STONE FRUIT - BACTERIA

Occurrence and importance: Crown gall mostly damages saplings in nurseries and young trees, causing significant economic losses. It frequently attacks stone fruit species, propagating materials, vines, ornamental trees and dicots such as sunflower, geranium and dahlia. Plants with galls on their roots or root collar should be destroyed. The sale of plants with galls is prohibited. The pathogen is strictly soil borne and only attacks through wounds. The disease typically develops during the growing season. In dormancy, the development of galls is interrupted, while vegetative processes and nutrient uptake promote it. The bacterium is transferred from the dead galls to the soil, where it remains infective for years. The galls block water and nutrient transport in the root vascular bundles, resulting in severe lesions.

Symptoms and other disorders causing similar symptoms: The bacterium produces galls on the roots and the root collar. At first, small, pea-sized, white nodules appear and develop rapidly. Later they grow, fade, die and disintegrate, gradually turning dark brown. Infected trees wither and die. Vegetative and generative development is stunted. The pathogen prefers moist soils rich in nutrients.

Life cycle: The rod-shaped bacteria live singly or form short chains. A. tumefaciens does not produce spores. The cell is surrounded by mucus. The infectivity of the isolated strain is highly variable and can only be detected in young galls. The pathogen induces the proliferation of cells, which then continues in the absence of the bacteria. Diseased cells differ from the healthy ones in that they reproduce in an unusual way.

Control: Controlling crown gall is not easy. As it typically infects wounds, any method that reduces the number of wounds on the roots and the root collar will promote successful control. As a partial solution, the soil and propagating material may be disinfected before planting. There is no cure for the infection, so prevention is extremely important. Plants from infested areas should not be used. The sale of trees with galls is prohibited. Nurseries should screen their sticks for the disease.

Occurrence and importance: Fire blight is caused by the bacterium Erwinia amylovora (Burill) Winslow et al. It attacks 129 plant species belonging to about 33 genus of the family Rosaceae.

The disease is particularly important in young orchards. The bark of shoots and branches turns soft and dark. Cracks and wounds exude bacterial ooze. The pathogen enters the leaf tissue through wounds and natural openings, travels to the petiole through the leaf veins and from there into the vascular bundles of shoots. Young shoot tips bend over into a hook. Diseased flowers turn brown and black. From the flower, the bacterium invades the stalk and attacks the developing fruit. Fruit infection is common, especially after heavy rain and hail. Pathogenic bacteria are also present in the healthy-looking plant tissue of asymptomatic flowers, leaves and fruit. The pathogen overwinters under the cracked bark of infected twigs, branches and trunks or in canker wounds and starts reproducing there in spring before flowering. Fire blight is spread by pollen, insects, rain, wind, birds and human activity.

The disease occurs in about 40 countries around the world.

In Hungary, it was detected in 2019 in Mirabolan rootstocks and in the scions grafted on Mirabolan as a new pests^[1]. The disease typically occurs in wet, rainy years.

Control: Preventive mechanical control by removing shoots that show signs of infestation. Annual dormant spraying with copper (considering the period when stone fruit species are sensitive to copper). Removal of infected shoot tips when they appear.

Host range: cherry, plum, sour cherry, apricot, peach, almond.

Occurrence and importance: A common disease of stone fruit, particularly damaging to cherry, sour cherry and plum. It is present in most of Europe, with the most severe cases reported from England. Damage rate on flowers and shoots may be as high as 20-60%. Yield losses may be equally severe. In young orchards, partial or total mortality of the tree stock may result in serious economic damage.

Symptoms and other disorders causing similar symptoms: Symptoms most often occur around buds and on twigs. Infected twigs often fail to sprout and young shoots wither.

Life cycle: As the bacteria die by mid-summer, it may only be isolated in winter and spring. Pseudomonas mors-prunorum is a rod-shaped bacterium, 2.5 µ long and 0.5 µ wide, and moves by means of polar flagella. It infects plants through wounds, but in the autumn season it is also able to enter through leaf scars and multiply in the vascular bundles. In spring, the pathogen is transferred from canker cells to the young parts, where it persists as an epiphyte. In the autumn, before the leaves fall, when the weather is wet and the air humid, the bacterium multiplies and infects the plant. It attacks the buds and the surrounding tissue during the winter, causing them to die in the spring.

Control: Scheduling pruning properly in late spring can significantly reduce the risk of infection. Unnecessary injuries to plants should be avoided. Sealing plant wounds promotes rapid callus formation and thus reduce the likelihood of infection. Repeated spraying with chemicals containing copper at leaf fall and when the tree is dormant will also reduce the risk of infection. The number of bacteria multiplying on the surface of the leaves can be significantly reduced by this method.

Pseudomonas syringae triggers a very quick disease process. The sudden destruction is called apoplexy ('stroke') in everyday language. During summer months the bacterium lives on the surface of the branches and leaves without causing any symptoms, but in rainy autumn it can multiply and enter the cambium through wounds. Withering in spring is the result of an infection during winter. The decayed cortical tissue is replaced by cancerous wounds in open or closed forms. The stem is the most sensitive to the bacterial infection that may be triggered by bark splitting as a consequence of frost. 8-10-year-old trees are the most sensitive to the apoplexy disease.

The decay of the cortical tissue can be observed with difficulties from outside but a cross-section clearly shows the damage as it is brown and smells unpleasant. In such cases resin flow is common.

Disease cycle: As the bacteria infects through wounds, infections generally start from pruning sites. Decay occurs in spring or early summer. Physiological effects also play an important role in triggering apoplexy along with pathological factors. The presence of Leucostoma cincta fungus affects the seriousness of the disease to a large extent. This fungus weakens the plant and provides space for the disease to spread.

Control: Take advantage of late spring pruning. It is vital to seal wounds and sterilise pruning tools. Trunks must be left intact. Spraying with chemicals containing copper at leaf fall and at the end of winter will also reduce the risk of infection.

Stunted growth, mosaic mottling, distorted leaves and fruits (the latter with wrinkles and chlorotic or necrotic spots), reduced fruit size and the abortion of flowers have also been reported.

Transmission & Epidemiology: PVY is transmitted in a non-persistent manner, by at least 25 aphid species. Its most efficient vector is Myzus persicae (the green peach aphid), which colonises peppers. As Myzus persicae is able to retain the virus for more than 6 days.

Control:

• Remove/ destroy potato crops after the final harvest in order to minimise PYV spread to new crops.
• Destroy volunteer plants before planting to reduce PYV inoculum and aphid populations
• PYV-resistant varieties

 

Throughout insect vectors:

• protect hotbeds with nets to prevent early infection
• use coloured sticky traps to monitor vector populations
• control of the vector population by chemical, biological and/or integrated means
• oils

 

  

CUCUMBER MOSAIC VIRUS

Pathogen: Cucumber mosaic virus (CMV)
Host range: CMV has a very wide host range that includes more than 1000 plant species
Distribution: worldwide

Importance: CMV causes severe damage during flowering and in the yield. Its impact depends on the geographical area. Although it is distributed worldwide, the most significant losses are experienced under warm climates.

Symptoms: Young leaves often display a light-yellowish green mosaic mottling, which may develop into diffuse chlorotic lesions. Leaves get distorted, with curled main veins. On old leaves, chlorotic and/or necrotic concentric rings may appear, as well as irregular spots.

Fruit symptoms include reduced size, dark green spots, irregular ripening and/or sunken lesions with necrotic centres. The extent and severity of CMV symptoms is significantly affected by the age of the plant at the time of infection. When infected young, plants typically develop severe symptoms, including mosaic mottling, small and deformed leaves and reduced fruit size. In some cases, the disease may destroy the entire crop.

Transmission & Epidemiology: CMV is transmitted in a non-persistent manner by more than 86 aphid species. Myzus persicae (the green peach aphid) and Aphis gossypii (the cotton aphid) are two of the most efficient vectors.

CMV may also be transmitted by seeds.

 

Control:

Use virus-free propagative material (seeds, etc.)

Control of weed reservoir hosts

• eliminate weeds in the vicinity of the crop
• remove and destroy infected plants.

Chemical control of aphids

• protect hotbeds with nets to prevent early infection
• use coloured sticky traps to monitor the vector
• control of the vector population: chemical, biological and/or integrated control

Resistance breeding

The most effective methods of control are growing resistant varieties.

 

 

ALFALFA MOSAIC VIRUS

Pathogen: Alfalfa mosaic virus (AMV)
Host range: AMV infects a wide range of hosts, with about 600 species in 70 families being susceptible. Occasionally it may infect woody species.
Distribution:

Importance: Worldwide occurrence, commonly it does not cause economically significant damage, but in some cases, it may significantly reduce yields.

Symptoms: The bright yellow mosaic mottling on young leaves and their increasingly severe distortion are easily confused with the symptoms of other viruses.
On fully developed leaves, characteristic AMV symptoms may be observed including white blotches arranged in a mosaic pattern. In the summer, these symptoms are less important.
Fruits may be distorted and reduced in size and develop necrotic spots. These symptoms are particularly pronounced in the late cultivars.

Transmission & Epidemiology: AMV is transmitted in a non-persistent manner by aphids such as Myzus persicae Sulz. It may also be transmitted mechanically or by Cuscuta species in the field.

Control: 
Reduce viral inoculum levels:

• eliminate weeds in the vicinity of the crop
• remove and destroy infected plants.

 

Vector control to minimise transmission:

• protect hotbeds with nets to prevent early infection
• use of coloured sticky traps to monitor the vector
• control of the vector population: chemical, biological and/or integrated control

Produce virus-free seeds (e.g., seed treatment)

Isolation from other hosts (pepper, tobacco, peas etc.)

 

 

CAPSICUM CHLOROSIS VIRUS

Pathogen:   Capsicum Chlorosis virus (CaCV). It is a tospovirus (prototype TSWV), a member of the genus Orthotospovirus (family Tospoviridae) only identified on the island of Crete in EU (Greece) (EFSA Panel on Plant Health (PLH), et al. 2022).
Host range: CaCV infects plant species in the family Solanaceae (i.e. pepper, tomato) and ornamental plants.
Importance: Trade of plants (excluding seeds), ornamental plants, cut flowers, fruits and movement of soil and machinery contribute to further spread of the virus and/or viruliferous thrips to larger distances.
Symptoms:  CaCV can induce severe symptoms on its hosts, mainly on leaves and fruits. Main symptoms are:  frequently consisting of chlorosis, mottle. The young leaves show chlorosis, curling and deformation, whereas chlorosis, ringspot and line patterns develop on old leaves.

Transmission & Epidemiology: CaCV is transmitted in a persistent manner by thrips (similarly to TSWV).

Control:

Preventive measures should be applied to hinder thrips-transmission (similarly to TSWV).

 

TOMATO MOSAIC VIRUS

 

Pathogen:  Tomato mosaic virus (ToMV). It is an important member of the genus Tobamovirus.
Host range: The host range of ToMV is very wide (similarly to TMV).
Importance: ToMV has been reported from countries where tobacco, tomatoes or peppers are grown. ToMV is of greater economic importance than TMV and mostly damages greenhouse crops.
Symptom: Its most typical symptoms include mosaic mottling, deformed leaves, necrotic lesions and stunted growth.
The symptoms of ToMV are similar to those of TMV, but more intense, including dark greyish-brown stripes on the stems and branches, followed by the necrosis of the foliage and defoliation.
Transmission & Epidemiology: ToMV (similarly to TMV) is transmitted mechanically, by contact between healthy and infected plants or contaminated objects, similar to the transmission of TMV.
It is also transmitted by seeds in the case of certain members of the family Solanaceae.
It stays infective in plant debris and on contaminated objects for a very long time (persistent).
It may also be transmitted by Cuscuta species. 

Control: 
Preventive measures should be applied to hinder transmission.

• use healthy seeds
• disinfect tools
• isolate crops, remove and destroy infected plants
• use ToMV-resistant varieties

 

 

CANDIDATUS PHYTOPLASMA SOLANI (PEPPER STOLBUR)

 

Pathogen: Candidatus Phytoplasma solani (Stolbur phytoplasma)
Host range: Stolbur is able to infect practically any solanaceous plant and has also been found in sugar beet and field bindweed.
Distribution:

Importance: Stolbur regularly damage crops in droughty years in southern, eastern and central Europe. There is no chemical method available to control it.

Symptoms: The most important symptoms are the reddish discolouration of green parts, upward rolling of leaves, yellowing and defoliation. Flowers are malformed, have green petals and may develop into leaves. The disease urges the development of numerous shoots while stunting growth. The plant does not produce fruit or fruits are deformed.

Transmission & Epidemiology: Stolbur overwinters on perennial weeds, especially in the rhizomes of the field bindweed (Convolvulus arvensis). Its vector is the cicada Hyalesthes obsoletus (sometimes other cicada species, too). The insects pick up the disease when sucking on infected plants.

Stolbur is transmitted in a persistent manner. Infected cicadas, flying from plant-to-plant actively spread the disease during the summer. The incubation period of stolbur is long, so usually it is first detected in pepper fields in the late summer. Its vector is polyphagous and thus infects further bindweed specimens, promoting the persistence of the pathogen.

Control:

Proper weed control is of paramount importance, not only on the field itself, but also in its surroundings. Take special care to eliminate field bindweed.

There is no stolbur resistant cultivar. Dealers and distributors may say otherwise, but this is misleading.

Monitor the insects in the crop. When cicadas are spotted (they are difficult to find unless they jump or fly right in front of your eyes), precautions should be taken.