Tomato Bacterial Canker (Some Reference Material)
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A. A. MacNab, Plant Pathology Dept., Penn State University

A.  Introduction  
B.  Symptoms
C.  Cause
D.  Disease Cycle and Development
E.  Control
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A.  Introduction:  
        This disease was observed in Michigan in 1909 and the cause was reported 
one year later.  Earlier reports suggest the disease was present in New York in 
1892.  The disease has been called Grand Rapids disease, bacterial tomato wilt, 
stem rot, stem canker and bird's eye spot.  Today, bacterial canker generally is 
the accepted name.  Bacterial canker occurs on all continents and has been 
reported from most tomato growing areas.  Losses are associated with stunting, 
wilting, cankering, and sometimes death of systemically infected plants, and 
with fruit spotting resulting from secondary infections.  Losses, reported for 
both field and greenhouse crops, vary greatly among years, fields, and 
greenhouses.  Bacterial canker is one of the most dreaded and potentially 
devastating disease of tomato.  Heavy losses reported include up to 80% of the 
trellesed crop on individual farms in North Carolina in the early 1960's, up to 
80% severe infection in some fields in East Africa in 1945, up to 60% in Kenya 
in 1962, and an average of 5 to 10% yearly loss and up to 60% loss to individuals 
involved in greenhouse production in Ontario from 1965 to 1971.  Hosts reported 
in nature, in addition to tomato, include the solanaceous weeds Solanum 
mammosum (spiny Porto Rican weed), S. douglasii (perennial nightshade, 
S. nigrum (black nightshade), and S. triflorum.  Several other plants including 
pepper and eggplant are susceptible when they are artificially inoculated.
 
B.  Symptoms:
        Bacterial canker symptoms appear on all parts of tomato plants.  Plants 
can be affected at any stage of development.  Many symptoms develop from 
systemic infection of plants; a few symptoms develop from secondary infections 
which may remain localized in the plant.

        Symptoms on systemically infected plants appear first on oldest leaves; 
these leaves turn downward, leaflets curl, and finally shrivel.  Frequently, one 
side of a leaf is affected; leaflets on one side die while those on the other 
side remain healthy.  Petioles bearing affected leaves may turn downward but 
do not wilt.  When top leaves become infected as a result of systemic 
movement of the bacteria, the leaves may wilt.  Symptoms reported 
infrequently on succulent tissue produced during wet weather include pale 
green spots of collapsed tissue between veins, and a clear water soaked 
appearance on the external and younger parts of infected stems and petioles.   
Characteristic coloration inside affected stems can be found by cutting the 
stem lengthwise; just inside the woody cylinder, tissue is first creamy white 
to yellow, and later reddish-brown.  This discoloration is most conspicuous in 
the upper part of the plant where the bacteria spread from the woody tissue to 
the  more succulent inner pith and outer bark tissue.  The pith is easily 
separated from the woody tissue when the discoloration occurs.  At advanced 
stages, cankers form in discolored tissue.  Characteristic symptoms develop 
within tissue at the base of petioles.  In cross section, this tissue contains 
creamy white to yellow mealy-appearing areas in the pith or cortex, 
sometimes contains cavities, and in later stages is reddish brown.  Symptoms 
seldom are evident in roots.  Characteristic symptoms may develop on fruit 
that become infected when bacteria move systemically in stem vascular 
tissue into young fruit.  Fruit infected when very young are stunted and 
distorted.  Fruit infected later may have no external symptoms; however, 
the calyx scar tissue may be discolored, the calyx attachment may be 
weakened, and vascular yellowing may be present within fruit, sometimes 
extending to the seed cavity and to seeds.  Some seeds in early-infected 
fruit are most likely to be spotted or entirely dark and do not mature.

        Secondary infection can appear on fruit, peduncles, pedicels, calyx and 
young stems, especially on plants in field culture.  Initially, spots on fruit are 
small, round, white, superficial, and slightly raised.  Spot centers become 
pustular, break open, and have a rough yellow to brown surface; a white halo 
usually persists, thus resulting in the typical and characteristic "bird's eye 
spot".  The spots remain small, usually less than 1/4-inch in diameter.  There 
is no watersoaking associated with the spots.  Fruit spotting, when present, 
usually is accompanied by spotting of peduncles, pedicels, the calyx and young 
stems.  Such spots are small, tan colored, usually superficial, and may appear 
as open cankers less than 1/10-inch wide.  Inconspicuous leaf spots can occur 
and usually are creamy white and raised.

        Thirteen distinctive diagnostic features listed for bacterial canker are:  
(1) irregular one-sided leaf wilting or withering, (2) yellow to black streaks 
on stems and petioles, (3) cankers on stems, petioles, and leaf midribs, 
(4) yellow to reddish discoloration and hollow areas within the pith, (5) firing 
of foliage, (6) "birds-eye" spotting of fruit, (7) brown, pimple-like spotting of 
peduncles and pedicels, (8) blister-like spotting of foliage, (9) presence of 
yellowish bacterial ooze that can be squeezed from infected portions of stem 
tissue, (10) adherence of affected petioles and leaves to stems, (11) absence 
of chlorotic foliage, (12) absence of extensive discoloration in roots, and 
(13) formation of adventitious roots on stems.
 
C.  Cause:
        The canker bacterium (Corynebacterium michiganense pv. michiganense 
(Smith) Jensen) is rod shaped when freshly isolated from plants, about 
1 x 0.5 u in size, gram positive, not acid fast, non-spore forming, and is now 
considered motile.  The pathogen grows well on ordinary PDA.  The bacteria 
can oxidize carbohydrates, is non-lipolytic, can liquefy gelatin slowly, and 
hydrolyses starch weakly or not at all.  Amino acids required for growth 
include biotin, nicotinic acid and thiamine.  The optimum temperature for 
growth is about 79 F; minimum and maximum temperatures are 34 and 95 F, 
respectively.  The pathogen can be maintained in a viable and virulent 
condition in nutrient agar at 55 F for at least 58 months.  Yellow, white, and 
pink forms of the bacteria occur; the yellow and white forms are most virulent.
 
D.  Disease Cycle and Development:
        The bacterial canker pathogen can survive in the absence of living 
tomato plants on and in seed, up to 2.5 to 5 years in soil, 2 years in compost, 
10 months associated with wooden tomato stakes, in dead stems and 
possibly other refuse from diseased plants, and in perennial solanaceous 
weed hosts.  The pathogen also can persist in association with living tomato 
plants when tomatoes are grown continuously throughout the year; this can 
occur where greenhouse and field culture periods overlap in the temperate 
zone and where successive field plantings overlap in tropical and 
semi-tropical areas.

        Widespread dissemination of the pathogen probably has occurred via 
seeds and transplants.  More localized spread, and sometimes inoculation, 
occurs by wind, rain, running water, insects, and by man and implements 
used during transplanting, cultivation, trellesing, pruning, pollinating, 
spraying, and harvesting.

        Primary disease cycles can start from any of the sources of inoculum 
that survive.  Infection appears possible through stomates but is more likely 
through wounded areas.  Broken hairs and trichomes likely are important 
infection courts.  Such wounds may be caused by movement of plants 
associated with wind, rain, and cultural practices.  After infection, the 
pathogen can move systemically through the xylem from which it invades 
the phloem, pith, and cortex.

        Secondard spread can occur in seedbeds and in production fields.  
Inoculum may be bacterial cells exposed on the surface of cankers and on 
stem, leaf and fruit spots.  Another source is bacteria inside plants; these 
bacteria can be moved to other plants on knives and implements during 
pruning and cultivation.  The pathogen can be spread and infection can occur 
as a result of "clipping", a pruning practice sometimes used in outdoor 
transplant production beds.  Apparently, secondard spread can be very 
effective since incidence of disease in seedbeds is reported to have increased 
from 1% infection associated with infected seed, to 100% infection of 
transplants.

        Disease is promoted by environmental conditions that favor succulent 
growth of tomato plants.  Specific conditions that favor disease development 
include an air temperature of 75 to 90 F, a predisposing period when soil or 
air temperature is several degrees higher or lower than 75 F, optimum 
moisture conditions for plant growth, relatively low light intensity, high 
nutrient concentrations, and a pH of 8.  Symptoms appear sooner in younger 
plants than in older plants.  Symptoms are more severe in sandy soil than in 
organic soil.  Fruit infection, which results in "bird's eye" symptoms, is 
favored by sprinkler irrigation which wets fruit; this symptom seldom occurs 
in greenhouses where fruit are not sprinkled during watering.
 
E.  Control:
        The most effective controls are those which reduce initial inoculum 
important in primary disease cycles.  The disease probably can be prevented 
by following an adequate crop rotation, eradication of solanaceous weeds, 
using only disease-free seeds and transplants, spraying seedlings two to four 
times in plant beds with streptomycin sulfate at 200 ppm, and use of 
pathogen-free stakes and other materials used in trellesing.  Three effective 
seed treatments are a 132 F hot water soak for 30 minutes, a 1.05% sodium 
hypochlorite soak for 20 or 40 minutes, and a 5% hydrochloric acid soak for 
5 or 10 hours.

        Secondary spread in production fields can be minimized by avoiding work 
in tomatoes when they are wet, and can be slowed to provide about 50% control 
by use of copper sprays applied at regular 5- to 7-day intervals.  Where needed 
copper sprays can be combined with sprays used for control of fungus blights 
and fruit rots.  Some researchers who recommend copper sprays for bacterial 
canker control also believe that the act of spraying is correlated with 
increased bacterial disease pressure, presumably because the air pressures 
from sprayers are breaking hairs and trichomes and creating infection sites 
for the bacteria.

        Various resistance sources are present in at least three species of 
Lycopersicon.  Varieties with resistance include Bulgaria 12, Utah 737, Utah 20, 
and H2990.  Campbell 28 and Heinz 1350 are less susceptible than Highland 
which is very susceptible.  Resistance is associated with several quantitative 
and incompletely dominant major genes that are influenced by modifying genes.

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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.

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