Tomato Late Blight (Some Reference Material)
============================================
A. A. MacNab, Plant Pathology Dept., Penn State University                               
                                
A.  Introduction  
B.  Symptoms        
C.  Cause
D.  Disease cycle and development     
E.  Control
===========

A.  Introduction:  
         The causal pathogen from potatoes was first described in 1845 by 
Montagne and from tomato in 1847 by Payen in France.  However, it was 1863 
before deBary established beyond doubt that this fungus was the cause of 
late blight.  The disease occurs worldwide where tomatoes are grown.  Late 
blight is thought to have originated in Central America and to have appeared 
almost simultaneously in Europe and North America about 1830.  It occurred 
in France in 1840, was destructive in Germany in 1841, and occurred in North 
America in 1843.  Then, from 1844 to 1847, it occurred in epidemic and 
catastrophic proportions throughout Europe and North America.  It was 
directly responsible for the Irish Famine of 1845 and 1846.  Since that time, 
epidemics have occurred periodically when weather and other conditions 
favored disease development.  Some of these epidemics occurred in 1878 in 
England when entire plantings were destroyed; 1906, 1927 and 1928 in 
California; 1940 in Ontario; 1946 and 1947 throughout the eastern half of 
North America when 80 to 90% of early seedbeds in Florida were a complete 
loss, over 50% of the crop was lost in eastern states from New York to 
Florida, and 25% of the crop was lost in midwestern states; 1960 in Ontario; 
and1976 in southern Georgia and some northern states where infected 
transplants were used.  Heavy losses can occur in transit; symptoms can occur 
on infected but symptomless fruit within 5 days of harvest.  The late blight 
fungus also affects potato and eggplant but not pepper.                  
                                
B.  Symptoms:        
        Late blight symptoms can develop on leaves, stems, branches and both 
green and ripe fruit.  On leaves, pale green to brown spots, sometimes with 
a purplish tinge, appear on the upper surface of leaves.  Leaf spot margins 
often are pale green or water soaked.  The spots may enlarge rapidly until 
entire leaflets are killed.  In moist conditions, a downy white mold usually 
develops near the margin of leaf spots on the underside of leaves.  When 
petioles and stems are affected, portions of plants beyond blight lesions may 
dry up rapidly.  Lesions can expand rapidly and result in extensive, if not 
complete defoliation with 14 days.  In dry weather, affected foliar parts may 
appear dry and shriveled.

        Tomato fruit can become infected when foliage is affected.  On tomato 
fruit, greenish-brown greasy-appearing spots may enlarge until the entire 
fruit is involved.  The fruit tissue remains firm at first with varying depths 
of discolored tissue below the skin.  In moist weather, a white downy fungus 
growth may appear on the affected fruit rot surface.  Secondary organisms 
may invade affected fruit and cause a soft-rot.                  
                                
C.  Cause:  
        The causal fungus is a Phycomycete (Phytophthora infestans (Mont.) 
de Bary).  Usually, the fungus is identified from fungus structures produced 
on infected plants but can be isolated and grown in pure culture on some 
media such as lima bean agar.  Long sporangiophores emerge from leaves 
through stomata and bear thin-walled, oval, colorless sporangia which are 
about 21-38 u x 12-23 u in size.  The sporangia spores may germinate 
directly to produce a germ tube, but when in cool dew, germinate to produce 
up to eight zoospores, each of which is motile by two flagella and can cause 
new infections.

        Two physiologic races of the fungus have been identified on the basis of 
their reaction on different tomato varieties.  The races are named race T-0 
and race T-1.  Race T-0 is the original race which can be controlled by using 
plants containing the Ph (formerly named TR1) gene for resistance.  Race T-1 
is more aggressive and is not controlled by the Ph gene for resistance.          
                                
D.  Disease cycle and development:       
        The most important sources of inoculum for primary disease cycles are 
infected potato tubers and infected tomato transplants.  The fungus also is 
capable of survival in seeds and in dead vines although such occurrences are 
considered rare.  Infected potato tubers may survive in fields or storage; 
infected stored potatoes may be culled out and dumped outdoors, and 
sometimes infected potatoes may be planted.  When infected potatoes sprout, 
the fungus can grow into the sprout and produce spores on the sprout surface 
during favorable environmental conditions.  The late blight fungus survives 
mild winters on plants in southern Florida; spores can be blown northward by 
prevailing winds when environment is favorable.  An effective method of 
spread is on infected tomato transplants.  Oospores, produced during the 
sexual stage, frequently are found in Mexico and South America and may be 
important survival structures; they germinate by production of up to four 
germ tubes which bear sporangia spores. 

        Sporangia can serve as inoculum for primary disease cycles.  Sporangia 
production is favored by temperatures between 65 and 70 F and relative 
humidity near 100%; under such conditions, sporangia can mature in from 
3 to 10 hours.  Sporangia are released from dried flattened sporangiophores 
by twisting of sporangiophores caused by increasing relative humidity.  The 
spores can be disseminated up to 30 or 40 miles by wind, or over short 
distances in dew and splashing rain.  They rapidly lose viability when the 
relative humidity is below 95%; at 80% RH they can survive only 5 hours.

        Once spores land on a host leaf, a film of water must be present 
continuously until infection is established; otherwise, infection will not 
occur.  Sporangia may germinate in one of two ways as determined by 
temperature.  At temperatures below about 70 F, the sporangia germinate 
in from 1 to 3 hours to produce up to 8 zoospores.  Optimum temperature 
for zoospore formation is 54 F.  Zoospores swim in the water film, lose 
their flagella and encyst, and germinate to form an appressorium from which 
an infection peg penetrates the leaf.  Zoospore germination can occur within 
2 hours.  Optimum temperature for zoospore germination is 54 to 59 F, and 
for germ tube development is 70 to 75 F.  At temperatures between about 
70 to 86 F the sporangia germinate directly to produce a germ tube without 
producing zoospores; this occurs relatively slowly taking from 8 to 48 hours.  
The optimum temperature for direct germination is 77 F.

        The fungus penetrates the leaf directly through the cuticle and outer 
epidermal cell wall and rarely through stomates.  After ingress, it grows 
intercellularly and produces haustoria in mesophyll cells.  The optimum 
temperature for rapid colonization is from 72 to 76 F.  Initial symptoms 
including chlorosis may appear in 2 to 3 days but usually symptoms are evident 
in the field about 5 to 7 days after, but sometimes 10 days after inoculation.  
Soon after symptoms appear, sporangiophores emerge through stomates and 
produce sporangia.  These sporangia serve as inoculum for secondary repeating 
disease cycles.

        Ideal environmental conditions which favor epidemic development include 
periods when the temperature drops to 70 F and the relative humidity rises to 
100% early during the night, then slowly falling temperatures for the next 
8 hours, dew formation by the end of this time, heavy dew at 50 to 55 F for 
2 hours, morning temperatures rising slowly to about 70oF under cloudy skies, 
and dew persistence for 2 to 6 hours after the temperature rises.  Symptoms 
generally can appear 5 days after inoculation if there is a minimum of 
11 or 12 hours when the relative humidity is 100%, there are at least 4 hours 
of dew, and the temperature is less than 70 F.  Abundant infection requires 
100% RH or moisture on leaves for 25 hours at 65 to 70 F, conditions likely to 
occur during foggy, drizzly or rainy periods.  In Italy, environmental conditions 
necessary for an epidemic include minimum daily relative humidity of 65%, and 
a mean relative humidity greater than 90% for 6 hours on 3 to 4 days with 
temperatures from 50 to 55 F.  Temperatures above 95 F after penetration can 
stop disease development even after infection occurs; however, the fungus can 
survive inside living plant tissue and can resume disease development when 
cool moist conditions return.                             
                                                            
E.  Control:       
        Try to eliminate all early inoculum by destroying potato cull piles, 
preventing growth of volunteer potatoes, planting tomatoes as far as possible 
from potatoes, and using only inspected tomato transplants and potato tubers 
which are certified to be free of disease.  Since 1947, the Georgia Department 
of Agriculture has prohibited shipment of any tomato transplants into Georgia 
from southern Florida, and has allowed shipment only of inspected and 
certified transplants from central and northern Florida.  By excluding inoculum 
early in the season, there is less chance of late blight development on Georgia 
and other southern-grown tomato transplants, and consequently less chance of 
late blight being introduced on southern-transplants into northern areas.

        When environmental conditions favor late blight development, fungicides 
provide control if applied as preventive sprays.  Detailed fungicide 
information is provided in yearly revised Commercial Vegetable Production 
Guides.

        Several late blight forecasting systems have been developed to help 
growers identify periods when environment favors disease development and 
when fungicide coverage is most important.

        There are two types of resistance to late blight on tomatoes.  The first, 
called race-specific or vertical resistance, is controlled by a dominant gene 
and is very effective against a specific race of the fungus.  Plants with 
race-specific resistance react to infection by forming small, dead, 
non-spreading spots.  A weakness in this type of resistance is that new races 
of the fungus can develop which can overcome the resistance.  At least two 
races of the tomato late blight fungus exist now.  Examples of plants with 
race-specific resistance include the small fruited Red Cherry, and West 
Virginia accessions 36 and 106.  The second type of resistance is controlled 
by several genes and sometimes is called horizontal resistance.  Plants with  
horizontal resistance form small, atypical leaf spots which produce 
relatively few spores.  This resistance, although not as complete as 
race-specific resistance, has an advantage of being effective against all 
races of the late blight fungus.  Examples of old varieties with horizontal 
resistance include Southland, Wisconsin 55, Adelaide Dwarf, Australian 
Earliana, Burwood Prize, Chemin Early REd, Danish Extra Early, Determinate 
Shipper, Dobbie's Champion, Dobbie's Holyrood, Dwarf Earliest Red, Garden 
State, Marvana, Potentate, Primrose Gaye, Ssan Marzano, Venturia, 
Vetomold, Westlandia, and possibly Danmark.  From Europe, the varieties 
Atom and Ruzovy Ker are field resistant and may be able to be grown under 
reduced fungicide spray programs.

-------------------------------------------------------------
A. A. MacNab,
Plant Pathology Department, The Pennsylvania State University.
Revised:  July, 2004

Where trade names are used no discrimination is intended, and no endorsement by the Cooperative Extension Service is implied.

Back