Bacterial and Viral Diseases of Plants | Botany

In this article we will discuss about the bacterial and viral diseases of plants.

Bacterial Diseases of Plants:

The first recorded observation on a bacterial disease of plants dates back to the work of Burrill (1881), who discovered the causative organism of pear blight. This work was confirmed by Waite (1891), who isolated the etiological agent and proved its pathogenicity. Since then a large number of bacterial plant pathogens have been isolated and described. It is safe to assume that there are as many bacterial diseases of plants as of man and animals.

Before an organism can be stated definitely to be the causative agent of a plant disease, it must be isolated from the plant tissue and its pathogenicity proved beyond doubt. Koch (1883) postulated certain requirements that should be met before an organism could be said to be the cause of a specific disease. These requirements have been generally accepted by both plant and animal pathologists.

The bacterial diseases of plants may be placed into five groups on the basis of the location and character of the lesions produced:

(1) Soft rots,

(2) Vascular diseases or wilts,

(3) Blights,

(4) Intumescence diseases, and

(5) Local lesions or spots.

1. Soft Rots:

Organisms responsible for soft rots reduce the plant tissue to a soft, very moist, pulpy mass. The condition may be better recognized as a state of rottenness. The attack may or may not be due to a specific organism.

The organisms producing soft rots differ from other forms found in soil in that they attack healthy plant tissue by the secretion of an extracellular protopectinase. The enzyme dissolves the pectin or cement-like material that binds the plant cells. The action is probably hydrolytic, resulting in the liberation of soluble sugars which are utilized by the bacteria for food. The plant becomes reduced to a mass of separate cells, which become converted later into a slimy, pulpy material.

In most cases, the specific organism is accompanied or closely followed by many saprophytic soil bacteria and fungi. These organisms find a favourable environment in the exposed cells and produce relatively large quantities of ammonia by the deaminization of the amino acids present in the proteins of dead plant tissue.

The ammonia produces a destruction of the neighbouring plant cells and rapidly reduces the plant to a slimy, pulpy, foul-smelling mass. The unpleasant odor is due to the secondary invaders. Plants decayed by pure cultures of the specific disease organisms do not give off an objectionable odor.

The organisms causing soft rots are members of the genus Erwinia. The important species include the following: E. ananas, the cause of brown rot of the fruitlets of pineapple; E. aroideae, the cause of soft rot of calla, potato, eggplant, cauliflower, radish, cucumber, cabbage, parsnip, turnip, and tomato; E. atroseptica, responsible for black rot of stem and tuber of potato and other vegetables; E. carotovora, the cause of black rot in carrot, cabbage, celery, cucumber, eggplant, iris, muskmelon, hyacinth, onion, parsnip, pepper, potato, radish, tomato, turnip, and other plants; E. chrysanthemi, responsible for a soft rot on many fleshy vegetables; E. dissolvens, isolated from rotting corn stalks; and E. rhapontici, the cause of crown rot of rhubarb.

2. Vascular Diseases or Wilts:

The bacterial wilts constitute a group of very important and destructive diseases of plants. The infecting organisms multiply and accumulate in large numbers in the vascular system, causing an interruption in the flow of sap in the plant. A complete interruption in the flow of sap results in a rapid wilting of the plant. A partial interruption results in the growth of a sickly plant which makes poor headway and finally dies. In some cases death is due to the action of secondary invaders.

Some important organisms causing wilt diseases are Xanthomonas stewartii, the cause of wilt disease of com; Corynebacterium insidiosum, the agent of vascular disease of alfalfa; C. michiganense, the cause of canker of tomato; Erwinia tracheiphila, the etiological agent of wilt of cucumber, cantaloupe, muskmelon, pumpkin, and squash; Pseudomonas solanacearum, the cause of brown rot of potato, tobacco, and tomato; Xanthomonas vasculorum, the causative organism of gummosls of sugar cane.

3. Blights:

Organisms producing blight diseases are capable of penetrating considerable distances between cells, leaving the neighbouring tissue intact. The bacteria grow in the plant juices without producing any digestion of the tissues. The rods produce usually a dis-colouration of the leaves and branches. Death is due probably to an interference with the flow of plant sap.

Some of the organisms producing blights are Erwinia amylovora, the agent of fire blight or pear blight, isolated from the blossoms, leaves, and twigs of pear and apple trees; Pseudomonas medicaginis, the etiological agent of stem blight of alfalfa, isolated from brown lesions on the leaves and stems; P. mori, the cause of mulberry blight, isolated from blighted shoots; P. pisi, the agent of stem blight of field and garden peas, isolated from water-soaked lesions on stems and petioles; Xanthomonas jugtandis, the cause of walnut blight, isolated from black spots on the leaves and nuts of English walnuts; and X. phaseoli, the cause of blight of bean, hyacinth bean, lupine, and other plants.

4. Intumescence Diseases:

Some bacteria produce galls or tumors on plants. These excrescences or abnormal growths are produced by the action of certain organisms on the meristematic tissue of the plants. Tissues infected in this manner are grouped under the intumescence diseases.

In some infections the galls remain small; in others they may assume large proportions. Sugar beets have been known to carry tumors larger than the original plants. The bacteria are believed to elaborate some irritating metabolic product that causes rapid division of the neighbouring plant cells. Some believe that tumor infections in plants are similar to cancerous growths in man and animals. Intracellular organisms are not necessary for the development of the characteristic lesions.

The important organisms producing intumescence diseases include Agrobacterium gypsophilae, the cause of galls on Gypsophila paniculata and related plants; A. rhizogenes, the agent producing hairy root of apple and other plants; A. rubi, the cause of cane gall on raspberries and blackberries; A. tumefaciens, the etiological organism of galls on Paris daisy; A. pseudotsugae, the cause of galls on Douglas fir in California; Corynebacterium fascians, the agent of fasciation on sweet pea, chrysanthemum, geranium, petunia, tobacco, etc.; Pseudomonas savastanoi, the etiological organism of olive galls; P. tonelliana, the cause of oleander galls; and Xanthomonas beticola, the cause of galls on sugar beets and garden beets.

5. Local Lesions or Spots:

In many plant diseases the attack is restricted to a small area around the point of entry. These diseases are grouped under local lesions or spots. The organisms responsible for leaf-spot diseases produce a vigorous attack on the plant, with the result that the cells become heavily infected and strongly dis-coloured. The dis-coloured areas dry up and frequently fall out, leaving holes in the leaves.

Some of the organisms causing leaf-spot diseases are Pseudonwnas angulata, the agent of angular leaf spot of tobacco; P. maculicola, the cause of cauliflower spot; P. mellea, the etiological agent of leaf spot of tobacco; Xanthomonas cucurbitae, the cause of leaf spot of squash and related plants; X. malvacearum, the agent of angular leaf spot of cotton; and X. ricinicola, the cause of leaf spot of castor bean.

Mode of Infection:

The mode of entry of bacteria into the plant is usually through wounds. Roots, leaves, and stems are easily injured mechanically by means of agricultural implements, by animals, etc. Plants become easily infected following injury to the roots, whereas sound plants remain free from bacterial attack.

Hailstones are known to produce injury to plants and make them vulnerable to infection. However, the usual cause of plant injury is through the bite of various insects. Sometimes the insects carry the etiological agent on their mouth parts, making it possible to injure and infect the plant in one operation.

In many of the leaf and fruit infections, the organisms gain entry through natural openings known as stomata. The organisms pass from the stomata into the intercellular spaces. The bacteria greatly reduce the resistance of the cells by suffocation or poisoning and make it possible for the etiological agent to enter the affected plant cells.

Bacteria may enter plants by way of the hydathodes or organs for the excretion of water. An excessive elimination of water results in the collection of considerable moisture on the plant surface. Bacteria readily collect in the water droplets, making it possible for some to gain entrance to the plant.

Lenticels are also unprotected openings, which may offer bacteria a path for invasion of the plant. These organs are cortical pores in the stems of woody plants through which air penetrates to the interior.

Many insects are responsible for plant infections. Their proboscises or legs act as carriers of bacteria that are capable of attacking the plant. This is especially true of those plants which produce nectars designed to attract bees and other insects for the fertilization of flowers.

Viral Diseases of Plants:

A virus may be defined as a disease-producing agent, often referring to one too small to be seen with the usual light microscope.

Viruses show the following characteristics:

i. They are very small, being generally below microscopic visibility. However, they may be seen by the electron microscope.

ii. They maintain themselves only within certain specific living cells.

iii. They produce typical and similar disease in suitable hosts in unbroken series.

iv. They are antigenic, being capable of stimulating antibody production when introduced into an animal body.

v. They show great capacity for variation.

Iwanowski (1892) was probably the first to report the existence of ultramicroscopic particles capable of producing disease. He showed that the agent causing tobacco mosaic disease passed through a filter that retained all of the bacteria then known. Since that time many filter passing agents causing diseases of plants, animals, and bacteria have been discovered. Viruses vary considerably both in size and shape.

Tobacco mosaic virus is rod-shaped; the viruses of tomato bushy stunt, southern bean mosaic, tobacco ring-spot, brome grass mosaic, turnip yellow mosaic and squash mosaic are spherical in shape. They are non-motile and are not known to multiply by fission as do the bacteria.

There are probably more plant diseases caused by viruses than by bacteria. They are the causes of some of the most destructive diseases of agricultural crops. It is safe to say that almost all cultivated plants are affected by at least one virus. It is not uncommon to encounter plants affected by two or more viruses.

For example, the potato is susceptible to at least 25 viruses, and the tobacco plant to at least 12 virus infections. Because of these multiple infections it is often very difficult, if not impossible, to identify a virus by the symptoms produced.

Nature of Plant Viruses:

The exact nature of plant viruses is not clearly understood. Some believe they are living particles of submicroscopic size which develop by multiplication of pre-existing forms. Others are of the opinion that plant viruses are not living organisms but autocatalytic bodies capable of producing an injurious action in a susceptible plant cell with the result that the cell is stimulated to produce more virus of the same kind.

The cell is eventually destroyed, after which the autocatalytic agent spreads to other cells of the host. Supporting this belief is the work of Stanley (1935), who isolated the virus of tobacco mosaic (TMV) disease from infected tobacco and cucumber plants in the form of fine, needle- shaped rods or crystals in a high state of purity which were capable of reproducing the disease in healthy plants.

Chemical Structure of Plant:

Viruses. Stanley (1935) isolated from Turkish tobacco plants, diseased with tobacco mosaic, a high-molecular weight crystalline ribonucleoprotein that possessed the properties of TMV. Repeated recrystallization failed to change the infectivity of the crystals. The virus crystals have been shown to be composed of pure ribonucleoprotein molecules.

Similar crystals have also been obtained from unrelated plants diseased with TMV. The reports of Stanley on TMV have stimulated work on other agents causing plant diseases, with the result that a number of different viruses have been obtained in crystalline form.

Tobacco Mosaic Virus:

Many strains of TMV have been recognized in nature. The virus nucleoproteins isolated from various sources are similar in physical and chemical properties, yet different from each other and from ordinary TMV. A virus may become modified after cultivation in an unnatural host.

Such a modified virus is probably accompanied by a change in the physical and chemical properties of the specific nucleoprotein. Therefore, typical symptoms of a plant virus disease are produced only by a non-mutated strain inoculated into a natural host plant.

Molecular Weight of TMV:

By means of chemical and X-ray determinations, Franklin and Holmes (1956) reported that the molecular weight of TMV was about 40 x 10⁶, or approximately 40 million. Ginoza and Norman (1957) by means of X-ray inactivation studies concluded that the molecular weight of the infectious nucleic acid portion of the nucleoprotein was between 2 and 3 million. The two components were present in the proportion of about 1 part nucleic acid to 10 parts protein.

Reconstitution of Tobacco Mosaic Virus:

Fraenkel-Conrat and Williams (1955) isolated native protein and ribonucleic acid from TMV by treatment with pH 10.5 buffer and the detergent sodium dodecyl sulfate. Free ribonucleic acid was shown to be infectious, whereas the protein component was devoid of this characteristic. At pH 6.0 a mixture of these components was shown to reconstitute active virus.

Typical lesions of tobacco mosaic were produced in susceptible plants, indicative of regeneration of up to 5 per cent of the original infectivity. Electron micrographs revealed rod-shaped particles indistinguishable from the original TMV particles. The rods contained about 5 per cent of ribonucleic acid as a central core surrounded by a helix of protein.

In later communications, Fraenkel-Conrat (1956) and Fraenkel-Conrat and Singer (1957) reported on mixed reconstitution experiments performed with protein and nucleic acid fractions isolated from different strains of TMV. The reconstitution of virus particles from protein and nucleic acid of different strains yielded very active preparations, one of which showed higher infectivity than one of its parent strains. The nature of the disease provoked by mixed virus preparations resembled in each case that characteristic of the virus supplying the nucleic acid.

In contrast to these properties, the serological characteristics of mixed virus preparations were those of the virus supplying the protein. In other words, immunological specificity is primarily an attribute of the protein, and infectivity of the nucleic acid.

Agents Responsible for the Dissemination of Viruses:

Probably all viruses causing plant diseases are disseminated by insects.

Other methods, of less importance, include:

(1) Wind,

(2) Water,

(3) Soil,

(4) Seed, and

(5) Pollen.

1. Wind:

Wind plays a minor role in the dissemination of plant viruses. However, there may be exceptions. For example, TMV is very resistant to desiccation and may be wind- borne in the form of dried, crumbled plant tissue. The virus is capable of readily infecting healthy plants through slight wounds.

2. Water:

Water appears to be of little importance in the spread of plant viruses. Here again there may be exceptions. It is possible to infect healthy plants with tobacco necrosis by bathing the roots in water containing the virus. The virus can infect healthy plants without artificial wounding.

3. Soil:

The soil itself is not an agent for the transmission of plant viruses. Infection may occur through roots and other underground parts of plants by soil water or by insects working in the soil. Since it is very difficult to observe underground parts of plants, the mechanism of infection by this route remains obscure.

However, it has been definitely shown that wheat mosaic virus may be transmitted underground through roots or the crown, or both. The virus is capable of surviving in the soil for some time and is difficult to remove by thorough washing. The mechanism for the entrance of the virus into plants is not known.

4. Seed:

Seed transmission of plant diseases does occur for some viruses. Bean mosaic virus is transmitted in this manner in about 50 per cent of plants under experimental conditions. The results are usually inconsistent. A plant may show both healthy and infected seeds. Plants of the family Leguminosae appear to be more susceptible to infection by this route than plants of other families.

5. Pollen:

Virus infections may be transmitted to seeds by pollen from infected plants. In the plant Jimson weed, up to 79 per cent of the seeds may become infected. Bean seeds may also be infected in this manner.

Insect Transmission:

The most important agents for transmitting plant viruses are insects. Some insects transmit the virus mechanically, others biologically. The former method occurs usually in those insects which have chewing mouth parts. The latter method occurs only in the sucking insects, but transmission by these insects is not always biological.

According to Leach (1940), biological transmission of plant viruses by insects has usually one or more of the following attributes:

i. An apparent multiplication or increase of the virus in the insect’s body.

ii. An incubation period in the body of the insect, i.e., a necessary period after feeding on infected plants before the insect becomes infective or viruliferous.

iii. A degree of specificity between the insect and the virus that it transmits.

iv. An obligatory relationship.

v. A relation between the age or life stage of the insect and its ability to transmit the virus.

vi. Congenital transmission of the virus from one generation to the next.