Dr.TitoCaffitito.caffi@unicatt.it

Disease andPest Managementtoward asustainable viticoltureMasterVENIT A.A.2017-2018

FAO

Backgroundand…foreground

Backgroundand…foreground

Backgroundand…foreground

The Triumph of the Fungi: A RottenHistory. By Nicholas P Money. Oxford and New York: Oxford University Press. 197 p; ISBN: 0-19-518971-X. 2007.

http://www.apsnet.org/members/outreach/opro/Documents/storybk.pdf

Stem rust onwheat

Robigus

Robigalia

NicholasP.Money.“TheTriumphofFungi”

Stem rust onwheat

TheRobigalia was afestivalinancient Romanreligionheld April25,named forthegod Robigus.Its main ritualwas afoxsacrifice (andasheep,you never know)toprotect grain fields fromdisease.TheRobigalia was one ofseveral agricultural festivals inApriltocelebrateandvitalize thegrowing season,butthedarker sacrificial elements ofthese occasions arealsofraught withanxiety about crop failure andthedependence ondivinefavor toavert it.

“Based onthis primeval wisdom,wemight try executing someone withafever tooffsetglobalwarming”

Secondary cycles (7-10days)when 16°-22°Candmoisture is not limiting

Uredospore->windblownGermination ->15-20°C(dew)Penetration ->through stomata

Latency ->8-14days

Puccinia triticina

SaintAnthonyMonk

Ergotamine=Lisergic AcidDietilamide =LSD

SaintAnthony’sFire– Ergotism

IntheMiddleAges,theErgotism was known as "holy fire"or"SaintAnthony's fire",named after monks oftheOrderofSt.Anthonywho were particularly successful at treating this ailment(don’t mixit upwiththevirusHerpeszoster).

Thesymptoms canberoughly divided into convulsivesymptomsandgangrenous symptoms.Convulsivesymptoms includepainfulseizures andspasms,diarrhea,paresthesias,itching,mentaleffects including maniaorpsychosis,headaches,nauseaandvomiting.

Gangrenous symptoms includedesquamation orpeeling,weak peripheralpulses,loss ofperipheral sensation,edemaandultimately thedeath andloss ofaffected tissues.

SaintAnthony’sFire– Ergotism

Ryeergot– Claviceps purpurea

TheCommonwealthin1897

SirThomasLipton(1850-1931)

Coffeerust– Hemileia vastatrix

20 1. INTRODUCTION

End of June

A

Mid-July

Mid-August

Mid-September

Mid-October

B

FIGURE 1-17 The late blight of potato and the Irish famine. (A) Itinerary of the advance of the potato blightbetween June, when the blight was first detected in Belgium, and the end of October 1845, by which time it spreadfrom Italy to Ireland and from Spain to the Scandinavian countries. (B) A young lesion on a potato leaf covered withsporangiophores and sporangiospores of the fungus (oomycete). (C) A potato plant killed completely by the blight(right) next to a healthy-looking resistant plant (left). (D) External and internal appearance of potato tubers infectedwith the late blight disease. The oomycete is still found near the surface. (E) Advanced invasion and rotting of potatotuber infected with late blight. (F) A period drawing of a family digging for potatoes to avoid starvation during theIrish famine. [Photographs courtesy of (A) W. E. Fry, Cornell University, (B) D. P. Weingartner, University of Florida,(C and D) Cornell University, (E) USDA, and (F) Illustrated London News, 1849.]

of the excess water, their tissues becameswollen and rotted. The Reverend Dr.Miles Berkeley, however, noticed thatthe mold covering potato plants about torot was a fungus (oomycete) similar butnot identical to a fungus he observed ona sick onion. The fungus on potato,however, was identical to a fungusrecovered from sick potato plants innorthern Europe. Berkeley concludedthat this fungus was the cause of thepotato blight, but when he proposed itin a letter to a newspaper, it was con-sidered as an incredible and bizarretheory unsupported by facts. The puzzleof what caused blight of potato contin-ued unanswered for 16 years after the1845 destruction of potatoes by theblight. Finally, in 1861, Anton deBary(Fig. 1-16A) did a simple experimentthat proved that the potato blight was

caused by a fungus. DeBary simplyplanted two sets of healthy potatoes, oneof which he dusted with spores of thefungus collected from blighted potatoplants. When the tubers germinated andbegan to produce potato plants, thehealthy tubers produced healthy plants,whereas the healthy tubers dusted withthe spores of the fungus produced plantsthat became blighted and died. Nomatter how many times deBary repeatedthe experiment, only tubers treated withthe fungus became infected and pro-duced plants that became infected.Therefore, the fungus, which, we knownow, is an oomycete was named Phy-tophthora infestans (“infectious plantdestroyer” from phyto = plant, phthora= destruction, infestans = infectious),was the cause of the potato blight.DeBary also showed that the fungus did

not just reappear from nowhere the fol-lowing growing season but instead sur-vived the winter in partially infectedpotato tubers in the field or storage. Inthe spring, the fungus infected youngplants coming from these partially rottentubers, produced new spores on theseplants, and the spores then spread toother cultivated potato plants that wereinfected and killed. With this experimentdeBary actually disproved the theory ofspontaneous generation, which statedthat microorganisms are produced spon-taneously by dying and dead plants andanimals, and ushered in the germ theoryof disease. The honor for this proof,however, is reserved for Louis Pasteur,who proved the theories while workingwith bacteria at about the same time,1861–1863, that deBary published hiswork with the potato blight fungus.

HISTORY OF PLANT PATHOLOGY AND EARLY S IGNIF ICANT PLANT DISEASES 21

The Expanding Role of Fungi as Causes of Plant Disease

Following the observation by French farmers around the mid-1600s and, independently, by Connecticutfarmers in the early 1700s that wheat rust was worsenear barberry bushes, the farmers came to believe thatbarberry fathered the rust, which then moved to wheat.The request by farmers for legislation to force towns to eradicate barberries and in that way to protect thewheat plants from rust followed. At about the sametime, spores of the rust fungus were observed with the compound microscope for the first time in England(Hooke, 1667). In Italy, Micheli 60 years later (1729)described many new genera of fungi, illustrated theirreproductive structures, and noted that when he placedthem on freshly cut slices of melon, these fungal struc-

tures generally reproduced the same kind of fungus that produced them. He proposed that fungi arose from their own spores rather than spontaneously, butnobody believed him. New information about plantpathogenic fungi continued to be developed, but mostof it was not accepted by the scientists of the time for along time.

As mentioned previously, in 1755, Tillet in Franceshowed that wheat smut is a contagious plant disease,but even he believed that it was a poisonous substancecontained in the smut dust, rather than a living microor-ganism, that caused the disease. In 1807, Prevost, alsoin France, repeated and expanded Tillet’s experimentsand appeared to have demonstrated conclusively thatwheat smut was caused by a fungus. His conclusions,however, were not accepted because the scientists wereblinded by the belief that microorganisms and their

FIGURE 1-17 (Continued)

E F

DC

Potatofamine– Phytopthora infestans

“Plant pathology is a science that studiesplant diseases and attempts to improvethe chances for survival of plants whenthey are faced with unfavorableenvironmental conditions and parasiticmicroorganisms that cause disease”George N. Agrios

PlantPathology – 5th EditionAuthors: GeorgeAgrioseBookISBN: 9780080473789Hardcover ISBN: 9780120445653Imprint: AcademicPressPublished Date: 25th January2005PageCount: 952

IntroductiontoPlantPathology

A plant disease is any abnormal conditionthat alters the appearance or function of aplant. It is a physiological process thataffects some or the entire plant functions.

Disease may also reduce yield and qualityof harvested product.

Disease is a process or a change that occursover time. It does not occur instantly likeinjury.

Damages caused bydiseases

Direct Indirect

Primary Secondary

• Loss of:• Productivity• Quality• Value

• Higher costs (selection,replanting,etc.)

• Disease controlcosts (PPP,application,etc.)

• Cropping techniques• Duration ofvineyards• Residual effects• ...

• Socialproblems• Ecological issues

• Pollution• Zootoxicity• Landscape• Ecosystems• …

• Health issues• Farmers• Rural inhabitants• Consumers

Causes ofDisease

Biotics

• Parasitic plants• Fungi• Bacteria• Fastidious Bacteria

• Phtoplasms• Spiroplasm

• Viruses• Viroids

Diseases

Abiotics

• Unfavourable conditions(lack/excess)

• Phytotoxic substances

Disorders

Causeofdisease- abiotics

Causeofdisease- abiotics

Causeofdisease- abiotics

Causeofdisease- abiotics

Magnesium deficiencyPotassium deficiency

Iron deficiency(limeinduced chlorosis)

…

Herbicides drift

Causeofdisease- abiotics

8 1. INTRODUCTION

development and spread of the disease and also possi-ble control measures. On this basis, plant diseases in thistext are classified as follows:

I. Infectious, or biotic, plant diseases1. Diseases caused by fungi (Figs. 1-4A and 1-4B)2. Diseases caused by prokaryotes (bacteria and

mollicutes) (Figs. 1-4C and 1-4D)3. Diseases caused by parasitic higher plants (Fig.

1-5A) and green algae4. Diseases caused by viruses and viroids (Fig.

1-5B)5. Diseases caused by nematodes (Fig. 1-5C)6. Diseases caused by protozoa (Fig. 1-5D)

II. Noninfectious, or abiotic, plant diseases (Fig. 10-1)1. Diseases caused by too low or too high a

temperature2. Diseases caused by lack or excess of soil

moisture3. Diseases caused by lack or excess of light4. Diseases caused by lack of oxygen5. Diseases caused by air pollution6. Diseases caused by nutrient deficiencies7. Diseases caused by mineral toxicities8. Diseases caused by soil acidity or alkalinity

(pH)

9. Diseases caused by toxicity of pesticides10. Diseases caused by improper cultural practices

HISTORY OF PLANT PATHOLOGY AND EARLYSIGNIFICANT PLANT DISEASES

Introduction

Even when humans lived as hunters or nomads and theirfood consisted only of meat or leaves, fruit, and seeds,which they picked wherever they could find them, plantdiseases took their toll on hunted animals and onhumans. Plant diseases caused leaves and shoots tomildew and blight, and fruit and seeds to rot, therebyforcing humans to keep looking until they could findenough healthy fruit or food plants of some kind tosatisfy their hunger. As humans settled down and be-came farmers, they began growing one or a few kindsof food plants in small plots of land and depended onthese plants for their survival throughout the year. It isprobable that every year, and in some years more thanin others, part of the crop was lost to diseases. In suchyears food supplies were insufficient and hunger wascommon. In years when wet weather favored the devel-opment of plant diseases, most or all of the crop was

Fungi

PlasmodiumSpore

Morphology

Morphology

Adults Egg Juvenile Protozoa (flagellates)

Dodder Witchweed Dwarf mistletoe Broomrapes

Viroids

Multiplication Spiroplasma

Colony Spores

Bacteria

Mollicutes

Parasitichigherplants

Viruses

Nematodes

Types of mycelium

Morphology and flagellation Fission Streptomyces

FIGURE 1-3 Morphology and ways of multiplication of some of the groups of plant pathogens.

Causeofdisease- biotics

Terminology(1)

>>PARASITE<<an organism that lives on or in another organism and obtains food from thesecond organism (e.g. fungus, bacteria, virus, phytoplasma, viroid, RLO’s,parasitic plants, nematode)

PATHOGENICITYthe ability of a pathogen to cause the disease by interfering with one or more ofthe essential plant cell functions

SYMPTOMthe expression of the disease caused by the manifestation of the physiologicalreaction of the plant due to harmful activity of the pathogen (e.g., oil spots)

SIGNSphysical evidence of the presence of disease agent (e.g., sporangiophores on thelower side of the oil spot)

Terminology(2)

SYNDROMEthe sequential appearance of disease symptoms on a plant during thedevelopment of the disease or total sum of the symptoms exhibited by a disease(e.g., necrotic spots --> blight --> fungal growth --> death of organ)

>> BIOTROPHS <<do not kill plant cells. They penetrate the cell wall and establish a continuousrelationship or move from cell to cell (e.g., rusts, powdery mildew)

>> FACULTATIVE PARASITE <<usually grows andcompletes lifecycle ondeadmaterial,but candosoonlivingtissue (e.g.,Sclerotinia)

FACULTATIVESAPROPHYTEusually grows andcompletes lifecycle onlivingtissue,but candosoondeadmaterial (e.g.,Phytopthora infestans)

Withineachspeciesthereisahighgeneticvariability.Groupsofindividual(populations)withsimilargeneticcharacterrepresentataxon(pl taxa).

Geneticvariabilityisaboutmanycharacters,whatisinterestinginplantpathologyare:ü theparasiticbehaviour;ü thefitness;ü thesensitivitytoPPP.

Pathogenicity =>attributeofaspecies,itisthecapabilitytocausedisease(ononeormorehosts).

Virulence =>attributeofasinglesubject(orgroupofsubjects),itisthecapabilitytocausethediseaseinaspecifichost

Aggressiveness =>attributeofasinglesubject(orgroupofsubjects),itisabouttypeand/orseverityofsymptoms

Terminology(3)

forma speciale

specie

razza

patotipo

Forma speciale (f.sp.): taxon con specificità di virulenza per specie vegetali; il taxon prende di norma il nome dalla specie vegetaleEs: Blumeria gramis f.sp. hordei; f.sp. tritici; f.sp.avenae; ecc.Questa terminologia è comunemente applicata ai funghi, mentre per i batteri si usa il termine di patovarietasEs: Pseudomonas syringae pv. tabaci; pv. pisi; pv. tomato; ecc.

Razza: taxon con specificità di virulenza per varietàvegetali; il taxon è di norma individuato da una sigla alfa numerica

Patotipo: taxon con specificità di aggressività; la terminologia che individua questi taxa è varia; per i virus si usa il termine ceppo

Terminologia dei taxa di rango subspecifico

forma specialerazza

Species

Formaspecialis

Pathotype

Race

Formaspecialis (f.sp.)Þ taxonwithspecificvirulenceforahost

species.Usuallyusedforfungi(e.g.Blumeria graminis f.sp.hordei;f.sp.tritici;f.sp.avenae)

Þ forbacteriaweusepatovarietas (pv.).E.g.Pseudomonassyringae pv.tabaci;pv.pisi;pv.tomato

Race=>taxonwithspecificvirulenceforonevariety

Pathotype=>taxonwithspecificaggressiveness

Terminology(4)

Parasiticplants

ü Theymakeupabout1%ofangiospermsallaroundtheworld

üNochlorophyllü Theyderivesome/allnutrientfromanotherplant

ü Theirseeds cansurviveintothesoilformanyyears

üModifiedrootsnamedhaustoriaüCancause100%yieldloss

Schematic diagram oftheshapesandsizes ofcertain plant pathogensinrelationtoaplant cell.

Bacteria,mollicutes,andprotozoaarenot found innucleated livingplant cells

Fungi

üVastmajorityarebeneficialüCancauseplant,human,andlivestockdiseases

üMostcannotbeseenwithoutamicroscope

ü LackchlorophyllüComposedofgrowingstructureofdelicate,threadlikefilamentscalledhyphae

üReproducebyformingspores

Bacteria

ü Extremelysmallorganismrequiringmicroscopetobeseen

ü Bacteriapopulationcanincreaseinnumberinshorttimeperiod

ü Cellsclumptogetherinmassescalledcolonies

ü Obtainfoodfromdeadordecayingorganicmatterorlivingtissue

ü Spreadplanttoplantbywind-drivenrain

ü Gainentrancethroughnaturalplantopeningsorinjuries

Viruses

ü Mostfamiliarbecausetheycausehumanandanimaldiseasessuchasinfluenza,polio,rabies,smallpox,andwarts

ü Causesomedestructiveplantdiseases

ü Measureonlyaboutone-millionthofaninchinsize

ü Arenotcompletelivingsystemsü Surviveonlyinlivingcellsü Transmittedbyinsectswhichare

calledvectors

Nematodes

ü Round,slender,threadlikeworms

ü Someareparasitesonanimals,insects,fungi,othernematodes,andplants

ü Plant-parasiticnematodeshaveastylet

ü Mostliveinthesoilandfeedinoronplantroots

ü The suspected causal agent must be present in every diseasedorganism (e.g., a plant) examined.

ü The suspected causal agent must be isolated from the diseased hostorganism (plant) and grown in pure culture.

ü When a pure culture of the suspected causal agent is inoculated intoa healthy susceptible host (plant), the host must reproduce thespecific disease.

ü The same causal agent must be recovered again from theexperimentally inoculated and infected host, i.e., the recoveredagent must have the same characteristics as the organism in step 2.

Koch’s postulates

18 1. INTRODUCTION

abnormally rounded wheat kernels but he, too, failed to show or suggest that they were the cause of theproblem.

In 1755, the Frenchman Tillet, working with smuttedwheat, showed that he could increase the number ofwheat plants developing covered smut (Figs. 1-8A and1-8B) by dusting wheat kernels before planting withsmut dust, i.e., with smut spores (Fig. 1-15). He alsonoted that he could reduce the number of smutted wheatplants produced by treating the smut-treated kernels

with copper sulfate. Tillet, too, however, did not inter-pret his experiments properly and, instead of conclud-ing that wheat smut is an infectious plant disease, hebelieved that it was a poisonous substance contained inthe smut dust, rather than the living spores and funguscoming from them, that caused the disease. More than50 years later, in 1807, Prevost, another Frenchman,repeated both the inoculation experiments and those inwhich the seeds were treated with copper sulfate, asdone by Tillet, and he obtained the same results. In addi-tion, Prevost observed smut spores from untreated andtreated wheat seed under the microscope and noticedthat those from untreated seed germinated and grewwhereas those from treated seed failed to germinate. He,therefore, concluded correctly that it was the smutspores that caused the smut disease in wheat and thatthe reduced number of smutted wheat plants derivedfrom copper sulfate-treated seed was due to the inhibi-tion of germination of smut spores by the copper sulfate.Prevost’s conclusions, however, were not accepted by theFrench Academy of Sciences because its scientists andother scientists throughout Europe still believed thatmicroorganisms and their spores formed through spon-taneous generation and were the result rather than thecause of disease. In 1855, a nematode was observed ingalls of cucumber roots, but again they were thought tohave appeared there spontaneously. These beliefs con-tinued to be held and expounded by scientists until theearly 1860s, when, in 1861–1863, Anton deBary (Fig.1-16A) proved that potato late blight was caused by afungus and Louis Pasteur (Fig. 1-16B) proved that microorganisms were produced from preexistingmicroorganisms and that most infectious diseases werecaused by germs. The latter established the “germ theoryof disease,” which changed the way of thinking of sci-entists and led to tremendous progress. Significant

FIGURE 1-15 Teliospores of the fungus Tilletia, the cause of thecovered smut or bunt of wheat. (Photograph courtesy of M.Babadoost, University of Illinois.)

A B CFIGURE 1-16 (A) Anton deBary. (B) Louis Pasteur. (C) Robert Koch.

RobertKoch

TheDiseaseTriangle

InoculationContact Colonization

Reaching thepenetration site

Penetration

Incubationdevelopment invasion feeding

Symptoms onset

Evasion

Dissemination

Epiphytic

Endo

phytic

Epiphytic

Symptom

atic

Asym

ptom

atic

incubazione (incubation

period)penetrazione

Analisi dei sistemi: diagramma relazionale

Elementi base del diagramma relazionale1.

Sana

Latente

infeziosità(infectious period)

spostamento(displacement

period)

sintomi

evasionelatenza

(latency period)

dispersione

inoculazione

Latente

Visibile

Infeziosa

Sterile

Healthy

Latent

Visible

Infectious

Sterile

incubazione (incubation

period)penetrazione

Analisi dei sistemi: diagramma relazionale

Elementi base del diagramma relazionale1.

Sana

Latente

infeziosità(infectious period)

spostamento(displacement

period)

sintomi

evasionelatenza

(latency period)

dispersione

inoculazione

Latente

Visibile

Infeziosa

Sterile

Inocula(on))))))

Penetra(on)

Symptoms)Dispersal)

Evasion)

1. Inoculazione

contattocolonizzazione

2. Penetrazione

3. Incubazione

sviluppoinvasione

azione trofica

comparsa dei sintomi

4. Evasione

5. Disseminazione

Inoculation

Penetration

contact

Incubation

colonization

DevelopmentInvasion

Trophic rel.

Symptom onset

Dissemination

Evasion

84 2. PARASIT ISM AND DISEASE DEVELOPMENT

F

G

E

FIGURE 2-4 (Continued)

Spore

Direct with haustoria

Direct penetration

Penetration throughnatural openings

Penetration throughnatural wounds

Direct, intercellular mycelium

Through stoma

Through wounds Through natural cracks betweenmain and lateral roots

Fungus kills and maceratescells ahead of its advance

Through lenticelThrough hydathodes

Guttationwater droplet

Direct, intercellular mycelium with haustoria

Direct, subcuticular only

Direct with appressorium (A),penetration peg (PP), andintracellular mycelium (IM)

Spore Spore Germ tube

A PP

IM

Subcuticular myceliumSuperficialmycelium

FIGURE 2-5 Methods of penetration and invasion by fungi.