Bacterial Soft Rots of Vegetables 359
soil, after they are set or formed in the soil. T h e se infections usually take place through wounds, since the softrot bacteria cannot pene -trate tissues directly. However, under certain conditions the bacteria can invade tubers through lenticels. T h e inoculation of bacteria into fleshy organs and their further dissemination are greatly facilitated by the seed-corn maggot and other insects which very effectively spread infection both in storage and in the field. T h e soft-rot bacteria can live in all stages of the insect. Moreover, the bodies of the insect larvae (maggots) b e c o me contaminated with bacteria w h en they crawl about in infested soil or on rotting s e ed pieces. Therefore, when such in-sects attack healthy plants or storage organs by boring holes into them, not only do they carry the bacteria to the plants, but they put the bac-teria into the plants where they can surely cause the disease. E v en when the plants or storage organs are resistant to soft rot and can stop its advance by formation of wound-cork layers, if borers are present they destroy the w o u nd cork as fast as it is formed, so that the wounds never heal and the soft rot continues to spread.
Whe n the soft-rot bacteria enter w o u n ds or are otherwise brought in contact with parenchymatous cells, they fee d and multiply at first on the liquids released by the broken cells on the w o u nd surface or on liquids in the intercellular spaces. Inoculation is followed by rapid multiplication of the bacteria, which produce increasing amounts of pectolytic and, in lesser quantity, cellulolytic enzymes. T h e pecto-lytic enzymes break down the pectic substances of the m i d d le lamella and of the cell wall and cause maceration of the tissues. T h e cellulo-lytic enzymes cause partial breakdown and softening of the cellulose of the cell walls. As a result of the action of these and other enzymes water from the protoplasts diffuses into the intercellular spaces; the cells plasmolyze, collapse, and die. T h e bacteria continue to m o ve into and to multiply in the intercellular spaces, while their enzymes advance a h e ad of them and prepare the tissues for invasion. Intact cells are not ordinarily invaded by bacteria, but collapsed cells with broken-up walls are. Whe n tuberous or rhizomatous plants are in-fected in the field, bacteria can m o ve into and spread through the xy-lem vessels of the plants where they interfere with the u p w a rd move-ment of water.
T h e elimination of the cementing properties of the m i d d le lamella through liquefaction of its pectic substances, and the exosmosis of water from the protoplasts into the intercellular spaces result in the softening of the invaded tissues and their transformation into a slimy mass. This mass consists of innumerable bacteria s w i m m i ng about in the liquefied substances and a m o ng the unbroken walls of collapsed parenchymatous cells or of unaffected lignified tissues. Although the
epidermis of most tissues is not attacked by the bacteria, cracks of var-ious sizes are usually present and the slimy mass extrudes through them into the soil or, in storage, it comes into contact with other fleshy organs, which are subsequently infected.
Control
T h e control of bacterial soft rots of vegetables is b a s ed almost exclu-sively on sanitary and cultural practices. All debris should b e removed from warehouses and the walls should b e disinfested with solutions containing formaldehyde, copper sulfate, or mercuric chloride.
Wounding of plants and their storage organs should b e avoided as much as possible. Only healthy plants, tubers, fruit, etc., should b e stored. Whe n ne w infections appear in storage, infected organs should be removed quickly and burned. Products to b e stored should b e dry and the humidity of warehouses should b e kept low if infections are to b e avoided. Temperatures around 4 °C in storage houses inhibit devel-opment of ne w soft-rot infections. Leafy vegetables should b e cooled to 4 - 6 °C immediately on arrival.
In the field, plants subject to soft rot infection should b e kept free of surface moisture by planting in well-drained areas, by allowing suffi-cient spaces among plants for adequate ventilation, and by avoiding overhead irrigation. Plants very susceptible to soft rot should b e ro-tated with cereals, corn, or other nonsusceptible crops. Although s o me varieties are less susceptible than others, few are noted for their resist-ance to soft rot and none is immune.
Chemical sprays are generally not r e c o m m e n d ed for the control of soft rots, except for soft rot of tomato fruit which can b e r e d u c ed by repeated applications of Bordeaux mixture. Spraying or dusting with insecticides, however, to control the insects which spread the d i s e a se has b e e n effective in reducing infections both in the field and in stor-age. Certain antibiotics, such as streptomycin, have b e e n shown to reduce infections when sprayed on plants in the field or on stored products in warehouses. Unfortunately these cannot b e u s ed b e c a u se they leave unacceptable residues on the crops.
Selected References
Ark, P. Á., a nd C. M. T o m p k i n s. 1938. A soft-rot bacteriosis of p u m p k in fruits. Phyto-pathology 28: 3 5 0 - 3 5 5 .
B o n d e, R. 1955. Antibiotic treatment of s e ed potatoes in relation to s e e d - p i e ce decay, blackleg, plant growth, a nd y i e ld rate. Plant Disease Reptr. 39 : 120-123.
Bacterial Wilt of Cucurbits -midity index for p r e d i c t i ng the occurrence of bacterial soft rot of Irish potatoes.
Phytopathology 49: 7 0 1 - 7 0 5 .
Smith, W. L., Jr. 1955. Streptomycin sulfate for the reduction of bacterial soft-rot of p a c k a g ed spinach. Phytopathology 4 5 : 8 8 - 9 0 .
Walton, G. S., a nd R. A. C a p p e l l i n i. 1962. Pectolytic a nd cellulolytic e n z y m es p r o d u c ed by Erwinia carotovora. Phytopathology 52 : 9 2 7 (abstr.).
Bacterial Wilt of Cucurbits Occurrence and Importance
Bacterial wilt of cucurbits is found in all the United States, although it is most severe in the eastern half of the country. It also occurs in central and northern E u r o p e, in South Africa, and in Japan. It affects many cultivated and wild species of plants of the family Cucurbita-ceae. C u c u m b er s e e ms to b e the most susceptible host to the d i s e a s e, followed in susceptibility by muskmelon, squash, and pumpkin. Wa-termelon is extremely resistant or i m m u ne to bacterial wilt.
Bacterial wilt affects plants by causing s u d d en wilting of foliage and vines and finally death of the plants. It also causes a slime rot of squash fruit in storage. T h e severity of the d i s e a se varies widely in different seasons and localities from an occasional wilted plant up to a destruction of 7 5 - 9 5 % of the crop. T h e percentage of infections and severity of the d i s e a se in an area are closely related to the prevalence of c u c u m b er beetles in the area, to the condition of vigor in the host plant, and to the weather conditions.
361
F i g. 68. Bacterial wilt of c u c u m b er c a u s ed by Erwinia tracheiphila. (Photo by cour-tesy of the D e p a r t m e nt of Plant Pathology, Cornell University.)
Symptoms
T h e first symptoms of bacterial wilt appear as drooping of one or more leaves of a vine; this is soon followed by drooping and wilting of all the leaves of that vine and quickly afterward by wilting of all leaves and collapse of all vines of the infected plant (Fig. 68). Wilted leaves shrivel and dry up; affected stems first b e c o me soft and pale but later they, too, shrivel and b e c o me hard and dry. Symptoms in less suscep-tible plants or under unfavorable conditions d e v e l op slowly and may b e accompanied by r e d u c ed growth and, occasionally by excessive blossoming and branching of the infected plants. Whe n infected stems
Bacterial Wilt of Cucurbits 363
are cut and p r e s s ed b e t w e en the fingers, droplets of bacterial ooze appear on the cut surface. T h e viscid sap sticks to the finger or to the cut sections and if they are gently pulled apart the ooze forms delicate threads that may b e extended for several centimeters. T h e stickiness and somewhat milky appearance of the sap of infected plants are fre-quently u s ed as diagnostic characteristics of the disease although they are not entirely d e p e n d a b l e.
T h e slime of stored squash progresses internally and may cause the spoilage of every portion of the fruit while the exterior surface of the fruit may appear perfectly sound. Usually, however, as the internal rot progresses there appear on the surface dark spots or blotches which coalesce and enlarge. T h e d i s e a se develops over several months in storage. Infected squash fruits are further invaded by soft-rot microor-ganisms and are completely destroyed.
The Pathogen: Erwinia tracheiphila
T h e pathogen of bacterial wilt of cucurbits is a rod-shaped bacteri-um, 1-2.5 μ long by 0.5-0.7 μ wide. In 4- to 5-day-old cultures many of the bacteria appear coccoid (i.e., spherical), with a diameter of 1.5 μ.
T h e ratio of coccoid to rod-shaped bacteria in culture increases with time until in 2-week-old cultures few rods remain. Later, however, the coccus forms disintegrate and only occasional rods may b e found in-tact. T h e bacteria exist singly or in pairs, do not produce capsules, and are facultatively anaerobic. E a ch bacterial cell has 4-8 peritrichous flagella.
Erwinia tracheiphila is very sensitive to drying and does not sur-vive in infected, dried, plant tissue for more than a few weeks. It survives, instead, in the intestines of striped cucumber beetles (Acalymma vittata) and spotted cucumber beetles (Diabrotica uncimpunctata) on which the cucurbit wilt bacteria are completely de-p e n d e nt for dissemination, inoculation, and overwintering (Fig. 69).
Development of Disease
T h e cucurbit wilt bacteria hibernate in the digestive tracts of a few overwintering striped cucumber beetles and spotted cucumber b e e -tles. In the spring these insects fee d on the leaves of cucurbit plants, on which they cause d e e p wounds. T h e bacteria are deposited in these wounds with the feces of the insects. S w i m m i ng through the droplets of sap present in the wounds, the bacteria enter the xylem vessels where they multiply rapidly and spread to all parts of the plant (Fig. 69). Penetration through stomata does not take place.
Fig. 69. Disease cycle of bacterial wilt of cucurbits caused by Erwinia tracheiphila.
Entire plant wilts and dies
~ Bacteria overwinter •in the striped and spotted cucumber é beetles
<\Beetles feed on /and contaminate J cucurbit plants
v Beetles lay egqs# ,jn near young cucurbit plants I ^Emerging adults become contaminated with LVU bacteria upon feeding xVlon infected r\t\ plants.
^.Larvae pupate NOjn soil
^The larvae attack (young cucumber /Xplants <^ Bacteria spread to 1 ^^rtrtsJ>ther vine \ Infected ' V ' fftpway^ vine wilts
Bacteria fill L and clog vessels Ί of the plant * Bacteria^lk spread to^^ adjacent \1 vessels throughl dissolved walls ll
Bacteria in vessels\ of vine vascular/ bundles \
Bacteria enter\v\ xylem vessels of leaf \v veins and move down \ the petiole and vine he cucurbit wilt bacterium Bacteria multiply in sap at the margins of wound
Bacteria are deposited with the insect feces . on leaf wounds ^
Bacterial Wilt of Cucurbits 365
As the bacteria multiply in the xylem they produce extracellular slimy polysaccharides which, together with the bacterial cells, cause a mechanical obstruction of the vessels and so reduce the efficiency of the water-conducting system of d i s e a s ed plants. Furthermore, gum deposits are commonly found in the xylem elements of infected plants and in s o me wilting plants tyloses are also present. In s o me instances the p r e s e n ce of gums and/or tyloses appears to b e as important in plugging the transpiration stream as the polysaccharides and the bac-teria. Whe n wilt symptoms b e g in to appear the transpiration rate of infected plants is lower than that of healthy ones and steadily de-creases as wilting proceeds. Stems of wilted plants allow less than one-fifth the normal water flow, indicating that an extensive p l u g g i ng of the vessels is the primary cause of wilting. It is also possible that wilting is e n h a n c ed by the softening of the vessel walls and collapse of the vessels d ue to the action of cellulolytic enzymes secreted by the pathogen and by the p r e s e n ce of toxic, wilt-inducing substances re-l e a s ed by the pathogen in the xyre-lem and transported to are-lre-l parts of the plant. T h e excessive b l o s s o m i ng and branching observed in plants showing slow d e v e l o p m e nt of the d i s e a se indicate an interference by the pathogen with the balance of growth regulators in the infected plants.
S p r e ad of the bacteria from one plant to another is achieved primar-ily through the striped and the spotted c u c u m b er beetles and to a smaller extent through other insects, such as grasshoppers. Whe n these insects fee d on infected plants their mouthparts b e c o me con-taminated with the wilt bacteria. Later the beetles move on to healthy plants and carry with them bacteria which they place in the ne w wounds they make upon feeding on the healthy plants. E a ch contami-nated beetle can infect at least three or four healthy plants after one feeding on a wilted plant, although s o me beetles are capable of spreading infection for more than three weeks after one wilt feeding.
Only a rather small percentage of beetles, however, b e c o me carriers of bacteria. Infections take place only w h en a film of water is present on the tissues and allows the pathogen to reach the w o u nd and m o ve into the xylem vessels. T h e first wilt symptoms appear 6 or 7 days after infection and the plant is usually completely wilted by the fifteenth day. T h e bacteria present in the vessels of infected plants die within one or two months after the d e ad plants dry up. T h e bacteria are also incapable of surviving the winter in the soil and in or on s e e ds from infected plants.
Fruit infection of squash plants usually takes place through infected vines, but it is also possible through the blossoms and the rind of the
squash by beetles which fee d on the blossoms and the fruits during the growing season.
Ther e is considerable variability in the virulence of different iso-lates of Erwinia tracheiphila. Also, the different cucurbit species and their varieties show varying degrees of resistance to this pathogen.
Furthermore, this disease is strongly influenced by certain environ-mental factors. T h u s, the greater the number of cucumber beetles in an area, the younger and more succulent the plants, and the more humid the weather, the greater the number of plants that will b e c o me d i s e a s ed and the more severe the symptoms.
Control
Bacterial wilt of cucurbits can b e controlled best by controlling the cucumber beetles; in addition to the d a m a ge they cause by chewing the plant parts, they also transmit the wilt-causing bacteria. Insecti-cides, such as carbaryl (Sevin), methoxychlor, and rotenone are u s ed to control cucumber beetles. Control of the early beetles is most im-portant in limiting or eliminating the primary infections of plants and the multiplication and secondary spread of the pathogen.
Sprays containing copper give fair protection to cucurbit plants from b e c o m i ng infected with the wilt bacteria, but copper stunts young cucurbit plants. Captan or ziram are sometimes u s ed with the insecti-cides, although their effectiveness is questionable.
Antibiotics such as streptomycin S T S, Terramycin and neomycin, when applied at fairly high concentrations (500 ppm) before inocula-tion of the plants with the bacteria, gave good control of the wilt in the greenhouse. Streptomycin and Terramycin also controlled the disease in the field. At these concentrations, however, they were toxic to the plants.
To avoid squash rot in storage only fruit on healthy plants should b e picked and it should b e stored in a clean, fumigated warehouse.
Several varieties within each cucurbit species are resistant to bac-terial wilt. T h e se should b e preferred to more susceptible ones.
Selected References
B u d d e n h a g e n, I., a nd A. K e l m a n. 1964. Biological a nd physiological aspects of bacterial wilt c a u s ed by Pseudomonas solanacearum. Ann. Rev. Phytopathol. 2: 2 0 3 - 2 3 0 . Burkholder, W. H. 1960. S o me observations on Erwinia tracheiphila, the c a u s al a g e nt of
the cucurbit wilt. Phytopathology 50: 179-180.
Bacterial Canker and Gummosis of Stone Fruit Trees 367
Yu , T. F. 1933. Pathological a nd physiological effects of Bacillus tracheiphilus E. F.
Smith on s p e c i es of cucurbitaceae. Nanking Univ., Coll. Agr. Forestry Bull. 5.
Bacterial Canker and G u m m o s is of Stone Fruit T r e e s Occurrence and Importance
This d i s e a se apparently occurs in all major fruit growing areas of the world. It has b e e n reported from E u r o p e, North and South America, Australia, Africa, and Japan. It affects primarily stone fruit and citrus trees. T h e s a me pathogen also affects pear, lilac, rose, and many other annual and perennial ornamentals, s o me vegetables and some small grains. T h e pathogen causing bacterial canker and gummosis occurs in numerous strains, each of which will attack s o me but not all the hosts that d e v e l op the d i s e a s e, although the host range of an isolate usually overlaps somewhat with the host ranges of other isolates. T h e d i s e a se is also known as b ud blast, b l o s s om blast, dieback, spur blight, and twig blight.
Bacterial canker and gummosis is one of the most important dis-eases of stone fruit trees in many fruit growing areas. Exact losses are difficult to assess b e c a u se of serious d a m a ge to trees as well as reduc-tion of yields. T h e d i s e a se affects trees by causing cankers on branches and main trunks, killing young trees, and reducing the yield of or killing older ones. T r e e losses which vary from 10 to 7 5 % have b e e n observed in young orchards. Bacterial canker and gummosis also kills b u ds and flowers of trees, usually resulting in yield losses of 1 0 - 2 0 % but sometimes up to 8 0 %. L e a v es and fruits are also attacked, resulting in weaker plants and in low quality or unsalable fruit.
Symptoms
T h e most characteristic symptom of the d i s e a s e, although not al-ways the most common or the most destructive on all hosts, is the for-mation of cankers accompanied by gum exudation (Fig. 70). Cankers on cherry, peach, apricot, and other trees usually d e v e l op at the b a se of an infected spur. T h e y then spread mostly upward and to a lesser extent down and to the sides. Infected areas are slightly sunken and darker brown in color than the surrounding healthy bark. T h e color of the cortical tissues of the cankered area varies from bright orange to brown. Narrow brown streaks extend into the healthy tissue above and b e l ow the canker. Cankers are first noticed in late winter or early spring. As the trees break dormancy in the spring, g um is produced by the tissues surrounding most cankers, breaks through the bark, and runs down on the surfaces of the limbs. Cankers in which gum is not produced are similar, but usually are softer, more moist, sunken, and may have a sour smell. Cankers on plums start as small, brown to red-dish-brown spots that enlarge as water-soaked streaks. In the spring the area b e t w e en the streaks b e c o m es uniformly brown and moist.
Usually little, if any, gum is e x u d ed from the affected p l um tissues, but a watery material may flow on the limb from cracks in the bark. As the infected area dries out cracks appear around the margin of the canker. Whe n the trunk or branch of a tree is girdled by a canker the leaves above the girdle show an inward curling and drooping, then a light green color, and then yellow. Within a few weeks the branch or entire tree above the canker is d e ad (Fig. 71).
Dormant b ud blast is more serious on cherry, apricot, and pear than
Dormant b ud blast is more serious on cherry, apricot, and pear than