Phytophthora infestans is anoomycete orwater mold, a fungus-likemicroorganism that causes the seriouspotato andtomato disease known aslate blight orpotato blight.Early blight, caused byAlternaria solani, is also often called "potato blight". Late blight was a major culprit in the1840s European, the1845–1852 Irish, and the1846 Highland potatofamines. The organism can also infect some other members of theSolanaceae.[1][2][3] The pathogen is favored by moist, cool environments: sporulation is optimal at 12–18 °C (54–64 °F) in water-saturated or nearly saturated environments, andzoospore production is favored at temperatures below 15 °C (59 °F). Lesion growth rates are typically optimal at a slightly warmer temperature range of 20 to 24 °C (68 to 75 °F).[4]
The genus namePhytophthora comes from the Greekφυτό (phyto), meaning "plant" – plus the Greekφθορά (phthora), meaning "decay, ruin, perish". The species nameinfestans is the present participle of the Latin verbinfestare, meaning "attacking, destroying", from which the word "to infest" is derived. The namePhytophthora infestans was coined in 1876 by the German mycologistHeinrich Anton de Bary (1831–1888).[5][6]
The asexual life cycle ofPhytophthora infestans is characterized by alternating phases ofhyphal growth, sporulation,sporangia germination (either throughzoospore release or direct germination, i.e. germ tube emergence from thesporangium), and the re-establishment of hyphal growth.[7] There is also a sexual cycle, which occurs when isolates of opposite mating type (A1 and A2, see§ Mating types below) meet. Hormonal communication triggers the formation of the sexualspores, calledoospores.[8] The different types of spores play major roles in the dissemination and survival ofP. infestans. Sporangia are spread by wind or water and enable the movement ofP. infestans between differenthost plants. The zoospores released from sporangia arebiflagellated andchemotactic, allowing further movement ofP. infestans on water films found on leaves or soils. Both sporangia and zoospores are short-lived, in contrast to oospores which can persist in a viable form for many years.
People can observeP. infestans produce dark green, then brown then black spots on the surface of potato leaves and stems, often near the tips or edges, where water or dew collects.[9] The sporangia andsporangiophores appear white on the lower surface of the foliage. As for tuber blight, the whitemycelium often shows on the tubers' surface.[10]
Under ideal conditions,P. infestans completes its life cycle on potato or tomato foliage in about five days.[7] Sporangia develop on the leaves, spreading through the crop when temperatures are above 10 °C (50 °F) and humidity is over 75–80% for 2 days or more.Rain can wash spores into thesoil where they infect young tubers, and the spores can also travel long distances on the wind. The early stages of blight are easily missed. Symptoms include the appearance of dark blotches on leaf tips and plant stems. White mold will appear under the leaves in humid conditions and the whole plant may quickly collapse. Infected tubers develop grey or dark patches that are reddish brown beneath the skin, and quickly decay to a foul-smelling mush caused by the infestation of secondarysoft bacterial rots. Seemingly healthy tubers may rot later when in store.
P. infestans survives poorly in nature apart from on its plant hosts. Under most conditions, the hyphae and asexual sporangia can survive for only brief periods in plant debris or soil, and are generally killed off during frosts or very warm weather. The exceptions involve oospores, and hyphae present within tubers. The persistence of viable pathogen within tubers, such as those that are left in the ground after the previous year's harvest or left in cull piles is a major problem in disease management. In particular,volunteer plants sprouting from infected tubers are thought to be a major source of inoculum (orpropagules) at the start of a growing season.[11] This can have devastating effects by destroying entire crops.
Themating types are broadly divided into A1 and A2.[12][13] Until the 1980s populations could only be distinguished byvirulence assays and mating types, but since then more detailed analysis has shown that mating type andgenotype are substantially decoupled.[14] These types each produce amating hormone of their own.[13][12] Pathogen populations are grouped into clonal lineages of these mating types and includes:
Discovered byJohn Niederhauser in the 1950s, in theToluca Valley in Central Mexico, while working for theRockefeller Foundation's Mexican Agriculture Program. Published in Niederhauser 1956.[13][15] A2 produces a mating hormone α2.[12] Clonal lineages of A2 include:
P. infestans isdiploid, with about 8–10chromosomes, and in 2009 scientists completed the sequencing of itsgenome. The genome was found to be considerably larger (240Mbp) than that of most otherPhytophthora species whose genomes have been sequenced;P. sojae has a 95 Mbp genome andP. ramorum had a 65 Mbp genome. About 18,000genes were detected within theP. infestans genome. It also contained a diverse variety oftransposons and manygene families encoding foreffector proteins that are involved in causingpathogenicity. These proteins are split into two main groups depending on whether they are produced by the water mold in thesymplast (inside plant cells) or in theapoplast (between plant cells). Proteins produced in the symplast includedRXLR proteins, which contain anarginine-X-leucine-arginine (where X can be anyamino acid) sequence at theamino terminus of the protein. Some RXLR proteins areavirulence proteins, meaning that they can be detected by the plant and lead to ahypersensitive response which restricts the growth of the pathogen.P. infestans was found to encode around 60% more of these proteins than most otherPhytophthora species. Those found in the apoplast includehydrolytic enzymes such asproteases,lipases andglycosylases that act to degrade plant tissue,enzyme inhibitors to protect against host defence enzymes andnecrotizing toxins. Overall the genome was found to have an extremely high repeat content (around 74%) and to have an unusual gene distribution in that some areas contain many genes whereas others contain very few.[1][18]
Study ofP. infestans presentssampling difficulties in the United States.[20]: 43 It occurs only sporadically and usually has significantfounder effects due to each epidemic starting from introduction of a singlegenotype.[20]: 43
The highlands of centralMexico were considered to be the center of origin ofP. infestans, although others have proposed its origin to be in theAndes, which is also the origin of potatoes.[21][22] A study published in 2014 evaluated these two alternate hypotheses and found conclusive support for central Mexico being the center of origin.[23] However, their study did not include either an extensive global sampling ofP. infestans or historic genomes. Support for a Mexican origin – specifically theToluca Valley[20] – came from multiple observations including the fact that populations are genetically most diverse in Mexico, late blight is observed in native tuber-bearingSolanum species, populations of the pathogen are inHardy–Weinberg equilibrium, the two mating (see§ Mating types above) types occur in a 1:1 ratio, and detailedphylogeographic and evolutionary studies.[22][23][24][25][26][27][28] For instance, while sexual recombination is regarded as evidence for a Mexican origin,P. infestans is mostly asexual and does not widely engage in sexual reproduction, despite the migration of the A2 mating type into Europe. Furthermore, the sister lineages ofP. infestans, namelyP. mirabilis andP. ipomoeae are endemic to central Mexico.[29]
Others have proposed an Andean origin forPhytophthora infestans. In 2002, Ristaino assessed the evidence for both the Mexican and South American origin hypotheses [24]. She pointed to the absence of potato exports during the 1840s, which posed a challenge to the notion of a Mexican origin for the blight's migration to the US and Europe [24]. Furthermore, historical accounts of a similar disease in the Andean region and the presence of the cosmopolitan US-1 lineage in South America since at least the 1980s (yet absent in Mexico) were invoked by Ristaino, potentially supporting the idea of a South American origin [24]. In 2016, the Ristaino lab with collaborators Mike Martin and Tom Gilbert, at the University of Copenhagen, conducted the largest whole genome sequencing project to date with historic and modern day lineages ofP infestans (25). Analysis of these more extensive genomic dataset that included bothP. infestans andP. andina isolates documented an Andean origin of the species [25]. Lineages of Andean origin were found to be more closely related to historicalP. infestans lineages from the famine era, implying an Andean origin with later subsequent migration and diversification occurring in Mexican lineages [25]. Significant admixture between the historicP infestans andP andina was also documented [25]. Several close relatives of P infestans have been found inthe Andes inSouth America, includingP. andina,P urerae and P betacei.
Coomber et al., examined the evolutionary history ofPhytophthora infestans and its close relatives in the 1c clade using whole genome sequence data from 69 isolates ofPhytophthora species in the 1c clade and conducted a range of genomic analyses including nucleotide diversity evaluation, maximum likelihood trees, network assessment, time to most recent common ancestor and migration analysis [26}. They consistently identified distinct and later divergence of the two MexicanPhytophthora species,P. mirabilis andP. ipomoeae, fromP. infestans and other 1c clade species.Phytophthora infestans exhibited more recent divergence from other 1c clade species ofPhytophthora from South America,P. andina andP. betacei. Speciation in the 1c clade and evolution ofP. infestans occurred in the Andes.P. andina – P. betacei – P. infestans formed a species complex with indistinct species boundaries, hybridizations between the species, and short times to common ancestry. Furthermore, the distinction between modern Mexican and South AmericanP. infestans proved less discrete, suggesting gene flow between populations over time. Admixture analysis indicated a complex relationship among these populations, hinting at potential gene flow across these regions. HistoricP. infestans, collected from 1845-1889 from herbarium collections, were the first to diverge from all otherP. infestans populations. Modern South American populations diverged next followed by Mexican populations which showed later ancestry. Both populations were derived from historicP. infestans. Based on the time of divergence ofP. infestans from its closest relatives,P. andina andP. betacei in the Andean region, the data support the Andes as the center of origin ofP. infestans, with modern globalization contributing to admixture betweenP. infestans populations today from Mexico, the Andes and Europe [26].
Migrations from Mexico toNorth America orEurope have occurred several times throughout history, probably linked to the movement of tubers.[30][31] Until the 1970s, the A2 mating type was restricted to Mexico, but now in many regions of the world both A1 and A2 isolates can be found in the same region.[13] The co-occurrence of the two mating types is significant due to the possibility of sexual recombination and formation of oospores, which can survive the winter. Only in Mexico andScandinavia, however, is oospore formation thought to play a role in overwintering.[22][32] In other parts of Europe, increasing genetic diversity has been observed as a consequence of sexual reproduction.[33] This is notable since different forms ofP. infestans vary in their aggressiveness on potato or tomato, in sporulation rate, and sensitivity tofungicides.[34] Variation in such traits also occurs in North America, however importation of newgenotypes from Mexico appears to be the predominant cause of genetic diversity, as opposed to sexual recombination within potato or tomato fields.[13] In 1976 – due to a summer drought in Europe – there was a potato production shortfall and so eating potatoes were imported to fill the shortfall. It is thought that this was the vehicle for mating type A2 to reach the rest of the world. In any case, there had been little diversity, consisting of the US-1 strain, and of that only one type of: mating type, mtDNA,restriction fragment length polymorphism, and di-locus[clarification needed]isozyme. Then in 1980 suddenly greater diversity and A2 appeared in Europe. In 1981 it was found in the Netherlands, United Kingdom, 1985 in Sweden, the early 1990s in Norway and Finland, 1996 in Denmark, and 1999 in Iceland. In the UK new A1 lineages only replaced the old lineage by end of the '80s, and A2 spread even more slowly, with Britain having low levels and Ireland (north and Republic) having none-to-trace detections through the '90s.[35] Many of the strains that appeared outside of Mexico since the 1980s have been more aggressive, leading to increased crop losses.[13] In Europe since 2013 the populations have been tracked by the EuroBlight network (see links below). Some of the differences between strains may be related to variation in the RXLR effectors that are present.
P. infestans is still a difficult disease to control.[3][36][37][38] There are many chemical options inagriculture for the control of damage to thefoliage as well as the fruit (for tomatoes) and thetuber[39] (for potatoes). A few of the most common foliar-applied fungicides areRidomil, a Gavel/SuperTin tank mix, andPrevicur Flex. All of the aforementioned fungicides need to be tank mixed with a broad-spectrum fungicide, such asmancozeb orchlorothalonil, not just for resistance management but also because the potato plants will be attacked by other pathogens at the same time.
If adequate field scouting occurs and late blight is found soon after disease development, localized patches of potato plants can be killed with adesiccant (e.g.paraquat) through the use of a backpack sprayer. This management technique can be thought of as a field-scalehypersensitive response similar to what occurs in some plant-viral interactions whereby cells surrounding the initial point of infection are killed in order to prevent proliferation of the pathogen.
If infected tubers make it into a storage bin, there is a very high risk to the storage life of the entire bin. Once in storage, there is not much that can be done besides emptying the parts of the bin that contain tubers infected withPhytophthora infestans. To increase the probability of successfully storing potatoes from a field where late blight was known to occur during the growing season, some products can be applied just prior to entering storage (e.g.,Phostrol).[40]
Around the world the disease causes around $6 billion of damage to crops each year.[1][2]
Potatoes after exposure. The normal potatoes have blight but thecisgenic potatoes are healthy.Genetically modifiedKing Edward (right) next to King Edward which has not been genetically modified (left). Research field,Swedish University of Agricultural Sciences, 2019
Breeding for resistance, particularly in potato plants, has had limited success in part due to difficulties in crossing cultivated potato with its wild relatives,[36][37][38] which are the source of potential resistance genes.[36][37][38] In addition, most resistance genes work only against a subset ofP. infestans isolates, since effectiveplant disease resistance results only when the pathogen expresses a RXLR effector gene that matches the corresponding plant resistance (R) gene;effector-R gene interactions trigger a range of plant defenses, such as the production of compounds toxic to the pathogen.
Potato and tomato varieties vary in their susceptibility to blight.[33][36][37][38] Most early varieties are very vulnerable; they should be planted early so that the crop matures before blight starts (usually in July in the Northern Hemisphere). Many old crop varieties, such asKing Edward potato, are also very susceptible but are grown because they are wanted commercially. Maincrop varieties which are very slow to develop blight includeCara, Stirling, Teena, Torridon,Remarka, and Romano. Some so-called resistant varieties can resist some strains of blight and not others, so their performance may vary depending on which are around.[33][36][37][38] These crops have had polygenic resistance bred into them, and are known as "field resistant". New varieties,[36][37][38] such as Sarpo Mira and Sarpo Axona, show great resistance to blight even in areas of heavy infestation. Defender is an American cultivar whose parentage includesRanger Russet andPolish potatoes resistant to late blight. It is a long white-skinned cultivar with both foliar and tuber resistance to late blight. Defender was released in 2004.[41]
Genetic engineering may also provide options for generating resistance cultivars. A resistance gene effective against most known strains of blight has been identified from a wild relative of the potato,Solanum bulbocastanum, and introduced by genetic engineering into cultivated varieties of potato.[42] This is an example ofcisgenic genetic engineering.[43]
Melatonin in the plant/P. infestans co-environment reduces the stress tolerance of the parasite.[44]
Blight can be controlled by limiting the source ofinoculum.[33] Only good-qualityseed potatoes and tomatoes obtained fromcertified suppliers should be planted. Often discarded potatoes from the previousseason and self-sowntubers can act as sources of inoculum.[45]
Compost, soil or potting medium can be heat-treated to kill oomycetes such asPhytophthora infestans. The recommended sterilisation temperature for oomycetes is 120 °F (49 °C) for 30 minutes.[46][47]
There are several environmental conditions that are conducive toP. infestans. An example of such took place in the United States during the 2009 growing season. As colder than average for the season and with greater than average rainfall, there was a major infestation of tomato plants, specifically in the eastern states.[48] By usingweather forecasting systems, such asBLITECAST, if the following conditions occur as thecanopy of the crop closes, then the use offungicides is recommended to prevent anepidemic.[49]
ABeaumont Period is a period of 48 consecutive hours, in at least 46 of which the hourly readings oftemperature andrelative humidity at a given place have not been less than 10 °C (50 °F) and 75%, respectively.[50][51]
ASmith Period is at least twoconsecutive days where min temperature is 10 °C (50 °F) or above and on each day at least 11 hours when the relative humidity is greater than 90%.
The Beaumont and Smith periods have traditionally been used by growers in theUnited Kingdom, with different criteria developed by growers in other regions.[51] The Smith period has been the preferred system used in the UK since its introduction in the 1970s.[52]
Based on these conditions and other factors, several tools have been developed to help growers manage the disease and plan fungicide applications. Often these are deployed as part ofdecision support systems accessible through web sites or smart phones.
Several studies have attempted to develop systems for real-time detection viaflow cytometry ormicroscopy of airborne sporangia collected in air samplers.[53][54][55] Whilst these methods show potential to allow detection of sporangia in advance of occurrence of detectable disease symptoms on plants, and would thus be useful in enhancing existingdecision support systems, none have been commercially deployed to date.
Fungicides for the control of potato blight are normally used only in a preventative manner, optionally inconjunction with diseaseforecasting. In susceptible varieties, sometimes fungicide applications may be needed weekly. An early spray is most effective. The choice of fungicide can depend on the nature of local strains ofP. infestans.Metalaxyl is a fungicide that was marketed for use againstP. infestans, but suffered seriousresistance issues when used on its own. In some regions of the world during the 1980s and 1990s, most strains ofP. infestans became resistant to metalaxyl, but in subsequent years many populations shifted back to sensitivity. To reduce the occurrence of resistance, it is strongly advised to use single-target fungicides such as metalaxyl along withcarbamate compounds. A combination of other compounds are recommended for managing metalaxyl-resistant strains. These includemandipropamid,chlorothalonil,fluazinam,triphenyltin,mancozeb, and others. In the United States, theEnvironmental Protection Agency has approvedoxathiapiprolin for use against late blight.[56] In Africansmallholder productionfungicide application can be necessary up to once every three days.[57]
In the past,copper(II) sulfate solution (called 'bluestone') was used to combat potato blight.Copper pesticides remain in use on organic crops, both in the form ofcopper hydroxide and copper sulfate. Given the dangers ofcopper toxicity, other organic control options that have been shown to be effective includehorticultural oils,phosphorous acids, andrhamnolipidbiosurfactants, while sprays containing "beneficial" microbes such asBacillus subtilis or compounds that encourage the plant to produce defensive chemicals (such asknotweed extract) have not performed as well.[58]During the crop year 2008, many of thecertified organic potatoes produced in the United Kingdom and certified by theSoil Association as organic were sprayed with acopper pesticide[59] to control potato blight. According to the Soil Association, the total copper that can be applied to organic land is 6 kilograms per hectare (5.4 lb/acre)/year.[60]
Ridging is often used to reduce tuber contamination by blight. This normally involves pilingsoil ormulch around thestems of the potato blight, meaning thepathogen has farther to travel to get to the tuber.[61] Another approach is to destroy the canopy around five weeks beforeharvest, using a contactherbicide orsulfuric acid to burn off the foliage. Eliminating infected foliage reduces the likelihood of tuber infection.
Maps of the geographic locations (occurrences) of the potato disease in the northeastern US and southeastern Canada from (a) 1843, (b) 1844 and (c) 1845 drawn from text analytics of US Commissioner of Patent Reports, 1843–1845. Image from Saeffer et al., 2024.
The first recorded instances of the disease were in the United States, inPhiladelphia andNew York City in early 1843.[62] Winds then spread the spores, and in 1845 it was found fromIllinois toNova Scotia, and fromVirginia toOntario. It crossed theAtlantic Ocean with a shipment of seed potatoes forBelgian farmers in 1845.[63][64] The disease being first identified in Europe aroundKortrijk, Belgium, in June 1845, and resulted in the Flemish potato harvest failing that summer, yields declining 75–80%, leading to an estimated forty thousand deaths in the locale.[65] All of the potato-growing countries in Europe would be affected within a year.
The effect ofPhytophthora infestans in Ireland in 1845–52 was one of the factors which caused more than one million to starve to death[66] and forced another two million to emigrate. Most commonly referenced is theGreat Irish Famine, during the late 1840s. Implicated in Ireland's fate was the island's disproportionate dependency on a single variety of potato, theIrish Lumper. The lack ofgenetic variability created a susceptible host population for the organism[67] after the blight strainsoriginating in Chiloé Archipelago replaced earlier potatoes of Peruvian origin in Europe.[68]
Since 1941, Eastern Africa has been suffering potato production losses because of strains ofP. infestans from Europe.[71]
France,Canada, theUnited States, and theSoviet Union researchedP. infestans as abiological weapon in the 1940s and 1950s.[72] Potato blight was one of more than 17 agents that the United States researched as potential biological weapons before the nation suspendedits biological weapons program.[73] Dr. Mannon Gallegley, deceased faculty from WVA worked in the late blight bioweapons program in the 1940s. It is unclear whether the pathogen was ever deployed. Whether a weapon based on the pathogen would be effective is questionable, due to the difficulties in delivering viable pathogen to an enemy's fields, and the role of uncontrollable environmental factors in spreading the disease.[74]
Late blight (A2 type) has not yet been detected in Australia and strict biosecurity measures are in place. The disease has been seen in China, India and south-east Asian countries.
A large outbreak ofP. infestans occurred on tomato plants in the Northeast United States in 2009.[75]
In light of the periodic epidemics ofP. infestans ever since its first emergence, it may be regarded as a periodicallyemerging pathogen – or a periodically "re-emerging pathogen".[76][77]
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