1. The document discusses various defense mechanisms in plants, including preexisting structural defenses like cuticular wax, cuticle thickness, and epidermal cell wall structures. 2. It also describes defense structures that develop after a pathogen attack, such as cytoplasmic reactions, cell wall thickening, gum deposition, and formation of layers. 3. Biochemical defenses are also summarized, including the release of inhibitory compounds and production of phenolic compounds and phytoalexins after infection.

1. Defense Mechanismin Plants.
Structural Defense:
In plantssome structuresarealreadypresent to defend the attackwhilein
others, the structurestodefend the host develops after the infection. In this
way, structuraldefensecanbe characterized as,
(A) Preexisting defensestructuresand
(B) Defense structuresdeveloped after the attackof thepathogen.
(A) Preexisting Defense Structures:
I.Cuticular Wax
Wax-mixturesoflong chainaliphaticcompoundsget deposited onthe
cuticular surfaceofsome plants. Depositionof wax on the cuticularsurface
is thought to play a defensive role by forming a hydrophobic surfacewhere
water is repelled.
As a result, the pathogendoes not get sufficient water togerminateor
multiply. In addition, a negativechargeusuallydevelops on theleaf surface
due to the presenceof fattyacids – the maincomponent of cuticle. The
negativechargeprevents/reducesthechanceof infectionbymany
pathogens.
(ii) Cuticle Thickness:
The thicknessof cuticleis most importantfor those which try to enter the
host through theleaf surface. The cuticlethicknessobstructsthepath of
pathogen. In addition, a thickcuticlechecksthe exit of the pathogenfrom
insidethe host, thus reducing thesecondaryinfection.
(iii) Structure of Epidermal CellWalls:

2. Tough and thickouter walls of epidermalcells may directlyprevent the
entry of thepathogencompletelyor makethe entry difficult. Thepresence
or absenceof ligninand silicic acid inthe cell walls mayshow variationin
resistancetopenetrationof the pathogen.
Most outer walls of epidermalcells of riceplantsare lignified and are
seldom penetrated byblast diseaseof ricepathogen. In resistant varietiesof
potatotubers(resistant toPythium debaryanum) theepidermalcells
containhigher fibrecontent thanthe susceptibleones.
(iv) Structure of Natural openings:
Structureofnaturalopeningslike stomata lenticelsetc. also decidethefate
of theentry of the pathogen. In Szincum varietyof citrus, the stomata are
small and possess very narrow openingssurrounded by broad lipped raised
structureswhich prevent entryof water dropscontaining citruscanker
bacterium.
In the sameway, the size and internalstructuresoflenticels may play a
defensive role against thepathogens. Varietieshaving smalllenticels in the
apple fruitsprevent the entry of thepathogenwhile those having large
openingseasily allow the pathogentoenter.
Nectariesprovideopeningsinthe epidermisand mayplay a defensive role
due to high osmotic concentrationof thenectar. In resistant varietiesof
apple, presenceof abundant hairsinthenectariesactsasa defense
mechanism whilesusceptiblevarietiesaredevoid of abundant hairs.
Internal Defense Structures:
There aremany preexisting internaldefense structuresinsidetheplant that
prevent theentry of pathogenbeyond thesestructures. In some plants, cell
walls of certaintissuesbecomethickand tough due to environmental
conditionsand thismakes the advanceof the pathogenquitedifficult.

3. In caseof stems of cereal crops, vascular bundles or extended areasof
sclerenchyma cells checks the progressof rust pathogen. Leaf veins
effectively obstruct thespread of pathogenlike the angular leaf spot
pathogen.
(B) Defense Structures Developedafter the Attack of the
Pathogen:
After the pathogenhassuccessfully managed toovercomethe preexisting
defense mechanismsof the host, it invades the cells and tissuesof the host.
In order to check the further invasionby the pathogen, thehost plants
develop some structures/mechanismswhich maybedefense reactionsin
the cytoplasm, cell wall defense structures, defensestructuresdeveloped by
the tissuesand ultimatelythedeath of the invaded cell i.e. necrosis. These
will be briefly discussed here.
i) Defense Reactions in the Cytoplasm:
The cytoplasm of the invaded cell surroundsthe hyphae of the pathogen
and the nucleusof the host cell getsstretched tobreak intotwo. In some
host cells, the cytoplasm and the nucleus of the infected cells enlarge.
The cytoplasm becomesgranular and dense and develops granular
particles. Theseresult in the disintegrationofthe pathogenmycelium and
thus theinvasion stops. Such cytoplasmic defencemechanismscanbeseen
in weak pathogenslike Annillaria and some mycorrhizalfungi.
(ii) Cell Wall Defense Structures:
Cell wall defense structuresareof limited help to the host. These include
morphologicalchangesinthe cell wall of the host.

4. Three types of cell wall defense structures are generally
observed:
(i) Cell walls thickeninresponse to thepathogenby producing a cellulose
material, thuspreventing theentry of the pathogen
(ii) The outer layer of cell walls of the parenchyma cells in contact with
invading bacterialcellsproduce an amorphousfibrillar materialthat traps
the bacteriathuspreventing them tomultiplyand
(iii) Callose papillaeget deposited on the inner layers of the cell walls due to
invasionby fungal pathogens.
In raw cases, the hyphaltips of the infecting fungalpathogenpenetrating
the cell wall and thereafter growing intothecell lumen get enveloped by
callose materialthat, later becomeinfused with phenolicsforming a sheath
around the hyphae.
(iii) Defense Structures Developedby the Tissues:
The following four developments take place in the tissues after
penetration:
(a) Gum Deposition:
Plantsproducea varietyof gummysubstancesaround lesions or spots as a
result of infection. These gummysubstancesinhibit theprogressof the
pathogen. The gummysubstancesarecommonlyproduced instone fruits.
(b) Abcission Layers:
Abscissionlayersare usually formed to separatetheripefruitsand old
leaves from the plant. But in some stone fruit trees, theselayers develop in
their young leaves in response to infectionby several fungi, bacteria or
viruses. An abscissionlayer is a gap formed betweentwo circular layersof
cells surrounding thepoint of infection.
Thisgap is created bythe dissolutionof one or two layers of the middle
lamella, one or two layers of cells surrounding theinfected loci resulting in
the infected locus becoming unsupported, shrivels, diesand falls down

5. along with the pathogen. Abscissionlayer formationprotectsthehealthy
leaf tissue from the attackof thepathogen.
(C) Tyloses:
Tyloses areout growthsof protoplastsof adjacent liveparenchyma cells
protruding intoxylem vessels through pitsunder stress or in response to
attackbythe vascular pathogens. Their development blocks the Xylem
vessels, obstructing theflow of water and resulting in the development of
wilt symptoms.
However, tyloses are formed in some resistant plantsahead of infectionand
the prevent the plant from being attacked.
(D) Formation of Layers:

6. Some pathogenslikecertainbacteria, somefungi and even some viruses
and nematodesstimulatethehost to form multilayered corkcells in
response to infection, these develop as a result of stimulationofhost cells
by substancessecreted by thus, pathogen.
These layers inhibit thefurther invasionby the pathogenand also block the
flow of toxic substancessecreted bythe pathogen. Cork layers also stop the
flow of nutrientsof the host thus also depriving the pathogenof the
nutrients.
Examplesof corklayer formationasa result of infectionare: soft not of
potatocaused by Rhizopus sp., potatotuber diseasecaused by Rhizoctonia
sp., Scab of potatocaused by Streptomycesscabiesand necrotic lesionson
tobaccocaused bytobaccomosaic virus.
II. Biochemical Defense:
It includes:
(A) Preexisting BiochemicalDefense:
(i) Inhibitors Released in the Prepenetration Stage:
Plant generally exudes organic substancethrough aboveground parts
(phyllosphere) and roots (rhizosphere). Some of the compoundsreleased by
some plants areknown to have an inhibitoryeffect on certainpathogens
during theprepenetrationstage.
(ii) Lack of nutrientsessentialfor the pathogenisanother preexisting
biochemicaldefense mechanism.
(iii) Absence of Common Antigen in Host plant:
(B) Post-Infection-Biochemical Defense Mechanism:

7. In order to sight infectionscaused by pathogensor injuriescaused by any
other means, the plant cells and tissuesproduceby synthesis many
substances(chemicals) which inhibit thegrowth ofcausalorganism.
These substancesaregenerally produced around the siteof infectionor
injurywith the mainaim at overcoming theproblem.
Some such important chemicals are described below:
i)Phenolic Compounds:
ii)Phytoalexins:
(iii) Substances Produced in Host to Resist Enzymes Produced
by Pathogen:
(iv) Detoxification ofPathogen Toxins and Enzymes:
(v) Biochemical Alterations:
Plant disease epidemiology:
Plant disease epidemiology is the study of disease in plant populations.
Much like diseases of humans and other animals, plant diseases occurdue
to pathogens such
as bacteria, viruses, fungi, oomycetes,nematodes,phytoplasmas,protozoa
, and parasitic plants. Plant disease epidemiologists strive for an
understanding of the cause and effects of disease and develop strategies
to intervene in situations where crop losses may occur. Typically successful
intervention will lead to a low enough level of disease to be acceptable,
depending upon the value of the crop.

8. Epidemic and epidemiology:
When a pathogen spreads to and affects many individuals within a
population over a relatively large area and within a relatively short time, the
phenomenonis called an epidemic.
An epidemic has been defined as any increase of disease in a population.
A similar definition of an epidemic is the dynamics of change in plant
disease in time and space. The study of epidemics and factors influencing
them is called epidemiology.
Epidemiologyis concerned simultaneously with populations of pathogens
and host plants as they occur in an evolving environment ie, the classic
disease triangle.
Epidemiology
Thus epidemiologycan be defined as the study population of pathogen in
the population of host and the resulting disease under the influence of
environmental and human factors.
Epidemiologyhelps in answering entire questions by describing disease
developmentpattern during the single seasonand from year to year.
Factors responsible for the establishment of an epidemic:
1. Nature of the host
i. Accumulation of susceptible individuals
ii. Heightened disease proneness of the host
iii. The presence of appropriate alternate host
2. Nature of pathogen
I. The presence of aggressive pathogen
ii. High reproductive capacity of pathogens

9. iii. Efficient dispersal of pathogen
iv. Unexacting growth requirements
3.Environment:
i. Accumulation of susceptible individuals
ii. Heighted disease proneness ofhost.
iii. Presence of appropriate alternate hosts.
iv. Presence of an aggressive pathogen.
V .High reproductive capacity of the pathogen.
vi. Ready disseminationof pathogen.
vii. Unexciting growth rate of pathogen.
viii. Optimal weather conditions (Meteropathology):