor growth. stunting  Leaves appear dull. dark green. or redpurple. especially on the underside. Restriction in growth may be noticed. and especially at the midrib and vein. blue green. .  Petioles may also exhibit purpling.

uniformly light green. Leaves small.  Uniform chlorosis does not occur . followed by yellowing and poor spindly growth.

scorched.  Margins become brown and cup downward.  Mild symptoms appear first on recently matured leaves.  Premature senescence Blotchy ripening of tomato: Green & Yellow area merging into Red .  Growth is restricted and die back may occur. or have necrotic spots (may be small black spots which later coalesce).Leaf margins tanned.

or necrotic.  Stunting prominant  Premature senescence .  Symptoms may appear later on older leaves.  Some mottling occurs in interveinal areas.  Chlorotic areas eventually become brown. transparent. Chlorosis is less marked near veins.

Iron. Zinc.Short internodes. chlorosis purplish necrosis. chlorosis & necrosis of leaf. drying & shedding of leaves. brown spots. Boron.Stunting. pitting of fruits etc.Chlorotic mottling & browning etc.terminal buds may die distortion & curling of leaf. . Copper.Leaf and twig necrosis Magnesium.• • • • • • Calcium.Chlorosis.Poor root growth. heart rot symptoms.

• Distortion and curling of leaf • Pitting of fruits . • Margins of leaves developing from the growing point are first to turn brown.• Poor root growth • Growing points usually damaged or dead (die back).

and veins eventually become chlorotic. drying and shedding of leaves .  Symptoms are rare on mature leaves Brown spots. Distinct yellow or white areas appear between veins.

stunting. expanding leaves may be chlorotic. especially at shoot terminals. or split along the vascular bundles.  Stems may be rough. necrotic or distorted followed by death of growing points. hence. Young.  Heart rot symptoms occur . cracked.  Internodes may be short.

. Internodes are shortened.  Leaves may be abnormally small .with chlorosis purplish necrosis.

 Wilting and necrosis are not dominant symptoms.  Twig necrosis not uncommon . then necrotic. Leaves wilt. become chlorotic.

 Marginal chlorosis or chlorotic blotches which later merge.  Leaves show yellow chlorotic interveinal tissue on some species. and curl upward. brittle.  Chlorotic areas may become necrotic.  Younger leaves affected with continued stress. . Symptoms usually occur late in the growing season. reddish purple progressing to necrosis on others.





Thank you .