Topic 2 Crop Prot 67 - 110

Crop ·Protection . . . t ~ ..
Contributors:
4 Ms.
Fe D. Alzona
. .
2
Prof.Johnny Balidion
3
Prof. Priscilla. M. Barcia}
Dr. Grace F. ·Barroga
1
·Dr. RizaldoBayot ·
Dr. 'feresita u~ Dalisay
· Dr.,I-Ienry T. Facundo
s· Ms. Ester A"Magsino
Prof. Janet B. Matanguihan
Dr. Marina P. Natural
Dr.· Joey I. Orajay
·Prof. Hedelina M. Ramirez
. Dr. Stephen G. Reyes ·-· · 1 .
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. ·· ·. CROP PROTECTION 67 .· ·• .
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PLANT PATHOLOGY
,1·.
• From: "pathos" (Greek)== suffering

"logos" . =to study ·; ·' .
Ill Study of the suffering plant (do plants really suffer?)
• has two important components
l. as a Science
2. as an Art
As a science
• Understand the nature of plant disease ·'
1. cause- etiology of plant disease
2. plant- pathogen interaction
3. determine factors affecting disease development
4. study methods of control or management of diseases
As an Art
111
Process where science is made usefol; is doing or applying knowledge gained in science.
l. Plant disease diagnosis ·
2. Assessment and forecasting
3. Recommend control measure
ill 11
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/;I lJltinrnte obj~~ctive M Plant Pathology
To control or manage plant diseases so that .losses will be brought to a minimum.
Charaderistics of Pla1it Disease

·1. /\ malfunctioning process that results in suffcl'ing
2. Generally harmful/detrimental . ·
3. Produces symptoms- histological and morphological abnormalities
4. Caused by an agent ' ·
Vital Processes of Plant:s Affected by Disease , (
1. Root absorption
2. Uptake of water and minerals
3. Photosynthesis
4. Respiration !""·
5. Transport of photosynthates
6. Reproduction
Importance of Plant Diseases

1. Plant diseases endanger food supply .~
2. Reduce the quantity and quality of plant produce.

3. Cause financ ia 1 losses
4. Limit the kinds of plants and i11dustrics in an area. , ·
5. Make plants poisonous to humans .
6. Increase cost of production dne to conlrol mc~tsltres
68 Aggie Board Reviewer
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Types of Losses due fo Diseases
l. Losses due to reduction in yield.
2. Losses due to .deterioration during storage, marketing or transport
3. Losses clue tor.eduction in quality. ·
4. Losses from produce contaminated with toxins that cause various disorders and /or death
to animals and man. ,
5. Losses due to predisposition of host to attack by other pathogens> .
. 6. Losses from increased cost of production mid handling.
Definitions and terininology

• Pathogen- any agent that causes disease especially the biotic or living agent.
II or
Parasite- an organism that depends wholly partly on anoihei' ·organism for its food.
l. · Is a pathogen always a parasite? ·
2. I~ a parasite always a pathogen?
Parasite
• Obligate parasi;te- subsist on_living organisms and attacks only' living tissues (ex. Virus,
rust fni1gi, downy mildew fungi, etc.) · . .· . .
• Facultative parasite- an organism, which has the ability to become a parasite but is ·
ordinarily n s~1prophyte . ·
Saprophyte- an organism that lives on dead organic or inorganic matter.
• Facultativc saprophyte- has the ability to bcco1nc a saprophyte but is ordinarily a parasite.
Host- reters to the plant that is being ;lttuckcd by a parasite: A foo'd rclati~nship between the ·
host and the parasite is implied. ·
Susccpt~ is a JJlant that is susceptible to a disease·whether or nofthe ·pathogcn is parasitic. · ·
• an
Pathogenic ity.,. is the capacity of organism j.p ca,1,1so-.disease. ·. . .
• Path.ogenesis- refers to~ s'ci:ics o(e·vents that lead to disea.se dcvelopmci~t. iilthe plant
• V irulcncc- rcfoi:s to the quantitati vc amount of disease th"at- ~11 iso.late (the pathogen) can
cause in a group ()fplants. A characteristic of a pathogen: . .
Plant Disease Diagnosis- defined as idcntific.:tion of diseases based on sy1nptorns and signs
• Symptom- manifestation or expression of a plant as a result of a disease.
• Sign- a pathogen or a part of a pathogen found on a host plant. .
Symptom~- evidences of disease in the plant

• Symptom complex- different symptoms exhibited by the plant
• Syndrome::. sympt9m + sign
e Classification of symptoms i::""~<:J\\f - "· "" 9ro"'\:.1,
0
a. Local or systemic ·;.•.

b. Primary or sccondm)'
c. Microscopic ,~r Macroscopic
" Local syr.nptoms- Expressed as physiological or structural cl~anges in a limited area of the
tissues of the .host (g3_g~2. sQQ.!~, c_~mk~rs)
(flOP PROTECTION . '6 9 .
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................._._ _ __ ~-......-..w---.-_....,.. .....w.. _,_ ..... ... _,,..._,_,,.... ~.-- .....~ ..... .. . .. ~ ......... .
.. Systemic symptoms- Expressed as the reaction of a greater pait of or all of the plants
(dwarfing, wilting, yellowing)
Primary vs. Secondary sy1hptoms (same disease) .

" Primary- the direct result of pathogeri activity o:n the i11vaded t~ssues .··
• Secondary- the physiological etlects 011 distant and uninvaded·hrgans
•, , •,.
Microscopic vs. Macroscopic syh1ptorns .

• Microscopic- c:x:pressions of disease in cefl structure or arrangement that can be studied
only under the microscope . · · · . . ·. . .
• Macroscopic- expressions of the disease in the plant or its parts that can be studied m
with the unaided eye · . ., . .
M.acroscopic symptoms . ·· ; ·.
" Pre-necrotic·· stage preceding death of cells
• Necrotic- characteristics of dead cells and tissues
General types of symptoms

1. Necrotic ·
• Involve the death of protoplast
• Examples- Spot, canker, blight, scorch
2. Hypoplastic
11 Inhibition or failure in the differentiation/develoRment of some aspect ofplant
· growth . . · . · , ·
• Examples~ Stunting, chJorosis, mosaic, curling and rosetting
3. Hyperplastic
• Expressed with the cxcessive·multiplication, enlargement.or overdevelopment of
plant organs "
• Prolonged retention of green color
• Gall formation,· scab, knots . · ·.
a. Hypertrophy- overdevelopment due to the h1crease in the sizt: of th"'
b. Hyperplasia- abnormal increase in the number of cells
-.S_ig_i_1s of Pathogens
--·-;- Strncturcs of the pathogen or pathogen itself; rnay be. the resu 1•
pathogen and the. host (ooze, odor) ·
• Examples- fungal mycelia, conidia, oospores, tel''

sclcrot:ia I bodies, chi a ir:y:~ospores; nematode.>
cells; virus particles; seed of p_hanerogmr
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70 Aggie Board Reviewer .2RoP PnOTECTION 71
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Koch's postulates- Criteria used to confirm the identity of the causal agent of a new or unknown
disease :
1. Association- the pathogen or signs ofthe pathogen must be found associated with the
disease in all the disease<;! pla1::t<> cx:imin.ed. · ,
2. Isolation- the pathogen must be isolated and grown in pure cultur~ on nutrient media, and
its characteristics described. Obligate ,parasites must be isolated a11d grown on. a h~althy
but susceptible host plant. The characteristics of the obligate parasite must also be
described. ·
3. inoculation- the pathogen from pure culture must be ·inoculated on healthy. plants.of the
same species or variety on which the disease appears, and it must produce the same
disease on the inoculated plants. ·
4. Re-isolation- the pathogen must be re-isolated from the ·inoculated plants and grown once
more in pure culture. Its characteristics must be exactly like tl1ose observed in steps 1
and 2 . ·
Classification of Plant Diseases according to:

I. affected plant organ
2. symptoms
3. type of affected plants
4. Lypc of pathogen
a. infectious diseases- biotic agents
b. non-infectious diseases- abi 0tic
- ~ I ~
L
1:
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· Abiotic stress or injury
Jf L Non-living ..
·:~ J 2 .. Not spi'ead from disd1scd to healthy plants ' ·~·~·'~ " " '·~ ·
.~ 1 3. Non~infectious . .. .· " ' •:i, ·. ,, .. ·~·"': "~ ' · ~· .
.of
. . . ' . • . \l, {-l < • • •
4. Kn·ow1·cdge envitonmcntal factors before and during disease occurrence necessary for
cbrrec.t diagnosis. ·
Kincls of Abiotic Diseases or injury or stresses
A. Injury caused by adverse physical factors

I .Injury caused by too low temperatures··
o Freezi.ng injury- caused by ice ·crystals formed within cells and in between cells
GI Chilling injury- 1ow temp slightly.above freei;ng. Pitting and water soaked
symptoms
2. Injury caused by too high tempcn\ture-.sun scald, heat necrosis of potato ·
3. Stress caused by lack of oxygen- black heart of potato
4. Stress caused by too much or tob little ligh.t
5. Injury caused by adverse 1netedrological conditions.
B. lujnry caused by air pollutants

1. ()-zone J •
2. Pcroxyacylnitratcs (PANS)
3. Hydrogen fluoride (HF)
. (ROP PROTECTION 71
.· .· ... ,.
•( .;
4. Ethylene
5. Nitrogen oxide
6. Particulates- volcanic ash, cement dust
C. Stress caused by mineral deficiencies and mineral excesses
D. Diseases caused by improper agricultural practices
E. Diseases caused by naturally occurring toxic chemicals
HO'W TO PRl~VENT THES.E STRESSES OR IN.JURIES

t . avoid the factor
2. protect the plants
3. supply the factor
4. good management of the crop to produce healthy plants
PARASITIC or BIOTlCAGENTS OF PLANT DISEASES
l. Vi.ruses and viroicls (subcellular entities) ·

2. Bacteria and phytoplasmas (prokaryotcs)
3. Fungi and :funga I-like protists
4. Nematodes · ·
). Parasitic flowering plants
Ci. Protozoa
7. otl1ers
VIRUS
m Ultra1nicroscopic made up of nucleic acid and a protein coat
.,, Oblig'.lte parasites (replicate only in cytoplasm of living hosts)
e Nucleic acid core (RNA or DNA);4-20 K bases; Infectious part
o Prolein coat-
1. Provide a protective sheath for the nucleic acid
2. Facilitate movement of virus. from cell to cell
3. For ~ransrnission o.i:· \·fr '.l:'-:1:r; by vectors
'frnnsmission and Spread of viruses

l. Mechanical means
2. Grafting
3. Nematodes
4. Soil-borne fungi and fungal-like organisms
5. Infected vegetative p !anting materials
6. Infoctcd seeds ·
7. Mites
8. Insects- Aphids, leafhoppers, plant hoppers, thrips, whiteflies, mealy bugs, etc.
i''I ,
Jn sect transmission ;.. Virus-V cctor Relationship
J. non-persistent viruses- (stylet-bome)
2. scmi-·pt:rni::;tcnt-(lurcgut-bornc)- viruses ·can stny in the vector for days.
3. P~rsislent viruses- · ·

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a, Circulative - replicate only in plants btit vim s pas ::;~ s through the gut inlo the
lrncmolymph and then the salivary glands ·
b. Propagative - replicates both in plants and vectors
VIRUS DISEASE SYMPTOMS

o Range from no symptoms to death of plants
·-~ " Local lesions
J
o Systemic symptoms
l. Rc_d uction in plant size
2. Mosaic patterns
3. Yellows
4. Ringspots/color break in flowers
CONTROL OF VIRUS DISEASES

• Difficult to control once established in an area
1. Prevention through quarantine arid certification
2. Use virus free seeds and planting n:iaterials
J, Roguing of diseased plants
4. Hot water treatment of planting m'a teriab
5. Control of vectors
6. Cross-protection
7. Genetic engineering
VIROJDS
I. Stable and lice ribonucleic acid (RNA) that can infect plant cells
2. 250-375 base pairs
3. Closely associatcct'with the nuclei, especially the chromatin of the cells they infect
Examples of diseases caused by viroids ·
I. Potato Spindle tuber
2 . Cadang-caclang of coconut:
3. Apple scar skin
4. Avocado blotch
BACTERIA ,, ..
Typically one-celled, J 1'
i •
Possess a i.rnit. membrane and cell wa II I
l·t
Reproduce by binnry fis sion !

No membrane-bound organelles; i 'i,:,1'
'1
Prokaryolic; lack nuclear membrane & lack a well-defined nuclet1S, !1\:

.,
DNA ns nuclear material
So me linve plasmids , which nre ~~xtra chromosomal DNA that are self replicating .j '
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(ROP PROTECTION 73 j
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Charncteristics of Plant Pathogenic Bacteri~1
1. Mostly rod-shaped
2. Mostly aerobic
3. Mostly flagellated
4. Mostly Gram negative
5. Mo stly non-spore-forming · . ' 1·
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Genera of Plant Pathogenic Bacteria I
Old Genera (Prior to 1980)

I. Agrobacterium
2. Pseudomonas
3. En11inia .
_.,'
•. 4. Xanthomo11as
5. COJ:J'llebacteria (not valid anymo1~e) i'l'··•t~u1 \'·'"-" t""
·New Genera of Plant Pathogenic Bacteria (after 1980)

- - - - - --- -,-----
From Pseudomo11a~· · Other Genera j,
l. Acidovorax · 1. Acetobacter i.
2. Burkholderia 2. Bacillus
3. Ralstonia 3. Clostridium
4. Pseutlomomzs 4. Gluconobacter
From Erwinia 5. Nocardia
L Brenneria 6. Rhizobacter ·
2. Enterobncter . 7. 1f}fJll iJ1.._'{01llOnil.s.
3. Pantoea 8. Serratia
4. Pectohacterium 9. Spiroplasma
5. Envinia 10. Streptomyces
Fomur C01:y11ebacteria (Gram positives) 11. )(yfella .
.1. Ariltrobacter 12. Xylophilus
2. Clavibacter I
3. Curtobacterium
. ±
'1
4. Lt•ij:wmia
5. Rathavibacter . I .
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BACTERIAL CLASSllilCATlON .
1'
Traditional im~thods of charnderizaHon to group bactcriff into genera:
l. Morphological- size, shape, flagella
2 . Cultmal- growth characters in media
3. Biochemical- reactions in substrates
4. Physiological- carbon·& nitrogen requirements
5. Pathological- pathogenicity to plants
·'•
I~
:· Molecular techniques
· 6. DNA base composition · I
I
7. DNA-DNA homology- useful for bacterial species identification

8. DNA-rRNA homology- detects similarities between genera or families
9. RFLP- for strain identification l. •
I
Bacterial Ecology- the scientific study of interactions ani.ong organisms, between ·organisms ,
and their environment, or surroundings
I. /\<;; parasite inside hosts ·
2. On plant surfaces (buds)
3. Partly in plant debris in soil
4. In or on seeds; other planting materials
5. hdnsccts
. pi
Bacterial diseases and their pathogens 'i'l,,1'
I. Potato blackleg- Pectobacterium carotovorwn ·1' ,,
' '
~ 1,
2. Potato soft rot- P. carotovorum .,·
3. Bacterial wilt of solanaceaus and non solanaceous crops- Ralsiq.nia solanacearum 1,
i
4. Stalk rot of corn- Pectobacterium chrysanthemi ·'
.·
5. Ratoon stunting disease of sugarcane-Leifsonia xyli subsp. xyli
6. Crown gall of roses and many dicots- Agrobacteriwn tumefaciens
7. Rice leaf blight- Xanthonwnas 01yzae pv. oi·yzae
8. Rice Leaf streak- Xa11thomonas my.we pv. 01yzicola
.r ;
9. Cassava blight- Xanthomonas axo110podi.~:pv. inanihotis
I 0. Citrus canker- Xanthomonas axonopodis pv. citri ·
l I. Angular spot of cotton- Xanthomonas axonopodis pv. malvacearum
Genera of Non·-typical Plant Pathogenic Hac:teria

I . Streptomyces sp.
2. Nocardia sp.
3. Fastidious bacteria
4. Plzytoplasma
5. c\'piroplasma
Fastidious vascular hacteria (previously called rickeHsia-likc organisms [RLO/)

I. Cannot be grown in simple media · ·
2. Generally rod-shaped; no flagella
3. Cell wall undulating or rippled
4. Gram-negative
5. Phloem (citrus greening, periwinkle club leaf) or xylem-limited (Xylella, Lcifsonia)
Mollicutes -· Bacteria without cell wnlls

1. Phytoplasnur
a. Spheroidal to ovoid, irregular to filamentous (pleomorphi('.)
b. Phloem sieve tubes
c. Transmitted by lcaJhoppers, psyiii~s in d plant hoppers
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· CROP PROTECTION 75
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d. Grow in insect body (propagative)
e Not yet grown in culture
r Resistant to pcnici !!in, not to tetracycline
2. Spiroplasmas ~
a. Can be spherical to slightly ovoid, branched non-helical filaments
b. Can be cultured in nutrient media
c. Reproduce by fission
d. No flagella but motile ifhelical
c. On agar, ty1)ical fried egg appearance
Control of Bacterial Diseases

1. Cultural Practices
a. Sanitation to reduce inocu !um
b. Crop rotation
c. Proper wateiing and draining
2. Seed treatm~nt- weak adds or sodium hypochlol'ite
3. Hot water treatment
4. Antibiotics (?) and copper fungicides
5. Resistant varieties
PLANT PA 1'HOGENIC PROTJSTS
1. They arc not considered as fi.mgi anymore but protozoa-like or fungal -like.
2. Their cell walls are not made up of chitin but of cellulose and other glucans
Protozoa-like protists - uniceliul&, :µlasmodial, or very sin>ple multicells, phagotrophic

(feeding by engulfing food) ·
a. Phylum: Myxomycota
b. Phylum: Plasmodiophoromycota (endoparasitic slime molds)
Phylum Myxomycota- true slime molds . . .

Vegetative body is a plasmodium (a membi·anc-bound single cell containing multiple
nuclei).
• Fruiting body is sporangium (a small spore container whi~h may be sessile or stalked),
actha lium ( masses of completely fused sporangia) or pseudoaetl}alium (fiuiting body
composc<l of sporarigia closely crowded together). ·
Saprophytic- feed on decaying .organic matter; bacteria, etc.
Disease of low lying plants like turf grasses; strawben-y, vegetables
Phylum Plasrnodiophoromycota- (Endoparasitic slime molds)

Plasmodium as vegetative body
" Zoosporangium as fruiting body ·
• Obligate cndoparasite of vascular plants
• One class- Plasmodioph') f·omycete
76 Aggie Board Heviewer

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· .... .. wt•:t11J1lil~~~-- ..- - - -..... - .. - - - - - - - -- - - - - - ·· - · - - ··- - - -· · · - - - --- ..•. - -
Fungal-like Protists-havc mycclia mid cr;.nidia but cell walls are rnade up of cellulose and
glucans, not chitin as true fungi would have.
Phylum: Oomycota
Class: Oomycetes
Order: 1. Saprolegninles
· 2. Peronosporales
Class: Oomycetes :'.
Have wcll'.·dcveloped aseptate (coenocytic) rnycelia co1itaining cellulose and glucans · ·
Frniting body is a zoosporangium for asexual reproduction
a. · Sporangia borne on mycelium or sporangiophore,
b. Spores- zoospores or conidia
Sexual reproduction
Hetero gametru}gia
female- oogonium= globose
male- anthericlium= club-shaped; forms · a fertilization tube
Fusion of male and female ·gametes produce oospores ·diploid; germinate into
diploid rnycelia
· Ord1fr: Peronosporales
Three Families
a. Pythiaceae - damping off & root rots
b. Peranosporaceae - downy mildew
c. A lbuginaceae - white rust .
Genera under Family Pythia<:eue
l . Genus: J~vthitm1
a. Damping off diseases
b. Rots of vegetables
c. Turf diseases
2-. Genus: Pkytophtlrora
a. Root rots
b. Rots or fleshy tissues
Family: Peronosporaceae
Obligate parasites of plants; cause downy mildew diseases
Spoi"angia borne in sporangiophores
• Sporangiophorcs are branched; determinate in growth ·
Aller sporangia foll of( sporul1giophore withers and drit,s.
Branching of sporangiophorc- distinguishing feature of the genus
Downy mildew diseases- the pathogens belong to the oomycdes

l. tobacco·· Peronospom tnbacina ·
2. lettuce- Bremia lactutae ·
3. Sugarcane Perondscleospora .i·acchari
4. cucurbits- Pse;;Joperonospor:-1cubensis
5. sorghum- Peronosclerospora sdrghi
6. grapes- Plasmopara vilicola
7. corn- Peronosclerospora philippbiensis
(ROP PROTECTION . 77
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Family: Albuginaceae .
Obligate parasite of flowering plants
SjJoranglophorcs short, club-shaped, indeterminate in .growth
Spornngia globose, in chain . · ·
Example : white rust of kangkong
Fungi (true fungi)
Four Phyla with Plant Pathogens .

1. Phylum: Chytridiomycota
2. Phylum: Zygomycota
3. Phylum: Ascomycota
4. Phylum: Basidiomycota
The Trne Fungi-general charactel.·istk:s =
I. Heterotrophs- obtain food from organic matter (living or non-living); cannot make its
O\:<,'n food; devoid of chlorophyll
2. Nutrition is by absorption
3. Non-motile (a fow, the chytridiomycetes, have motile reprod9ctiv~ cells)
4. Reproduce by spores (sexual/ asexual)
5. Primary stored carbohydrate is glycogen
6. Usually filamentous & multicellular (hyphac/ mycelia made up 'o fchitin) · ·
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Phylum: Chytridiomycota I
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• Contains a single class- Chytridiomycctc i
• About 150 genera; 1000 species .
• The only member or Kingdom Flmgi tl1at form rnotilc cells '(zoosporcs or garnctes)
• Thallus is cocnocytic; either globose or ovoid, elongated byphu or well developed
rnycclimn
• Zygote formed converted into: resting spore or resting spora11gium
lmport.ant plant pathogenic chytrids

J. Olpidium brassicae- root disease of crucifcrs (vector oflettuce big vein virns)
2. .~ynchytrium endobioticmn- biack wart of potato ·
3. Synchytrium psophocarpi-· orange galls of calamismis (winged bean)
4. Physoderma maydis- brown spot of com ··
Phylum Zygomycota
• . Produce non-motile asexual spores in sporangia
• Sexual spore is zygospore formed irisidc a zygospornngium after union of two
isogamctangia
e Produce well-developed aseptrite mycelium
• Cell wall has chit in and glucan
o Habitat- tcrrcstial, saprobic, human pathogens, weakly plant path.ogcnic;ecto-cndo
rnycorrhizal
"'--------. --....... ----~ --·· -----· ,. ____.... . .....
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• ___f':. _ ..__ .. _ ... _........_ .. _ .__ · -· -· - .. - · · - " ' - - - - - · - - -- - - - · · - ~-·-
Order: Mucorales
.. Rhizopus
• Jvlucor
• Choanephora
Order: Glomales (mycorrhiza)
• G/omus
• Gigaspora
Phylum Ascomyc.ota
Sac fungus - sexual spores (ascospores) formed within a sac known as ascus. ,
" Te leomorph- the sexual or perfect stage of ascomycetes
e Anai11orph- the asexual or conidial or imperfect stage
,. During the gro wing season, plant pathogens exist as mycclia/conidia.

• Perfect stage occurs only at end of growing season.
.. Ascosporcs generally act as prirnt1ry inoculum . .
., Sexual reproduction through an ascogoniuni(~) fertilized by antheridium or spermatium
(o ), a minute male sex spore.
Dcuterornycctes or imperfect fungi- the imperfect stage of Phylum Ascomycota. Many plant
pathogens belong to this c lass .
• Asexual or co11idial forms of most of the Phylum Ascomycota ~md rarely of the Phylum
Basidiomycota
"' Sexual reproduction and sex ual structures are lacking oi· unknown
'l'hrcc groups of Dcutcromycefos or imperfect fungi .

1. Hypomycctcs .. Fungi that produce conidia on free conidiophorcs' or groups of
conidiophoi"cs ·
2. Coelomycctes .. Fun gi that produce accrvuli or pycnidia th;:~t bear conidia and
conidiophorcs · '
3. Mycelia sterilia- No asexual nor sexual spores
ii)1Jhomycetcs- no f~uiti~g st~~~ct~re ----- , Cocl<;mycete;-- ------------

Genera I m Pycnidia-forming
I. A/ternaria . I. Dip!odia
2. Asperg il/us I 2. Phornopsis
3. Penicilli11111 l J. Phyllosticta
4. Cercospora ! 4. Septoria . ,i
6. Fusori11111 al Acervuli-forming
7. Bipolaris J. Gloeosporium
8. Oidium 2. Colletotrichum
9. Pyricularia 3. Sphaceloma I;
.'I
I 0. Verticilliurn ~ :
l 1. Cladosp orium
______1_ _ _ _ _ _ _ ________ ""·-·- - -- - -'" -
(ROP PROTECTION 79
..- j .
.... --.- ·,- - - .
•·c--·- · - ·- -
.. ---
--~·--.- - ... ---. -- --------
Mycelia sterilia
• the sterile fungi; no asexual nor sexual spores produced
e sclerotial bodies produced
1..
Examples : Rhizoctonia solani. Scleroth1m rolfsii
Phylum Basidiori1ycota
Club and mushroom fungi
Sexual spores are basidiospores produced externally on a club-like,· one- or four-celled
spore producing structure called a bar>idium
Most are fleshy
Includes rusts and smuts
Orders under Phylum Basidiomycota
l. Order Uredinales·- Rusts
2. Order Ustilaginalcs- Smuts
3. Order Exobasidiales- lacks basidiocarp
4. Order Agaricales- the mushrooms ,
5. Order Aphyllophorales- the polypores
Order Uredinales - The rusts

Attacks mostly leaves and stems; some form. swellings and even gal}s.
About 140-150 genera; 5000 species.
Most rust fungi are very specialized..: attack only certain gem;ra, varieties.
a. F'ormae speciales- · ·
. Puccinia graminis Csp. tr;rfci;'~ attack~ wheat only
Puccinia graminis fsp. hordei= attacks barley only ,
b. Pathogeni~ (physiologic) race= P.g. t:sp. tritici attacks some, varieties ~fwheat
(within crop species).
Most. produce 5 dlsl.ind fruitin'g structures and 5 spore .forms.
Frnltlng structures Spore forms
basltiiurn Basidiospores (n)
sperrnogoniurn Spermatia (n)
aecium Aeciosporns (n+n)
uredlnlum Uredlnlospores
(uredosporos) (n+n)
tellu111 Teliospores (n+n)== 2n

(teleutospores)

-----------
- lti~~(;!'l&aM~:t.il'fttll°'l"''~lk..._..._ _ _. -.. ,,., ... , _
...--- _ _ ,. __ .. ,,_ · - - - - ·· ·- ·· ··· .. ...
Ex:nnplcs of rust diseases

I. Peanul rust- Puccinia arachidis
2. Corn rust -- Puccinia maydis, P. polysora
3. Coffee rust- flemeliae vastaM.x
4. soybean rust Phakopsora pachyrizi
5. bean rnst- Uromyces phaseoli
Order Ustilaginales - the smuts-
Attack ovaries of grains, develop in them and in the fruit or kernel; some attack leaves,
stems and floral parts. ·
Some infect seeds or seedlings, grow internally until they reach the inflorescence.
Cells affected are destroyed and replaced by black spores . . , · . ·
Produce teliospores and teliospores produce basidiospores: ·
Basidiosporcs germinate, gcnn tubes unite with compatible ones and then infect; or
penetrate tissue directly. ·· ·
Haploid mycelia cannot invade tissues, only dikaryotic ones.
Examples:
1. Corn smut- Ustilago maydis
2. Com headsmut and sorghum· smut- Sporisorium reilianum
3. Sugarcane smut """ Ustilago scitaminea ·
Order Agaricales- the mushrooms .

Armillaria
ivfarasmius
P!eurotus
Amanita.- poisonous
Calvatia- pui1ball
Order Aphyllophorales - shelf or bracl<et fungi

Cortichun- rcsupinate
Ganoderma
Po~}1porus
A ethalium (Sclcrotium)
NEMATOLOGY
Nematod es
• Derived from th e Greek words "nema/nematos" "thread" and "edos" ="resembling ·
or likeness"
Morphologically, they are vermiforrn/vrorm shaped ( exc~pt for the female ~f some . .
genera which swells upon maturity), unsegmented, pseudocoelomate, bilaterally
symmetric<il animals without motile cilia.
• Mc:i jorily are marine aquatic species: som.e arefre.e living terrestrial and animal
parasites. Only 10% of the 30,000 described species are known as plant parasites.
(ROP PROTECTION 81 .
Phytonematology
• Deals with nematodes that parasitize plants.
.. . Begun with the invention of microscope
• Turbatrix ace/i (wheat gall nematode) fast plant parasitic nematode (PPN)
described. . .. , .\
• Ca enorhabdilis efegans (a free living nematode) l.lsed as a modelorganism (for.
animals) for genetic and physiological studies: the complete genome was sequenced
in 1995.
I. Techniques
Reasons for sampling:
• Nematodes are too small to be seen with bare eye.
• Symptoms caused are not typical
• Need for quantitative estimation ofdensity
Sampling theori es:

1. Spatial distribution - nematode distribu~ion within the field is generally patchy owing to
th eir small size and slow rate of active movement.
2. Vertical distribution - refers to the dispersal of nematodes in a soil .profile. This is mainly
influenced by density of feeder roots which is higher in the lipper 30 cm of soil, though
it can grow deep er inperennial crops. .
3. Temporal/seasonal distribution - influenced by climatiC pattern (wet and dry) and host
availability. Nematode density is highest during near harvest stage of crop.
Extraction techniques:
A Motility - dependent/ active methods - extracts slender and active stages of
nem a todes.
Examples: Bearmann funnel and its modification and H20 incubation method
B. Motility-independent/ passive methods - extracts even sluggish (slow moving) .
nematodes.
Examples:
- Wet si eving method (depend s on nematode size)
- Maceration - sieving (depenc:. s 0:·:1nematode size)
.. 'Elutriation method (depends on sedimentation difference of nematode and soil .
particle)
- Centrifugal flotation (depends· on specific gravity)
11. Morphology . . .
The cross section of nematode looks.like a "tube within a tube". The outer tube consists
or the following:
• Cuticle· a serni··permeable outermost covering or.the nematode body; made lip
of protein (keratin and collagen as opposed to chitin of insect cuticle); shed off
during molting to allow grm.·vth. · ·
- - - -- · ------·-·--- ·
• Epidermis- a thin layer which functions mainl:y for secretion of new cuticle
during molting. .. . . . . . .
o Muscles - allow movement by alternate contraction and relaxation of dorsal and
ventrnl muscles.
Digestive system- the inner tube is essentially the digestive system. It begins from
the mouth opening to the anus (for female) or Cloaca (the common-.opening of digestive and
reproducUvc system for male)
The stylet is a protrusible structure in the mouth of nematodes which distinguishes
plant parasitic from living forms. It is the structure they use for puncturing plant cells and
withdrawing their contents. · · .
Three types of stylet:
· • Stomatostylet- with distinct cone, shaft and imobs~· inside is hallow;
possessed by Order Tylenchida (the order where most of the knownand
most important PPNs belong) .
e Odontostylet- a hallow spear, possessed by members of the Order
Dorylaimida where the virus vector genera Xiphinera, Longidorus and ..
Pa ralongidorus belong. . .. · .· . · .
., Onchiostyler- a bent solid needle-like stylet possessed by members of the
· Order Triplonchida where two other virus-vector genera belong
(Trichodorus and Paratrichodorus).
Nematode Biology
/\. Life Cycle

Zygote -7 embryogenesis -~Juvenile stages -7 adult
/\ft:er the zygote is formed, it will undergo embryogenesis wherein the initially
single cdled zygote will divide. At the end of embryo genesis, a complete individual is
formed which is formed the 1st juvenile (Jl). This will molt (M2) and JZ will emerge. All
these occur in the egg. The egg will hatch from it. J2 will emerge. This is .the feeding or
infective stage for most PPNs becaus8 t Ms i:J the stage where they will st~rt looking for and
feeding in/on host root<;. Two more juvenile stages (J4 and 14) will emerge after each
tnoltings (MZ, M3 and M4). For few PPNs, J4 is the infective stage. After M4, adult
nematodes (either male or fem ale) will emerge which are capable of mating and producing
offsprings. Male nematodes are usually non-parasitic and leave the roots and die after
copulation.
B. Parasitic/feeding strategy
Types of PPNs based on location of feeding . .
• Ectoparasite - feeds superficially (epidermal cells) using their stylet. Body (or large
part of it) remains outside the root cells. ·
(ROP PROTECTION 83
" Endoparasite - ·cap'a ble of entering the roots during their i.nfective stage or in some
genera, in all stages, They establish feeding site in the cortical, endodermal or stellar
tissues, .
Types of PPNs based on mobility .

• Migratory - moves to another cell once the initial feeding site is exhausted.
•"
Essentially, they are 'vermiform. · · ·
• Sederitary - stays longer in the cell (in case of ectoparasite ), or establish a
permanent feeding site in the innertissuys (in case ofendoparasite), As feeding and .·
development proceeds, body size increases.
Combining the two classifications, we will havi; the following:
1. migratory ectoparasite e.g.' Longidorus_. Xiphinema, Trichodorus, Paratrichodorus

2. sedentary ectoparasite e.g. Criconemoides, 'Hemicyclophora
3. semi-ecto, serni-endoparasite (feeds.in inner tissues, l;;trge partofthe body remains
outside, becomes swollen) e.g. Tyienchulus, Rotylenchu/us · ·
4. sedentary endoparasite e.g. Meloidogyne, Globodera, Nqccobus, Hirschmanielja
C. Reproductive stage
1.. Amphimixis - mode of reproduction where males are needed.
2. Parthenogenesis- mode of reproduction wherein only females are produced (or
males are rare and not needed) arid offspring:; are clone of the female.
3. Sex reversal - phenomenon observed in juveniles of parthenogenic species of
Meloidogyne during unfavorable condition. Depending on the onset ofthe .
unfavorable condition, gonad of"destined to be" female juveniles develops into
non-functional testis.
n. Survival Strategy
Dormancy- lowered met<ibolism
Types of dormancy . .
• Dia pause- state of arrested c:,evelopment which persist until specific .
requirements for developnient are satisfied even .if favorable condition
return.
• Quiscence- spontaneous reversible response to unpredictable unfavorable
conditions.
----------------·--
Egg stage- the survival stage of nematodes; the egg shell provide protection. Once the ]2
emerge, they are more prone to external stresses. ·
Survival strategies of selected PPNs:

• Egg sac/gelatinous matrix- Meloigyne spp.
• Cysts- Globodera, Hetrodera
o Daucer- Rolylenclwlus
• Coiling/damping- Ditylenchus, Anguina
V. Nematode Ecology
/\. Biotic influences
• Parasites of Nematodes
o Nematode trappers
o Endozoic parasites
o Egg parasite . . . .
• Predators of nematodes: tardigrades, insects, protozoa, other i1ematodes
B. Abiotic Facto~ · ' ·
~ Soil texture and structure
• Moisture
• Aeration
' VI. Nematode diseases important to the Philippines
• Slow cleclii1e of citrus (Tylenchulus semipenetrans)
• Spreading decline of citrus (Radopholus similis)
• 'J'oppling di.scl\se ofbarrnna (R;:idopholus similis}
Root knot: ofvariouso·ops (Meloidogyne spp.)
False Root knot (Naccobus spp.)
• Ufra disease of rice (Aphelenchoides besseyi)
• Rice root knot (mentek) (Hirschmaniella oryzae)
• Yellow dwarf disease of black pepper (Radophollls similis)
• Red ring di sease of coconut (Radinapbelenchus cocophilus)
. . '.
Vil. Methods of Nematode Management .

• Prevention- quarantine at farm, country and international level
Crop rotation- altering susc;eptible host with 'n on··l1ost: crop
• Trap crops- susceptible crops intentionally planted but are uprooted before the
nematode complete its life cycie. E.g. Crotolaria
• J\ntagonistic crops- exudes chemicals that are eithrr repellant or nematicidal ,
o e.g. Tagates patella- produces a-t~1ertienyl .· · · ·
o 13rassicas- produces isothiocyanates
• Land rnanagement and cultural practices
o Early planting
o Plowing
o Flooding
o Orga1iic soil amendments
• Phys ical m ethods
CROP PROTECTION 85
---~w.~· -, , - ·-Jil•- .......
..... _ .,_~-......"""-.....---...... Joo• . - .... ------- ·~ .. ..,, . -- - --- -·--- •w --- •~w ••••- • •
o Steaming
o So larization
o Field bumming
o Heat treatment of planting materials
• Resistant /tolerant varieties
" Biological controls e.g. BIOACT
" Chemical control
o Fumigants- methyl bromide; ethylene dibromide; chloropicrin
o Non-fumigants- fenamiphos, thionazin, aldicarb, oxamyl, methomyl ·
PARASITIC HIGHER PLANTS

Classification:
A. Hemiparasites - c·ontains chlorophyll but without roots so it depends on host for
water ::incl minerals.
a.. Examples: witchweed;.Triie mistletoe and leafy mistletoe; Loran thus sp.
B. True parasite - have little or no chlorophyll and .no roots either so entirely
dependent on host for water and minerals.
a. Examples: dodder; Broomrapes; Bunga ng tubo (Aeginelia indica)
FLAGELLATE PROTOZOA
~ Possess one or more long slencl.e r flagella

" Mo s tly one-celled and generally motile
•Plant protozoa -- Phytomonas .
• - Can be found on sieve tubes of non-laticiferous plants
~ Coconuts and oil palms - heart rot of coconut
.~ !~
~:i t~ • Coffee- phloem necrosis of coffee .
MECHANISM OF VARIABILITY IN PATHOGENS
I. GENERAL MECHANISMS OF VARlABILITY
/\. Sexual Reproduction

• Segregation and recombination of genes during meiosis
0 Genetic crossovers (exchange of chromatids and the gen·es they carry)
• Haploid gametes are diffe;ent l'r~ m parents and from each other
l3. Mutation · . ·
• Abrupt changes in the genetiC material which is inherited by the offspring
• Can occur spontaneously or through mutagenic agent .
II. SPECIALIZED MECHANISMS OF VARIABILITY
A. Sexual-like processes in Fungi i '1 •
• Heterokaryosis - cells of fungal hyphae contain two or more nuclei that are
genetically different
-------- ------- - - · - - - - - - - - - - - - - -
86 Aggi e Boa rd Reviewer
•••••••••••MRm!llillliilMl!.bl!Ml!tmtPrrr..,~llfll••~1a11~•1t1•-•••
· ., •am'• --------------
• Heteroploidv ··cells, tissues or whole organisms have chromosomes in.the nuclei

that are different in number from the normal number of chromosomes
.. Parasexualism - genetic recombination .~ccur in the fungal l~eterokaryosis during
meiosis
B. Sexual-like processes in Bacteria ,

a Conjugation - two compatible bacterial cells come into contact and exchange genetic
material through a conjugation bridge or pilus
• Transformation - bacterial cells incorporate genetic material from ruptured
bacterial eels ·
• Transduction - a phage or a virus that infects bacteria, transfers genetic material
from one bacterial cell to an0ther
DISEASE CYCLE
. .
Iii Sequence of events that leads to, and is involved in disease production
• Activities of the pathogen away :from and .in the host
• Not the life cycle of the pathogen
• Continuous process
.. ': :.·.... ~ ' ·.": ... . . ·: . ~· ~·~·· : .1, •
:~ . .
l'ATMO !~l: N(:!!itS STA<l~ . ··- . . - .
TYPES OF DISEASE CYCLE
(~-~·-
~-·- .
MONOCYCLE ·
POLY CYCLE
A General Disease Cycle
MONOCYCLIC DISEASE
One disease cycle in llllC crop growing season or one year - ~"··t\;v~\.. · ·\ <-" ~'''"J( - s't""I\< .... 1:. ~\ ·~'"
I.t ale of inoculurn build-up is slow - tz 'N . .
' ' • - ~<A(,t-C\/1<!\I W1 I\
Rate of disease mcrease 1s slow .
· - \'.'".i'"'V\•\" v-"11::
Soilbnrnc diseases like bacterial mid fusarial wilt; rusts of trees; smuts .
POLYCYLIC DISEASE
• 2-30 disease cycles in one cropping season or one year
,, Rate of inoculum build-up is fast
• Rate of disease increase is 50-100%
·-- --------------------~-----·------
Cnop PROTECTION 87 .
I I Al
'·
o Late blight of potato, gn1in rusts, ric~ blast, leaf spot ofmungbean' viruses with insect
vectors
o EPIDEMICS
Saprogenesis Phase
• Smvival phase
• Weakest link in the disease cycle
• Pathogen population is at its lowest
IP Target for most control strategies
Mechanisms for Pathogen Survival

1. Formation of specialized structure- nematode cysts, teliospores, oospores, sclerotial
bod ics, clcistot:hccia, zygospores
2. Dormancy.- ~·est period intem11)ting development; long enough for the pathogen to resume
parasitic activity; synchronize with renewed host activity. Ex. Claviceps ascosporcs (rye
flowers) &Plasmodiophora spores (ally! .isothiocyanate from·crucifers)
3. Fungistasis- a control mechanism which restricts germination of propagµlcs deposited in
the soil · · ·
4. Survival in hosts or vectors- quiescent vegetative condition in host tissues.
5. In alternate hosts
6 . Survival as saprophytes- degrade and make use of a wide range of organic nutrients
Geographic Distribution of Plant Pathogens

o Distribution- movement of a plant pathogen to and its establishment in a geographical
area not previously invaded by that pathogen.
" Transport, dispersal, dissemination- movement within an area of distribution
Ecological significance of dispersal ·
e A fundamental feature of the life cycle of all living organisms
o Space and nutrients are limited
• Adaptation is very narrow; parasites need Jiving hosts
8 Dispersal in terms of
• Spatial spread
• Time scale
Structures well adapted for dispcr:. a~

• ln vital assoc. with host
I. Yiralparticles
2. Bacterial cells
3. r-4~ ungal. n1yce]ia , conidia
4. Nematode larvae & adults
• In non-vital assoc .
1. Oospores
2. Tcliospores
3. Zygosporcs
4. Sclerotial. bodies
5. Seeds olparnsitic lloweringplant;,

Main Routes of Dispersal
1. Aerial environment
2. Soil environment
3. Man and other vectors
.. )
Probl.c rns facing the pathogen after dispersal
I. Unfavorable environmental conditions
2. Uninhibited germination or hatch
t Absence of a host to infect following dispersal
4. Consumption of energy reserves during dispersal
INOCUl,ATJON
" ( 't rnl :wl ()f'pall11l gl·11 will1llH.: 11(! :·;1
l ·,.._· p i: 1~; i! iu n u!· i 11uculll il) ifllcY ~ 111 ! n f t:ci.? ~.nt cou rt
.. lnoct!lum : any part of the pathogen that can initiate disease
• Infection court: the susceptible part which could be natural opening, a wound, or intact
plant surface ·
TYPES OF INOCULUM
• FUNGI: spores/conidia, mycelial fragments, sclcrotial bodies
• NEMATODES: eggs, larvae, adults .
• PHANEROGAMS: seeds
c Bacterial cells, phytoplasnrn cel!R, protozoan cells, virus and viroid particles
'"
'
SOURCES OF INOCULUM
'
~ I . lnfocted living plants
''°t
2. Plant debris
3. [nfcstcd soil
'!. Infected seed and vegetative propagating materials
5. Vectors like insects, nematodes
6. Contaminated containers, storage areas and cquip1rn;nt .
Agl·nts of inoculation
1. Man in the process of doing farm work
2. Insects- casual or specific vectoring
3. Nematodes~ virus diseases
4. Ivfites- virus diseases
5. Fungi and fungal-like organisms- virus diseases
6. £3y chance- wind and rain splashes, near and far
Speciaiizcd transmission- Bacteria -insects

I. l~rwinia tracheiphila- striped cucmnber beetle (cucumber wilt)
2. Pecrobacteri11m carotovorum subsp. atroseptica - seed corn maggot (potato soft rot)
3. Pseudomr_inas savastanoi-· olive fly (Olive knot) ·
---------
Cnor PnoTECTtON 89
' ' :d: 1
Specialized transmission - Virus -Insects

4. Rice tungro virus- green leaf hopper, Nephotettix virescens
5. A.baca bunchy top virus- Pentalonia nigronervosa ·
6. tomato spotted wilt vims- 7 species ofthrips
Penetration or Ingress
• Entrance of pathogen into the host
e Passive: pathogen plays no active part. Vectors cany the pathogen into the plant cells or
tissues.
• Active: pathogen participates. Flagellar movement, germination of spores, appresorium
mld penetration pegs
Avenues for penetration

l. Wounds
a. Mechanical wounds- grafting, pruning, dest1ckering, plowing, ·w eeding, transplanting;
spraying, harvesting
2. Through nntural openings _ . _
1. Stomata- rust spores, downy mildew pathogens, Xanthomonas axonopodis pv. citri
2. Lenticels- occur in barks or woody sterns, tubers '
3. Hydathodes-- water pores
4. Ncctarthodcs, broken glandular ancl foliar trichomes
Direct Penetration
• Through intact epidermis- wax, cutin, pectin, cellulose :fibrils
• l3ttctcri~, virnscs & some fungi cannot penetrate directly
INFECTION
ft Occurs when the pathogen has become established in the plant tissues after penetration
and obtains nutrients from the host. -
• Penetration alone docs not imply successful infection and d]scase product*on.
Latent infection- the state in which the host is infoctcd with the pathogen but docs not
show any symptoms.
Pathogen stops growing and remains dom1ant.
Jn mango fruits w/ anthracnose; symptoms appear only after fruits start to ripen as the
fungus resumes parasitic activity.
COLONIZATION/ INVASION
Growth I multiplication or movement of the pathogen in 01-,tlu·ough host tissues

Produce harmful chemicals like enzymes, toxins, hormones; etc
Colonization by Fungi- growth by producing mycelia and spores

a. Intercellular invasion- hyphae are in between cells -
b. .Intracellular invasion:. spores and hyphae in xylem vessels
c. Intcrcellular invasion (hyphae) but with intracellular haustorium

Colonization of Bacteria~ multiplication of more.bacterial cells .
a. Intercellular- in between cells . .
b. Intracellular~ in xylem and phloem vessels
Colonization of Viruses- multiplication of virus particles

a. Always intracellular- inside epidermal cells, the palisade ce~ls, the spongy mesophyll,,
vascular systems.
Colonization of Phytoplasnrns- binary fission, budding, etc'. to produce m_o re cells.

a. Colonize phloem sieve tubes and phloem parenchyma. ·.
Factors affecting spore germination

I. Mo islure- free water is required for germination.
a. 100%RH- Pu ccinia coronata & P. graminis .
b. 90- 100%RI-I- Ustilago spp., Bot;.ytis cinerea, Peronosclerospora ph;/ippiriensis ·
c. 75%RH- Some species of Pe1iicillium and Aspergillus
d. 0-98%RH- E1ysiphe polygoni & Uncinula necatur. Free water inhibits some
Erysiphaceae, esp. if spores are completely immersed.
2. Temperature
Cryophilic organisms- optimum below l 5°C
Mesophilic - 15-20°C
Semi-thermophilic- 25-30°C
Thcrrnophilic- ubow 35°C
• of
Optimum for germination may not be optimum for growth genn tube or for general
vegetative growth . . Ex. P. ir!fe.s·tans·· short exposure to 40°C increased germination, then
Lo 20()C. .
Cl Can also influence method of germination. P. ir!f'e.stans"libe~ate zoospol;CS at 12- l 3 °C;
gch11 tubes at higher temperature. ·
3. Light
~ N;1tm;il visible light - '1000- frnooA huvc little c.~nt..~ct bt1t intense light: mi1y cnusc heating
thu s inhibit it.
4 UV rays- injurious and mutagcnic
• Neur UV- 3100AOOOA peaking at 3650Ainduces sporulation
• Light near the red end can inhibit
• Shorter wavelength accelerates germination
4. pH
• Fungi germinate best under slightly acid conditions (about pl15-6.5 with a range of
pH 3-8). ,
• Plant exudates mayrender the pH at the infection droplet unsuitable for gcnnination and
subsequent growth of the germ tube. : . .
• Over-all effect is complex- involves availability of nutrients ~nd other factors.
5. Oxygen and C0 2 concentration ·
Spores germinate with oxygen concentr~tion of 50% and above . .
An increase in C0 2 cone. stimulates germination (60-70%).
1:- -- -·-·--·----- -- --- -----···-·-- -·- --·-

(ROP PROTECTION 91
..
~r-·----------..,,-.......--..................._..._..,.w· ------·...._...··~---------~------~----~-
• \\later logging limits oxygen and can inhibit spore germination; can also. increase C02
accumulation that also inhibits germination. . ·· . .
6. Biological Factors
Nutrient in spores -some will germinate in pure water because. the spore contains all
nutrients needed.
Exuda tes from plant tissues- stimulate spore germination. Ali ecological aclvantage~ for
specialized parasites.
Pollen- diffusates stimulate germination.
Root secretions- egg hatching, Striga sp. ·seed germination
Age of spores
• Auto tropism- influence of surrounding spores in detennining whether and where the
germ tube emerges.
MECHANISMS OF PA THOGENICITY
How pathogens ~1ttack 1:ila.nts,

• How pathogens cause disease,
How pathogens bring about "malfunctioning of the normal physiology" of affected
suscept.
1. Interference with the uptake of water and inorganic elements from the soil.
I. Root-rotting ·microorganisms
2. Colonization of xylem vessels
3. Crushing of xylem hy gall forming nematodes
4 . . Formation oftyloses-enlargcd xylem parenchymu cells
5. EPS and vessel macromolecules resulting from brcakdowffof cell walls ..
2. lnterferer.l~~ with ~ranslocation of organic compounds . ·. . .
Plfotosyt1t'1fatcs~ pass thi·(:i\igh plasrr:odesrnata tc the phloem elements, then to cell
protoplasm
• Phloem necsosis by viruses
11 Yellowing · · .I·
::
•i
• Unfilled grains or small tubers
3. Reduction Of plant's photosynthetic. capacity
• Reducing the effective surf~1ce .for photosynthesis like leaf spots, blight, curl, • .,
·.. niosu.ic, mohlc,: d111kcr, 1-ical~, dicback, wilt, etc. ''
i'1;
'I•
• · D~sfru~iion of: Criloroplast~ and r~dti;ction ()f chlorophyll ·
19 I? locking reactions for production of chlorophyll resulting .in chlorosis.
4. Increased transpiration ',:
• Powdery mildew, downy mildew nnd rust pathogens destroy the cuticle und ,,; "'
epidermis
.. Increase pcrmc<1bility of leilfcells
• Detrimental water loss through increased transpiration
o Will
I - - - - --- - -- ··· - - - - - - · · -·- - - - - -

\ 92 Aggie Board Hf~ viewer
·------·--- --- ----·- ··- -- -·----·- - -~----~-·~~~~------------.........-.............
5. Changes in growth of suscept

Plant growth invo Ives a series of well-rq:.,'l.tlated and coordina~ed processes as
metabolism is controlled by growth regulating hormones and feedback mechanisms.
Hormones associated with plant diseases

1. Auxins (IAA) and cytokinins
1. required for cell division and differentiation
2. promotes synthesis of mRNA =>proteins, enzymes=> structural proteins
3. Increased auxin (IAA) levels 0ccur in many plants infected by fungi, bacteria,
viru.scs, 1no llicutcs mid nematodes. ·
Examples:
I . Corn smut caused by Ustilago maydis
2. Club root of cabbage c:m:1sed by Plasmodiophora brassicae
3. Peach leaf curl-Taphrina deformans cause puckering, curling and other leaf ·
distortions. Auxin is involved. Palisade parenchyma cells respond more than the
1.;. ~
spongy mesophyll and result in uneven growth, causing leaf to curl.
.;
4. Crown Gall- Agrobacteriw11 tumefacien
lncrease in IAA is due to: ·

Pathogens induct~ increased IAA levels in their respective hosts
Decreased degradation of lAA through inhibition ofIAA o.xiclase
2. Gihbcrillins - Stimulate stem elongation by stimulating cell division and

elongation
1.:xample- Foolish disease of rice caused by Gibberella.fitjikuroi which led to the discovery of
the gibbcreUins.
3. Eth~1 lene
• a simple, gaseous hydrocarbon synthesized by all plant tissues and by some
microorganisms
• the natural aging andripening hormone, physiologically active in trace amounts (0. 1
ppm)
• levels of production and internal concentration vary widely among different fruits
and plants . '"
Applied exogenously it is effective ;.n very low concentrations (below 0. 1 ppm)
• in excess, it produces a variety of plant responses such as: epinasty, premature
senescence, ancl shedding ofleavcs
• in a number of viral diseases, leaves with necrotic local lesions produced more
ethylene than th()sc vvith systemically infected plants without necrotic lesions
6. Dea th of cells n nd tissues
A. Eu:Lymcs in plant disease

• Enzymes are large protein molecules that catalyze all interrelated reactions in the cell.
• Enzymes involved degrade the pl ant cell wall that is col.11posed primarily of
polysac charides (pectic substnnces, cellulose, hernicellulosc), structural glycoproteins
:ind li g nin .
(ROP PROTECTION 93 .
Pectic enzymes ,
I. Assist in the p~netration of the host. Expose the cellulose and hemicellulosc fractions of
cell wall.
2. Degradation resu Its in the weakening of cell walls or tissue maceration which facilitates
inter-and intracellular invasion of the tissues.
3. Provide nutrients to the pathogen in infected tissues. (exo-enzytnes)
4. Involved in the induction of vascular plugs and occlusions in vascular wilt diseases (endo-
enzymcs) ·
Cellulose Enzyme degradation

1. Endo-1,4 P-D glucanasc- cleaves internal glucosidic bonds within an unbroken
glucan chain.
-0-0-o-o-o-o-o-o-o-o-o-o-o-o-o-<1-o-
f j· .
'.•
2. 1,4 P-D glucan <.·eUobiohydrolase- cleaves cellobiose dimers from exposed non-
" reducing ends
-o-o-o-o-o-o-o-o-o-o-o-o.:.o-o-o-o-o-
-o-o-o-o-o-o-o-of o-o- t
3. r3-glucosidase- hydrolysis ccllobiose (o-o) to glucose (o) (o)
~· I
o-o o-o o-o cellobiose
\, :
I t t t
Hcmicellulose fraction- found in the matrix of both prima1"y and secondary cell walls.
II A xyloglucan with glucose backbone linked f3 1,4. Xylosc units are attached to the
backbone, and both galactose and fucose are bonded .to xylosc.
ill Requires many enzymes to degrade the hemicellulose.
B. Toxins in Plant Diseas(~

Toxins- Chemicals that act directly on living host protoplasts, seriously damaging or
killing cells resulting in necrosis
Extremely toxic, effective in low concentrations
Affect pcnncability ofnwmbrancs
Inactivate or inhibit en?:ymcs
As antirnetabolite- inJuu: deficiency for an essential growth factor.
I. lJost Specific toxin~

• Toxic only to hosts of the pathogen producing the toxin. Little or no toxicity to non-
susceptiblc plants.
V iru Jenee of the pathogenic strains varies with their capacity to produce the toxin.
Has a role in the establishment of the pathogen in the host.
- - -·---------·--·----···----·-----------------
94 1\9gie Board Revi ewer
--- -·---·---·--·-·-:-··-- -·.-...·--···------
Examples of Host specific toxinll . .

l. Hclminthosporoside (HS toxin)- produced by Cochliobolus (Helminthosporiwn sacchari),
the cause of eye spot of sug<"trcanc.
2. Victorin (HV toxin)- Cochliobolus (Helndnthosporium) victoria,!! causing foot or root rot
and leaf blight of 9ats.
3. T-toxin- Coch!iobo!us heterostrophus (Helminthosporium maydis)- causes Southern corn
leaf blight. ·
4. I-JC tox in- C'ochliobolus (Hclmintho.s1Joriwn) carbonum causes leaf spot of corn.
Resistant corn has gene that codes for HC toxin recluctase that detoxifies the toxin.
5. PC toxin- Periconia circinata causes milo disease of sorghum. Only isolates that
produce the toxin are pathogenic.
II. Non-host specific or non-host selective toxins

Produce all or part of disensc syndr~nm· on host plants and non-host plants. Not selective.
Enhance cl iseasc but not essential for the pathogen to cause disease.
Examples of non:-hosC specific fungal toxins

I. Fusarial wilt toxins
a. Fusaric acid- many species of fosarium
b. Phytonivein-Fusariurn oxysporumf ~qJ. nh eum 1
c. Phyto lycopersin- F. o. f sp. lyr.opersici

d. Lycomarasmin- F.o. f sp. Lycopercisi, melonis, vm;;njectum
2. Ophiobolin (Cochliobolin)-Cochliobolus miyabeanus
3. Hclminthosporal- Cochliobolus (Helminthosporium) sativus
.\ ;
.~ 4. Fusicoccin- Fusicoccuin arnygdali
;\j: • 5. Pyriculurin- Pyricularia grisea
. '
, Examples of 11011-host Specific Bacterial Toxins
;~ ~ I, · Tabtoxin- Wildfire disease of tobacco- Pseudomonas .~vringae pv. tabaci
2. Ph ~1s co lotoxin- Pseudomonas savastanoi pv. phaseolico!a (halo blight of beans) and P.s.
pv actinidae (bacterial canker of Kiwi fruit) ·
3. Coronatinc- Pseudomonas ::iTrh1gae pv: atropurpurea .
. l
4. Rhizobitoxin-Produced.by some isolates of the root-nodule bacterium, Rhizobium
japonicurn, when plants are under stress.
5. Syringomycin and Syringopcptin-Producc<l by Pseudomonas syringae pv. syringae
6. Amylovorin - Erwinia amylovora causes fi re. blight of apples arid pears
lViECHANISMS O.F DISEASE RESISTANCE

~Y,
'
• Bow plants defend themselves against pathogens
I
•i
. Resistance - Charnctcristic of host that inhibits or suppresses the growth and
dcvl~ loprncnl of'tlw
parasite I pat hogen
CHOP PROTECTION 95
Types of rcsistan ce
I. Pre-formed Resistance-· Resistance present in plant even without the presence of the.
pathogen
2. Induced resistance -Activ0 only in the presence of inducers
Preformed Resistance
A. U:xternal Physical Barriers
1. Trichomes
8,. Effect of trichomcs on insect transmission of plant pathogens
Intcrfore w/ feeding and oviposition
Hooked hairs catch tarsal claws
Glandular hairs secrete alkaloids that are toxic or secrete chemicals that repel
insects
I '
b. Effect of trichomcs in fongi .
Spores, germ lubes and appressoria can't adhere to surfaces
Malic acid in glandular hairs toxic to A1ycosphaerella blight
2. Culicle
a. Consists of pectin, cut in, wax layers
b. Acts as· water repellent (electrically charged surface)
c. A toxic barrier
d. A mechanical barrier
3. Stomata b<lse<l on:
Stomatal density
Spatial arrangement
·• Structure (cuticular ridge)
Time of opening and closing
4. Root cap und mucilage
) . Thick seed coat
(i . Thick epidermis
13 . Internal Physical. Barri.crs

t. Subcrized Tissues
An insoluble polymer tightly attached to cell walls of underground parts, barks and
paiderm!;
iv1cchanical and chemic8! b:ffrkr
2. Lignified Tissues
Phenolic polymer
Plant cell wal.ls and iuterccllular spaces
Endo dermis of roc>ts
3. Ccllulosic walls- more difficult to degrade 1'•
4. :iviiddle Lamella- lignified or calcified pectic substances

S. Deposition of Gums, Resins, and Tannin-like substances- serve as partial barriers, can be
rungitox ic
G. Deposition ol'Silicic Acid
96 A~1gic Bo.:ird neviewer

•••••••••••••••••••1t;amam•YfM••• nwrnnm rrnmr , ' t:r:: 'W
7, Stru ctural features of the vascular elements - narrow and more branching contribute lo
res istance
C. Defense through ladi: of essential factors in the host

1. Lack of reco gnition between host and the pathogen
2. Lac k of host receptors and scm:itivc ~:ii e s for toxins
3. Lack of essential nutrients Jor the pathogei1
D. Pre-form ed Chemical Factors

I. Phcnolics- pyrocatcchol and pyrocatcchuic acid arc fotmd in onions resistant to onion
smud ge caused by Colletotrichwn circinans
Phlorid zin and phlorctin- found in apples resistant to Erwinia amylovora
2. Tannin s ~ found to be powerful inhibitors of the pcctolytic and hydrolytic enzymes

3. Saponins- naturally occurring chemicals' that bind to sterols in fung·a l cell membranes;
alters permeability , .
• Avcnacin- found in oats that are resistant to root rot pathogens . .
t '
111 Tomatine- in tomato resistant against Fusarium oxysporum f. sp. lycoperCisi
4. Enzy mes involved in resistance ,
! >.
~ Pcro xidases- involved in oxidation reaction

0 Po lyph eno I oxidas c- converts phenols to qui nones
"' Lytic enzymes
I ' A. chitinasc- against fun gal cell walls
B. r3-l ,3 g JUC<lll(ISC- also against fongaJ -likc oornycctc cell walls
/
B. Induced Resistance
" Active only in the presence of .inducers . . .
• Indu ced response to infection includes: a cascade of responses such as the production
o f nove l antimicrobial com1:iounds (phytoalexins), proteins, and formation of physical ·
harri ers to penetration.
Rl'rognHion of the Pathogen hy the Plant

Fung i and bnctcria release in their ,i mmediate environment various substances like
g lycoproteins, carbohydrates, fatty acids, and peptides which could act as elicitors of
recognit ion by the plant.
Inducers
I. Ph ysiL:itl presence 0 rpil llwgcns Iikc n111ga l spore::; on plant surface
2, O thers req uire penetration before induction
3, Non-specific clic itors (innate response that discriminates between self and nori.-self)
4. A VR gene pro ducts in Gene fo r gem~ rcsistan ~e model (races of pathogens)
5, Other molec ul es
- ----------- - ---
CROP PROTECTION 97
A. Induced structural defenses
This type of defense includes the formation or one or more types of structures for defense
which could involve:
I. the cytoplasm (cytoplasmic defonse),
2. the cell wall (cell wall defense),
3. histological defense (host tissw~s ahead of pathogen), and
4. the death ~fthc invaded cells (necrotic or hypersensitive reaction).
I. Cytoplasmic Defense Reaction
Cytoplasm and nucleus of the invaded cells enlarge and the cytoplasm becomes granular,
dense and filled with various particles causing disintegration of the fungal mycelium (observed
in weakly pathogenic Armil!aria strains). .,
2. Cell Wall Defense Structures

I ~
J')
Involve morphological changes in the cell wall of the invaded cells.
~ J
,· Three types of such structures have been observed in piant diseases
I
.
A. outer layer of the cell wall of parenchyma - in contact with an incompatible bacteria
swells and produces an amorphous, fibrillar material - surrounds and traps the I
' bacteria a ncl prevents rnu it ip 1icat ion I
t : B. Cell will.ls thicken - ccllulosic materia l: infused with phenolic substances that arc
~ cross-linked; resistant to penetration. ,
"
~
' C. Callose papillae - deposited on the inner side of the cell wall (fungal invasion):
1"
' envelopes the penetrating hyphal tips forming a sheath infi.tsed with phenolic
subs tances.
I
.,
J. H.istological Defense Structures
a. Formation of cork layer (with sube1in or lignin)-Cork layer is composed.of dead
cells that inhibit furth er iiwasion by the pathogen; also block the spread of any toxic
suhs. !hat the pntliogcn may secrete. .
b. Formation or Abscission Layers - formed on young active leaves; consists of u gap
between two circular layers of cells of leaf surrounding the locus of infection;
c. Formation of Ty loses - overgrowths of the pro top last of adjacent living
parenchyrnatous ·cells which protrude into xylem vessels through half-bordered pits . .
Tyloses have ccllulosic walls. /
d. Deposition of Gums-around lesiorn; or injury through mechanical means
• they form quickly in the interccllular spaces and within the cells surrounding the
locus of infection ·
• an impenetrable banicr around the pathogen which becomes isolated
B. Induced Biochemical Defenses

t'.
A· l. Defense thru hypersensitive response (HH.)
• HR is locn lized plant. cell death at the site of infiltration. Occurs in incompatible
interactions.
-----·- --------·- -------------------

98 Ag9ie Board Reviewer
~
I
• The cell death surrounding the pathogen creates a physical ban-ier to movement of the
pathogen .
• Ln addition, compounds released from the dead cell can be toxic to the invading
~· pathogen.
2. Production of anti-microbial substances in ~1ttacked cells (Phytoalexins)
" Secondary metabolites produced in response to p<lthogen attack, stress, and injury
" produced by healthy cells adjacent to localized damage and necrotic cells in response
to materials diffusing from the damaged cells
Examples ofphytoalcxins
I. Phascolin in beans
2. Pisatin in pea
3. Glyceoli:n in soybean, alfalfa and clover
4. Rishitin in potato
5. Gossypol in cotton
6. Capsidiol in pepper
3. Pathogenesis related proteins- proteins that m~e related to disease process
Examples-
! . Endo f3- 1,3-glucanase
.. f 2. Type l, U, IV, V,VI, VII chitinase
3. Protease inhibitor
tJ.. Encloprotea:sc
5. Peroxidase
<). Ribonuclcasc
7. Defonsin
'l'J'.
;
8. Lipid-trans for protein
4. Production of other defcnse-1·e!ated proteins
a. Lectin- chitin-binding lcctins in cereals
b. Ribosome inactivating proteins (R1Ps)- an antiviral protein, reduces virus replication
c. Lipoxygcnases- produce volatile and non-volatile fatty acid d~rived 2° metabolite toxic
to invading pathogens
}, '
5. Detoxification of Pathogen Toxin
Dct()xirication of some toxins like HC toxin and pyricularin, are known to occur in plants
and rnay play a rok in resistance.
6. Protection of plants against Pathogens

Cross protection: less virulent strain of a virus is inoculated into the plant - more resistant
to more virulent strain
Locnl and Systemic Acquired Resistance

.. f-;AR confers quantitati ve protection against a broad spectrum of microorganisms
• Chemical activators of SAR cornprisc inorganic compounds, natural compounds, and
t;y nth c tic compounds.
(ROP PROTECTION 99
;ti
Systemic signal transduction (leading to systemic acc1uired resistance or SAR)
Systemic inducers ·
QI Salicylic acid (SA)
• Oligogalacturonidcs
,. Jasmonic acid (.TA)
• Systemin
• Fatty acids
i: Ethylene
GENES FOR DISEASE RESISTANCE

• Defense Genes
• Resistance Genes
Defense genes- Sequence of DNA that encode various proteins that are responsible for synthesis
and sccumulation of defense arsenals in plants · ..,
. ~ '
• quiescent in healthy plants but activated when patho'gens come in contact,
re lettsing signals
• s ignals arc transforrccl to the plant nucleus through signa:l transduction pathway
activating defense genes
Defense genes may function as:
'i 1. involved in-production of antimicrobial compounds like phenolics, phytoalexins,
''
;'.j
·:d pathogenesis-related (PR) proteins and active oxygen species.

. ., n: inforcemcnt ol'cdl \Vall by accurnulnting hydroxyprolinc-rich, glycoprot.eins, callus,
lignin and phenolics.
3. Non--cnzymatic action which includes antifungal action, elicit.or-releasing activity,
increase in mechanical strength of host cell wall and others involved in the release of
secnnd message and systemic signal molecules.
(R) Genes
H(~ sistanc:c
o Resistance genes arc regulatory genes. Sequences of DNA that regulate the functions of
the defense genes ·
• Products of the resistance genes share striking similarities and they appear to be involved
in signal transduction syslcm to activate defense genes
Role of R gene Products:
1. Recognition - likely the "receptors" or binding sites for the "elicitors" (Avr proteins)
2. Signaling- participating '.n signal transduction cascades
(,
; ,. R genes and Resistance

... I I. Elicitor molecule produced by uvr gene of pathogen is recognized by a specific plant receptor
encoded by an R gene.
2. Aft.er recognition, one or more kinase enzymes may become activated that then amplify the
signal by phosphorylating, and thereby energizing, other kinases and other enzymes.
3. This leads to cascade of biochemical reactions leading to hypersensitive reactions (HR).
100 A99ie Board Reviewer

EPIDEMIOLOGY
I> Study or diseas e development in plant populations

to Epidemics- (Vander Plank) an increase in disease incid ence within the plant population
with time.
~ Epiphytotics- (purist) epidemics of plant disease
Endemic dis eas e- disease that is nntive or indigenous to a particular place
Exotic disease- a disease that was introduced from some other area
('.
Pandemic disease- a disease of worldwide or widespread occurrence throughout a

continent or region.
•i
Other factors involved in disease development

I.. Plant susceptibility
2. Pathogen virulence
3. The duration and intensity of the various environmental factors
4. Time
5. Presence of
vectors
6. Intervention measures by man
Ep.idemic more likely to occur if: .
l. Asingle crop variety is planted over a wide area
2. Plants are predisposed to infoction by excessive nitrogen fertilization or by injuries
3. There is abundant inoculum, inoculum is rapidly formed, efficiently liberated, spread,
and inoculated. . .
Disease increase at any one time is dependent on:

I. Initial amount of inoculum or disease (X 0 )
2. Rate of disease increase (r)
3. Duration or period of time involved
• Accdg. to Vander Plank, this is similar to the increase in money invested at
different interest rates. (Initial amount, interest rate, duratioil of investment)
Relation of epidemiology to control practice ~i :
X =X
• 0
ert
Where: X::=: amount of disease

\= initial inoculum
e= base of naturnl logarithm
F ' rate of disease increase
t= time
Control measures ~H"e geared fowards reducing initial inoculum and reducing the rate of ·
disease inc1·casc
I
I'·
\ '
CROP PROTECTION 101
I
Development of epidemics
• Plotted against time, disease incidence shows a sigmoid epide1'nic curve (polycyclic)
" Epidemics begin at a point where sigmoid curve begins to leave the horizontal line to
approach the vertical line
~ After onset of epidemic, disease incidence becomes logarithmic, until suscephble tissues
decrease.
.. Epidemic cnds-
o A. no susceptible tissues,
o B. unfavorable environment prevent further increase. Curve levels-off.
Types of diseases
l. Compound interest or polycyclic clisea~es
Pathogens arc readily spread from plant to plant during the disease cycle (rusts,
powdery mildews, Cercospora, etc)
Repeating disease cycles occur with several generations of the pathogen
2. Simple interest or monocyclic diseases

o No plant to plant spread during the primary cycle, or
• Only one gcncrntion of pathogen occurs during the growing season as in root knot and ·
vascular wilts caused by soil-borne pathogens
Control prnctice~dhat reduce the amount of initial'inoculum

I. Roguing of diseased plants.
2. Chemical eradication
3. lJot water treatment
4. Destroying infested plant debris ;,,,
5. Soil tlnnigation
" 6. lbng varieties with vertical resistance
·~
Control prndices that reduce race of dise.r,sc increase

1. Modification of enviromncnt
2. Cultural prncticcs that hinder growth and reproduction of pathogen (Jess fortilization,
r:iising rurrows, clean culture)
. l. Planting varieties witli horizontal resistance
DISEASE ASSESSMENT
Disease assessment is necessary in:

1. Evaluating resistance of varieties.
2. Disease survey and evaluation of incidence and severity in a locality.
J. Effectiveness of fungicides and how much contro 1 was attained.
4. Effectiveness of management package in controlling the disease.
·- -- -·- ---·- ------·- - -

• ' " • ·• • • •. •• · --- · ~ •• ·• • ' • M h -·~- · • • . . _ _ •.• - • • • • • • • • · • - •' • • • • - • • • - - ·· - - - -· • o•
Assessiug amount of disease

l. Determining% incidence(% diseased phints, organs or tissues)
.[NurnlJer of_~1foctcd p~ _ _J
'%disease incidence --· [- :;:- - · - - - - - . X I 00
L~~~J number of plants
Disease incidence best used for:

• diseases that exhibit systenm; synptoms such as wilts, damping ofC root rots, those ' .
caused by viruses
• disease that affect entire organs such as fruit rots, inflorescence smuts
• presence of disease is directly translated to yield loss
2. Use of descriptive disease ratings on a numerical scale (Disease severity)
• diseases that show various amounts of infection in different parts of the plant like leaf
spots, rust pustules, stem rusts, anthracnose
• Presence of disease does not directly translate to yield loss.
Fur example:
Rating scale -foliar rice blast (Percent leaf area infected)
ti1\g _ __
~
ff~
DESCRIPTION
scale ·
------- -- · - - - -- -- - - - --- - - - - - - - - - - - - - - - i
0
- ----- -- No
--lesion/infection --- ·-
______l____ §mall to large brown spcck1 1-5'l-~J~afarea infected~-
~- ----~---_:_ __JJ'.pical blast lesion, 6-_! 5% lai --·----·--------i
----~!._ ___ ~al _bl~!l_csio1~, 16-25% lai_________________--;
....____ ]_____ _Ixp_i~I blast lesion, 26-59% la~.--,--------·--------l
9 More than 50% lai
--.- ---- -- - ----------------------'
To compute for % disease severity
n(O) + n(l) + n(3) ..... n(9) X 100
Nx9
\\"here n= number of infested plants classified by grade (scale)

N"' total numbcrof samples
9= represents the highest value in the rating scale; varies on the rating scale used
- - - -------,·-------- - -~ ·- ---- --------- · - ~-- ...

Cr.op PROTECTION 103
·, '
<-lf.%:fJA:l:i.011 13'.59To'
Cercospora leaf spot of rraungbean
For examp le:
------~~-at-in_g___ F b e r o.fPlants Rating x no. of plants (n x r)
()
-·---·· - - ·0- - - - ---- ----- 0
-- -
1 - ---+- 3 3
---- ·- -- ---------
3 12
-- ~·
36
- ·-
5
- ------- -- · -- -~- --·
10
- 50
7 1 7
-·- -- - - - - - - + --·
---- ---·- - 9
- - -·- -!----- -0- f-·
0
I:.N=2 6 .. :ENxR= 96
[_~6=i
% D.S. = ---------------------- x 100 = 41 %
PLANT DISEASE SURVEYS

• Wide scale appraisal of the sever ity and prevalence of disease in a countty, a region or a
continen t.
• Prevulcncc~ How oJlen 1hc dis8<:tSC occurs in the locality (Whole year?, occasional?).
Ouj cctives:
1. Dclc.rminc the gcogrnph1cal distribntion of certain diseases, certain pathogens or ce1tain
physiologic races. ·
2. Detect and monitor newly introduced pathogens.
3. Determine the distribution of alternate hosts.
tJ.. Quarantine
-----------------··--·- -·------·---
-, s ,•• rrm=-
- ---------lllllllllllilllillllllillliRMl!il-iUlllllllllli!fllljNJ-IB_i _ _I I I FJ"!l7
.:
Plant d[scase surveys

Aid in evaluation of the relative importance of diseases a,nd assist in the development of a
cooperative control program.
Canied out by trained personnel
Aerial photography of diseases with symptoms .
Spore trappiDg
Space vehicles that orbit the eai1h
Molecular biology tools
FORECASTING OF PLANT DISEASES
I, Predicting the 'i ncidence and severity of plant disease

2, To properl}'guide farmers in making decisions on disease control .
3. To save crop growers a lot of money that otherwise would be thrown away on control
measures that are not necessary.
General Procedure
1. Study under controlled co11dition the eiwironmental conditions required by the pathogen for
tiding over adverse conditions, for the development and spread; .
2, From the data obtained,

a , a climatological model is prepared;'
b. model.includes the sequence of climatic conditions during specific times of the day as
they affect the variOli's events
of the disease cycle (spore germinatioi1, penetration;
colonization, spornlation, spore dispersal, etc,) ··
2. From the data obtained,
' I
a, a climatolo gic.~! n.1od.:: \ i~ prepared; ~ . >

1
1
1
1 1
0
r 0 1' • •: I
1
:
1 1
1
1
' :
I b: 1'nodel incli:\afW·tr1e s~q~uencc of climatic conditic:i1is during specific times of the day as
they affect the various events of the disease cycle (spore germination, penetration,
colonization, sporulation, spore dispersal, etc.)
2, From the data obtained,
a, a climatolo_gic ~ l . rnodel ,i s prepared; ~- .. ..·: . , ., .·. , . . . .

b. model includes the ·s<xil.1enc'd of cliq{~i:tic' c6nd iti61is during s~1ccific times of the day as
they affect the various events of the disease cycle (spore germii1ation, penetration,
colonization, sporulatio1'1, spore dispernal, etc.) .
c. Model is field tested noti11g cli~ease development in relation to the weather, and the
necessary refin ements are made. ·
------- ·¥ ·-- -·- - - ------- · ---- - - ~----------------------
(ROP PROTECTION 105

PRlNCIPLILS AND METHODS OF PLANT DISEASE MANAGEMENT
(PLANT DISEASE CONTROL)
• The raison d'etre of the science of plant pathology is the control of plant diseases
• ivlust be economical
• Most arc preventive in nature
Purpose:
J. Prevent di sease development
2. Maintain a tolerable disease incidence
3. Minimize yield losses
Four General Principles

I. exclusion
2. eradication ·
3. protection
4. resistance
Ji:X CLlJSJON principle

• Prevention of a "new pathogen" from being introduced into a locality where it is
currently unknown. ·
Methods of Plant Disease control {those that exclude the pathogen)
a. Quarantine - regula~ory actions to prevent the introduction or dispersal of non-native
organisms (exotic diseases); Legal methods
b. Inspection and seed certification
c. Use of pathogen-free propagating materials
ERAIHCATJON prindplc
• Elimination of pathogens that have becom~ established within the plant or in an area
Mechanical and physica l methods to eradicate pathogens
Utilize so me physical component of the erivironmenl, such as temperature, humidity, or
light , to the detriment of pathogens
/\. PHYSICAL
I. I lent trcatm~nt (hot water, hot air, soil sterilization, soil solarization)
2. Jrradiation- UV mys, X rays and Gamma rays
J. Light' wavdcnlhs that prevent sporulation
4. Drying stored grains
13. CHEMlCAL
1. Systemic chemicals
2. Soil fumigants
3. Disinfcstation of warehouses
4. Control of insect vi.:;ctors
i.
106 Aggie Board Hevi ew e. r

Chemical Control
1. Employs the use of chemicals thafare generally toxic
2. Used as disinfectants or tl.1migants or chemicals that target specific kinds of pathogens
( fi.1 ng icides, bact er ic ides, ncrnatic ides)
J. Ef!Cctive at concentrations that will not harm the plant -.
Know your chemical
° Chemical must have low risks to rn.an and animals and minimal effect on normal
microflora of plants and soil
~ Pathogens should not develop resistance against them
" Suitable for long storngc in ambient conditions
Antibiotics - against bacteria

• Chemicals produced by micro-organisms w~1ich destroy or injure living organisms,
especially bacteria ·
• Vcry few, very expensive
• Strcptomych1 used as stop-gap measure
• Development of resistance fo antibiotics
Issues related to use of chemicals

1. Pathogen resistance
2. Risk of poisoning humans and animals
3. Contamination of livestock products
4. Harri1 beneficial insects and microflora
5. Contamination of food products, waterways and soil
Ri sks tQ humans- when and bow they become risks
I. Preparation or application of chemicals- i~1haled, ingested or absorbed through the skin
· • safoty precautions must be followed
2. Consumption of plan ls or their products
11 various regulations exist with regard consumable products like wit:h··holding
period and MRL ·
3. Environmental concerns- copper and sulfur sprays that drip off in soils affecting a broad
range of microorganisms or washed off in waterways
4. Public awareness- less use, best application, lower doses, better understanding of
threshold levels
C. Biological Control
• A pathogen kept in check by the m\crobial community- natural control which ,js a form
of biological control
·• Employs natural enemies of pests or pathogens to eradicate or control their population.
"' Involve introduclion of exotic species 01' USC of naturally existing biological control
agents in the ccosy~;tern
Jvlcchanisms ofbiological control

I. Parasitisrn-hypcrparasitism or mycoparasitism
2. Predation- invc1iebrntcs, bacteria feeding nematodes, amoeba attackfog yeasts, small
spores, and fungal hyphac ·
---------- - - - - - - - - - - - - - - - - - -
(ROP PROTECTION 107
. ..~:.~·1
. .. ·
..
:ij
3. Competition- between organisms that require the same resource for growth and survival.
Also, competition for infection sites ofrelated microorgm1isms.
4 . .Induced resistance- cross protection, systemic acquired resistance. Prepares plants for
attack by virnlent pathogens . ·
5. ·Production of antimicrobial substances- but antibiotics are easily lost in the environment
and broken down by other organisms. ·
D. Cultural management to eradicate pathogens

1. Roguing or removal and destruction of infected plants
2. Removal of alternate hosts
1. Sanitation
4. Crop rotation
5. Creating unfavorable conditions
PROTECTION PRINCIPLE
Prevention of infection through
· l . Chemical barriers
2 . . Biological control
3. Crop management
4. Manipulation of environment
Putting a chemical barrier between the pathogen and the host
l. before inoculation
2. to prevent spore germination
J. or kill germinating spores
Cultural Management Practices for protection and eradication
• Mcasmcs undert<1ken by man to prevent and control disease by manipulating plants. Only
frll'lns of control that arc economically viable for low value crops.
A. Reducing initial levels of inoculum (Xo)
I. Selecting appropriate.planting materials

a) Planting resistant varieties
h) Planting a number of mixed cultivars
c) Using cerlillcd seeds
l
(.
2. Destruction of crop residues- burying or burning or removal of crop residues arc
important practices performed bet\veen cropping seasons
• Disadvantages of burning-loss of nutrients, smoke pollution, increased soil erosion
and greenhouse effect.
3. Elimination of l.iving plants that carry pathogens
a) Rcm1iant or diseased crop plants
b) Wild plants or weeds as alternate hosts
4 . . Crop rotation- successive planting of different crops in the same area, sometimes with
fallow , or resting period in between crops.
• rotate crops over periods that are longer than the survival period of pathogens

- - · 111.c m!U arr:mr n nonm · rr:i ·p p:;
B. Reducing rnte of disease spread (r)
I. Wider spacing of plants

a) . Reduces speed with which disease moves between plants
b) Reduce moisture levels to inhibit infection-
~ water plants in the morning to reduce wet periods when the sun rises and dries leaves;
• lmming or training plants to reduce canopy cover.
2. Adjust sowing practices
a) Change time of planting - exploit weather conditions.
b) Depth of sowing- chance of infection at pre-emergence attack
c) Dire ct ion o [sowing
3. Change µ'!anting density- transfer of inoculuJ.n, micro climate, wet periods longer
4. lntercropping- the practice of planting more than one crop in ~lternating rows.
a) lncrease the distance between plants of the same species
b) Creating a physical bari-icr between plants of the same species
c) Labor intensive but beneficial
d) Proper combinution of phi1its
5. l'vl.ulching and soil amendments- used to conserve moisture attd organic matter and reduce
erosion in the soil, decrease soil temperature, weed inhibition and seedling protection.
a. Organic matter- straw, sawdust, manure, aquatic plants, coir dust
• Crop residues as mulch should notprovide food and attractive environment to
pathogens.
b. Manufactured products- plastics, asphalt paper, paper
6. Flooding- reduce weeds, reduce fi.mgal propagules, insects and nematodes but may also
help in dissemination of pathogens
7. Irrigation- irrigation water mny carry propagules, overhead sprinklers splash inoculum,
etc. Trickle or drip irrigation as alternative.
Ii. Roguing - rcrnoval and destruction of diseased plants. Practical in small plantings,
.cl election is early and labor is cheap.
9. Fertilizers and crop nutrition- healthy vi gorous plants better. N,P, Kand Ca for plants and
pathogen.
a) N- delays crop maturity, alter activity of soil micro flora, change microenvironment
" due to increased canopy cover and crowding of foliage, therefore higher risk of
infection.
b) Phospho1'us·· sometimes encourages disease. Not well understood.
c) Potassium- generally inhibits disease dcvelop1i.1ent. Promotes healing of wounds.
Sometimes
.
effects are variable. . I
cl) Calcium- necessary component of plant cell walls for resistance.
I0. Strip farming - areas of one ~rop are separated from each other with strips of another.
Cro ps do not share the same pathogens
RESISTANCE PRINCIPLE
• Invo lves modifying certain physiological or physical features of the host so that it
can rc2£1 infection
~ Resistance is the relative ability.of the plant to overcon1~ the effects of a pathogen ·
. (HOP PHOTECTION 109

--.u•11 5 nrn rs x®m T m
METHODS IN RESISTANCE
I. Jmproving the growing conditions of plants (cultural management)

:?.. Use of resistant varieties
• Vertical resistance (few major genes)
• Horizontal resistance (many minor genes)
o Mo st effective and economical
Resistant varictit!S developed by/ used:

1. Selection
2. Gene pyramiding- involves incorporation of several resistance genes in one host
v<1 riety. Reduces X0 ;caution: development ·of "super pathogen"
J. Mu It iline varieties- a mixture of several lines with similar agronomic charactc;:ristics
. but with different genes for resistance
Gene deployment- involves the use of d.iffor;:: ntT~sistancc genes or varieties in various
geographical areas where the pathogen I race is absent.
IMPORTANT PEST MANAGEMENT PRINCIPLES
., Plant diseas es <111<l /or pests can never be eliminated, only managed at economically
acceptable level.
., Pest management requires knowledge and judgment: know the enemies (the pests), know
the battleground ( the environn1ent), know the crop (the host)
Ill Proyi ~lc thc _~rop with every possiblt:! advantage. Use all weapons .in the arsenal of
integrated j)est: management.
• Continuous pest management is basic to efficient production.
• Least po ssible cost and minimize losses.
St rategic objectives in disease management

I. Reduce the initial inoculurn.
2. Reduce the rate of increase and spread of the pest.
· Remember: X ""' X0 e'1

• Use proper tactics; develop and employ suitable weapons to carry out strategy
Example of a Disease Management Package

I. U 1:c chemicals if available and effective
2. Resistant varieties ·
3. Seed treatment
4. Crop rotation
5. Pro pe r planting dal e and site
6. Prope r seeding rate and depth
7 . Proper harvesting and storage
g, Keep abreast of latest dcveldpments
--··-- - -·--- -- - ·-·--····--···-----·---·--- - -

11 O Aggie Board Review er

Topic 2 Crop Prot 67 - 110

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Topic 2 Crop Prot 67 - 110

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Crop ·Protection . . . t ~ ..

• From: "pathos" (Greek)== suffering

To control or manage plant diseases so that .losses will be brought to a minimum.

Charaderistics of Pla1it Disease

Vital Processes of Plant:s Affected by Disease , (

Importance of Plant Diseases

2. Reduce the quantity and quality of plant produce.

68 Aggie Board Reviewer

Definitions and terininology

Symptom~- evidences of disease in the plant

a. Local or systemic ·;.•.

(flOP PROTECTION . '6 9 .

Primary vs. Secondary sy1hptoms (same disease) .

Microscopic vs. Macroscopic syh1ptorns .

General types of symptoms

• Examples- fungal mycelia, conidia, oospores, tel''

Classification of Plant Diseases according to:

Kincls of Abiotic Diseases or injury or stresses

A. Injury caused by adverse physical factors

B. lujnry caused by air pollutants

HO'W TO PRl~VENT THES.E STRESSES OR IN.JURIES

PARASITIC or BIOTlCAGENTS OF PLANT DISEASES

l. Vi.ruses and viroicls (subcellular entities) ·

'frnnsmission and Spread of viruses

72 Aggie Board Reviewer

VIRUS DISEASE SYMPTOMS

CONTROL OF VIRUS DISEASES

Reproduce by binnry fis sion !

Prokaryolic; lack nuclear membrane & lack a well-defined nuclet1S, !1\:

Old Genera (Prior to 1980)

·New Genera of Plant Pathogenic Bacteria (after 1980)

-=~~-=~!!!!!!_<:_!!~'.~-=~=-= -=-·· .-_,_-_-::~~--------'

74 Aggie Board Reviewer

7. DNA-DNA homology- useful for bacterial species identification

Genera of Non·-typical Plant Pathogenic Hac:teria

Fastidious vascular hacteria (previously called rickeHsia-likc organisms [RLO/)

Mollicutes -· Bacteria without cell wnlls

Control of Bacterial Diseases

PLANT PA 1'HOGENIC PROTJSTS

Protozoa-like protists - uniceliul&, :µlasmodial, or very sin>ple multicells, phagotrophic

Phylum Myxomycota- true slime molds . . .

Phylum Plasrnodiophoromycota- (Endoparasitic slime molds)

76 Aggie Board Heviewer

Downy mildew diseases- the pathogens belong to the oomycdes

Fungi (true fungi)

Four Phyla with Plant Pathogens .

The Trne Fungi-general charactel.·istk:s =

lmport.ant plant pathogenic chytrids

,. During the gro wing season, plant pathogens exist as mycclia/conidia.

'l'hrcc groups of Dcutcromycefos or imperfect fungi .

ii)1Jhomycetcs- no f~uiti~g st~~~ct~re ----- , Cocl<;mycete;-- ------------

______1_ _ _ _ _ _ _ ________ ""·-·- - -- - -'" -

Order Uredinales - The rusts

Frnltlng structures Spore forms

basltiiurn Basidiospores (n)

sperrnogoniurn Spermatia (n)

aecium Aeciosporns (n+n)

tellu111 Teliospores (n+n)== 2n

80 Aggie Board Reviewer

Ex:nnplcs of rust diseases

Order Ustilaginales - the smuts-

Order Agaricales- the mushrooms .