Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide


Phytophthora infestans
(Phytophthora blight)



Phytophthora infestans (Phytophthora blight)


  • Last modified
  • 29 March 2018
  • Datasheet Type(s)
  • Invasive Species
  • Pest
  • Natural Enemy
  • Preferred Scientific Name
  • Phytophthora infestans
  • Preferred Common Name
  • Phytophthora blight
  • Taxonomic Tree
  • Domain: Eukaryota
  •   Kingdom: Chromista
  •     Phylum: Oomycota
  •       Class: Oomycetes
  •         Order: Peronosporales

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Top of page
Leaflets are blighted due to infection by P. infestans.
TitleInfected potato leaflets (detail)
CaptionLeaflets are blighted due to infection by P. infestans.
CopyrightMauritius Sugar Industry Research Institute
Leaflets are blighted due to infection by P. infestans.
Infected potato leaflets (detail)Leaflets are blighted due to infection by P. infestans.Mauritius Sugar Industry Research Institute
Stem lesions and wilted leaves on potato plant infected with P. infestans.
TitleInfected potato stem
CaptionStem lesions and wilted leaves on potato plant infected with P. infestans.
CopyrightWilliam E. Fry
Stem lesions and wilted leaves on potato plant infected with P. infestans.
Infected potato stemStem lesions and wilted leaves on potato plant infected with P. infestans.William E. Fry
Phytophthora infestans on tomato.
TitleSymptoms on tomato plant
CaptionPhytophthora infestans on tomato.
CopyrightRob Williams/CAB International
Phytophthora infestans on tomato.
Symptoms on tomato plantPhytophthora infestans on tomato.Rob Williams/CAB International
Phytophthora infestans leaf sporulation symptoms (Late blight) on potato leaf in the field
CaptionPhytophthora infestans leaf sporulation symptoms (Late blight) on potato leaf in the field
CopyrightThorsten Kraska, University of Bonn, Germany
Phytophthora infestans leaf sporulation symptoms (Late blight) on potato leaf in the field
SymptomsPhytophthora infestans leaf sporulation symptoms (Late blight) on potato leaf in the field Thorsten Kraska, University of Bonn, Germany
Phytophthora infestans leaf sporulation symptoms (late blight) on potato leaf in the field.
CaptionPhytophthora infestans leaf sporulation symptoms (late blight) on potato leaf in the field.
CopyrightThorsten Kraska, University of Bonn, Germany
Phytophthora infestans leaf sporulation symptoms (late blight) on potato leaf in the field.
SymptomsPhytophthora infestans leaf sporulation symptoms (late blight) on potato leaf in the field. Thorsten Kraska, University of Bonn, Germany
Phytophthora infestans symptoms (late blight) on potato stem in the field.
CaptionPhytophthora infestans symptoms (late blight) on potato stem in the field.
CopyrightThorsten Kraska, University of Bonn, Germany
Phytophthora infestans symptoms (late blight) on potato stem in the field.
SymptomsPhytophthora infestans symptoms (late blight) on potato stem in the field. Thorsten Kraska, University of Bonn, Germany
Infected potato tubers exhibit wet and dry rots.
TitleTuber blight on potato
CaptionInfected potato tubers exhibit wet and dry rots.
CopyrightWilliam E. Fry
Infected potato tubers exhibit wet and dry rots.
Tuber blight on potatoInfected potato tubers exhibit wet and dry rots.William E. Fry
Blighted tubers, showing typical reddish-brown 'marbling' of infected flesh.
TitleP. infestans on potatoes
CaptionBlighted tubers, showing typical reddish-brown 'marbling' of infected flesh.
Copyright©Anna L. Snowdon
Blighted tubers, showing typical reddish-brown 'marbling' of infected flesh.
P. infestans on potatoesBlighted tubers, showing typical reddish-brown 'marbling' of infected flesh.©Anna L. Snowdon
Lesions are firm, large, irregular, brownish-green blotches; the lesion surface has a greasy rough appearance.
TitleSymptoms on tomato fruit
CaptionLesions are firm, large, irregular, brownish-green blotches; the lesion surface has a greasy rough appearance.
CopyrightThomas A. Zitter
Lesions are firm, large, irregular, brownish-green blotches; the lesion surface has a greasy rough appearance.
Symptoms on tomato fruitLesions are firm, large, irregular, brownish-green blotches; the lesion surface has a greasy rough appearance. Thomas A. Zitter
Late blight of fruit.
TitleP. infestans on tomato
CaptionLate blight of fruit.
Copyright©Anna L. Snowdon
Late blight of fruit.
P. infestans on tomatoLate blight of fruit.©Anna L. Snowdon
Lemon-shaped sporangia  (29-36 x 19-22 µm) on sporangiophores.
TitleSporangia on sporangiophores
CaptionLemon-shaped sporangia (29-36 x 19-22 µm) on sporangiophores.
CopyrightR.V. James
Lemon-shaped sporangia  (29-36 x 19-22 µm) on sporangiophores.
Sporangia on sporangiophoresLemon-shaped sporangia (29-36 x 19-22 µm) on sporangiophores.R.V. James
Oospores of P. infestans
CaptionOospores of P. infestans
CopyrightRichard Shattock
Oospores of P. infestans
OosporesOospores of P. infestansRichard Shattock


Top of page

Preferred Scientific Name

  • Phytophthora infestans (Mont.) de Bary

Preferred Common Name

  • Phytophthora blight

International Common Names

  • English: blight of potato; downy mildew of potato; late blight of potato; late blight of tomato; potato blight; potato late blight
  • Spanish: mildiu de la patata; mildiu del tomate; tizon tardio
  • French: mildiou de la pomme de terre; mildiou de la tomate
  • Russian: fitoftoros
  • Chinese: wan yi bing
  • Portuguese: mela da batata; requeima da batata

Local Common Names

  • Germany: Braunfaeule: Kartoffel; Braunfaeule: Tomate; Kraut und Knollenfaeule: Kartoffel; Krautfaeule: Tomate
  • India: aaloo ka jhulsa
  • Ukraine: phytophthorosis

EPPO code

  • PHYTIN (Phytophthora infestans)

Taxonomic Tree

Top of page
  • Domain: Eukaryota
  •     Kingdom: Chromista
  •         Phylum: Oomycota
  •             Class: Oomycetes
  •                 Order: Peronosporales
  •                     Family: Peronosporaceae
  •                         Genus: Phytophthora
  •                             Species: Phytophthora infestans

Notes on Taxonomy and Nomenclature

Top of page The taxonomic understanding of species of Phytophthora and related organisms has been improving rapidly (Brasier, 1992; Brasier and Hansen, 1992). It is now clear that oomycete fungi are not related to ascomycete and basidiomycete fungi. Erwin and Ribeiro (1996) discussed the change in understanding of the taxonomic position of this group of organisms. It has long been held that organisms producing zoospores with two, unequal flagella are closely related. This characteristic includes the genus Phytophthora as well as some algae. In some classification schemes these organisms were grouped into the large kingdom Protoctista. However, a recent classification scheme, discussed by Erwin and Ribeiro, is that of Dick (1995a, b) in which the kingdom Chromista is supported. The genus Phytophthora occurs within the family Pythiaceae, which is included either in the phylum Oomycota or the phylum Peronosporomycota, depending upon interpretation. However, regardless of the groupings of more general taxa, it is very clear that the genus Phytophthora, the closely related genus Pythium, and the downy mildews (i.e. Bremia, Sclerospora, Peronospora, etc.) are unrelated to ascomycetes and basidiomycetes.


Top of page P. infestans is a coenocytic oomycete with rare cross walls. Asexual reproduction is via sporangia that are ellipsoid to lemon shaped with a small pedicel. Sporangia are 29-36 x 19-22 µm. Sporangia germinate either directly to form a germ tube (at temperatures of 15-24°C), or indirectly via zoospores (at temperatures below 18°C). Zoospores (ca 7-12 per sporangium) have two flagella, one forward-directed tinsel type and a backward-directed whiplash type (heterokont). Zoospores are usually uninucleate, but binucleate zoospores have been detected.

In culture, the mycelium is white and fluffy; the colony is somewhat slow growing. Growth rates can vary dramatically among isolates, but fast-growing isolates can cover a 9-cm plate within 7-10 days. Some isolates produce a lumpy appearance: this has sometimes been associated with the A2 mating type.

Oogonia rare in host or single culture, but developing promptly on pairing isolates of opposite compatibility type, 38 (max. 50) µm diameter, tapering at base. Antheridia amphigynous, elongated cylindrical, 17 (max. 22) x 16 µm. Oospores average 30 µm, aplerotic, wall 3-4 µm (Stamps, 1985).


Top of page P. infestans is intimately associated with its potato host and has apparently travelled around the world with potatoes (Cox and Large, 1960; Fry et al., 1993).

Potato tubers are readily infected and seed tubers are distributed all around the world, thus the occurrence of P. infestans is sometimes more closely allied to the distribution of seed tubers than to an indigenous pathogen population that survives in the absence of its agricultural hosts. Any location that receives seed tubers from an area where late blight is present is thus also likely to have late blight. Most locations in Asia, South-East Asia and Australia, Africa, the Americas and Europe can have late blight, especially if seed tubers are imported from an area where late blight is persistent. Thus, one location can have a population of P. infestans in one year, but not the next. Alternatively, a location could be free of late blight in one year, but have it the next. Locations that might reliably avoid late blight are those at very northerly or southerly latitudes, and at particularly high altitudes. Similarly, some lowland tropical locations are persistently too warm for late blight. Reports of the disease, therefore, do not necessarily imply an indigenous population of the pathogen. Instead, such reports indicate that the climate can support growth of this oomycete at least in some growing seasons.

Recent Migrations of P. infestans

Until the 1980s, only the A1 mating type of P. infestans was widely and commonly distributed (Goodwin et al., 1994b). Both mating types (A1 and A2) were common in Mexico, but were apparently not common in other locations. Outside Mexico, populations of P. infestans were dominated by a particular clonal lineage (US-1) (Goodwin et al., 1994b). This situation changed dramatically during the 1980s and 1990s. Isolates of P. infestans with the A2 mating type were first reported from Switzerland (Hohl and Iselin, 1984) and subsequently from many countries in northern Europe (Fry et al., 1993). Subsequently, isolates with A2 mating type were reported from Japan and Korea. By the early 1990s, isolates with A2 mating type were common throughout the USA and Canada (Fry et al., 1993). In addition to A2 mating types, isolates of A1 mating type that were quite different from US-1 began to appear in other locations worldwide (Colombia, Ecuador, USA, Canada, western Europe, Burundi and Rwanda) (Fry and Goodwin, 1995).

The occurrence of exotic strains of P. infestans (A1 and/or A2) indicates migrations of P. infestans. The primary origin of these exotic strains is Mexico in all cases where an origin can be ascribed. In many locations, the exotic strains are associated with an increased severity of late blight on potatoes and/or tomatoes (Spielman et al. 1991; Goodwin et al., 1994b, 1995b). After a very long time in which P. infestans populations had been asexual, sexual reproduction has become a component of the life history of this organism in parts of western Europe and the USA and Canada (Sujkowski et al., 1994; Drenth et al., 1995; Goodwin et al., 1995b).

Distribution Table

Top of page

The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes


BangladeshPresentHossain et al., 2009
ChinaPresentCMI, 1982
-BeijingPresentZhang et al., 2001
-ChongqingPresentZhang et al., 2001
-FujianPresentZhu et al., 2004
-GansuPresentZhu et al., 2006
-GuangxiPresentZhu et al., 2008
-GuizhouPresentJin et al., 2008
-HebeiPresentZhang et al., 2001
-HeilongjiangPresentZhu et al., 2004
-JiangsuPresentYu et al., 2007
-JilinPresentZhu et al., 2004
-LiaoningPresentZhang et al., 2007
-Nei MengguPresentZhang et al., 2001
-QinghaiPresentYe et al., 2008
-ShanxiPresentZhang et al., 2001
-SichuanPresentZhang et al., 2001; Zhu et al., 2004
-SichuanPresentZhang et al., 2001; Zhu et al., 2004
-YunnanPresentZhang et al., 2001
Georgia (Republic of)PresentMetreveli and Ordzhonikidze, 2002
IndiaPresentCMI, 1982
-AssamPresentJhilmil et al., 2001; Phukan, 2008
-AssamPresentJhilmil et al., 2001; Phukan, 2008
-BiharPresentJhilmil et al., 2001
-HaryanaPresentLakra, 2004
-Himachal PradeshPresentJhilmil et al., 2001; Arti et al., 2013
-Indian PunjabPresentJhilmil et al., 2001
-Jammu and KashmirPresentDar et al., 2004
-MaharashtraPresentIlhe and Warade, 2007
-MeghalayaPresentShantanu et al., 2008
-Tamil NaduPresentJhilmil et al., 2001
-Uttar PradeshPresentJhilmil et al., 2001
-UttarakhandPresentJhilmil et al., 2001
-West BengalPresentDe and Basu, 2002
IndonesiaPresentCMI, 1982
IranPresentCMI, 1982
IraqPresentCMI, 1982
IsraelPresentCMI, 1982
JapanPresentCMI, 1982
JordanPresentCMI, 1982
KazakhstanPresentCMI, 1982
Korea, DPRPresentCMI, 1982
Korea, Republic ofPresentCMI, 1982
LaosPresentCMI, 1982
LebanonPresentCMI, 1982
MalaysiaPresentCMI, 1982
NepalPresentCMI, 1982
PakistanPresentCMI, 1982
PhilippinesPresentCMI, 1982
Saudi ArabiaPresentCMI, 1982
Sri LankaPresentCMI, 1982
TaiwanPresentCMI, 1982
ThailandPresentCMI, 1982
TurkeyPresentCMI, 1982
VietnamPresentCMI, 1982


AlgeriaPresentCMI, 1982
AngolaPresentCMI, 1982
CameroonPresentCMI, 1982
EgyptPresentCMI, 1982
EthiopiaPresentBekele and Sommartya, 2006
GhanaPresentCMI, 1982
KenyaPresentCMI, 1982
MadagascarPresentCMI, 1982
MalawiPresentCMI, 1982
MauritiusPresentCMI, 1982
MoroccoPresentCMI, 1982
NigeriaPresentCMI, 1982
RéunionPresentCMI, 1982
RwandaPresentCMI, 1982
SomaliaPresentCMI, 1982
South AfricaPresentCMI, 1982
SudanPresentCMI, 1982
TanzaniaPresentCMI, 1982
UgandaPresentCMI, 1982
ZambiaPresentCMI, 1982
ZimbabwePresentCMI, 1982

North America

BermudaPresentCPPC; CMI, 1982
CanadaPresentPresent based on regional distribution.
-AlbertaPresentCMI, 1982
-British ColumbiaPresentCMI, 1982
-ManitobaPresentCMI, 1982
-New BrunswickPresentCMI, 1982; Wijekoon et al., 2014
-Newfoundland and LabradorPresentCMI, 1982
-Nova ScotiaPresentCMI, 1982
-OntarioPresentCMI, 1982
-Prince Edward IslandPresentCMI, 1982; Wijekoon et al., 2014
-QuebecPresentCMI, 1982
MexicoPresentCMI, 1982; López et al., 2013
USAPresentPresent based on regional distribution.
-AlabamaPresentCMI, 1982
-AlaskaPresentCMI, 1982
-ArizonaPresentCMI, 1982
-ArkansasPresentCMI, 1982
-CaliforniaPresentCMI, 1982
-ColoradoPresentCMI, 1982
-ConnecticutPresentCMI, 1982
-DelawarePresentCMI, 1982
-FloridaPresentCMI, 1982
-GeorgiaPresentCMI, 1982
-HawaiiPresentCMI, 1982
-IdahoPresentCMI, 1982; Wharton et al., 2015
-IllinoisPresentCMI, 1982
-IndianaPresentCMI, 1982
-IowaPresentCMI, 1982
-KansasPresentCMI, 1982
-KentuckyPresentCMI, 1982
-LouisianaPresentCMI, 1982
-MainePresentCMI, 1982
-MarylandPresentCMI, 1982
-MassachusettsPresentCMI, 1982
-MichiganPresentCMI, 1982; Dangi et al., 2016
-MinnesotaPresentCMI, 1982
-MississippiPresentCMI, 1982
-MissouriPresentCMI, 1982
-MontanaPresentCMI, 1982
-NebraskaPresentCMI, 1982
-New HampshirePresentCMI, 1982
-New JerseyPresentCMI, 1982
-New MexicoPresentCMI, 1982
-New YorkPresentCMI, 1982
-North CarolinaPresentCMI, 1982
-North DakotaPresentCMI, 1982
-OhioPresentCMI, 1982
-OklahomaPresentCMI, 1982
-OregonPresentCMI, 1982
-PennsylvaniaPresentCMI, 1982
-Rhode IslandPresentCMI, 1982
-South CarolinaPresentCMI, 1982
-South DakotaPresentCMI, 1982
-TennesseePresentCMI, 1982
-TexasPresentCMI, 1982
-VermontPresentCMI, 1982
-VirginiaPresentCMI, 1982
-WashingtonPresentCMI, 1982
-West VirginiaPresentCMI, 1982
-WisconsinPresentGevens and Seidl, 2013a; Gevens and Seidl, 2013b; CMI, 1982
-WyomingPresentCMI, 1982

Central America and Caribbean

Antigua and BarbudaPresentSchotman, 1989
BahamasPresentSchotman, 1989
BarbadosPresentSchotman, 1989
Costa RicaPresentCMI, 1982
CubaPresentCPPC; CMI, 1982
DominicaPresentSchotman, 1989
Dominican RepublicPresentCPPC; CMI, 1982
El SalvadorPresentCMI, 1982
French West IndiesPresentSchotman, 1989
GuadeloupePresentCPPC; CMI, 1982
GuatemalaPresentCMI, 1982
HaitiPresentCPPC; CMI, 1982
HondurasPresentCMI, 1982
JamaicaPresentCPPC; CMI, 1982
MartiniquePresentCPPC; CMI, 1982
MontserratPresentCPPC; CMI, 1982
NicaraguaPresentCMI, 1982
PanamaPresentCMI, 1982
Puerto RicoPresentCPPC; CMI, 1982
Saint Kitts and NevisPresentCPPC; CMI, 1982
Saint LuciaPresentCPPC; CMI, 1982
Saint Vincent and the GrenadinesPresentCPPC; CMI, 1982
Trinidad and TobagoPresentCPPC; CMI, 1982

South America

ArgentinaPresentCMI, 1982
BoliviaPresentCMI, 1982; Coca Morante, 2016
BrazilPresentCMI, 1982
-BahiaPresentCMI, 1982
-Espirito SantoPresentCMI, 1982
-GoiasPresentReis et al., 2006
-Minas GeraisPresentCMI, 1982
-ParaibaPresentCMI, 1982
-Rio Grande do SulPresentCMI, 1982
-Santa CatarinaPresentWamser et al., 2008
-Sao PauloPresentCMI, 1982
ChilePresentCMI, 1982
ColombiaPresentCMI, 1982; Cárdenas et al., 2011
EcuadorPresentCMI, 1982
GuyanaPresentCPPC; CMI, 1982
ParaguayPresentCMI, 1982
PeruPresentCMI, 1982
UruguayPresentCMI, 1982
VenezuelaPresentCMI, 1982


AustriaPresentCMI, 1982
BelarusPresentPliakhnevich and Ivaniuk, 2008
BelgiumPresentCMI, 1982
Bosnia-HercegovinaPresentCMI, 1982
BulgariaPresentCMI, 1982
CyprusPresentCMI, 1982
Czech RepublicPresentCMI, 1982
Czechoslovakia (former)PresentCMI, 1982
DenmarkPresentCMI, 1982
EstoniaPresentCMI, 1982
FinlandPresentCMI, 1982
FrancePresentCMI, 1982
GermanyPresentCMI, 1982
GreecePresentCMI, 1982
HungaryPresentCMI, 1982
IcelandPresentCMI, 1982
IrelandPresentCMI, 1982
ItalyPresentCMI, 1982
LatviaPresentCMI, 1982
LithuaniaPresentCMI, 1982
LuxembourgPresentCMI, 1982
MacedoniaPresentCMI, 1982
MaltaPresentCMI, 1982
MoldovaPresentTrotus and Naie, 2008
NetherlandsPresentCMI, 1982
NorwayPresentCMI, 1982
PolandPresentZarzycka and Sujkowski, 2000
PortugalPresentCMI, 1982
-AzoresPresentCMI, 1982
RomaniaPresentCMI, 1982
Russian FederationPresentFilipas, 2009
-SiberiaPresentMalyuga et al., 2003
SerbiaPresentMijatovic et al., 2007
SlovakiaPresentCMI, 1982
SloveniaPresentCMI, 1982
SpainPresentCMI, 1982
SwedenPresentCMI, 1982
SwitzerlandPresentCMI, 1982
UKPresentCMI, 1982
-Channel IslandsPresentDeahl et al., 2009
-England and WalesPresentDay et al., 2004; Day et al., 2004
-England and WalesPresentDay et al., 2004; Day et al., 2004
-ScotlandPresentDay et al., 2004
UkrainePresentCMI, 1982
Yugoslavia (former)PresentCMI, 1982


American SamoaPresentBrooks, 2002
AustraliaPresentPresent based on regional distribution.
-New South WalesPresentCMI, 1982
-QueenslandPresentCMI, 1982
-South AustraliaPresentCMI, 1982
-VictoriaPresentCMI, 1982
-Western AustraliaPresentCMI, 1982
Cook IslandsPresentCMI, 1982
FijiPresentCMI, 1982
New CaledoniaPresentCMI, 1982
New ZealandPresentCMI, 1982
Norfolk IslandPresentCMI, 1982
Papua New GuineaPresentCMI, 1982
SamoaPresentCMI, 1982

Risk of Introduction

Top of page Risk Criteria Category

Economic Importance High
Distribution Worldwide
Seedborne Incidence Low
Seed Transmitted Yes
Seed Treatment Yes

Overall Risk High

Notes on phytosanitary risk

Until very recently, there were strict controls on the movement of exotic strains of P. infestans. Typically, locations that did not have the A2 mating type prohibited import of potatoes from locations with the A2 mating type. The very recent and rapid distribution of isolates of A2 mating type (Fry et al., 1993) has stimulated a re-evaluation of that policy. Nonetheless, different strains of P. infestans have different characteristics and it may still be important to restrict or reduce rapid distribution of this pathogen.

Hosts/Species Affected

Top of page Although generally considered to have a limited host range and to be a near-biotrophic pathogen, P. infestans has been reported to cause infection on a large number of species. Erwin and Ribeiro (1996) list 89 host species, but more than 25% of these were included because artificial inoculations resulted in lesions. In agriculture, the two most important hosts are potatoes and tomatoes.

P. infestans is a potentially devastating pathogen on potatoes in almost all locations where they are grown (Cox and Large, 1960). It is also a serious pathogen on tomatoes in cooler climates. In addition to these globally important agricultural crops, P. infestans attacks wild and cultivated species of Solanum in the Americas. It is reported on a large number of species of Solanum in central Mexico (Rivera-Pena and Molina-Galan, 1989), on hairy nightshade (Solanum sarrachoides) throughout the Americas, and on pear melons (S. muricatum) in the Andes of South America (Turkensteen, 1978).

Some populations of P. infestans have been identified that favour one host over another. In Ecuador, two populations of P. infestans exist which can be distinguished by isoenzyme patterns for glucose-6-phospahte isomerase (Erselius et al., 2000). One population (EC-1) is only found on potato and the other population (US-1) is only found on tomato. Similar preferences were also reported from isolates collected in France and the USA (Legard et al., 1995; Lebreton et al., 1999).

Isolates of the genus Phytophthora closely related to infestans have also been found in South America on Solanum betaceum, a tree fruit, and on the wild species Solanum brevifolium and Solanum tetrapetalum (Ordoñez et al., 2000). These isolates are morphologically identical to P. infestans but represent novel genotypes based on analyses with neutral genetic markers. For this reason, the taxonomy of these isolates is uncertain.

Although P. infestans has been associated with many hosts it is not clear to what extent these hosts may be attacked in nature by the same pathogen genotype. Separate genotypes have been associated with different hosts in South America (Erselius et al., 1999) and even with potato and tomato in different parts of the world (Oyarzun et al., 1998; Vega-Sanchez et al., 2000). Therefore, although the host range of P. infestans is potentially wide, many pathogen genotypes may be specific to certain hosts.

Host Plants and Other Plants Affected

Top of page
Plant nameFamilyContext
Capsicum annuum (bell pepper)SolanaceaeOther
Capsicum frutescens (chilli)SolanaceaeOther
Datura metel (Hindu datura)SolanaceaeWild host
Datura stramonium (jimsonweed)SolanaceaeWild host
Hyoscyamus niger (black henbane)SolanaceaeWild host
Ipomoea purpurea (tall morning glory)ConvolvulaceaeWild host
Lycium barbarum (Matrimonyvine)SolanaceaeWild host
Lycopersicon pimpinellifolium (currant tomato)SolanaceaeOther
Nicotiana glauca (tree tobacco)SolanaceaeWild host
PetuniaSolanaceaeWild host
Petunia hybridaSolanaceaeWild host
Pharbitis nil (Japanese morning glory)ConvolvulaceaeWild host
Physalis angulata (cutleaf groundcherry)SolanaceaeWild host
Physalis ixocarpaSolanaceaeOther
Physalis peruviana (Cape gooseberry)SolanaceaeOther
Rumex acetosa var. hortensis (garden sorrel)PolygonaceaeWild host
Solanum (nightshade)SolanaceaeWild host
Solanum cardiophyllumSolanaceaeOther
Solanum demissumSolanaceaeOther
Solanum dulcamara (bittersweet nightshade)SolanaceaeOther
Solanum ehrenbergiiSolanaceaeOther
Solanum incanum (grey bitter-apple)SolanaceaeWild host
Solanum indicumSolanaceaeWild host
Solanum laciniatum (kangaroo apple)SolanaceaeWild host
Solanum lycopersicum (tomato)SolanaceaeMain
Solanum marginatum (white-edged nightshade)SolanaceaeWild host
Solanum melongena (aubergine)SolanaceaeWild host
Solanum muricatum (melon pear)SolanaceaeOther
Solanum muricatum (melon pear)SolanaceaeOther
Solanum nigrum (black nightshade)SolanaceaeWild host
Solanum physalifoliumSolanaceaeOther
Solanum sarrachoides (green nightshade)Other
Solanum stoloniferumSolanaceaeOther
Solanum tuberosum (potato)SolanaceaeMain
Solanum verrucosumSolanaceaeOther
Solanum viarum (tropical soda apple)SolanaceaeOther

Growth Stages

Top of page Flowering stage, Fruiting stage, Post-harvest, Pre-emergence, Seedling stage, Vegetative growing stage


Top of page The symptoms of late blight on potatoes and tomatoes may vary, depending on the age of the lesion and the immediate preceding environment (previous 12 h). Very young lesions on potato or tomato foliage appear as irregularly shaped, small (2-10 mm) lesions with or without a small surrounding area of collapsed but still green tissue. Lesions later turn brown. Older lesions are larger and assume a circular appearance unless delimited by the leaflet margin. They are usually not delimited by the veins. Older lesions are typically surrounded by a zone of collapsed tissue that is not yet necrotic. The non-necrotic tissue may also appear somewhat chlorotic. If there are many lesions on a single leaflet, the entire leaf can turn chlorotic.

Sporulation may be evident on the collapsed tissue and on the outermost portions of the necrotic areas of a lesion if it has been in a saturated atmosphere (100% RH) for more than 7 or 8 h. The length of time required for sporulation is dependent on temperature and host resistance. On resistant cultivars, sporulation might not appear until some hours after it would appear on a susceptible cultivar. Optimal temperature for sporulation is usually regarded to be 15-20°C. Temperatures above or below this range will reduce the rate of pathogen growth and thus extend the time required for sporulation. Under optimal conditions for sporulation it is easily visible as a noticeable fuzzy white growth on lesion margins. Sporulation occurs from lesions whether they are on leaflets or on stems.

When the immediately preceding conditions have been dry, there is no sporulation and the lesions may appear dried up with no remnants of sporulation.

Blighting of the entire plant (even entire fields) occurs during moist warm periods. Patches of infected plants have a characteristic odour.

Infected potato tubers exhibit wet and dry rots. On tomato fruits, lesions are firm, large, irregular, brownish-green blotches; the lesion surface has a greasy, rough appearance.

List of Symptoms/Signs

Top of page
SignLife StagesType
Fruit / lesions: black or brown
Leaves / abnormal colours
Leaves / fungal growth
Leaves / necrotic areas
Leaves / wilting
Vegetative organs / dry rot
Vegetative organs / soft rot
Whole plant / seedling blight
Whole plant / unusual odour

Biology and Ecology

Top of page Where P. infestans exists as an asexual organism it is essentially an obligate parasite. It requires a living host (crop debris or solanaceous weeds) for long-term survival. Whereas sporangia may survive days or weeks in soil, they cannot overwinter or overseason. Mycelium of the fungus cannot survive in the absence of a living host cell. However, in locations where sexual reproduction occurs, the resulting oospore can survive for months or years in the absence of living hosts (Drenth et al., 1995).

Asexual Life History

The details of infection have been known for decades (Crosier, 1934). Infections usually start from sporangia which germinate either directly via a germ tube or indirectly via zoospores. Zoospores can swim for some minutes, after which time they encyst and germinate. A germ tube penetrates a living host and establishes a near-biotrophic relationship for the first few days in a compatible interaction. If the interaction is incompatible, host cells die rapidly (hypersensitive response). In the compatible interaction, lesions become visible within a few days; the exact time is dependent on temperature and host resistance. Under optimal conditions (18-22°C), infections can be visible in less than 3 days.

Within a day or two after the lesion first becomes visible, the fungus is capable of sporulation. Moderate temperatures (10-25°C) and very wet conditions (leaf wetness or 100% RH) are required for sporulation. Sporangia are borne on sporangiophores within 8-12 h during favourable conditions. Sporangia secede during changing relative humidity and can be captured in air currents; they can also be splash dispersed. They can survive for hours in unsaturated atmospheres when protected from solar radiation (Minogue and Fry, 1981), so dispersal distances of hundreds of metres or kilometres are possible (Van der Zaag, 1956). Sporangia landing on a host can germinate and penetrate living cells within 2 h under favourable conditions. In most cases, however, germination and penetration require more than 2 h. Under favourable conditions, large numbers of sporangia can be produced from a single lesion (more than 100, 000 sporangia per lesion) (Legard et al., 1995); the disease can thus progress rapidly under cool, wet conditions.

Potato tubers (surviving in soil, surviving in storage, or surviving in dumps or other locations for discarded materials) are very important in the survival of the asexual phase of P. infestans. Infected tubers that are protected from freezing in the cold temperate zones harbour viable P. infestans. If these tubers are planted or if plants are produced from these tubers, the fungus can again sporulate under favourable conditions and initiate a new series of asexual generations.

Seed tubers are crucial in the long-distance dispersal of P. infestans. It seems highly likely that they were the vehicle for transport of P. infestans in the very earliest migrations (19th century). Detection of exotic genotypes in seed tubers shipped across a continent (2000 km) and in subsequent epidemics in plants produced from those seed tubers (WE Fry, Cornell University, USA, unpublished results) confirms that tubers shipped very long distances have transported P. infestans, and intercontinental transport seems highly likely.

Tuber infections are highly variable from place to place, from one year to the next, and among cultivars. However infections as high as 60-80% are possible. More typically, low percentages of tubers are infected (not detectable to 2-3%). The probability that any given tuber will initiate a new epidemic on foliage is quite low. But because of the very high reproductive potential of this organism, a very low rate of transfer of pathogens from tubers to new foliage can still lead to devastating epidemics. Infection of potato tubers (especially seed tubers) is crucially important in long-distance dispersal of P. infestans. Conditions that enable the tuber to survive also enable the pathogen to survive. When that tuber gets to another location and is placed in conditions that favour the fungus (moderate temperatures and high moisture), the fungus can resume activity. It can sporulate directly on a potato tuber. If the tuber is planted or otherwise buried in the ground, the fungus can sporulate from the tuber and grow up the stem or perhaps be splash dispersed by rain-drops from the tuber in soil. When sporangia contact host tissue, the cycles of infection can be resumed.

Sexual Life History

When individuals of opposite mating type (A1 and A2) come into physical contact, sexual structures (antheridia and oogonia) are produced by each thallus. Meiosis is gametangial. After fertilization, the oogonium develops into an oospore which can survive adverse conditions better than the hyphae or sporangia. After a period of dormancy (weeks or months), oospores become capable of germination. Germination in the laboratory can occur on water agar at 18°C in the presence of blue light. It is clear that oospores can survive winter in northern temperate zones (Drenth et al., 1995), but the precise conditions stimulating germination are not yet known. Oospores germinate via a germ sporangium. This sporangium can then germinate via zoospores or via a germtube. If the fungus contacts a host plant it can initiate the asexual phase.

Natural enemies

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Natural enemyTypeLife stagesSpecificityReferencesBiological control inBiological control on
Bacillus subtilis Pathogen Russia
Colletotrichum coccodes Pathogen Russia
Pseudomonas putida Pathogen Russia

Notes on Natural Enemies

Top of page There is very little work reported on natural enemies of P. infestans, and none has been employed in managing this oomycete.

Seedborne Aspects

Top of page Incidence

P. infestans has long been known to be seedborne on tomato (Reed, 1912; Boyd, 1935). Vartanian and Endo (1985a) recovered the pathogen from seeds at incidences of up to 93% when seeds were plated directly on selective medium after harvesting from blighted fruit. However, the recovery rate dropped to 0% when the seeds were air-dried for 72 hours at 22°C. Histological studies on freshly harvested seeds showed that the pathogen was present in the gel surrounding the seed, in the seed coat, in the funiculus and between the endosperm and seed coat (Vartanian and Endo, 1985a). Rubin et al. (2001) showed that abundant oospores developed in the vascular tissues, pericarp, columella, and placenta of tomato fruits at the mature green stage, when coinoculated with A1 + A2 sporangia of P. infestans. Oospores were also formed on the surface of fruits kept in a moisture-saturated atmosphere. Occasionally, oospores were enclosed between the epidermal hairs of the seed coat. In a few seeds, oospores were detected inside the embryo.

P. infestans has not been reported as seedborne on true seeds of potato. However, it is seedborne on tuber seed pieces. Tuber infections are highly variable from place to place, from one year to the next and among cultivars. However, infections as high as 60-80% are possible. More typically, low percentages of tubers are infected (not detectable to 2-3%). The probability that any given tuber will initiate a new epidemic on foliage is quite low. However, because of the very high reproductive potential of P. infestans, a very low rate of transfer of the pathogen from tubers to new foliage can still lead to devastating epidemics.

Effect on Seed Quality

Infected seeds recovered from blighted tomato fruits were discoloured (Vartanian and Endo, 1985a).

Pathogen Transmission


Transmission of P. infestans to tomato seedlings at rates of 34 and 18% was demonstrated for moist, discoloured seeds in sterilized soil in the greenhouse and under field conditions in natural soil, respectively. No transmission of the pathogen was found in the greenhouse or field for moist, non-discoloured seeds or from discoloured seeds that had been air-dried before planting (Vartanian and Endo, 1985a).

Other sources

Potato and tomato crop residues provide an overwintering source of P. infestans, which then sporulates and can be transmitted by wind to tomato plants (Vartanian and Endo, 1985a, b).

Infection of potato tubers (especially seed tubers) is crucially important in long-distance dispersal of P. infestans. Conditions that enable the tuber to survive also enable the pathogen to survive. When that tuber is placed in conditions that favour the fungus (moderate temperatures and high moisture), the fungus can resume activity. It can sporulate directly on a potato tuber. If the tuber is planted or otherwise buried in the ground, the fungus can sporulate from the tuber and grow up the stem or perhaps be splash dispersed by rain-drops from the tuber in soil. When sporangia contact host tissue, the cycles of infection can be resumed.

Seed Treatment

Fermentation reduced seedborne infection of tomato seeds, but air-drying for 72 hours at 22°C or oven-drying for 6 hours at 29-5-37.7°C was needed to eliminate the pathogen (Vartanian and Endo, 1985a).

Potato tuber infections probably result from sporangia that have been washed from foliage through the soil to the tuber. Theoretically, tuber infections can be prevented by systemic fungicides if the pathogen is sensitive to these fungicides. For example, metalaxyl was very effective at preventing tuber infections caused by metalaxyl-sensitive strains of P. infestans (Fry et al., 1979). However, metalaxyl has almost no effect against strains that are insensitive. A number of materials have recently been evaluated for efficacy as protective seed treatments for late blight. Dimethomorph plus mancozeb, cymoznil plus mancozeb, and propamocarb hydrochloride plus chlorothalonil had increased stand emergence when inoculum was applied following seed treatments (Powelson and Inglis, 1999).

Seed Health Tests

Culture plate (Vartanian and Endo, 1985a)

- Place tomato seeds on rye seed agar, supplemented with pimaricin, ampicillin, rifampicin and pantachlronitrobenzene.
- Incubate at 21°C in the dark and evaluate plates at 1, 2, 5 and 14 days.

Plant Trade

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Plant parts liable to carry the pest in trade/transportPest stagesBorne internallyBorne externallyVisibility of pest or symptoms
Bulbs/Tubers/Corms/Rhizomes hyphae; spores Yes Yes Pest or symptoms usually visible to the naked eye
Flowers/Inflorescences/Cones/Calyx hyphae; spores Yes Yes Pest or symptoms usually visible to the naked eye
Fruits (inc. pods) hyphae; spores Yes Yes Pest or symptoms usually visible to the naked eye
Leaves hyphae; spores Yes Yes Pest or symptoms usually visible to the naked eye
Stems (above ground)/Shoots/Trunks/Branches hyphae; spores Yes Yes Pest or symptoms usually visible to the naked eye
True seeds (inc. grain) hyphae Yes Yes Pest or symptoms usually invisible
Plant parts not known to carry the pest in trade/transport
Growing medium accompanying plants
Seedlings/Micropropagated plants


Top of page Introduction

Late blight of potatoes or tomatoes can be a devastating disease with dramatic and disastrous economic consequences. It is known as the most devastating disease of potatoes and one of the most devastating plant diseases of any crop. When conditions favour pathogen development and there are no steps taken to suppress the disease, late blight can completely destroy the above-ground parts of plants (stems, leaves, tomato fruits) and can also affect potato tubers. The disease is a very serious economic threat in the vast majority of potato-production systems, and in many tomato-production systems. In locations where disease pressure is high, protectant fungicides may need to be applied as frequently as twice per week.

The Irish potato famine provides a grim indication of the destructive potential of P. infestans. The disease was first detected in Ireland in 1845 and for the succeeding several years it devastated the potato crops (Bourke, 1993). More than a million Irish died from starvation and at least another million emigrated. The population of Ireland declined steadily after 1845 from a high of about 8.5 million to just over half that by the end of the nineteenth century.

The Global Late Blight Initiative

The International Potato Center, known by its Spanish acronym, CIP, has made an attempt at estimating global losses due to potato late blight. The information that follows can be found on the CIP web page.

The acceptance of the late-blight-resistant cultivars to be developed under the global late blight initiative (GILB) is consistent with the economic benefits to be derived by reducing fungicide inputs and crop damage in developing countries. For the purpose of projecting potential returns on investment, CIP has conservatively estimated current losses from late blight at approximately 15% of annual production in developing countries. Assuming that a third of global potato production now occurs in developing countries (FAO/CIP, 1995), an equivalent or proportional share of these losses must occur there as well. Thus, 15% of one-third of 275 million tons (annual global potato production) is equivalent to 13.75 million tons. According to the CGIAR Technical Advisory Committee, a reasonable estimate of global producer prices for potatoes is US$200 per ton. Hence, the annual economic value of crop losses from late blight in developing countries is said to total $2.75 billion. In 1976, late-blight-related crop losses occurred despite increases in fungicide use. At the time, estimated global fungicide costs exceeded $1 billion annually. Again, for the purpose of the GILB, CIP conservatively estimates current fungicide costs to be on the order of $100 million annually in developing countries, that is, an average of $15 per hectare. Hence, crop losses (production forgone) and increased costs (expenses incurred) for late blight begin to approach the $3 billion mark. It should be noted that these figures represent only current losses.

Crop Losses


Late blight is a major problem throughout Northern and Eastern Europe. In Poland it causes significant losses (Piekarczyk and Babilas, 1986) that have been estimated at about 22% (Pietkiewicz, 1991). In Romania, in experiments conducted in 1982, there were losses of about 40% on the susceptible cultivar Bintje and losses of between 6 and 30% on other cultivars (Cupsa et al., 1983). In 1990 late blight was reported as increasing in importance as potato acreage increased (Bicici and Cinar, 1990).

The severity of late blight was recently reported to be increasing in Hungary, but quantitative data were not given. The increased severity was associated with the presence of the A2 mating type, as well as increased specific virulence and fungicide resistance of the pathogen population (Bakonyi and Ersek, 1997).

In Denmark, yield losses were simulated for pesticide-free agricultural systems. Losses due to potato late blight were among the highest of all crop systems considered, indicating the potential destructiveness of this disease in that country (Jorgensen et al., 1999).


Fungicide use comprises one of the simplest ways to estimate economic loss attributed to a disease and therefore is frequently used in developing countries. A survey done in Eastern African countries in the early 1990s (Kalyebara, 1994) demonstrated that fungicide use in this part of the world was highly variable, even among neighboring countries. In Zaire, fungicides were almost never used, in Burundi somewhat more and in Rwanda, most farmers sprayed at least 3 times. In Kenya, commercial farmers sprayed 5-7 times; smaller semi-commercial farmers spray 3-5 times. The most common product was Dithane, but Ridomil was used to some extent. Although production losses were not estimated in this survey one can probably assume to some degree an inverse relationship between fungicide use and losses; in those countries where fungicides were used more, production losses would be less. Workers in those parts of the world and even recent simulation efforts indicate that fungicides are generally poorly utilized, and frequently under-utilized in sub-Saharan Africa (Hijmans et al., 2000).

This view is consistent with a study undertaken in Burundi in 1989-90, where 32,000 t of potatoes were produced on 10,000 ha of land. Late blight was the most important disease causing yield losses up to 40% (Higiro and Danial, 1994).

Late blight is also important in western Africa. Yield reductions were found to vary between 25 and 71% in experiments done in Cameroon in 1990 and 1991. These data reflect comparisons of fungicide-treated and untreated plots under experimental conditions. Disease was more severe in Bansoa than it was in Dschang (Fontem and Aighewi, 1993).


Experiments conducted in India demonstrated loss potential of 39 and 37% due to late blight in two consecutive years. Two sprays of fungicide were able to control disease in these years (Rao and Veeresh, 1989). Bisht (Bisht et al., 1997) estimated that yield losses can be much higher, about 65%, in higher altitudes of India.

Yield losses in Bhutan were estimated as between 20 and 90%, but this was for a complex of disease including late blight, early blight (Alternaria solani), wart (Synchytrium endobioticum), black scurf (Rhizoctonia solani), brown rot (Ralstonia solanacearum), blackleg (Erwinia carotovora subsp. atroseptica) and potato virus Y (Shrestha et al., 1986).

Late blight was apparently introduced recently in Pakistan (Khan et al., 1985). At that time (1980s) it caused complete crop loss in some cases, presumably due in part to lack of control measures. Workers in the region indicate that late blight is still an important problem (CIP, unpublished data).

Andean region

Fungicides cost Andean farmers a lot of money. A recent survey estimated costs of about $150.00 per ha for a single season (Ortiz et al., 1999). This survey, however, was done in a particularly dry period and probably underestimates costs. The cost of spraying a field 15 times, which is not uncommon during rainy periords, would be closer to $600.00, depending on the type of fungicides used.

Based also on farm surveys, Andrade and Revelo (1994) estimated losses in Ecuador in 1992 to be about US$ 2.4 million. They added that 1992 was a dry year and that this figure would double in a wet year. Ecuador is probably a good indicator for fungicide use in other Andean countries.


The economic consequences were estimated for one epidemic occurring in 1995 in the Columbia Basin of the state of Washington in the USA. The mean number of fungicide applications per field varied from 5.1 to 12.3, depending on cultivar. Total per acre expenses (application costs plus fungicide material) ranged from $106.77 to $226.85, depending on cultivar and location. Approximately 28% of the crop was chemically desiccated before harvest as a disease management practice for the first time in 1995, resulting in an additional mean cost of $34.48/acre or $1.3 million for the region. Harvested yields were 4 to 6% less than in 1994. The total cost of managing late blight in the Columbia Basin in 1995 is estimated to have approached $30 million (Johnson et al., 1997).

Avoiding Crop Losses

Avoiding disease can be an effective disease management strategy. Farmers in the Andes plant susceptible potatoes at high altitudes where low temperatures reduce late blight pressure (Thurston, 1994). However, this strategy is frequently used in such a way that farmers trade off yield potential for decreased risk of disease. One survey in Ecuador estimated that between 30 and 40% of potato production in the province of Cotopaxi (central Ecuador) was done in the dry season to avoid late blight (Instituto Nacional de Investigación Agropecuaria, unpublished data). Yields in the dry season are considerably lower. Similarly, much of the potato production in the highlands of Ethiopia occurs during a period known as the "short rains". Yields are low during this period because of limited water supply, but the risk of losses due to blight is also reduced. Overall production in this country could be increased by the introduction of potato cultivars with resistance to late blight that could be planted in the main rainy season.

Late Blight on other Hosts

Late blight can be a devastating disease of tomato. Although tomato is generally an intensively-cultivated crop and farmers therefore justify the expense of fungicides, several factors make late blight a particularly difficult problem. First, there is very little resistance available in commercial tomato cultivars (Oyarzun et al., 1998), which means that with favourable weather conditions it is difficult to manage the disease even with fungicides. Second, unlike potato, the edible portion of tomato is directly exposed to fungicide applications. This complicates management practices near harvest time. Finally, pathogen populations from tomato and potato appear to be separate and adapted only to one host (Oyarzun et al., 1998). This means that tomato workers can not readily apply information gathered on the pathogen population from potato. Late blight is the most important disease of tomato in some developing countries.

P. infestans (or a very closely related species) is a pathogen of other cultivated hosts that only occur in specific regions of the world. One host is tree tomato (Solanum betaceum), which is economically important in certain parts of the Andes. Late blight of tree tomato appears to be important in specific climatic zones. In one valley in Ecuador known as San Jose de Minas, tree tomato production was abandoned because of late blight. Late blight of pear melon (S. muricatum) is also a limiting factor for producers in the Andes. The pathogen populations of tree tomato and pear melon are also host adapted and do not pose a threat to potato. Both tree tomato and pear melon are cultivated outside of the Andean region but it is not known if blight attacks these crops in other parts of the world.


Top of page Lesions may be incubated in a moist chamber for 12-24 h: the subsequent characteristic sporulation may be observed.

P. infestans can grow on a variety of culture media, but not all isolates will grow on all media. Commonly used media are rye agar, V-8 juice agar, pea agar, cornmeal agar, corn seed agar, and lima bean agar. A listing of recipes is presented in Erwin and Ribeiro (1996).

Diagnostic kits or techniques that employ biochemical or molecular methods may be helpful. Diagnostic kits, such as enzyme-linked immunosorbent assay (ELISA) that rely on antibody-antigen reactions may not be sensitive to species and may cross-react with Pythium, but can provide initial indication of the presence of an oomycete. Amplification of DNA using the polymerase chain reaction (PCR) may be helpful. Some primers for PCR are apparently specific to P. infestans (Trout et al., 1997) and their use in diagnosis should be helpful. Alloenzyme markers have been used to detect specific genotypes of the fungus in certain simple clonal populations (Goodwin et al., 1995a).

Detection and Inspection

Top of page For potatoes, the first plant parts to be inspected should be the seed tubers. Lesions can be readily seen on clean tubers with smooth white skins. Lesions are more difficult to detect on russeted or pigmented tubers. External inspection should be followed by observation of the flesh just underneath the periderm. Late blight causes a corky, 'granular', apparently discontinuous dry rot. Sometimes the rot penetrates only a few millimetres into the flesh; however, in other situations, or on other cultivars, the rot may extend for 1, 2 or 3 cm. Soft rot may follow infection by P. infestans and soft rot can sometimes overtake the late blight. The fungus will typically sporulate from tuber lesions if the tubers are placed in a moist chamber for 24 h at 18°C: positive confirmation of sporulation is often sufficient for diagnosis.

When the crop is growing, lesions can appear on any plant part. Typically, lesions are most likely to occur on plants in the wettest locations. These could be in a low spot in a field, or in locations that are shaded or that are likely to remain wet longer than other locations in the field. If a fungicide is used, the disease may appear first on plants that are difficult to spray with fungicide. The initial lesions can appear on stems or leaflets: on upper leaflets (presumably from an aerially dispersed sporangia), on upper stem segments, or on lower leaflets or lower stem segments (perhaps from an infected seed tuber). In locations where sexual reproduction is possible, the soil can serve as a source of inoculum and the first infections might again appear in the lower part of the canopy (leaves or stems).

If lesions are observed under dry conditions, diagnosis from visual symptoms may be more difficult. Incubation of lesions in a moist chamber for 12-24 h and subsequent observation for the characteristic sporulation is quite helpful.

Similarities to Other Species/Conditions

Top of page Late blight lesions can be mistaken for several other diseases. Under especially wet conditions, Botrytis cinerea can rot lower leaves of potato plants such that they resemble late blight lesions. However, the sporulation from B. cinerea is noticeably grey rather than white as for P. infestans. When conditions become quite dry and late blight lesions dry out, they can be mistaken for dried lesions caused by B. cinerea or sometimes for lesions caused by Alternaria solani (early blight). However, early blight lesions are typically zonate with a definite outer margin, whereas active late blight lesions are almost never zonate and typically do not have a definite outer margin.

Prevention and Control

Top of page Introduction

Both reduction in the amount of initial inoculum and suppression of pathogen growth rates are important in the suppression of late blight of potatoes and tomatoes. At this point, there is no biological control of known efficacy for use in suppressing late blight. Several fungicides have been shown to have a curative effect in tuber-borne P. infestans (Inglis et al., 1999). Thiophanate-methyl plus mancozeb applied to blighted potato seed pieces reduced the amount of surface colonized by P. infestans and when planted had higher emergence in two locations.

Reduce Initial Inoculum

For potatoes, it is important to plant healthy seed tubers, so that the pathogen is not imported with seed tubers. Other sources of inoculum in a growing region should be eliminated. These include any place where infected potato tubers might reside: piles of cull potatoes, or unharvested potato tubers that survive from one season to the next. Because sporangia of P. infestans can be dispersed aerially, late blight is a 'communal' disease. It is important that all growers in a production region collaborate to eliminate sources of inoculum. If this doesn't happen, a few fields with infected plants can jeopardize production in an entire region.

Tuber infections can be limited by increasing the depth of the soil barrier that protects the tubers. This can be achieved by constructing deep hills over the tubers to lessen the probability of tuber infections. Theoretically, tuber infections can be prevented by systemic fungicides when the pathogen is sensitive to those fungicides. For example metalaxyl was very effective at preventing tuber infections caused by metalaxyl-sensitive strains of P. infestans (Fry et al., 1979). However metalaxyl has almost no effect against strains that are insensitive.

Limit Pathogen Growth Rates

Late-blight-resistant cultivars and periodic application of fungicides limit pathogen growth rates. Both are effective and can be used together. In some agroecosystems, cultivars with very high levels of resistance are available and these alone are sufficient to suppress late blight. In other locations, such highly resistant cultivars are not available, and fungicides are also required. Note that some fungal strains are insensitive to some fungicides such as metalaxyl.

Many 'forecasting' schemes have been developed to improve the efficiency with which fungicides are used (Van Everdingen, 1926; Beaumont, 1947; de Weille, 1964; Krause and Massie, 1975; Connell et al., 1991). Most of these schemes identify when the first applications of protectant fungicide should be made in each season; such schemes operate in areas of defined seasons and not in the highland tropics where planting can occur throughout the year. In general, such schemes have successfully identified when periodic protectant fungicide applications should commence. Some forecasting schemes have also attempted to identify the subsequent frequency of fungicide applications. The efficacy of this approach is less certain.

If a hot spot of late blight appears in a field, growers should destroy that section of the field as rapidly as possible and perhaps also increase the frequency of fungicide application in surrounding areas.


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