The following points highlight the four major diseases of wheat. The diseases are: 1. Rusts of Wheat 2. Hollyhock Rust of Wheat 3. Loose Smut of Wheat 4. Bunt of Wheat.
Contents
Disease # 1. Rusts of Wheat:
Wheat is attacked by three different rusts:
(i) Black rust or stem rust or black stem rust Puccinnia graminis Pers. f. sp. tritici Eriks. and Henn.;
(ii) Yellow or stripe rust, P. striiformis West; and
(iii) Brown or orange or leaf rust, P . recondita Rob. ex Desm.
Rusts of various crops are mentioned in ancient history. The writings of the Romans bear evidence that their cereal crops were attacked with rusts. During subsequent years rusts were reported from different countries of the world, but without realizing the actual reason behind the incidence.
It was Persoon in 1797, who recognized that the stem rust was due to the attack of a fungus Puccinia graminis. But the true life history of P. graminis was not known until 1865 when De Bary, by inoculation experiment, was successful to demonstrate that P. graminis needs two hosts- wheat and barberry to complete its life history.
Black rust or stem rust or black stem rust. (Puccinnia graminis Pers. f. sp. tritici Eriks. and Henn.). This disease is present in greater or less amount practically in every country throughout the world, where wheat is grown, and epiphytotics have been recorded in many countries. The disease is most damaging in moderately moist areas and in moist seasons in areas with low average rainfall.
Symptoms:
Black stem rust is characterized by the development of the ‘red rust’ or summer stage represented by the uredial stage appearing on leaves and culms, followed a little later by the ‘black rust’ or winter stage represented by the telial stage.
With the onset of the disease, elongated brown or reddish-brown pustules or sori burst through the epidermis of the host tissue (Fig. 368C). These pustules or uredia or uredosori split open in an irregular manner having an elongated crater-like opening with ruptured host epidermis clinging to one or both sides of the opening.
The size, shape and number of sori vary with environmental conditions and particularly with the inherent resistance of the host.
The uredosori may develop without any surrounding chlorotic or dead cells or they may be seated in chlorotic areas which soon become dead. They may be few in number, or they may be very numerous and may coalesce to form more or less elongated brown or rusty powdery streaks.
Within these sori are masses of reddish or rust-coloured powder consisting of thousands of minute dust-like uredospores. Later in the season the black rust stage or winter stage or telial stage appears. This consists of elongated pustules or telia or teleutosori similar in shape to the uredosori but black in colour. The black colour is due to the presence of masses of dark teleutospores they bear.
The teleutosori are dark-brown to black and are smooth rather than powdery, although the epidermis of the host tissue is broken and the teleutospores are exposed. The dark teleutospores are more firmly attached in their beds than the uredospores, and their stalks are more rigid and thicker.
They are essentially resting spores adapted for perennating on straw or stubble. The teleutospores on germination produce promycelia which again produce sporidia (basidiospores). The sporidia cannot infect the cereal host, and infect only the alternate host, the barberry (Berberis vulgaris L.).
On the barberry, small circular yellowish spots appear on the upper surface of the leaf. These spots increase in size, become margined with a brighter colour or reddish-purple and show a central cluster of minute honey-coloured pustules—sperm o- gonia from which minute droplets of nectar ooze out.
At more or less opposite places towards the lower surface of the leaf, yellowish or orange-coloured spots appear. Close examination of these spots on the lower surface of the leaf shows a cluster of small cups with saw-toothed edges—the aecia or cluster cups. Often the host tissue developing aecia may become hypertrophied. Similar hypertrophied cluster-cup lesions may appear on the fruits and petioles.
Causal Organism:
Black stem rust is caused by Puccinia graminis Pers. f. sp. tritici Eriks. and Henn. This is a heteroecious fungus. Its principal hosts are graminaceous plants including wheat, oats, barley, rye, a large number of grasses and the alternating host is barberry.
A transverse section of an uredosorus shows that the mycelium is intercellular, the hyphae produce small-rounded or branched haustoria which penetrate in the host cells.
The uredospores are stalked single-celled, dikaryotic and golden-brown. The cell of the uredospore is oblong or ellipsoid with four equatorially arranged germ pores, and strongly echinulate. These spores must have a film of water in the host surface before they can germinate. The uredospores can infect graminaceous hosts repeatedly.
The teleutospores follow the uredospores on the same or similar dikaryotic mycelium. Two kinds of spores may frequently be found together in the same sorus. A teleutospore is stalked consisting of two thick-walled, smooth, superimposed cells, the top cell being rounded or blunted and thickened at the apex. Each spore is dark- brown, bur-black in mass.
Each constituent cell is furnished with a germ pore, situated apically in the top cell, and just below the septum in the lower cell. Each cell during development possesses a pair of nuclei contributed by the dikaryotic mycelium. When the teleutospore turns brown and matures in the teleutosorus, the paired nuclei in each cell fuse.
The mature teleutospore thus represents the diploid phase in the life history of P. graminis tritici. The teleutospores do not germinate forthwith but undergo a period of rest and remain dormant on stubble or straw for several months.
Like the uredospores, the teleutospores also germinate in presences of a film of water. One or both the cells of a teleutospore may give rise to a promycelium, during the formation of which the diploid nucleus undergoes a reduction division and four sporidia (basidiospores)—two of (+) strain and two of (—) strain, are formed.
The sporidia germinate on the barberry leaf in the presence of moisture. Two types of spermogonia (+) and (—) are developed near the upper epidermis of the barberry leaf. The spermogonia are flask-shaped structures embedded in the host tissue and opening out into a small ostiole at the epidermis. They bear spermatia and flex- uous (receptive) hyphae.
The spermatia are exuded at the ostiole in a copious nectar or honey-dew and are carried to respective (+) to (—) and (—) to(+) flexuous hyphae through insects establishing dikaryotic condition.
The dikaryotic condition so established perpetuates through hyphal connection to the protoaecium which develops close to the lower epidermis of the barberry leaf along with the development of spermogonia. Ultimately the protoaecium develops into an aecium.
The aecium when young is covered by a peridium which breaks with the maturity of the aecium. The aecium bears aeciospores in chains. The aeciospores are dikaryotic, single-celled and hexagonal in shape. The aecispores are readily dispersed by wind. They have about six germ pores in the wall.
These spores serve to return the rust to the cereal or other graminaceous host. The aeciospores germinate on the graminaceous host in the same manner as the uredospores. The spores being dikaryotic are responsible for the establishment of a dikaryotic mycelium which ultimately gives rise to uredosori on the graminaceous host.
Physiologic Races:
True, P. graminis can attack any of the graminaceous hosts indicated, but it is also true that much fewer than that number of graminaceous hosts are found to be susceptible in any particular locality. This is due to the fact that P. graminis is composed of many different physiologic forms, races or varieties.
Any particular form, race or variety can attack certain species or varieties of host plants but not all of the susceptible graminaceous hosts.
The mighty Rust investigation began in Australia following the epidemic in 1889. The classical researches of Anton de Bary and the Tulasne brothers had long since established the parasitism of the rust fungi.
Between 1892 and 1896 Carleton grew various cereals in pots in a greenhouse and tried to infect the wheat plants with uredospore’s from the rust on the oats. The attempt failed—the spores from the rust on the oats would not infect wheat, barley or rye. And with the exception of the rust on the wheat, which did infect the barley, he found that the rust on one cereal would not infect the others.
There was not one Puccinia graminis but several, to be distinguished from one another only by the kinds of wild or cultivated grasses on which they would grow.
Meanwhile, Professor J. Eriksson (1894-96) of Sweden had already sorted the single Puccinia graminis of his botanical forefathers into six special forms:
Puccinia graminis special form avenae, to be found on oats and some half-a-dozen wild grasses; Puccinia graminis special form tritici, to be found on wheat and barley and a few others of the grasses; Puccinia graminis special form secalis, on rye, and so forth. These special forms of the fungus which differed so widely in their ability to parasitize the different cereals could perhaps be regarded as species in the making.
Forms in which adaptation and natural selection had gone far to make profound physiological differences, but not far enough to alter the external appearance of the parts of the organisms in so far as those alterations could be seen by man with the aids to vision available.
Were these special forms of Puccinia graminis really species in an early stage of differentiation? Subspecies? Adapted species? Physiologic forms? Biologic races? Biologic forms? Physiologic races?
H. M. Ward (1905) encountered a similar type of specialization toward species of Bromus. He was of opinion that the host substrate influenced the pathogenicity of a given race.
E. C. Stakman and his associates made intensive study of the physiologic races of Puccinia graminis and indicated that the physiologic races are best defined by the effect upon different hosts. The physiologic races may or may not be stable. New physiologic races may arise in nature through gene mutations and also by genetic, recombinations of characters in the process of sexual reproduction.
Physiologic races in so far as barberry is concerned are unknown. All physiologic races of graminaceous hosts, in so far as is known, infect barberry. When this host is infected, the pathogenic difference between races no longer exists. As such, it appears that the monokaryotic mycelium of rusts has as a rule pathogenic properties distinct from those of the dikaryotic mycelium.
Disease Cycle:
The pathogen perennates as teleutospores which remain dormant on stubble or straw of graminaceous hosts for several months. They are known to be viable for at least 18 months. Teleutospores serve, indirectly, to convey the disease to the alternate host, the barberry. They must be wetted before they germinate.
The most favourable temperature for germinaton is 19°C. to 21 °C. P. graminis being heterothallic, of the four sporidia formed by the teleutospore germination two belong to (+) and two of (—).
The sporidia are dispersed by air currents and fall on the barberry host and infect young stems, petioles and leaves by direct penetration of the cuticle. Infection may take place during the day or night but is favoured mostly by daylight. Two types (+) and (—) of spermogonia are produced by the respective (+) and (—) sporidia.
The function of spermogonia was established by Craigie in 1927. Following transfer of (+) spermatia to (—) flexous hyphae and vice versa— spermatization by flies or raindrops, dikaryotic condition is established resulting in the formation of aecia and aeciospores. The aeciospores dropping from the aecia are caught up by air currents and are carried to the graminaceous hosts.
The aeciospores germinate in presence of a film of water, form appressoria, penetration always through the stomata, and each forms a vesicle in the substomatal chamber from which dikaryotic hyphae ramify intercellularly into the parenchymatous tissue resulting in the formation of uredosori.
The uredospores formed in uredosori germinate on graminaceous hosts to spread infection. These spores germinate by a germ tube in a film of water.
The tip of the germ tube swells to produce an appressorium from which a narrow hypha arises which passes through stomata and invades the substomatal space where it soon expands into a vesicle. From the latter an infection hypha emerges, which having penetrated a mesophyll cell establishes within it.
The hypha proceeds sending haustoria into the cells with which it comes into contact. From such an initial infection an uredosorus with mature spores becomes established in eight to fourteen days.
With the dissemination of the uredospores throughout the crops, fresh uredosori continue to be formed, but they usually cease to develop before the wheat begins to change colour and ripen. The development of teleutosori follows along with the slowdown of the formation uredosori as the host plant approaches maturity.
Disease cycle of Black stem rust of wheat is presented in Figure 369.
Annual Recurrence:
Since sporidia cannot infect the graminaceous hosts and the source of inoculum of wheat infection is the aeciospores it is logical to conclude that both wheat and barberry hosts are essential for the annual recurrence of the disease. The pathogen perennates as teleutospores in the stubbles and straw of graminaceous host.
Eriksson in 1894 in his ‘Mycoplasm theory’ suggested that during the active wheat growing season, the fungal hyphae attack the wheat host and thereby an intimate mixture of the fungus protoplasm and the host protoplasm is established resulting in the formation of what he designated mycoplasm.
When the seeds from rust infected wheat plants bearing mycoplasm are sown, the mycoplasm splits up into the host protoplasm and fungus protoplasm. The fungus protoplasm then becomes organized into fungal hyphae and thus the infection is re-established. But Eriksson’s theory did not receive wide support.
In areas where both wheat and barberry hosts are present, the infection of the former may be initiated by aeciospores. But this ideal condition does not prevail all over India. For example, in the plains of India where barberry plants do not grow for hundreds of miles but the wheat rust appears year after year. What is the explanation for it? Since the barberries are absent, aecial stage does not come into picture at all.
The summer heat in the plains is so intense that the survival of rust on weeds or on any other substrate is not possible. It is obvious then that the rust does not spend summer in plains.
Therefore, the first appearance of rust on wheat crop during next winter is due to the dissemination of inoculum which is most likely from uredospores from some source other than plains. The possibility of air-borne dissemination from other countries is rather nil due to natural barriers like, Indian Ocean and the Himalayas.
K. C. Mehta (1931) working in the Nilgiri Hills conclusively proved that the uredospores and teleutospores cannot survive in the plains during summer, but the uredospores can do so in the hills at an elevation of 3,000 to 5,000 ft. and above where the summer temperature is congenial and where the rust survives in the uredial stage on self-sown wheat plants or other graminaceous hosts particularly grasses, of which Briza minor has been found most suitable.
When regular wheat crop is sown in hills it is infected by the inoculum (uredospores) from Briza minor. From this infected wheat crop in the hills the disease spreads to the wheat plants growing near the foot of the hills —the Tarai regions, by wind-borne uredospores. Again from these infected wheat plants of the Tarai regions, the disease gradually spreads to the plains.
This is how Mehta explained the infection of wheat crop annually in the plains in spite of the absence of barberry plants in the plains. Mehta devised an aeroscope, a small weather cock fitted with a greased slide, on which he collected uredospores flying with air currents at different areas from hills, the Tarai regions and the plains.
Control:
Since black stem rust infection takes place during the growing season from spores produced on the barberry or on wheat plants, prevention of infection is a logical method of control.
Toward this end measures applicable are:
The growing of wheat varieties resistant to attack; interruption of the life cycle of the rust-so that an important infective spore type cannot be produced; eradication of grasses which serve as alternate hosts; treatment of growing wheat so that spores alighting on it do not produce infection; and improved cultural practices.
Wheat varieties entirely immune to black stem rust do not exist. However, varieties resistant in various degrees are numerous. Since a large number of physiologic races greatly complicates the problem of developing varieties resistant to black stem rust, continuous processes of breeding, improvement and replacements will be useful to evolve new resistant varieties.
Varieties of wheat that are not resistant to the fungus but that mature early may escape serious rust damage.
Control by interference with the life history of the rust fungus is another means to reduce the incidence of the disease. Since the perennating stage of the rust is able to infect only the barberry, eradication of the barberry should remove the link necessary for .carrying infection over from the crop of one year to that of the next.
Eradication of barberry not only serves to remove infection of wheat by aeciospores, but also, it eliminates the possibility of recombination of genes in the fungus and the production of new races. Eradication of barberry, however, does not prevent infection from- uredospores.
In India, one of the effective control measures is to discontinue wheat cultivation in the hills and eradication of grasses like Briza minor and Bromus japonicus which serve as hosts on which fungus harbours when wheat season is over.
Experimental work has shown that reduction in stem rust infection accompanied by increases in yields can be obtained if growing wheat is dusted with sulphur at intervals of 4 days before heading time.
Some positive results have also been obtained by chemical control of the disease. Immediately with the appearance of rust symptoms, the crop should be sprayed 3 to 4 times with dithiocarbamate fungicides (Di- thane Z-78, Dithane M-22, and Dithane S-31) at the rate of 1 Kg. per acre. Dusting of crop with sulphur for 2 to 3 times at the rate of 6 Kg. per acre is also recommended.
Four to five applications of Nabam and zinc sulphate starting from initial stage of attack of the disease have proved to be effective in controlling the disease.
Besides these, the use of organic nickel salts; some of the antibiotics, e.g., actidione and related products; sulpha-compounds such as, sulphadiazine, sulphapyrazine, and sulphapyridine have given satisfactory results. Soil or seed treatment with systemic fungicides—plantvax gives effective control of the disease.
Certain items in the cultural practices of wheat-growing may contribute to a reduction in losses due to rust infection. Drainage facilities, date of sowing and maturing of crop, and the use of fertilizers all play a part. A better opportunity i» afforded for rust infection and spread on low-lying wheat fields.
Hence wheat cultivation should be avoided in low-lying fields. Early maturing varieties of wheat are preferable as they have a greater chance of escaping rust infection than late-maturing varieties. Excessive use of nitrogenous fertilizers promotes excessive growth of the rust fungus. A judicious application of phosphates, however, is necessary to counteract the harmful effects of excessive nitrogenous fertilizers.
Yellow or Stripe Rust:
Yellow or stripe rust (yellow rust) rarely ruins the wheat crop in India to the same extent as black stem rust. It is particularly limited to Northern and Eastern parts of India.
The disease is often accountable for very serious losses in the field, due to destruction of the foliage, followed in some cases by sterility of spikelets or in the production of badly shrivelled grain. But in general, the infection is chiefly confined to the leaves, only in case of severe attack it spreads over to the leaf sheath, the stalk, and even to the glumes.
Due to infection, the green colour of the leaves first of all fades in long streaks, and later, as small pustules of uredosori arise along them, a distinct yellow striped effect is produced in the leaves (Fig. 368A). The uredosori appear as bright-yellow pustules.
They are sub-epidermal and remain covered for a much longer time than in the other rusts, but when they finally break through, the yellow uredospores are shed and dispersed by wind.
The uredospores are spherical to ovate in shape, dikaryotic, and very variable in size. The spore wall is colourless, minutely echinulate and may have six to sixteen germ pores which are scattered, whereas, in the black stem rust the germ pores are equatorial in position and are four in number.
As the host matures the teleutosori appear on the leaf sheaths, glumes, but rarely on the leaf blade. The teleutosori always develop abundantly on the leaf sheaths. It is very infrequent that the teleutospores and uredospores occur together in the same sorus, as is often the case in the black stem rust.
The teleutosori are compact, appear as dull black spots, arranged in rows very similar to the uredosori. They do not, however, as in the black stem rust, break through the epidermis at all, but remain as flat black crusts. The teleutospores are dark-brown and flattened at the top in contact with the host epidermis (Fig. 370A).
They are two-celled inserted with brown unicellular paraphyses. The teleutospores on being released can germinate immediately without any rest. It is a heteroecious rust but no alternate host has so far been found.
The uredospores are capable of withstanding very low temperatures and serve as the source of inoculum to spread infection through grass hosts from the hills, as is encountered in case of black stem rust incidence in India. There is also evidence that this rust can perennate as mycelium in the wheat leaf or in various grasses. With the advent of favourable season the perennating mycelium produces uredosori.
The effective control of yellow rust disease is through the development of resistant varieties of wheat by hybridization of favourable types of wheat. Satisfactory results have, however, been obtained by using calcium cyanamide as an effective fungicide.
Brown or Orange or Leaf Rust:
This is known as brown rust or orange rust or leaf rust of wheat. In general, it is rather common in the Northern and Eastern parts of India and occurs along with the yellow rust causing damage to the wheat crop in some parts of Bihar, the Punjab and the United Provinces.
This disease is favoured by the same climatic conditions as those which favour black stem rust, but brown rust can develop over a wide range of temperature, particularly at temperatures below 15°C.
Rust infection is mainly confined to the leaves, rarely occurring on the stems and ears. In cases of heavy infection photosynthesis is retarded, the affected leaves turn yellow and wither early. Consequently the ears become retarded reducing in the grade, yield, and quality of grain.
The uredosori appear only on the leaves, very rarely on the leaf sheaths and stalks. They do not arise in rows or Stripes as in yellow rust but are grouped in small clusters or irregularly scattered (Fig. 368B). The uredosori break out from under the epidermis as orange or brown specks.
They are round to slightly oblong in shape. The uredospores are brown and spherical with minutely echinulate wall (Fig. 370B) furnished with seven to ten germs pores.
The teleutosori are very rarely produced. When formed, they are scattered chiefly on the underside of the leaf and on the leaf sheaths having similarity with those of yellow rust and do not break through the epidermis. The teleutospores resemble those of yellow rust in size and shape but the teleutosorus is divided into small groups by the interpolation of paraphyses (Fig. 370C).
The teleutospores are oblong with slightly constricted at the septum and possessing rounded apex with prominent thickening.
Thalictrum flavum is the alternate host of this rust. Its role in the annual recurrence of this rust has not been established in India.
This rust, however, perennates as uredospores on self-sown wheat plants in the hills at an altitude of 5,000 ft. and above. It is probable that brown rust can perennate as mycelium in the host leaf, and if the infected host can survive, the mycelium may produce fresh uredosori.
Though the fungus has numerous physiologic races, yet raising resistant varieties to these physiologic races would be the effective control of the disease.
Disease # 2. Hollyhock Rust of Wheat:
Hollyhock rust of wheat disease has been studied with great interest since 1852. The original home of the disease is either Chile, where it was found to occur in 1852, or Australia, where its presence was recorded in 1857. It was found in Spain in 1867, in France in 1872, in England and Germany in 1873, in Belgium, Holland, Denmark and Italy in 1874; and in South Africa in 1875.
The first appearance of the disease in the United States on the hollyhocks was reported in 1886. This disease was introduced in the United States with imported seeds of Malope.
Since then the rust of wheat was spread all over the world. The fungus which produces this disease is too well known in general appearance and by the effects it produces. The sudden and widespread appearance year after year of the disease particularly on the Malvaceous plants has grown the keenest interest for the study of the disease.
In 1852 Bertero first observed in Chile the appearance of the Hollyhock rust on different kinds of Malvaceous plants on which it was very common. He sent his collections to Montagne, who diagnosed, described and named the causal organism of the disease Puccinia maluacearum Bertero, which is the cause of a widespread disease of Althaea, Malva and related genera of the family Malvaceae.
The fungus is one of the most noticeable of the Uredinales being truly plurivorous, i.e., attacks a number of hosts; so far from being confined to a species it is not even confined to a genus. It can spread on all green parts of all Malvaceous plants if they are grown side by side. In all the plants the appearance of the disease is identical and by artificial inoculations it was proved that it can be transferred from genus to genus.
Symptoms:
It is an autoecious rust of wheat which produces only one form of spore, the teleutospore, and has therefore been classified in the group Lepto-peccinia. The Uredo and Aecium forms are wanting. The teleutospores are formed in sori. The sori are again formed scattered simultaneously on the leaf blade, petiole and stem.
They are very prominent and stand up almost like beads from the surface of the host and are more abundant upon the under than the upper side of the leaf, but arise anywhere on the leaf even upon the long petioles. The sori are about 1 to 2 mm in diameter.
The infection is very much localized, that is, confined to a small area immediately in connection with the sorus. This is especially true of the leaves but on the petioles and stems the sori may be much longer than broad and running some distance up and down the petiole and stem from the point of infection.
The sori on the petioles and stems are covered by the epidermal layer of the host for a longer time than is the case with the sori on the leaves. Upon the petiole the mycelium works more readily and more extensively, giving the sorus more strikingly the appearance of an eruption.
Causal Organism:
Puccinia malvacearum Bert. The teleutospores are oblong to oblong-fusiform, two-celled, rarely somewhat elliptical, smooth light-yellow slightly constricted at the septum and acute to slightly rounded but not thickened apex. The two cells are more or less of the same shape and size, narrowed each way from the septum, hyaline and persistent.
Pedicels are firmly attached to the tissues of the host plant which bear them by well-developed mycelium and hence they remain attached to their host tissue until the mycelium causes the dissolution of all vegetable substances. The teleutospores germinate in a damp atmosphere upon the host plant as soon as they are mature without any resting period by throwing a four- celled promycelium.
The sporidia are formed in one of the two ways:
(i) The four cells of the promycelium may separate into four free and independent cells, each of these cells later sends out a little protrusion which elongates and swells up as the content of the mother cell is gradually passed into it, and thus a mature sporidium is formed, which readily breaks away from the basal cell and germinates;
(ii) In the other type, the four cells of the promycelium do not break apart but each sends out little sterigma, which gradually swells up until the sporidium is formed into which the content of the promycelial ceil is passed. The sporidium is then abstricted and germinates. The sporidia are oval or spherical or subreniforai. The sporidia are carried by wind readily and are lodged on the leaf, where infection takes place.
They are the source of secondary infection and can spread the disease very rapidly. The sporidia produce germ tubes in 24 to 48 hours, which immediately bore through the cuticular cells of the host.
Playwright observed two kinds of teleutospores:
(i) roundish masses of teleutospores are clear brown and germinate at once
(ii) the other form occurs more upon the veins of the leaves, but especially upon the stem, in more elongated sori.
These spores are darker in colour and do not germinate immediately. The entire sorus becomes detached from the stem and falls upon the ground where it probably remains until the next year.
Disease Cycle:
The fungus becomes active as soon as the winter is over. Epidemics are regulated by the frequency of rains and dampness in the summer season. Usually it is not active in the spring and early summer as it is in late summer or autumn. The host plants suffer severely in September and October.
The teleutospores germinate very rapidly at 15°C. with suitable moisture. The-first visible sign of infection is tiny white spot or pustule on the under surface of the leaf, indicating the grouping of hyphae. The rate of development of the hyphae is independent of the host, but varies appreciably with the temperature.
Germ tube formation starts within 24 hours after infection, penetration occurring at the point of the epidermal wall to which the sporidium is adherent. A minute pore is formed at the point of contact. The germ tube then slowly works itself in. Infection never occurs through a stoma.
The germ tube then elongates and in three days it becomes branched with many transverse septa. The branches (infection hyphae) then pass into adjacent cells and in the intercellular spaces. Profuse branching of mycelium takes place in all directions. This vegetative mycelium becomes both inter- and intracellular and ramifies very rapidly in all directions of the host tissue.
The change in colour of the pustule from white to pale-yellow marks the initiation of the dikaryophase. This somewhat suggests the homothallic nature of the fungus. The colour becomes deeper and deeper until finally the epidermis is ruptured, and the rusty brown teleutospores are exposed.
The teleutospores germinate as soon as they are ripe. At first, fusion between the two nuclei takes place. The diploid nucleus migrates in the promycelium where as a result of reduction division four haploid nuclei are formed. Ultimately from the four- celled promycelium four sporidia are formed. Sporidia are discharged at binucleate stage.
Under cultural condition sporidia produce germ tubes within 10 to 24 hours after infection. The fungus is readily transmitted from Althaea rosea to Malta rotundifolia or Malva crispa, and vice versa by artificial cross-inoculation.
Both intra- and intercellular hyphae cause disorganisation of the host tissue. The hyphae extend inwards in the intercellular spaces of the cortical parenchyma, making a very definite attack on the starch sheath. Strands of mycelium pass into tie vascular bundle by way of the less resistant phloem rays, and then ramify among the tissues of the phloem.
Branches of mycelium extend to the parenchyma within the circle of vascular bundles. The mycelial branches attack the tissues of the stem in the similar manner.
In the petiole there is a definite attack on the starch sheath, medullary rays and the phloem elements of the vascular bundle. The attack of the pathogen causes a marked diminution of starch in the cells of the endodermis and the phloem-rays. The nature of invasion is practically restricted in certain areas.
Due to the fungal attack the cellulose thickenings on the cell walls of the collenchyma tissue disappear gradually as the mycelium advances between the cells. During the early stage the cells elongate. The pericycle fibres of the vascular bundle of both stem and petiole turn out to be almost devoid of thickening.
Due to the attack of the pathogen transpiration rate of the host tissue in increased. This may be due to the fact that the infected host cells have lost their power to retain water. At the same time the enhancement of the rate of transpiration is further helped by the ruptured epidermis due to fungal attack.
The infected leaves wither and dry up very rapidly. Very often the leaves take a scorched appearance long before the appearance of flowers. Such an abnormality may be due to rapid growth of mycelium in the host tissue. In many cases even flowers fail to appear.
In some extreme cases entire annihilation of the hollyhocks has been reported, as a result of which many growers have discontinued to cultivate them.
Disease cycle of Hollyhock rust is very similar to the secondary cycle of Black stem rust of wheat as indicated in Figure 369.
Control:
Various control measures have been suggested by many workers which may be summarized as follows:
(i) Eradication:
Destroy all old infected stems and leaves immediately after flowering to reduce the source of primary inoculum.
(ii) Protection:
(a) Planting in crowded plots should be categorically avoided, as closer planting gives more chance for the spread of infection. So best way is to plant the seedlings in isolated rows.
(b) Application of copper sulphate fungicide to the soil in weak solution (1 to 3 per cent.) has some effect in reducing the virulence of the disease.
(c) Dusting once a week with a fine grade of sulphur before flowering is useful.
(d) Infection may also be satisfactorily controlled by frequent spraying with lime-sulphur (1 in 60 to 1 in 100) from spring to summer, or with Bordeaux mixture (4-4-0) spraying several times during the season. The application of sulphur spray should be completed before blooming otherwise it may cause burning of the flowers.
(e) Application in the infected areas with a sponge the following mixture is a cheap and effective method of control of the disease:
Permanganate of Potash—2 to 5 table spoonful’s.
Water — 1/2 gallon.
(f) Application of lime-sulphur in the seed-bed at a concentration of 1 in 40, yields good control of the ‘disease and at the same time causes no injury to the host plants.
(g) Application of summer spray with Bentonite sulphur prepared by fusing fluid sulphur is very effective. This fungicide does not produce any caustic effect to the host tissue and is more adhesive than any other sulphur. Moreover it is cheaper and is not washed away readily.
Disease # 3. Loose Smut of Wheat:
Loose smut of wheat is the most early recognized of all wheat diseases because of the characteristic dusty appearance of diseased heads, an appearance that has given it such common name as smut, black head, blasted head, snuffy ear and black smut.
An important difference between this and other smuts of wheat is that the infection is carried over from season to season within the seed and not as spores on the surface of the seed.
The incidence of the disease is common in almost all the wheat- growing regions of the world. Prior to 1888 not much differences Were indicated- aetween the loose smuts of wheat, bailey and oats. It was Maddox in 1895 who first showed the nature of loose smut of wheat. Maddox’s work was later confirmed by Brefeld in 1903.
Symptoms:
Loose smut is recognizable as soon as the affected head emerges rom the leaf sheath, usually about the same time as, or very often in advance of, the leads of healthy plants.
Loose smut of wheat is easily distinguishable from stinking smut and flag smut of wheat being characterized by the complete destruction of spike- ets, whereas stinking smut is confined to the kernels, leaving the glumes intact, and lag smut attacks the leaves and culms.
The smutted head consists of deformed spike- et filled with black, dry, powdery masses of spores, known as brand spores or jhlamydospores; at first covered by a delicate membrane, which soon bursts md exposes the powdery spores.
The glumes and kernels are completely disintegrated and soon after emergence the wind blows the powdery mass of spores having only the bare rachis which is not attacked by the fungus.’Usually all spikelets n a head are destroyed but occasionally only a part of a head is affected.
Ordinarily all the heads on a plant are affected, and while the smut is confined mostly to the jars, sometimes dark streaks of spore formation may occur also on the leaves and ess often on the stem. In dry weather the spores are blown in clouds throughout he crop when the healthy heads are in bloom. During intermittent brief intervals ,when the spikelets are open for pollination, infection of the flowers takes place.
Causal Organism:
Loose smut of wheat is caused by the fungus Ustilago \uda var. tritici Schaf. The chlamydospores are pale-olive, more or less spherical in hape or occasionally oval, minutely echinulate, and measure 5 to 9 /n in diameter.
They germinate by germ tube which develops to become a promycelium of four uninucleate cells. No sporidia are produced. The spores retain their vitality for 5 or 6 months, a much shorter period than in the other cereal smuts. The fungus is not ;apable of a saprophytic life in the soil.
The name for the fungus causing loose smut of wheat is mostly a matte, taxonomic opinion rather than of nomenclature. For quite some time the fungus w. named as U. tritici (Pcrs.’ Rostr, which was later replaced by the name U. nuda (Jens. Rostr. G. W. Fischer says that Ustilago nuda (Jens.) Rostr. and U. titici (Pers.) Rostr. are indistinguishable.
Since U. nuda was published first, it is the correct name. But some feel that the two species are distinguishable and therefore the name U. tritici should be retained. Again others prefer to use the name U. nuda var. tritici Schaf. than using the name U. nuda (Jens.) Rostr.
Disease Cycle:
The spore masses on smutty heads are broken up and scattered by wind, rain, and other agencies just at the time when the healthy heads of adjacent plants are in flowering stage. Innumerable spores lodge between the glumes and reach the feathery stigmas.
Spores caught up on the stigmas of the flowers, germinate on the moist stigmatic fluid, put forth promycelia. The promycelium becomes septate, but the dikaryophase is established by fusion of germ tubes derived from the individual unincleate cells of the promycelium and ultimately infection hyphae are produced.
Spores are short-lived, rarely survive more than a few days under normal conditions. Spore germination occurs in moisture and only <m the feathery stigmas of normal wheat flowers. It was earlier thought that the point of entry of the infection hyphae was the stigma of healthy flowers, but it has been shown that the normal entry point is the young tissue at the base of the ovary.
After entering in the ovary the infection hyphae pass through intercellular spaces and through the integuments and ultimately reach the ovule. The infection hyphae ultimately pass into the space between the endosperm and the nucellus and move round the bottom of the endosperm to reach the scutellum and the embryo.
Growth of the infection hyphae is exclusively intercellular, there are no haustoria, and the host cells are not affected in the slightest degree by the presence of the parasite. Simultaneously with this process, pollination, fertilization and embryo formation take place in the heads. The fungal mycelium continues to grow along with the development of seeds.
Fungal infection in no way hampers the grain formation. The fungal mycelium becomes somewhat thick-walled, remains dormant in the seed, and from superficial examination at harvest time, the infected grain cannot be distinguished from the perfectly normal grain.
In the matured seed there is copious mycelium in the scutellum. The mycelium remains dormant in the seed, until the lowing growing season. When an infected wheat seed is sown, it begins to sprout, Sue dormant mycelium resumes activity, grows into the young shoots up to the growing “points and keeps pace with the development of the plant. As each head forms, there is a great accumulation of hyphae which ultimately replace the spikelets with masses of dusty spores.
The spores are ready to infect the flowers of healthy plants. The spore masses are covered by a delicate silvery membrane which bursts usually before the head emerges from the sheath, forming very dark olive-brown powdery masses in place of the spikelets, of which only the ends of the awns ordinarily escape transformation.
The spores separate easily and in dry weather may be almost all blown off, leaving a bare stalk (the rachis) behind. In dry weather, clouds of spores are thrown into the air. In dry weather again the glumes of healthy flowers are rather wide open and the stigmas exposed on which the spores lodge and behave in the manner already described.
A diseased seed or plant cannot be distinguished from a healthy one until the plant begins to develop heads. As such, it is a case of seed-borne systemic infection and the fungus perennates as dormant mycelium in the seed. The severity of infection is influenced by moisture and temperature prevailing during the dissemination and germination of spores, and the duration of flowering stage.
In many regions the loose smut of wheat is of little economic importance because it occurs in small amounts. Again, there are areas where the damage is considerable since the infection is very severe.
Disease cycle of Loose Smut of wheat is presented in Figure 371.
Control:
Seed treatment with fungicides in the form of dips or dusts such as are employed with other diseases of cereals is of no value, since the infection is internally see-borne as a dormant mycelium. An effective method must kill the internal mycelium. The only effective method thus far developed for controlling loose smut of wheat is the hot water seed treatment.
This consists essentially of soaking the seeds in hot water for a sufficient time, the object being to destroy the infection within the seeds without harming the embryos. The exact method of providing the hot water and handling the seeds can be variable according to convenience.
The hot- water seed treatment method requires great care since by the same treatment mycelium will be destroyed but the embryo should be saved from the heating effect. The embryo being a very delicate structure special care should be taken at every step.
The recommended procedure will be: (t) carry out the treatment in small lots of seeds, (it) soak the seeds in cold water for 4 to 6 hours to ensure complete wetting of all the seeds, (tit) immerse the seeds in warm water at 120°F. for one minute for a brief dip, (iv) finally immerse the seeds in water held at 129°F. for 10 minutes or within a range of 124°F. to I30°F., (v) remove the seeds from warm water and dip in cold water to stop the action of heat, (vi) spread out seeds in a thin layer to dry, quickly to avoid moldiness or deterioration, and (vii) sow the seeds or dry thoroughly and store for later use.
Since even good sound seed has from 6 to 10 per cent, of the grains injured by the heat, it is necessary to increase the sowing rate. Bad seed may suffer more heavily. Besides hot water seed treatment the disease may, however, be controlled by having special seed-raising areas being protected from the prevailing winds at flowering time to reduce the risk from blown spores, and no wheat fields should be closer than 500 yards.
Field of other crops and surrounding trees acting as windbreakers often will help to reduce external infection. The seed-plot should be large enough to allow for loss in cleaning and selecting the seed and still provide enough for the field sowings.
Growing a crop in a dry area for a season, where the conditions of humidity would be so low as to inhibit spore germination at the flowering time may yield infection-free crop without seed-treatment. It is always recommended that seeds for sowing should be procured from certified disease-free supplying concern.
Some claims have been made from the Punjab that loose smut of wheat can be controlled by a sun heating method. In the Punjab, where summer temperatures are usually very high, sun heating treatment is in practice with great amount of success.
The seeds are spread in shallow flatbottom open containers and covered with water having water-level about 2 inches above the layer of seeds. The containers are then placed in the sun for about five hours from early in the mornilig. The water is then poured off from the containers and the soaked wheat seeds are spread in sun to dry.
The direct action of hot summer sun rays produces two effects: (i) the newly grown young hyphae developed from dormant mycelium get killed, and (ii) the seeds gets dried at the same time.
The most effective control is, however, to produce and introduce resistant vatieties. Great attention is being paid along this line with a considerable success. The whole programme of breeding resistant varieties often becomes complicated, since along with the new resistant varieties there develop fresh physiologic races of the causal organism almost simultaneously to defeat the whole purpose.
Loose smut of wheat can be effectively controlled by soaking wheat seeds in fungicides like Chlorex, Purex, Ceresan, and Vitavax.
Disease # 4. Bunt of Wheat:
Bunt of wheat, also called stinking smut of wheat gets its name from the characteristic odour of decaying fish given off by infected ears. This is one of the most severe diseases of Middle Ages to attract attention. In 1755 Tillet was the first to establish distinction between the bunt or stinking smut and the loose smut. Prevost, in 1807, described the germination of the bunt spores and the production of sporidia.
The true nature of the fungus was determined by Tulasne (1854), Kiilu (1874) and Brefeld (1883).
There are three principal bunts of wheat.
They are:
Rough-spored bunt, caused by Tilletia caries (DC). Tul.; smooth-spored bunt, caused by T. foetida (Wallr.) Liro; and Karnal bunt, caused by T. barclayana Sacc. and Sydow.
This disease occurs wherever wheat is grown all over the world. Its severity varies greatly, however, in different localities. The damage done by bunt fluctuates from season to season and in various localities. Losses are attributable to two separate and distinct items, namely, actual percentage of decrease in yield and the quality of the threshed grain.
Besides these, losses may be due to explosion of harvesting and threshing equipment instigated by the concentration of spores. Again the spores may produce allergic effect on man during handling of infected grains.
Symptoms:
The disease is not evident until the wheat plant is in the heading stage. The diseased heads are usually slim compared with healthy ones, and they retain their greenish colour longer. They stand more nearly erect than healthy heads, because of their lighter weight. Stunting of growth of diseased plants is also common.
The kernel, during growth, is transformed into a spore ball, which is shorter and plumper but lighter in weight than a normal wheat grain. The spore balls are recognizable by their colour which is darker than that of the healthy grains.
Diseased grains retain more or less the shape and size of normal kernels. When broken open the smut balls are found to be filled with black or dark-brown powdery substance composed entirely of spores. The offensive odour announces the presence of heavy infections in the field.
Causal Organism:
Tilletia caries (DC.) Tul. The chlamydospores are of various shades of brown and are black in mass. The spore wall has reticulations ranging from minute shallow meshes to deep indentations. The young chlamydospores are dikaryotic, the nuclei fuse in the mature chlamydospores. On germinating the chlamydospore sends out a non-septate promycelium during which meiosis takes place.
The promycelium produces at the apex a cluster of filiform, hyaline 8 to 16 sporidia—the primary sporidia which frequently fuse in pairs to form characteristic H-shaped structures. These H-shaped structures germinate to produce mycelium on which sickle-shaped, hyaline, secondary sporidia are borne. The secondary sporidia develop infection threads which penetrate the young seedling.
Disease Cycle:
Many of the spore balls are shattered during threshing and spores thus liberated lodge on the healthy kernels or are left in the soil and thereby carry the pathogen over form one crop to the next.
This is how the pathogen perennates. With the return of favourable season the chlamydospores germinate to produce promycelium bearing primary sporidia where dikaryotic condition is established by the formation of H-shaped structures between the compatible sporidia.
The H-shaped structures then germinate to produce mycelium from which secondary sporidia are produced. The secondary sporidia give rise to dikaryotic infection hyphae which penetrate the wheat seedlings. Infection takes place on the young seedlings before the first leaf emerges.
Conditions suitable for infection are:
(i) Temperature of 25°C., and
(ii) Moderate amount of soil moisture.
Following upon penetration of the coleoptile, the hyphae pass to the young shoot keeping pace with the growth of the host and cause little interference to it until the formation and development of the ears. Eventually hyphae accumulate in the ovaries, the cells of which are crushed and replaced by hyphal masses.
A rapid transformation of the hyphal mass into spores takes place filling the grain internal to the pericarp to constitute a spore ball.
Diseases cycle of Bunt of wheat is presented in figure 373.
Control:
In controlling the disease it should be carefully considered that the spores are either externally seed-borne or are in the soil where wheat seeds are sown.
Some of the effective control measures are as follows:
(i) Use of Clean Seeds:
Visibly spore infested seeds should be rejected. Seeds from fields where there was not bunt infection are always preferable.
(ii) Seed Treatment:
Seed treatment with appropriate fungicides is very effective not only in destroying seed-borne spores but also in checking infection from soil- borne spores.
Some of the commonly used fungicides are:
(a) Copper sulphate solution, 2 per cent., seeds to be dipped for 5 to 10 minutes.
(b) Formaldehyde solution, 1 pint of formaldehyde in 40 gallons of water, seeds to be dipped for 5 minutes.
(c) Dusting of seeds with copper carbonate.
(d) Dipping seeds in Bordeaux mixture of 4-4-50 to 8-8-50 strength for 10 to 15 minutes.
(e) Seed treatment with Ceresan M, Agrosan GN, Spergon, and Pangon has been found very effective.
(iii) Crop Rotation:
Rotation of wheat cultivation with some other crop enables to make the spores in the soil ineffective.
(iv) Cultural Practices:
Cultural practices that may reduce the rate of infection are:
(a) Seed sowing in relatively dry rather than moderately moist soil,
(b) Shallow rather than deep sowing in soil, and
(c) Early sowing.
(v) Use of Resistant Varieties:
Many satisfactory disease resistant varieties are now in use which has enabled to raise disease-free wheat. Continued effort along this line should be made to combat with the physiologic races that may upset the entire programme of breeding of disease resistant varieties. Even if resistant varieties are used, the seeds should be treated with a fungicide.