In culture the mycelium is white and the colony is somewhat slow growing.  Growth rates can vary dramatically among isolates, but fast growing isolates can cover a 9 cm plate within about 1 week.  Some isolates grow irregularly, producing patterns in agar.  This has sometimes been associated with A2 mating type.  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.  Recipes for many media are presented in Erwin and Ribeiro (Erwin and Ribeiro 1996).

Taxonomy

The genus Phytophthora, the closely related genus Pythium, and the downy mildews (i.e. Bremia, Sclerospora, Plasmopera, Peronspora, etc.) belong to the oomycetes, which are unrelated to true fungi, such as ascomycetes and basidiomycetes.  Oomycetes are stramenopiles, a group which includes golden and brown algae, and which is characterized by zoospores propelled by heterokont flagella (of unequal length).  Zoospores are formed in sporangia.  Nuclei in vegetative cells are generally diploid (Shaw and Khaki 1971), although polyploidy has been detected (Tooley and Therrien 1991).  Sexual reproduction occurs via the development of oospores that develop from the joining of oogonia and antheridia.  Oomycetes have cellulose in their cell walls.   Erwin and Ribeiro (Erwin and Ribeiro 1996) discuss the changes in the understanding of taxonomic position of this group of organisms.  Many pathologists now consider the following to the correct taxonomic classification of P. infestans:

Phytophthora infestans (Mont.) de Bary—Kingdom Chromista, Phylum Oomycota, Order Peronosporales, Family Peronosporaceae, Genus Phytophthora, of which it is the type species (Birch and Whisson 2001).

Biology and disease cycle

Once epidemics are underway, secondary infections initiate from wind- or splash-born sporangia.  Under favorable conditions, sporangia or zoospores can penetrate living cells within 2 hrs.  Zoospores can swim up to several hours, depending primarily on temperature, after which time they encyst and germinate.  After penetration, P. infestans establishes a near-biotrophic relationship that lasts several days. 

Germ tubes can penetrate most leaf epidermal cells, but various authors have detected that infection on the leaf surface is not random and that successful infections more readily occur near the stomatal complexes (Coffey and Gees 1991).  Germ tubes do not penetrate host tissue directly, but rather via formation of an appresorium and subsequently an infection peg (Pristou and Gallegly 1954).   After penetration, the pathogen forms a specialized hyphal structure, sometimes referred to as an infection vessel.  Hyphae extend from this and begin colonization of plant tissue intercellularly.  Intercellular hyphae form haustoria that penetrate cells to absorb nutrients (Hohl and Suter 1976).   After a certain amount of time, sporangiophores grow out of stomatal openings.  Sporangia are borne on sporangiophores.  The amount of time between infection and sporulation depends on many factors including temperature, humidity, and host and pathogen genotypes. 

Lesions become visible within a few days, the exact time dependent on temperature, and the genetics of the host and pathogen.  Under optimal conditions (18-22^oC), and with a susceptible potato cultivar, infections can be visible in less than 3 days.  Within a day or two after the lesion first becomes visible, the pathogen is capable of sporulation.  Moderate temperatures (10-25^oC ) and very wet conditions (leaf wetness or 100% RH) are required for sporulation.  Within 8-12 hrs of favorable conditions sporangia are borne on indeterminate sporangiophores.  Sporangia dislodge during changing relative humidity and can be captured in air currents or splash dispersed.  Sporangia can survive for hours in unsaturated atmospheres when protected from solar radiation (Mizubuti, Aylor et al. 2000), so dispersal distances of hundreds of meters or kilometers are possible.  Under favorable conditions, large numbers of sporangia can be produced from a single lesion (more than 100,000 sporangia/lesion). 

P. infestans, as an oomycete plant pathogen, has a complex pre-infection process involving sporangial germination, zoospore taxis, encystment, cyst germination, germ tube development, appresorium formation and penetration.  Any one of these steps may be further decomposed into sub-units.  For example, penetration may involve both physical pressure from the infection peg, as well as enzymatic activity (Bignell 1975).   Oomycetes have been studied to determine how environmental stimuli affect the pre-infection events mentioned above (Shang, Chen et al. 1999).  While complex stimulus-response relationships may be encountered for any particular step in the pre-infection process, it is evident that virtually all steps are influenced by one or more environmental stimuli.  By altering one or more of these orienting stimuli, researchers can potentially interrupt the process and thereby control disease.  As a result, components of pre-infection are studied for opportunities in both chemical (Kiefer, Riemann et al. 2002) and biological (Shang, Chen et al. 1999) control. 

Potato tubers are very important in the survival of the asexual phase of P. infestans.  In the cold temperate zones P. infestans may over-winter on tubers that are protected from freezing in storage, or within the soil or a refuse pile.  These infected tubers then give rise to new epidemics the following season. 

Seed tubers play an important role in the long distance dispersal of P. infestans (Fry, Goodwin et al. 1993).  It seems highly likely that tubers were the vehicles of transport of P. infestans in the very earliest migrations (19th Century), and the introduction of new genotypes of the pathogen has been associated with seed shipments (Fry, Goodwin et al. 1993). 

When individuals of opposite mating type (A1 and A2) colonize the same substrate (plant tissue or agar), sexual structures (antheridia and oogonia) are produced by each thallus and meiosis occurs in the gametes.  After fertilization, the oogonium develops into an oospore, which can survive adverse conditions better than other forms of the pathogen.  After a period of dormancy (weeks or months) oospores become capable of germination. 

Germination in the lab can occur on water agar at 18^oC in the presence blue light.  It is clear that oospores can survive winter in temperate zones (Turkensteen, Flier et al. 2000), but the conditions stimulating germination are not yet precisely known.  Oospores germinate via a germ sporangium.  This sporangium can then liberate zoospores or may germinate directly with a germ tube. 

Most potato growers know the general conditions that favor late blight development in potato.  Studies in developing countries demonstrate that farmers who have never seen a microscope or weather data logger realize that late blight is favored by wet conditions (Nelson, Orrego et al. 2001).   Within months of the appearance of late blight in Ireland in 1845, David Moore, curator of the Royal Dublin Society’s Botanic Gardens, cited in (Nelson 1995) wrote that “damp is conducive to the progress of the disease ….. dryness retards it”.  Since those initial observations, plant pathologists have attempted to quantify the effects of weather on late blight development, as well as elucidate factors other than humidity and temperature that may be of importance.  The sexual phase of the pathogen has only been present outside Mexico for a little over decades, so much of the published information deals with the asexual phase.  Some of the earliest, detailed work was done by Melhus (Melhus 1915) and Crosier (Crosier 1933) in the early part of the 20^th century.   Since then a number of authors have studied the effects of the external environment on one or more aspects of the biology of P. infestans.  This work was reviewed in detail (Harrison 1992), and has been complemented by some recent work at Cornell (Mizubuti and Fry 1998; Mizubuti, Aylor et al. 2000) and at the International Potato Center (Andrade Piedra, Forbes et al. 1999).  The earliest workers discovered that sporangia of P. infestans germinate either directly with a germ tube or indirectly, by liberating zoospores.  Germ tubes can also form secondary sporangia, which may serve to increase the longevity of the spore (Harrison 1992).  The principal factor determining sporangial germination appears to be temperature, although the exact temperature effect probably depends on the particular pathogen genotype being evaluated (Mizubuti and Fry 1998).  Regardless, 15^oC appears to be a point of differentiation, below which germination is indirect, and above which it is direct.  This is, however, not a threshold effect, and it is better to consider these phenomena as stochastic processes related to temperature optima, maxima and minima (Mizubuti and Fry 1998).  Interestingly, germination and zoospore activity can occur at very low temperatures, near 0^oC, although at a very slow rate.  Above 30^oC, sporangia don’t germinate (Crosier 1933).  It is not known how well laboratory studies on the effect of temperature on germination mimic what happens in nature.  Factors other than temperature can affect sporangia germination, including pH and osmotic potential of the water (Sato 1994).  

Temperature affects nearly all aspects of P. infestans development, so it is difficult to sum up the corpus of information existing on the effects of temperature on the pathogen.  The disease has been associated historically with “cool wet weather”, but optimum temperatures are probably near 20^oC (Harrison 1992).  What this means is that epidemics occur fastest at this average temperature, although disease can occur over a range from about 5^oC to 30^oC.  Since the disease is a complex process affected differentially by day and night temperatures, it is easy to imagine how the average daily temperature is only a crude parameter for judging epidemic rate.  Still, average temperature appears to be a practical estimator of overall epidemic rate and has been used to compare epidemics in different environments (Forbes 1998).  Most phases of P. infestans cannot survive temperatures above 30^oC (Harrison 1992), but the pathogen is more robust when inside plant tissue and has survived temperatures of 40^oC in stem tissue (Kable and Mackenzie 1980). 

Similarly, the effect of humidity on the pathogen development, and subsequent disease, is complex.   Generally, saturated air or leaf wetness is required for sporangia to germinate and for zoospore motility (Harrison 1992).  After infection has occurred, the mycelium is relatively protected from low humidity, but high ambient humidity, near saturation, is needed for sporangia formation (Harrison 1992). 

There is inconsistency in the literature relating to sporangial sensitivity to drying.  Most studies found that once dried, sporangia were no longer viable (Warren and Colhoun 1975).  However, Minogue and Fry (Minogue and Fry 1981) showed that sporangia could remain viable after drying if re-hydrated gradually.  Because of the putative sensitivity of sporangia to drying, early workers considered rain splashing as one of the primary dispersal modes for this pathogen (Hirst 1958).  More recent studies indicate that sporangia are dispersed in air and are generally released during the day when relative humidity is lower (Aylor, Fry et al. 2001).  Because of this wind-borne mode of dispersal, the sensitivity of sporangia to ultraviolet light is an important issue.  Under high light conditions, most sporangia are killed within 1 hr, but sporangia can last for very long periods on cloudy days (Mizubuti, Aylor et al. 2000).  Long-distance wind dispersal can virtually be inferred by the extremely rapid rate of overland, and over-sea, movement detected when P. infestans was introduced to Europe in 1845 (Bourke 1991).  

Historical migrations of the pathogen

P.  infestans, which has a global distribution on potatoes and tomatoes, is thought by most researchers to have originated in the highlands of central Mexico (Goodwin, Spielman et al. 1992; Grünwald, Flier et al. 2001) causing mild epidemics on native wild tuber-bearing Solanum species (Reddick 1939).  Mexico is considered the center of origin of P. infestans because both mating types (A1 and A2) were present when the disease was discovered in that location and there is a high genetic diversity for the pathogen in this region

(Niederhauser, Cervantes et al. 1954; Tooley, Sweigard et al. 1986; Goodwin and Drenth 1997; Grünwald, Flier et al. 2001).  In contrast, only the A1 mating type and low genetic diversity had been found outside Mexico until the mid 1980s (Hohl and Iselin 1984; Goodwin, Spielman et al. 1992; Grünwald, Flier et al. 2001).  An alternative hypothesis proposed the Andes, center of origin of the cultivated potato, as the center of origin for P. infestans (Abad and Abad 1997).  This hypothesis is based primarily on historical accounts of potato disease in the Andes, and appears to have little support in the scientific literature. 

Until recently, most isolates of P. infestans found outside North America belonged to the US-1 clonal lineage.  This led to a hypothesis that US-1 had caused the original epidemics in Europe in the 1800s (Goodwin, Cohen et al. 1994) and then spread globally, presumably with seed trade (Fry, Goodwin et al. 1993).  Originally researchers proposed that US-1 had spread from Mexico to the US and then from the US to Europe (Goodwin, Cohen et al. 1994).  Alternatively, some researchers proposed that US-1 was introduced into Europe directly from South America (Tooley, Therrien et al. 1989; Andrivon 1996).  However,  recent analyses of mitochondrial DNA of P. infestans in herbarium material presented evidence that a genotype different from US-1 was involved in the original epidemics in Europe (Ristaino, Groves et al. 2001).  This has not contributed to the debate about the origin of P. infestans, but it has dispelled earlier notions about historical migration patterns that led to the Irish Famine.  During the 1980s, the A2 mating type of P. infestans was detected in Europe (Hohl and Iselin 1984) along with several new alleles for known markers (Drenth, Goodwin et al. 1993).  A new global migration from Mexico had taken place. The pathogen population in Europe is now highly diverse and there is evidence for sexual reproduction in several European countries (Drenth 1994; Andersson, Sandstrom et al. 1998; Turkensteen, Flier et al. 2000; Flier, Kessel et al. 2002). 

Literature Cited

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Morphology  

Phytophthora infestans is a coenocytic oomycete.  Asexual reproduction is via sporangia that are ellipsoid to lemon shaped with a small pedicel.  Sporangia range in length from 29-36 µm and in width from 19-22 µm, and either germinate directly forming a germ tube (at temperatures of 15-24 C), or indirectly via zoospores (at temperatures below 15 C).  These temperature ranges may vary for different populations of the pathogen.  Zoospores  (ca 7 - 12 per sporangium) have two flagella, one tinsel type that is directed forward and a second whiplash type, which is directed backward.  Zoospores are usually uninucleate, but binucleate zoospores have been detected.

Sporangium of Phytophthora infestans

Sporangium and Sporangiophore of P. infestans