Plant Pathology

PLANT PATHOLOGY

Crop Diseases and their Management

Professor Y.S.Ahlawat Division of Plant Pathology Indian Agricultural Research Institute New Delhi-110012

(30-04- 2007) CONTENTS Wheat Diseases Rice Diseases Maize Diseases Sorghum Diseases Bajra Diseases Sugarcane Diseases Groundnut Diseases Sunflower Diseases Mustard Diseases Pigeonpea Diseases Soybean Diseases Gram Diseases Lentil Diseases Cotton Diseases Potato Diseases Tomato Diseases Brinjal Diseases Chilli Diseases Vegetable Crucifer Diseases Vegetable Cucurbit Diseases Pea Diseases Bean Diseases Mango Diseases Apple Diseases Papaya Diseases Citrus Diseases Peach and Pear Diseases Guava Diseases Grape Diseases Sapota Diseases Ber Diseases Custard Apple Diseases Coconut Palm Diseases Management of Plant Diseases

Keywords Crop disease, symptom, pathogen, control, disease cycle, economic importance

Wheat Diseases 1. Rusts of Wheat The rusts of wheat belong to genus Puccinia, family Pucciniaceae, order Uredinales and class Basidiomycotina. Wheat suffers from three rust diseases namely stem, leaf and stripe rust. Stem rust caused by P. graminis, leaf rust caused by P. recondita but currently P. triticina was suggested to be the preferred name, yellow rust of wheat is caused by P. glumarum but later changed as P. striiformis. Rust fungi which are morphologically identical but attack different host genes are known as special forms (formae specialis) for example, P. graminis on wheat is Puccinia graminis f. sp. tritici, P. recondita as Puccinia recondita f. sp. graminis and P. striiformis as Puccinia recondita f. sp. graminis. In each special form of these rusts are several pathogenic (physiological) races which can be detected on different varieties of the same species by inoculation and these varieties are known as differential hosts.

The rust fungi, being an obligate pathogen, must be cultured on living host plants under controlled condition in a glasshouse. Black and brown rust pathogens complete their life cycle on two hosts. For P. graminis tritici, wheat is the primary host and barberis is the secondary or alternate host. P. graminis tritici completing their life cycle on two hosts is known as heteroecious rust. This rust pathogen produces five different stages/spores to complete the sexual cycle and the stages are: pycnial, aecial, uredial, telial and basidial. Urediospores and teliospores are formed on wheat and basidiospores, pycniospores and aeciospores on alternate host (barberis). Such rusts are known as macrocyclic or long cycled rusts.

2. Black or Stem Rust of Wheat Stem rust of wheat is worldwide in its distribution and affects wheat wherever it is grown. It caused enormous losses to wheat production all over the world. This disease has caused greater damage than any other disease of wheat crop. In dry areas, the disease developed in epiphytotic form during wet season. Losses were higher in spring wheat areas of North America than winter wheat areas because of relatively high summer precipitation in spring wheat areas and the the plants exposed to longer period of favourable summer conditions. Now stem rust is largely under control worldwide.

Symptoms: The stem rust pathogen attacks all the above ground parts. In addition to wheat, this pathogen also infects its alternate host barberis (Barberis vulgaris). The black or brown colored elliptical blisters or pustules develop on upper and lower surfaces of leaves, stem and leaf sheaths of wheat generally parallel to their long axis and known as uredia (Fig.1a).

(a)Stem Rust (b)Leaf Rust (c)Stripe Rust (Puccinia (P. recondita) (P. striiformis) graminis tritici) Fig 1. Three rusts of wheat 2

These uredia are 1-3 mm wide and upto 10 mm long in size. The epidermis of the infected plants is ruptured releasing a powdery mass of brick red coloured uredospores. Later in the season these pustules turn black due to abundant production of shiny black teliospores alongwith the uredospores but finally the uredia are transformed into black colored telia forming teliospores. All the affected parts are ultimately covered with uredia or telia filled with either urediospores or teliospores or both. Stem rust is favoured by humid conditions and warmer temperatures of 15 to 35 C. Uredia contain upto 10000 urediospores.

The basidiospores infect barberis, the alternate host. On barberis, symptoms are developed on affected leaves as yellowish to orange colored spots. Later on the upperside of the leaves appear minute black colored bodies known as spermagonia or pycnia having nector. Horn- like or cup shaped aecia appear below pycnia or sometimes next to them. The host tissue swollen in and around the infection and whitish aecial wall protrudes at the margin of aecia. Aeciospores can also be a source of inoculum of wheat stem rust and can infect wheat similar to uredospores wherever alternate host is found.

Pathogen: Puccina graminis tritici (pers.) Erikss. Henri = Puccinia graminis f. sp. tritici is the causal pathogen.

Disease Cycle: Wheat, barley, triticale and a few related species are the primary hosts for P. graminis f. sp. Tritici .The pycnia and aecia develop on alternate hosts, Barberis vulgaris L. and Mahonia spp. wherever they are found.The pathogen completes its life cycle on two hosts, wheat and barberis being its heteroceous nature. The uredo and teleuto stages are found on wheat, barley or some grasses and pycnial and aecial stages on alternate hosts. The life cycle is given in (Fig 1a-1).

Fig 1a-1. Life and disease cycle of Puccinia graminis tritici (Source: Courtesy of V. Brewater)

The uredospores are brown, thick walled with spines and measure 25-30 X 17-20 µm. They germinate through the germ tube when come in contact to a proper host. The germ tube produces appressoria which in turn develop the infection peg. The infection pegs enter the host through stomata and finally hyphal strands develop and hyphae spread intercellularly. When fully established, the uredosori are developed, which erupt releasing the uredospores. Uredospores spread from field to field of wheat through winds.

At late in the season the telia are produced in mature uredial sori. The teliospres are dark brown, two celled and wedge shaped with thick walls measuring 40 to 60µm x 18 to 22µm. Teliospores are dicaryotic (n = n) and remain with the straw after harvesting where karyogamy occurs and the teliospores become diploid (2n). The teliospores germinate after a long resting period and exposer to freezing temperature. They undergo meosis producing a four celled basidium. Each cell produces a single haploid basidiospore (1n) which is hyline and travel through wind and infects barberis bush resulting the production of a pycnium (1n). The picnium produces receptive hyphae and picniospores of a single mating type (+ or -) that serves as female and male gametes of the fungus. Pycniospores of one mating type must be transferred to the receptive hyphae of the opposite mating type to initiate aecia and aeciospores development which is normally done by insects or splashing rains. Aeciospores are dicaryotic (n+n) and are produced in aecia on the lower surface of barberis leaves below the pycnia.

Aeciospores are hydroscopically released from the aecia, travel by wind and infect wheat resulting in the production of dicaryotic uredia with uredospores. The asexual stage is repeated several times during the season. However, the sexual stage is not found in India because of nonavailability of proper alternate host (s). In India, disease develops by air borne uredospores which needs free moisture and temperature above 20 C for spread. The pathogen perpetuates in Nilgiri hills during off season and becomes air borne. If peninsular and central India has rainfall during November then epidemics are severe. Late infection causes less damage in north India.

Control: Control of wheat stem rust has been achieved through the development of rust resistant varieties. Genetic analysis of five bread wheat cvs. Hd 2135, HD 2160, HD 2189, HD 2285 and Vaishali with four selected pathotypes 21, 21A-2, 40-1 and 117A of Puccinia graminis f. sp. tritici showed the presence of three dominant and one recessive gene for resistance in HD 2135, two dominant and one recessive genes in HD 2160, four dominant genes in HD 2189, three dominant and two complementry recessive genes in HD 2285 and five dominant genes in Vaishali. Test of allelism confirmed the presence of Sr 8a and Sr 30 in HD 2135 and HD 2160; Sr 8a in HD 2189; Sr5 in HD 2285 and Sr5 and Sr8a in Vaishali. World wide resistance genes of stem rust (Sr genes) have been identified from Triticum and related genera and incorporated in agronomically superior cultivars.

The cultivation of slow rusting varieties will be useful for certain regions. Therefore, commercial wheat varieties were evaluated for slow rusting phenomenon. Wheat cvs. HPW 42, Hs 207, and GW 190 showed slow rusting to both stem and leaf rusts. Among durum wheat cvs. HI 8316, HI 8381 and HD 4633 are slow ruster to stem rust.

Eradication of alternate host (barberis) from countries where it plays role in rust recurrence helped in controlling black rust. In India, the inoculum survives on self sown wheat at hills. Therefore, resistant varieties should be grown in hills as eradication of self sown plants is practically impossible. Use of early maturing varieties and early sowing is also helpful to

avoid damage due to black rust since this rust appears late in the season. Excessive irrigation increases the susceptibility to uredospores. Therefore, irrigation schedules recommended for a variety or cultivar must be followed.

Seedling and adult plant resistance and use of slow rusting varieties/cultivars are another area of interest to minimize the losses caused by stem rust. Slow rusting means the ability of a cultivar to retard rust development. This phenomenon is governed by genes. Several Sr genes are associated with slow rusting on wheat by stem rust pathogen.

Single foliar spray of new systemic fungicides such as Bayleton, Diniconazol can control stem rust. For the efficient use of fungicides mathematical prediction model to forecast stem rust based on environmental variables have been developed. The linear prediction equation developed for stem rust (Y=29.3733 + 1.820X1 + 1.7735X2 + 0.2515X3) may be useful in estimating the severity of the disease and thereby giving enough time to decide the economic use of fungicides for the disease management. In this equation, Y, X1, X2 and X3 were expected disease severity after one week, prevous disease severity, minimum temperature and maximum relative humidity in the next week.

3. Brown or Leaf Rust of Wheat Leaf rust of wheat is found in all the wheat growing countries. In India, this rust appears in northern and eastern part of the country in wheat crop earlier than yellow or black rust and causes much higher damage than other rusts. Epidemics due to this rust have been experienced in North western region during the year 1971-72 and 1972-73 causing losses in wheat production to the tune of eight and ten lakh tones respectively. Similary, during the year 1985-86 and 1986-87 this rust appeared in a severe form in North western states of India especially on late sown wheat.

Symptoms: As the name indicates the first symptom of the disease is the appearance of minute, round, orange sori, irregularly distributed on the leaves but occasionally they may appear on stem, leaf sheath and spikes. These sori are irregularly distributed on both the surfaces of leaves (Fig.1b). Maximum numbers of sori are seen on the flag leaf towards late in the season. Initially these sori are bright orange in colour but become brown at maturity. The epidermis is ruptured over the pustules and brown powder of large number of uredospores can be seen on the leaf surface. The affected leaves become yellow. At the time of maturity of the crop, the telia are formed on the lower surface of leaves. Telia are lead gray or black in colour and are covered with epidermis. The affected plants remain dwarfed and develop shrinkled grains. During severe infection plants may die before maturity.

Pathogen: Puccinia recondita Roxb. Ex Desm =Puccinia triticina Pers = Puccinia recondita f. sp. tritici is the causal organism. It is hererocious rust. The uredial and telial stages appear on wheat and some grasses. The alternate host is Thalictrum speciosissimum where the fungus produces its sexual gametes (pycniospores and receptive hyphae). In India, The alternate host does not to play any role.

Disease Cycle: Infection normally takes place from the inoculum survives on self sown wheat or grasses or overlapping of crops. Puccinia recondita attacks a wide number of grasses but it is primarily a pathogen of wheat. The rust inoculum survives on volunteer (self sown) wheat. The inoculum comes from volunteers in the form of uredospores. The pathogen over-summers in low and mid-altitudes of Himalayas and Nilgiri hills. Primary infection develops from wind deposited uredospores in eastern Indo-gangetic plains in middle of

January where it multiplies and moves westward by March. Temperature of around 20C with free moisture (rain or dew) causes epidemics. Uredospores germinate 30 minutes after contact with free water and temperature of 15 C to 25 C.

Fig 1b-1: Life and disease cycles of Puccinia recondita (Source: Courtesy of V. Brewater)

The germ tube grows along the leaf surface until it reaches to a stomata ; an appresorium is then formed, followed immediately by the development of penetration peg and a sub-stomal vesicle from which primary hyphae develops. A haustrial mother cell develops resulting in additional haustrial mother cells. The mycelium produces uredia where uredospores are developed. Maximum sporulation is reached in about four days following infection under favourable temperatures.

Uredospores are orange to dark red, echinulate, spherical and usually measure 20 to 28 µm. The telia are rare but when formed are found mostly on the under surface of leaves and do not rupture the epidermis of the host. The sori are divided into compartments by means of lengthy paraphysis among the teliospores. They are developed with unfavourable conditions or senescence. They are dark brown, two celled with thick walls and rounded or flattened at the apex. The teliospores remain under the epidermis with the leaves. Pycnial and aecial stages of the pathogen are similar to P. graminis tritici and are known to occur on 11 species of Thalictrum. The life cycle of the pathogen is shown in (Fig 1b-1).

Control: The control strategies described under black rust of wheat are also applicable for the management of leaf rust. In India, several races of leaf rust have been identified with variable virulence. Genetic analysis for leaf rust resistance in nine cultivars viz. HD 2402, HD 2643, HI 1077, HP 1731, PBW 343, UP 262 UP 2338, WH 147, and WH 542 with pathotypes 77-2, 104-2 and 106 showed the presence of one dominant gene for resistance in HD 2402, one dominant and one recessive gene in HI 1077, PBW 343, UP 262 and WH 542; two dominant and one recessive resistant gene in HP 1731 and UP 2338 and three dominant independent resiatance genes in HD 2643. Test of allelism confirmed the presence of leaf rust resistant gene Lr1 in HD 2643, Lr13 in HD 2329 and Lr 14a in HI 1077 and UP 262.

Cultivars HI 7747, HI 8461, HI 8488, HI 8490, HD 4637 and HD 4645 are slow ruster to leaf rust.

The linear prediction equation developed for leaf rust is: (Y= -83.531 + 1.522X2 + 1.753X3).

4. Yellow or Stripe Rust of Wheat Yellow rust of wheat is a major disease of wheat especially during winter or early spring or at high elevations. In India, this is an important disease because wheat is a winter crop. This rust pathogen infects wheat and barley in indogangetic plains. In Delhi and areas of Punjab this rust appears in the month of January-February. The disease is more damaging in northen and eastern parts of the country than southern and western regions.

Symptoms: The disease symptoms appear as pin head-like light yellow coloured sori in between the leaf veins and appear like a stripe (Fig.1c). In severe conditions, the sori may also develop on other parts of the plant such as lemma, stalk, glumes, awns and even on grains. When the infection is severe these sori may coalesce and the whole leaf show yellow powder on its surface due to release of urediospores in large numbers and yellow powder of these spores can be seen even on ground near the plants. Late in the season the dull black coloured telia appears on leaves, stalk and glumes. Like uredium they also develop in a line and covered with a membrane which does not burst like black rust. The light and shreveled grains are formed on affected plants and such plants remain stunted.

Pathogen: Puccinia striiformis West = Puccinia glumarum Schmidt Erikss & Henn is the causal pathogen.

Disease Cycle: Puccinia striiformis is a pathogen of grasses, and cereal crops, wheat, barley, triticale and rye. No alternate host of P. striiformis could be confirmed as yet under natural conditions. Puccinia striiformis is most likely hemiform rust in that the life cycle seems only to consist of the uredial and telial stages. The uredospores require the lowest temperature as compared to other wheat rust pathogens (minimum 0C, optimum 11 C and maximum 23 C) for their development. In areas near the equater, yellow rust tends to cycle endemically from lower to higher altitude and return following the crop phenology. In more northern latitudes, the cycle becomes longer in distance with moving from mountain areas to the foothills and plains. The pathogen spreads through air borne uredospores, when temperature is 10-20C. Pathogen survives in the cool temperature of hills and the primary infection takes place by middle of January in the foot hills and submountaineous parts of north western India. Also infection comes from across the western border; hence the probability of evolution of new races increases in this area. Yellow rust from Nilgiri hills can not come out of the zone due to high temperature in the peninsular and Central India.

Puccinia striiformis consists of Uredial and telial stages. Uredia develop uredospores on wheat which are yellow to orange in colour, more or less spherical, echinulate and 28 to 34 µm in diameter. Teliospores are dark brown, two celled and similar to size and shapes to those of P. triticina. Uredospores are the only source of inoculum for wheat, and they germinate and infect at cooler temperatures. In India, several pathogenic races in P. striiformis are known to occur.

Control: Most of the presently recommended varieties are resistant. Major emphasis should be given to host resistance and cultivation of resistant varieties is the main strategy for management.

Rust Reccurrence in India: Mehta from 1920 to 1950 studied the perpetuation of rusts in more detail and systematic manner. He conclusively proved that the Barberis species found in India do not play any role in the perpetuation of stem rust in India. Similarly it has been proved that Thallictrum species occurring in the hills are also not playing any role in the perpetuation of stem rust.

Mehta has shown that high temperature during summer in Indian plains followed by rains, wheat rusts in general, can not survive. They oversummer in cooler climates of hills on self sown wheat plants, ratoon tillers and also on summer crop grown in Nilgiri and Palini hills in south India. He later concluded that stem rust of wheat spreads from the sub-Himalayan ranges to the plains of India and asserted that central Nepal forms the “ most dangerous” foci of infection of this rust. Possible role of grasses in the hills in the annual reccurrence of stem rust could not be established although some of the grasses were susceptible to Puccinia graminis tritici under natural and glasshouse conditions in the hills and plains of India. Until early 1970s, rusts were one of the major causes of economic losses to wheat production Extensive wheat disease surveys conducted by the Indian Agricultural Research Institute showed that the stem rust ( P. graminis f. sp. tritici ) is introduced from Nilgiri and Palini hills of South India and spread every year northwards because of tropical cyclones that crosses coastal Andhra Pradesh and Tamil Nadu late October-November. The northernly winds associated with rain efficiently transport and wash down the inoculum over central India where one month crop is available. The fixed path between Nilgiri and Palini hills to Narmada and Tapti river belt is known as Puccinia path.

Initially, Mehta had shown the movement of leaf rust both from north and south Indian hills. Later, Joshi and his team supported this view and further demonstrated that leaf rust ( P. recondata ) spreads both from southern and northern hills. It is introduced from Nilgiri and Palini hills and is established in the plains of Karnataka and Tamil Nadu in South India. The rust population from southern foci moves northwards towards Maharashtra and Madhya Pradesh. The spread of leaf rust over the Indo-Gangetic plains is predominantly from the warmer north-eastern region and is influenced by the number of rainfall during winter month.

Stipe rust (P. striiformis) is a major problem only in cooler parts of the country especially north and north-western region. Its infection in south, central and eastern parts remains isolated and seldom become a serious threat to wheat. In north India, the inoculum moves from northern hills and get established in the plains of Punjab, Hariyana and western Uttar Pradesh. In the foot hills and northern Indian plains stripe rust spread much faster by uredospores than leaf rust due to favourable cool temperature but the spread after February is checked due to rise in temperature and this time the telial stage is developed which does not play any role in the spread of the disease.

A national stretagy for vertical resistance (VR) and adult plant resistance (APR) genes deployment has been proposed along “Puccinia path” for managing stem and leaf rusts. In this strategy, vertical resistance genes in different epidemiological sub-zones are deployed to minimize the possible break down of the cultivars from virulent pathotypes.

5. Loose Smut of Wheat Loose smut is a common disease of wheat throughout the world wherever wheat is grown. The disease incidence depends from variety to variety and the environment conditions prevail during crop season especially during flowering time. Cool, humid climate accompanied by light showers favour the loose smut infection. In India, disease incidence is more in northern areas than in southern parts where wheat is grown. Wheat yield is reduced in proportion to the smutted heads. In India, loose smut causes 3-4 per cent loss in yield annually

Symptoms: The plants produce smutted spikes which are easily recognized at the time of heading by their characteristic dusty black appearance of the ears (Fig.2). The smutted spike emerged from the boot leaf a few days (1-3 days) earlier than those of healthy plants but in some varieties smutted and healthy heads emerge simultaneously. The infected plants are stunted and produce less tillers in some varieties such as sonalika. All the spikelets of a smutted ear are filled with black powdery mass of spores. The spore mass is covered with a delicate silvery membrane of host origin which usually ruptures before the complete emergence of ears from the sheath exposing dark, olive brown powdery mass of spores in place of normal spikelets. The chaff and grains are completely transformed into black powder. The spores are blown away by the wind and by the harvesting time of crop, bare rachis remains of the smutted heads.

Fig 2. Loose smut of wheat Fig 3. Karnal bunt (Neovossia indica) of

Pathogen: Ustilago tritici (Pers.) Rostr. = Ustilago segetum var. tritici is the causal pathogen of the disease and belongs to the family Ustilaginaceae, order Ustilaginales and class Basidiomycotina. The mycelium in the seed is hyaline, septate and dikaryotic. It grows alongwith the plant and turns brown near maturity of plant. The cells of the mycelium are turned into brown spherical teliospores which are carried to healthy plants by wind. Disease Cycle: It is a seed borne disease and hence the primary inoculum comes from contaminated seeds. The mycelium remains dormant in the embryo of seed and cause infection to the next year crop. Maximum infection of loose smut fungus takes place during flowering time. The olive black teliospores from smutted heads are carried by wind, rain or insects to the open flowers of healthy heads. These spores are thick walled, echinulate and measure 5-9 µm. On the healthy spikelets the spores germinate quickly by forming a germtube which develops into basidium or promycelium with four uninucleate cells. Diplodization takes place between compatible cells of promycelium by means of short and long conjugation tubes. The resulting diploid cells produce binucleate hyphae. These hyphae invade the stigma and pistil and finally reach the young embryo in the seed. Penetration may also occur directly to embryo cells. Infection is favoured by cool, humid conditions during flowering period of the host plant. Control: The best method available is the use of certified seed and seed treatment with chemical like carboxin (Vitavex 75WP @ 2.5/ kg seed), carbendazim (Bavistin 50WP @

2.5g/kg seed), tebuconazol Raxil 2DS @ 1.25g/kg seed) if the disease level in the seed lot is high. If it is low to moderate, treat the seed with a combination of Trichoderma viride @ 4g/kg seed and half the recommended dose of carboxin.These are systemic fungicides and are absorbed by seed or in growing plants. Before these chemicals were investigated hot water treatment was in use and was very good method of controlling wheat smut specially in countries like India where summers are bright sunny and temperature rises upto 45 C. To carry out hot water treatment, the seeds are socked in ordinary water on a sunny bright day from 8 a.m. to 12 noon (The mycelium inside seed become active) followed by exposure to sun from 12 noon to 4 p.m. to dry (The active mycelium is killed by heat). Early roughing of infected plants in the field must be done.

The studies on the inheritance revealed that resistance is controlled by single dominant gene or by few genes. However, wheat breeding efforts in this direction are not adequate. As a result existing high yielding wheat varieties are susceptible to loose smut. Some promising strains of wheat viz, HD 2197, HD 2203, HD 2221, HD 4502, HD 4549, HI 7483, HI 7525, HI 7595, HI 7717, HI 8073, NP 789, NP 791 MACS-9, E 559, E 140, E 3320, WR 29, BW 7, BW 11, VL 428, VL 639 HDR 43, K 8027, HS 87, HB 1364, DL 108-3 etc. are reported to possess fairly good degree of resistance. These strains can be used as resistance donors for breeding for loose smut resistance.

6. Karnal Bunt of Wheat Karnal bunt was first reported by Mitra in 1931 from Karnal, a place now in Haryana state of India from where the name Karnal bunt originates. This fungal disease is causing severe losses to wheat in India, Pakistan, Mexico, Iraq, Afganistan and a few states of southwestern United States. Karnal bunt was found in traces and in isolated pockets of northwestern region of India earler and was considered a disease of minor importance till 1974. The surveys in India undertaken later showed that KB can cause losses upto 20% in susceptible cultivars such as WL 711 and WG 357 etc. Karnal bunt has been listed as quarantine pest in 21 countries. In addition to yield losses, the quality of grain is also deteriorated directly affecting its market and export value .The quality of the flour from wheat mixed up with infected grains and the finished product like “chapati.” etc. are fishy in odor. This odor is due to the production of a chemical, trimethylamine by the fungus. Wheat containing 3% bunted grains is unfit for human consumption. Affected grains however, appear nontoxic.

Symptoms: Karnal bunt is principally a disease of grains. The (grains are either partially affected or in severe cases the whole grain is converted into black powder of bunt spores (Fig.3). In a stool all the ear heads are not infected and in an ear all the grains are not infected. In severely infected spikelets, the glumes spread apart, forming a greater angle with the main axis and bunted grains may fall down on the ground. Initially the smut sorus is covered with a membrane (pericarp) but when it brust black masses of spores are exposed, resulting in bunt smell. The spores may blow off or may fall on ground and thus the inoculum is not resticted to only infected fields but can spread to distant places.

Pathogen: Tilletia indica Mitra or Neovossia indica (Mitra) Mundkur. Mitra reported the causal organism of Karnal bunt as Tilletia indica but later in 1944 Mundker renamed it as Neovossia indica.The bunt pathogen belongs to genus Tilletia = Neovossia, family Tilletiaceae, order Ustilaginales and class basidiomycotina. The Karnal bunt affects wheat, durum wheat, triticales and rye (susceptible only by inoculations). Five pathogenic populations viz, KBAg-1, KBAg-2, KBAg-3, KBAg-4, KBAg-5 are known to exist in N. indica. The teliospores of these pathotypes differ in the arrangement of surface rodlets and

can be divided into three broad groups (1) rodlets compact and regularly arranged (2) rodlets loose and irregular and (3) exines very loosely and irregularly arranged. KBAg-2 is virulent and contains highest contents of lipids, nitrogen, protein sugars and also has linolenic acid while less aggressive isolate KBAg-6 have lesser amount of these constituents and does not have carpic and pentadecenoic acid and thus both the isolates behave differently.All these isolates showed different Rf values in polyacrylamide gel electrophoresis analysis.

Disease Cycle: Mitra reported the karnal bunt as soil borne disease but now its airborne nature has been well established. The fungal spores are also carrired as contaminent on farm equipment, operational tools or by man moving from milling places. The spores remain viable in soil, wheat straw and farm yard manure for several years (2 to 10 years). The source of primary inoculum is either soil or seed contaminated with teliospores. The teliospores are spherical to oval, reticulated with curved spines and measure 22-49 um in diameter. Each teliospore consists of three layers, perisporium, episporium and endosporium.

Teliospores in the soil germinate at suitable temperature (15 to 25 C) and moisture. This condition normally prevails during February and first week of March in North Indian plains. Each teliospore produces promycelium on germination which produces as many as 110-185 primary sporidia at its tip. The primary sporidia are sickle shaped and were considered to be the infective entities. But now it has been established that two kinds of secondary sporidia- allantoid and filiform types play an important role in the disease cycle of the pathogen. The allantoid sporidia are only pathogenic and filiform sporidia help in the multiplication of inoculum on host/soil surface. Mature teliospoes contain a single diploid nucleus which divides meotically into two as the promycelium emerged. The daughter nuclei further divide mitotically and their number increases. Simultaneosly the sporidial initials are formed at the tip of promycelium which elongate and become filiform. The nuclei move towards the tip and finally the nucleus migrate into the sporidial initial. The mature sporidia are sickle shaped, detach from promycelium and then carried to the flower either by wind currents or by water splash. The sporidium elongates and the nucleus undergoes mitotic division producing two nuclei. The two nuclei become separated by a septum making the sporidium bicelled. The majority of sporidia are binucleate. The sporidia germinate and the germ-tube penetrates the developing grain through stigma or through the ovary wall. Normally infection takes place at the time of anthesis. Majority of grains are partially affected but in severe cases whole grain may be infected.

Control: Karnal bunt is difficult to control due to its mode of perpetuation. The control measures in the field are: to avoid sowing of highly susceptible cultivars in the endemic areas; use of disease free seed; avoiding excessive nitrogen fertilizers or irrigation particularly at flowering time and avoiding the late planting. Crop rotation and use of plastic mulches (soil solarization) is also helpful in management of the disease.

Seed treatment with fungicide may reduce the incidence but is not effective to eliminate the complete infection as the pathogen is soil borne. Since the disease is air borne also, one foliar spray by fungicide, propiconazole (Tilt 25EC20.1%) should be given at the time of anthesis. Integration of one spray of propiconazole with one spray of bioagent fungus, Trichoderma viridae (0.4%) gives almost cent percent control. The bioagent spray should be done before earhead emergence followed by spray of chemical at start of earhead emergence. Use of resistant varieties is the most effective method for controlling the disease. Among the present day varieties, PBW 502 is resistant while the others show various degree of susceptibility.

7. Powdery Mildew of Wheat Powdery mildew is a destructive disease when it appears in severe form. For example, in Canada the infection of the disease was observed up to 80 percent during years of heavy infections. In India, the disease is mostly confined to northern and southern hills but sporadically appear in plains and foothills of the country.

Symptoms The symptoms start as superficial greyish small patches of white cottony growth on leaves, stem, sheath and even on ear. The patches may appear on both surfaces of the leaves. The white cottony growth can cover the whole leaf and other aerial parts of the plant (Fig.4). The white patches turn into brownish to dull tan colour late in the season due to formation of cleistothecia. The mildew colonies are surrounded with chlorotic or yellow areas resulting decease in photosynthetic rate. The affected leaves die off prematurely. The cleistothecia remain on wheat debris. At times, development of the ears is checked partially or wholly.

Pathogen: Erysiphe graminis f. sp. tritici = Erysiphe graminis var. tritici (D.C.) E. Marchel. The fungus belons to family Erysiphaceae, order Erysiphales and sub-division Ascomycotina. E. graminis is an obligate parasite. Primary mycelium of the fungus forms appresorium and haustoria. Each haustorium is divided into finger-like structures which enter in the epidermal cells and supply food to the mycelium. Conidiophores develop on the mycelium which produces conidia or oidia in a basipetal manner. The mature conidia at the top are released first and others are released in the succession and blown away by wind currents to healthy plants and cause infection. This asexual cycle of the fungus is repeated several times during the crop season. At the end of the season, the sexual parts develop at the tips of mycelium. Two opposite mating type which are uninucleate fuse together and dikaryotization takes place. The dikaryotic cells develop secondary mycelium. A series of cells on this mycelium form ascogenous hyphae and convert into cleistothecia.The cycle is repeated till the death of the invaded cell. The cleistothecium is globose in the beginning but later depressed and its colour is also changed from white to brown or black. Each cleistothecium contains 9 to 30 oval shaped asci which are pedicellate. In each ascus there are 8 ascospores or sometimes four which are formed when affected leaves are dried. Several physiological races are present in the pathogen worldwide.

Fig 4 Powderu mildewq of wheat (Erysiphe graminis f.sp. Fig 5. Helminthosporium blight of wheat tritici)

Disease Cycle: The cleistothecia of the pathogen remain attached to the infected straw after the crop is harvested. The pathogen survives the off season in the cleistothecial stage. Under favourable conditions, the ascospores are released ( December-January ) bring about primary infection, secondary infection is by air borne oidia which reach to the crop by wind and develop typical mildew colonies, sporulate (asexually) and infect newly developing wheat leaves. The infection is favoured by the temperature (15-20 C) and high relative humidity. As the crop matures and temperature rises, the pathogen produces perithecia which remain dormant in straw and debris after harvest to provide the primary source of inoculum for the next season.

Control: Based on analysis of powdery mildew samples on 11 Pm lines (differential set) 41 pathotypes were recognized in the country. Different Pm genes combinations were found effective against powdery mildew and should be utilized for breeding resistant varieties. However, present day varieties are not resistant to powdery mildew. Hence, the disease severity is more in some pockets. Avoid excessively dense stands by using adequate seed. Powdery mildew fungi are unique among the plant pathogens showing high response to sulphur and related fungicides. Several systemic fungicides such as benlate (0.1 %), kerathane (2 lb /ha) etc. can control powdery mildew through foliar sprays. Seed dressing and soil drenching with 0.01 % calexin was also found effective. One spray of propiconazol (Tilt [email protected]%) on disease appearance is highly effective.

8. Alternaria Blight of Wheat Alternaria blight causes significant yield losses in wheat in the Indian subcontinent, from where it originates and has spread throughout the world. The disease was considered as minor but the increase in the severity of leaf blight may be due to new cultural practices and use of new germplasm. In India, The epidemic of the disease was observed during 1964 – 65 and 1965-66 in eatern Uttar Pradesh. It causes severe damage to certain wheat varieties and reported to have acquired severe proportions in the recent past.

Symptoms: Wheat plants with Alternaria blight are affected when they are 45-50 days old. The symptoms appear as discoloured, oval lesions on the lower surface of leaves (Fig5). The disease progresses upwards, lesions enlarge and coalesce to irregular, dark blotches, often with chlorotic margins. However, youngest leaves are not usually affected. Heavily infected fields show a brunt appearance, even from a distance. Severely infected seeds are discoloured and shriveled. During humid weather the pustules are covered with black spores and most of the leaves of severely affected plants become dry. A temperature around 25C, coupled with high humidity, favours the disease.

Pathogen: Alternaria triticina Prasada and Prabhu is the causal organism of the disease. The genus Alternaria belongs to family Dematiaceae, order Hyphomycetales, class Hyphomycetes and division Eumycota. The mycelium of the fungus is colourless in the beginning but later turn deep olive. The conidiophores are 17 – 28 µm. long and 3 -6µm wide. The conidia developed on conidiophores in acrogenous succession. Conidia are irregularly oval, ellipsoid conical, generally tapering into a beak, 15 -92 x 8-35 µm, with 1 - 10 transverse septa and 0-5 longitudinal septa, light brown to dark olive buff becoming darker with age. Two physiologic races were found in the pathogen.

Disease Cycle: Wheat is the only host of Alternaria blight. The disease is seed as well as soil borne. The inoculum survives as conidia on the surface of seeds and also as deep seated mycelium in seeds. The conidia germinate on the lower surface of the leaves at temperature

of 5-35 C but the optimum temperature for germination is 25 C with 100 % humidity. Large numbers of conidia develop on affected leaves in dark, dispersed by wind and infect healthy plants. The maximum infection takes place when the crop is 45-50 days old.

Control: Only certified seed must be used and shriveled seeds should be discarded. The seed infection can be eliminated by keeping the seeds in cold water for 4 hours followed by 10 minutes in hot water at 52 C. Seed treatment with Vitavex @ 2.5 g/kg or with 0.2 % Rovral can remove the seed infection. One spray of Fungicide, propi-conazol (Tilt [email protected]%) can control the disease. To manage soil infection the crop debris must be brunt. Only recommended doses of fertilizers should be used. In NP 52 a pair of recessive genes governs resistance and two pair in NP 824 and NP 809. Presently, no wheat variety is resistant to Alternaria blight.

9. Yellow Ear Rot of Wheat The disease is popularly known as “tundu” disease and vernacularly known as “tanan”. This disease was first reported from Punjab province of India. Now the disease is known to occur in India, Egypt, China and Australia.The disease occurs in the prence of a nematode known as ear cockle nematode, Anguina tritici and a bacterium, Corynebacterium michiganensis tritici and never observed individually. There is no grain formation in the ears of affected wheat. The disease incidence ranges between 0.5 to 50%. Sporadically, it is reported to be very serious in some places in Bihar and some eastern U.P. districts. The disease incidence depends on the degree of contamination of wheat seeds with galls at the time of sowing.

Symptoms: The symptoms appear as twisting and crinkling of lower and middle leaves of affected plants (Fig.6). A slime is produced which cover the whole ear and other parts of the plant like glume and stem resulting sticking of these parts together. Because of twisting and sticking, the growth of affected plant is retarded and stem becomes deformed. Near maturity of the crop, oozing of the slime is visible from tissue of affected plants under humid conditions. However, if the weather is dry the slime becomes hard and turns to dark yellow or brown in colour. Most of the grains in the ear are converted in to galls due to nematodes. The nematodes serve as a vector of the yellow ear rot pathogen. The disease occurs only in the presence of ear-cockle nematode, Anguina tritici. For the maximum expression of yellow rot disease disease a combination of 0.4 optical density of the bacterium and 10 larvae of the nematode is required.

Pathogen: Clavibacter tritici, a bacterium which belongs to genus Clavibacter, class Thallobacteria, division Firmicutes and Kingdom Prokaryotae is the causal organism.The bacterium is a gram-positive type, nonmotile and pleomorphic in nature. In synthetic medium, it develops yellow pigmented colonies.

Disease Cycle: The disease is developed only when both nematode (Anguina tritici) and bacterium (C. tritici) are present in plant. The bacterium alone is not capable to produce the disease. Under favourable conditions of low temperature of 10-15C and high humidity (70- 100%) the bacterium multiplies and expresses itself in the form of yellow slimes on the leaves of young plants. It has been observed that for the maximum expression of the disease a combination of 0.4 optical density of the bacterium and 10 larvae of the nematode is required. The causal bacterium remains in and around nematode galls. When seeds contaminated with galls are sown, The galls swell due to moisture in the soil and nematodes come out from swollen galls. The bacteria attached to these galls also move with nematodes either already attached to nematode body insiside the galls or stick to them while nematodes coming out of

the galls. Thus both the pathogens infect the host simultaneously and cause their own disease. The nematodes convert the grains into galls and these galls along with the bacterium are harvested with the crop. The cycle is repeated when such seeds are used. Control: The disease is managed by the use of certified seed, removal and burn of affected ears and summer ploughing of affected fields to kill the nematodes by natural heat during May-June. The galls from mixed seed can be removed by brine-water treatment as for ear cockle disease (next disease).

Fig 6. Yellow ear rot symptoms of wheat

10. Ear Cockle Disease of Wheat Ear cockle nematode is a parasitic nematode and found throughout the world wherever wheat is grown.The ear cockle nematode is still common in Eastern Europe, parts of Asia and Africa. It is widely distributed in most of the wheat growing parts of India and cause considerable loss to the crop annually. It is mostly found in some parts of northern India especially the states of Bihar, Jharkhand, eastern U.P. and Chhatisgarh

Fig 7. Ear cockle disease of wheat in field Symptoms: The first symptom is the basal swelling of the stem at the ground level with a whitish tinge. Infected seedlings are severely stunted and show characteristic basal enlargement of the stem, rolling, twisting and crinkling of leaves (Fig.7). As the plant does not have erect leaves, it remains stunted. The nematode infesting seedlings show profuse tillering which starts earlier than healthy ones. This increase number of tillers does not necessarily means an increase in the number of ear-heads, only few are only the productive tillers. The nematode juveniles reach upto the growing point and start feeding ectoparasitically and reach upto the developing ear. On initiation of the leaf primordia these nematodes act as endoparasite and initiate production of galls preferably on staminate tissue. The galls and the grains develop side by seed in the same floret. Number of galls produced in

a spikelet varies from 1 to 5 seedgalls in the beginning are greener and smooth but later turn brown or black as the head matures. Diseased heads are shorter than healthy ones and remain green longer than healthy heads. The galls are shed off the heads more readily. In case of severe infections the plant may die prematurely.

Pathogen: Anguina tritici (Steinbuch) Filipjev is the causal pathogen and belongs to family Anguinidae, order Tylenchida, class Secernenitea, and phylum Nematoda in the kingdom of Animalia. This is one of the few parasitic nematodes that infects above ground parts of the plant. The pathogen is a large nematode about 3.2 mm long and 120 µm in diameter. The nematode lays its eggs and produces all its juvenile stages including adult stages in seedgalls. The seedgalls contain thousand of infective J2 juveniles. These juveniles come out of seed galls on receiving moisture when seeds are sown and infect the growing point in the plumule.

Disease Cycle: Ear cockle disease perpetuates year after year through the seed contaminated with cockles or nematode galls. The seed contaminated with cockles or galls when sown, the galls absorb water from the soil, become soft and liberate the second stage juveniles which infect the seedling. In temperate countries the galls which fell down during the harvest of the crop are considered as one of the sources of inoculum but in India such a situation is not functional. In India, during rainy season juveniles emerge and perish in the absence of host plants. The juveniles enter the seed, both at brush and embryo ends. Juveniles entering seed embryo can reach the growing point of seedling and start feeding as ectoparasitically. On initiation of floral primordial, the juveniles become endoparasitic and start producing galls. The juveniles in the developing galls undergo three successive moults and developed into males and females. The number of adult nematodes in a gall vary depending on the size of gall ( 16-85). Each fertilized female lays eggs in hundreds inside the gall. The adults die soon after oviposition. The eggs hatch and develop into second stage juveniles. Near maturity of the crop each gall may contain upto 12000 juveniles in anhydrobiotic stage in which the organism does not show any visible sign of life and metabolic activity is hardly detected. The second stage juveniles are resistant to dessication and can survive in the galls upto 30 years. They produce only one generation per year.

Control: The disease can be controlled by using certified seed, free from galls. The seed can be cleaned by sieving or by seed floatation in fresh water. The seed lots are floated in 2-5% brine solution. The galls, which float on the surface, can be easily separated and destroyed away from the field. The seeds thus cleaned should be washed with clean water and used for planting.No resistant variety has been found except one cultivar Saber beg in Iraq. Since floatation is a very effective method to control, chemical or biological approaches has not been tried much. Crop rotation in affected fields is also recommended.

Diseases of Rice 1. Blast Disease of Rice Blast disease of rice is one of the earliest known plant diseases. Now it is of worldwide occurrence wherever rice is grown. In India, blast disease occurs in rice crop of all the states where rice is commercially grown. The disease is quite common in areas of high rainfall and in irrigated areas where the crop is highly doses with nitrogen. Several epidemics due to blast have been experienced in different parts of the world resulting losses in yield from 50 to 90 percent. In India, the yield loss during the year 1960-61 was estimated to 2,66,340 tonnes.

Symptoms: The blast symptoms appear on leaves and other above ground parts of rice plants although leaves and the neck of the panicle are more commonly affected.. The affected leaves developed water soaked, boat shaped white to grey lesions (Fig.8). The lesions may be from 0.5 cm to several centimeters in size and they are surrounded by a yellowish halo. The lesions enlarge and coalesce with each other covering the whole leaf surface and the leaves subsequently die off. Other parts of the plant such as stem, leaf collar, stem nodes and occasionally the internodes are also affected. On stem nodes, brown to black lesions are formed and cover 1 to 2 cm on both sides (Fig.9). After the heads are emerged, the fungus attacks the peduncle neck node, which is girdled. This stage is known as neck infection which is most destructive. If neck infection is at an early stage, the panicles become erect and grains do not fill but if the infection is late, the grains are partially filled. However, in such a situation the panicle base is broken due to grain weight and and weaking of neck tissue. Such panicles hang down (Fig.9) and are visible in a rice field even from distances.

Fig.8. Leaf symptoms of Fig.9 Node and Neck Blast symptoms of Rice Rice Blast Pathogen: Pyricularia oryzae Cavara (It is not distinguishable from P. grisea (Cooke) Sacc.) The pathogen belongs to family Moniliaceae, order Moniliales and sub-division Deuteromycotina.

Perfect or Teleomorphic stage is Magnaporthe grisea Kato and Yamaguchi (This stage has not been found in nature but developed experimentally in the laboratory). In nature, most of the pathogen isolates are of the same mating type (male) and do not cross with each other. The teliomorphs were produced in the laboratory by crossing appropriate isolates. The pathogen produces septate, branched, and hyaline to olivaceous mycelium which is localized in lesions. The conidiophores emerge from the leaf through stomata or by rupturing the cuticle. The conidiophores bear terminal pear shaped or pyriform conidia having 1 to 3 septa but majority is biseptate. The conidia develop in succession and each cell of the conidium is uninucleate. Conidia measure approximately 20-25 X 8.5-9.5 micron. The pathogen produces several toxins such as piricularin, and alpha picolinic acid etc.The blast pathogen have several physiologic races. In India, about 32 races have been reported but races 3(1C3) and 1(1D1) are more virulent.

The perfect stage of the pathogen is Magnaporthe grisea (Hebert.) Barr. which belongs to ascomycotina. Perithecia of this fungus occur singly or in groups without apparent stroma. The asci are beak-shaped, cylindrical to subclavate containing fusiform hyaline four celled ascospores. The asci arose from the base of perithecium and measure 7-10 X 55-90 micron. Ascospores measure 4-7 X 17-24 micron.

Several physiological races are recognized in P. oryzae based on infection types developing on different hosts by artificial inoculation. Cytological studies have shown that the chromosome number in nuclei varies from 2-12. The pathogenicity of individual conidia continues to segregate in each generation. Asynchronous division, nondisjunction and lagging chromosome appear to be the cause of differences in chromosome numbers. The unusual nuclear behaviour explains the pathogenic variability in blast fungus.

The nature of rsistance in rice varieties due to blast has been studied over the past 50 years. Silicification of the epidermal cells of rice plant is considered to confer resistance against blast as it prevents the entry of the pathogen. Heavy nitrogenous manuring decreases silicate accumulation in rice plants which makes the plants susceptible to the pathogen. Rice plants have several prohibitins which are phenolic in nature. The nitrogen nutrition greatly influences the concentration of prohibitins and their oxidation. In a resistant variety browning reaction or necrotic response is due to irreversible oxidation of polyphenols of the host tissue. There is an increase in the hydrogen peroxide level of the infected tissue leading the rapid death of infected tissue. The blast pathogen produces a few toxins such as alpha picolinic acid, piricularin and pyriculol. Phenolic compounds detoxify alpha picolinic acid while the resistant tissues detoxify piricularin to non-toxic substances.

It appears that there are several genes confer blast resistance to rice varieties. The higher is the degree of resistance of a variety, the fever are the races of the pathogen that would be virulent to that variety. The rice varieties fall under the botanical group of japonica, indica, javanica and glaberrina differ in their genetic behaviour nd can provide potential for breeding new blast resistant varieties of rice.

Disease Cycle: The pathogen overseasons as mycelium and conidia on rice straw and seed from contaminated crops. The inoculum may also survive on graminaceous weeds near the crop or on overlapping crops of rice. The pathogen produces and releases conidia in abundance at a favourable temperature and relative humidity of 90% or more. The conidia can be formed at temperatures between 15 and 32 C but the optimum is between 20 and 28 C. The mature conidia are released by wind and reach to the healthy plants. On landing to the healthy plants, the conodia adhere by producing mucilage at their tips. Conidia germinate in the presence of free water through a germ tube. The germ tube produces an appresorium which produces and accumulate melanins which help the appresorium to penetrate the host. The infection may also take place through stomata. Seedlings and young leaf tissues are comparatively more susceptible to infection. Under favourable conditions, new lesions may develop within 4 to 5 days after infection. Newly formed conidia are released within hours and continue for several days. Low temperature (about 20C) and excessive dew during night may increase the intensity of the disease. Most of the conidia are released after midnight to sunrise. This cycle is repeated several times till the crop is harvested or temperature rises

Control: Th grows resistant varieties is the best option. The registant genes have been identified in more than 13 rice cultivars. However, the resistance is break down due to appearance of new races. Therefore, resistant varieties need to be developed more frequently.

Rice cultivars like Java, Vani, Akashi, IR-8, IR-36 etc. are some of the promising resistant cultivars. Other methods like use of certified seed, burning of rice remains from the field, early sowing, avoid excessive doses of nitrogen and use of fungicides are also helpful in controlling the blast disease. Several fungicides are being used for controlling rice blast viz; mancozeb, edimfos, benomyl carbendazim and antibiotics such as blasticidin -S and kasugamycin at 20 ppm.. Systemic fungicides, pyroquilone and tricyclozone were found to provide better control as these fungicides interfere in melanin production by the appresorium thereby inhibiting the entry of the pathogen to the host plant. Rabcide 20% solution @ 1.5 kg/ha spray can control both leaf and neck blast.

2. Brown Spot Disease of Rice Rice brown spot is a historical disease because it caused a major outbreak in Bengal in India in 1942 when approximately two million people died of starvation. The disease is widely distributed in India, especially in West Bengal, Orissa, Andhra Pradesh and Tamil Nadu.

Symptoms: The symptoms first appear as brownish spot on leaves and glumes of the plant. The disease causes blight of seedlings. On seedlings, the pathogen produces small, brown lesions, which may girdle the coleoptile and cause distortion of the primary and secondary leaves. In some cases, pathogen may also infect and cause a black discolouration of rootsatt. Infected seedlings are stunted or killed. On the leaves of older plants, the pathogen produces circular to oval lesions that are grey at the centre and brown at the borders measuring about 0.5-2mm X 2-5mm (Fig.10). On moderately susceptible cultivars, the pathogen produces tiny, dark specks. When infection is severe, the lesions may coalesce, killing large areas of affected leaves. The pathogen causes main damage Fig.10. Brown spot of rice by attacking the leaves at seedling stage. At times the neck region may be infected causing similar symptoms to those of neck blat caused by P. oryzae. The affected plants become weak and the yield is drastically reduced. The grains show a black discoloration.

Pathogen: Helminthosporium oryzae Breda [Syn: Bipolaris oryzae Breda de Hann) Shoemaker] is the causal pathogen which belongs to family Dematiaceae, order Moniliales and sun-division Deuteromycotina. The perfect stage is Cochliobolus miyabeanus Ito and Kubribayashi. C. miyabeanus belongs to the subdivision Ascomycotina, the sac fungi. The brown mycelium is inter or intracellular in the host. The conidiophores are multiseptate upto 600µm long and 4-8 µm wide and develop singly or in bundles (generally 17). Conidia are generally curved, boat or club shaped with 6-14 septa, 63-153 x 14-22 µm and often with a minute, slightly protruding hylum, by which they are attached to conidiophores. The conidia are born singly and successively at regular intervals on the upper part of the conidiophore in a sympodial manner.The conidia are dispersed by the wind. These spores are asexual; they do not rise from sexual crosses, but rather act as a method of dispersing the pathogen. A consequence of this is that the pathogen can spread rapidly in devastating epidemics. The conidia germinate readily, producing germ tubes mostly from both the end cells. The perithecia of the perfect stage pathogen (C. miyabeanus) are globose with the outer wall dark yellowish brown and parenchymatous, and with ostiolar beak.The asci are cylindrical, slightly curved and contain 4-6 ascospores. The ascospores are hyaline, long cylindrical with 6-15 septa and measuring 6-9 X 240-268 micron.

Disease Cycle: The fungus overwinters mainly in infected plant parts. The pathogen is not soil borne. This disease occurs naturally on as many as 20 different wild species of Oryzae. A few collateral hosts like Digitaria sanguinalis, Echinochloa colona, Pennisetum typhoides Setaria italica and Cynodon dactylon, on which the pathogen is recorded, may serve as a source of primary inoculum. The conidia carried through infected rice seeds are are also the primary source of inoculum. The conidia germinate on the emerging seedlings and produce several generations asexually as the plants grow. They are blown away by wind and cause infection to the new crop and thus serve as the source of secondary infection. The optimum temperature for the germination of conidia is 25-30C and humidity 90% or above. If seedlings are affected crop yield is drastically reduced. The pathogen can spread fast and may cause devastating epidemics.

Control: As the disease incites discolouration of the tissues, phenolic prohibitins present in rice tissues are associated with disease resistance. The reducing agents such as ascorbic acid and glutathione enhance the tissue susceptibility. The pathogen produces a toxin, obliobolin. The varieties, BAM-10, CO-20, and IR-36 etc. are some of the resistant varieties. Plants growing in good nutritional conditions are generally resistant to the disease. The susceptibility to infection appears to be a deficiency in available silicon. Preventive treatment of the field with calcium silicate may be used in deficient soil. Seed treatment may ward off the seedling blight phase.

3. Bacterial Blight of Rice The blight disease is widely prevalent in Asian countries including India. With the introduction of rice variety Taichung Native-1 (TN-1) in India the disease spread rapidly as TN-1 is highly susceptible to rice blast. The disease is now found in all the rice growing areas of the country both on indigenous and exotic varieties. The disease was not considered serious until 1962 when epidemics broke out in Bihar and other parts of North India. Epidemics of this disease were also witnessed in non-traditional rice growing areas of Punjab and Hariyana.

Symptoms: Symptoms appear on the margins of leaf blade and sheath as small, linear, water- soaked areas that soon elongate and coalesce into irregular, narrow, yellowish and brownish stripes. Droplets of white exudates are found on the stripes. During severe infection, the leaves become yellow and start dying from the tip downwards. Small lesions are also seen on the kernels. As the disease progresses, several lesions may coalesce to form straw brown large lesions or blighted portions (Fig.11).

Fig.11. Bacterial Blight of Rice caused by Xanthomonas oryzee The disease develops mainly in rainy and humid weather and becomes more severe at the time of grain formation. If seedlings or young pants are infected they show wilting a stage

known as Kresek stage. This stage commonly occurs within 3-4 weeks after transplanting of the crop. Leaf blight phase is the most predominant form of the disease occurring between tillering and heading stage of the crop. When the affected leaves are cut and immersed in clear water in a test tube a turbid ooze of the bacterium, streaming from the vascular bundles can be seen.

Pathogen: The bacterium, Xanthomonas oryzae pv oryzae = X. campestris pv oryzae (Ishiyama) Dye is the causal organism. The bacterium is rod shaped 1-2 x 0.5 -0.8 µm in size occurring singly or in pairs, gram-negative, aerobic and non-spore forming with a polar flagellum which helps in movement. The bacterial cells are surrounded by mucus capsules which are soluble in water and precipitated by acetone. It is a kind of heteropolysacchride. Wax yellow coloured bacterial colonies are formed on synthetic media. It does not produce indole, nor does it reduce nitrate, and it may or may not liquefy gelatin and produce H2S. The pathogen is found in several strains. Five different pathotypes have been identified in Japan but in India only two pathotypes have been reported based on the reaction on international set of differentials.

Disease Cycle: The blight disease of rice is a vascular disease. The primay infection may result from the inoculum overwintering in seed or in crop residue or on overlapping crops. It may also survive in soil. The primary inoculum may also be build up from soil or plant stbbles and debris and can infect nursery seedlings. The bacterium infects some grasses like Leersia spp. which might play a role in the spread of the pathogen. It is disseminated through irrigation water and wind-borne rain. The bacteria enter in the host through roots, stem near ground or hydathodes in leaves. After infection it becomes systemic in the vascular bundles and move upward. The disease spreads fast at a temperature of more than 25 C with a combination of rainy weather or in crops where excessive fertilizer is used.

Control: Control measures are the use of resistant cultivars, certified disease free seed and crop rotation. A mere soaking of seed for 8 hr in Ceresan (0.1%) and steptacycline-crude agricultural preparation (3g in 1100 litre of water) is effective to eradicate seed infection. Spraying with copper fungicides alternatively with streptocycline (250 ppm) is effective in controlling bacterial blight. Varities like TKM-6 and IR-42 and Chinsurah Boro II are tolerant to disease.

4. Sheath Blight of Rice Sheath blight is one of the serious diseases of rice and sometimes important to other cereals as well. It is found worldwide wherever rice is grown. The banded leaf blight symptoms of this disease have been reported from Uttar Pradesh.

Symptoms: The symptoms develop as large, irregular, and oval to elliptical, green grey, water- soaked lesions on the sheath of leaves and have a straw coloured centre and a wide reddish brown margin (Fig.12). These lesions first develop near the water line on sheath or lower leaves when plants are in the late tillering or early internode elongation stage. These lesions usually develop just below the leaf collar about 1/4 inch wide and 1/2 to 1.1/4 inch long. With age, the lesions expand and the centre of the lesions may become bleached with an irregular tan to brown border. Seedlings and mature plants are blighted when humidity exceeds 95% and temperature in the range of 15-35C. Disease development progresses very rapidly in the early heading and grain filling growth stages during period of frequent rainfall and overcast sky. The grains in the lower parts of penicle are poorly filled. Additional losses result from increased lodging or reduced ratoon production due to reduced carbohydrate

reserves. Near maturity of the plants dark brown coloured sclerotia are produced superficially on or near the lesions and easily fell down on soil.

Fig.12. Sheath blight of rice

Pathogen: Rhizoctonia solani Kuhn. is the causal organism. The perfect stages is Hypochnus sasakii Shirai = Corticium sasakii (Shirai) Matsumoto = Thanatephorus cucumeris (Frank) Dark.The pathogen belongs to order Mycelia Sterilia of the sub-division Deuteromycotina. The mycelium is colourless when young but turn yellowish to light brown with age, consists of long cells and produces branches at the right angles to the main hypha and have a cross wall near the junction. The sclerotia are flattened on the lower side and are loosely attached and easily dislodge from the plant. The basidia are 10-15 x 7-9 µ and the sizes of basidiospores are 8-11 x 5-6.5µ. The pathogen grows over a wide range of temperature, the optimum ranging from 28-30C.

Disease Cycle: The primary source of inoculum comes from sclerotia and they survive between the crops. When the rice crop is planted, the sclerotia float on the surface of flooded water and infect the plants near the water line. Sclerotia can survive one to several years in soil. Further spread takes place by rain, irrigation and tools carrying soil contaminated with the pathogen. The infection can take place with a temperature ranging from 15 to35 C and 95% humidity. The pathogen can infect and survive on certain weed hosts which may also serve as the source of inoculum for further spread of the disease. The mycelium grows inside the tissues in all directions, initiating secondary spots, in turn producing sclerotia on the spots. The disease is highly destructive during humid and warm temperatures. High dose of nitrogenous fertilizers make the tissue more susceptible to the disease while high potassium induces resistance to the disease.

Control: New vaieties and changing cultural practices often combine many of the factors that favour disease development. In recent years, wide acceptance of susceptible varieties, because of their high yielding potential, has contributed greatly to the rapid increase in the incidence of sheath blight. To manage the disease, application of heavy doses of nitrogen should be avoided as it predisposes plants to infection. Close transplanting of rice plants and wet and poorly drained fields for cultivation of rice should be avoided. The fields may be kept clean with grasses and weeds. Other measures like crop rotation, multching during summer, biological control may be helpful. Resistant varieties if available should be used and foliar fungicides may be economical for reducing sheath blight infection. In heavily infected patches, soil drench with 0.1% wet Ceresan will be useful.

5. Tungro Disease of Rice Tungro disease is most destructive to rice in countries of Southeast Asia. Outbreaks of the disease are common in one part or the other in India. In severe cases of infection or infection during early stages of plant growth the yield loss may be as high as 100%. The damage

depends on the variety used, plant stage at the time of infection, strain of the causal virus and environmental conditions.

Symptoms: Affected plants show discoloration of the leaves which begins at the leaf tip and move down to the lower leaf portion (Fig.13). Young infected leaves show interveinal chlorosis and incomplete emergence. The tillering is reduced and plants become stunted. The flowering on infected plants may be delayed and most panicles are sterile or with partially filled grains with dark brown spots. The symptoms may be confused with nitrogen and zinc deficiencies or water stress or insect damage or other virus diseases like grassy stunt and orange leaf.

Pathogen: Tungro disease is associated with rice tungro bacilliform virus (RTBV) and rice tungro spherical virus (RTSV) (Fig.13). Both the viruses appear responsible to cause infection simultaneously by the leafhopper, Nephotettix virescens (Distant). RTBV can not be transmitted by leafhopper vector in the absence of RTSV. RTBV particles are bscilliform in shape measuring 100 to 130 nm in length and 30 to 35 nm in width and contain ds DNA of 8.3 kb. RTSV particles are isometric and 30nm in diameter and contain ssRNA of about 12kb.

Disease Cycle: The inoculum of the virus survives on rice or some wild relatives in the nature from where the infection takes place to the rice crop plants by the leafhopper vector. The vector can acquire the virus while feeding on infected plants within a feeding period of minimum 30 minutes and transmit it immediately when feed to healthy plants for a few minutes. After acquisition of the virus the leafhopper can transmit the virus from 5 to 8 days and after that become nonviruliferous or no virus is retained by the vector and would require reacquisition feeding.

Fig.13. Tungro disease of rice and its associated virus particles

Control: Planting of resistant varieties either to vector or virus is the most economical means of managing the disease. The resistant varieties to the virus are now available in India and neighboring countries. Eliminating the hosts of the viruses and vector and to destroy stubbles after harvest is also advisable.

Diseases of Maize 1. Stalk Rots of Maize Stalk rots are caused by several fungi and bacteria which affects the plants near maturity. Losses from stalk rot vary region to region and are estimated 10 – 20 %. Losses are caused either by poor filling of the cobs or due to lodging of affected plants. The following pathgens are associated with stalk rot of maize.

Bacterial Pathogens: Pseudomonas avenae sub-sp. avenae Manns. Enterobacter dissolvens (Rosen) Brenner et al. = Erwinia dissolvens (Rosen) Burkholder Erwinia carotovora sub-sp. carotovora (Jones) Bergey et al. = E. chrysanthemi pv. Zae (Sabet) Victoria et al.

Fungal Pathogens : Colletotrichum graminicola (Ces.) G.W. Wils., Telemorph: Glomerella graminicola (Politis), G. tucumenensis (Speg.) Arx & E. Muller. Physoderma maydis (Miyabe) Miyabe Diplodia maydis (Berk.) Sacc. Fusarium moniliforme J. Sheld var. subglutinans Wollenweb & Reinking Gibbrella zeae (Schwein) Petch. (Anamorph: Fusarium graminearum Schwabe. Setophaeria turcica (Luttrell) K.J. Leonard & E.G.Suggs (Anamorph : Exserohilum turcicum (Pass.) K.J. Leonard & E.G. Suggs = Helminthosporium turcicum Pass. Pythium aphanidermatum (Edson) Fitzp. Rhizoctonia solani Kuhn. = R. zeae Voorhees = R. solani sub sp. sasakii Cochliobolus heterostrophus (Drechs.) Drechs. Anamorph: Bipolaris maydis (Nisikado & Miyake) = Helminthosporium maydis (Nisikado & Miyake). Fusaium spp., Mucor sp., Spicaria spp. & Rhopographus zeae Pat.

Symptoms: Stalk rot and ear rot are the two important phases of the disease. In stalk rot, symptoms appear after a few weeks of pollination as premature dying of lower leaves which turn into dull grey appearance (Fig.14). The internodes become soft and appear tan to brown from outside and pink or reddish inside. The pith is completely rotten and the stalk may lodge. Plants may die if harvesting is delayed. In ear rot, ears may rot completely and a pinkish mold can be seen between ear and husks.

Pathogens: Gibberella zeae; Diplodia zeae; Fusarium species and Colletotrichum graminicola are the major pathogens involved in the rot complex but G. zeae dominates in the complex. The fungus produces ascospores in perithecia, mycelium, or chlamydospores in infected plant debris. G. zeae also produces mycotoxins which are toxic to human and animals.

Disease Cycle: The pathogens survive in soil from one growing season to another. The spores are blown off by wind into the base of leaf sheath and cause infection either by directly penetrating into the host or through wounds caused by insects such as stem borer. Conidia are produced on infected plant parts and serve as secondary inoculum. The disease is favoured by wet weather near or after silking. Higher plant density, high nitrogen and low potash doses and early maturity of hybrids also favour the disease.

Control: The preventive measures for disease management are use of resistant varieties, low plant density, proper fertility practices, insect control and timely harvesting.

2. Downy Mildews of Maize Downey mildews are found worldwide but they cause serious diseases in Asia and Africa on maize and other grain crops. These diseases cause considerable losses to the yield under favourable conditions of fungal growth. These diseases cause severe damage to hybrid maize like Ganga-3 etc. Several mildews are known as mentioned below: 1. Brown stripe mildew caused by Sclephthora rayssiae Kenneth et al. var. zeae Payak & Renfro. 2. Crazi top downy mildew caused by Sclephthora macrospora (Sacc.) Thirumalachar et al. =Sclerospora macrospora Sacc. 3. Green ear downy mildew caused by Sclerospora graminicola (Sacc) J. Schrot. 4. Philippine downy mildew caused by Peronosclerospora philippinensis (W.Weston) C.G.Shaw 5. Spontaneum downy mildew caused by Peronosclerospora spontanea (W.Weston) C.G. Shaw. = Sclerospora spontanea W. Weston. 6. Sorghum downy mildew caused by Peronospora sorghi (Weston & Uppal) C.G.Shaw = Sclerospora sorghi Weston and Uppal. 7. Sugarcane downy mildew caused by Peronosclerospora sacchari (Miyake0 Shirai & Hara = Sclerospora sacchari Miyake Symptoms: The symptoms appear on younger leaves as white or light green stripes which soon become white or light yellow on most of the leaves of affected plants. The sporangia develop on branched sporangiophores which emerge in groups from the plant tissues through stomata. A white mat of the fungal growth can be seen on the lower or both the surfaces of leaves during wet weather. The stem may also be affected if infection occurs during early stages of plant growth.

Pathogens: Sclerophthora rayssiae, Peronosclerospora maydis; P. philippinensis; P. sorghi and P.sacchari are commonly distributed downy mildew pathogens.These pathogens belong to the group Oomycetes and family peronosporaceae. The first two pathogen attacks maize but the rest two are the pathogens of sorghum and sugarcane respectively but also infect maize.

The S. rayssiae produces sporangia at the tips of sporangiophores at their branches. Sporangia are white in colour in the beginning but turn to greyish light brown later. The sporangia germinate by protruding a germ tube and finally produce zoospores at higher temperature. The P. philippinensis fungus produces numerous hyaline, thin walled, ellipsoidal conidia on dichotomously branched conidiophores.

Disease Cycle: Downey mildews are soil and seed borne in nature. The spores in the soil or on seeds germinate through a germ tube and infect plant tissues through roots or collar region. This is called as primary infection. The infection becomes systemic and reaches at the upper parts of the plants. The fungus develops sporangia in large numbers on the younger leaves of affected plants. The sporangia blown away by wind or through rain water or insects and infect healthy plants. This is the secondary spread of the disease where they form zoospores which cause the secondary infection.

Control: The control of mildew diseases is difficult. The sprays with systemic fungicides such as metalaxyl and propamocarb etc. can be used to manage the disease. However, the best control is to use resistant varieties or hybrids, if available.

3. Leaf Spots of Maize Leaf spots of maize are caused by several bacteria and fungi and they develop their respective symptoms on leaves of maize plants. Leaf spots of various sizes are caused by different pathogens.The following bacteria cause leaf spot symptoms on maize plants.

Bacterial leaf spot caused by Xanthomonas campestris pv. Holicola (Elliott) Dye; Chocolate spot caused by Pseudomonas syringae pv. Coronafaciens (Elliott) Young et al.; and holcus spot caused by P. syringae pv. Syringae Van Hall.

The following fungi causing spots or lesions on leaves are: Brown spot caused by Physoderma maydis (Miyabe) Miyabe; Curvularia leafspot caused by Curvularia species such as C. clavata P.C. Jain; = C. maculens (Bancroft) Boedijn (telemorph : Cochliobolus eragrastidis (Tsuda & Ueyama) Sivanesan ; C. lunata (Wakk) Boedijn (telemorph : (Cochliobolus lunatus R.R. Nelson & Haasis) ; C. pellescens Boedijn (Teliomorph : Cochliobolus pellescens (Tsuda & Uema) Sivanesan ) ; Gray leafspot caused by C. zeae- maydis Tehon & E.Y. Daniels ; Didymella leaf spot caused by Dodymella exitalis (Morini) E. Muller ; Phaeosphaeria leafspot caused by Phaeosphaeria maydis (P.henn) Rane, Payak & Renfro = Sphaerulina maydis P. Henn and zonate leafspot caused by Gloeocercospora sorghi Bain & Edgerton ex Deighton. Leaf spots are also caused by several species of Alternaria such as Alternaria alternata and A. tritici. Zonate leafspot, grey leaf spot and brown leaf spot are important and described in this chapter.

4. Zonate Leaf Spot The disease symptom appears as oval and black brown lesions near the leaf veins. These spots enlarge and may coalesce and cover the leaf surface. Affected leaves may die and fall down. The pathogen, Gloeospora sorghi develop slimy masses of conidia on the surface of lesions which are dispersed by wind or rain. High temperature and humidity favour the disease development more rapidly. When the lesions are old , small sclerotia are formed in the infected tissues and survive overseason in infected tissues or contaminated seeds and become the primary source of inoculum when the crop is sown. The disease can be managed by using certified seed, crop rotation and the use of fungicides like benomyl, Bordeaux mixture, maneb etc.

5. Grey Leaf Spot The disease is caused by Cercospora zeae-maydis. The leaf spots are brown, narrow and long which become ash grey in humid weather. The lesions may coalesce covering the whole surface of the leaf. During severe attack the affected leaves may fall down. The fungus produces long, slender, colourless to dark, curved multicellular conidia on conidiophores. The conidia developed on tips of conidiophore and can be easily blown off by wind and cause infection to healthy plants. Most cercospora species produce mycotoxin, cercosporin which kills cells in light. The pathogen overwinters on or inside seed and also on affected leaf tissues as mycelium or spores. The disease is retarted by dry weather. Most of the Cercospora species have teleomorph as cochliobolus but teleomorph of grey leafspot fungus is not known. The control strategies are applicable as with zonate leaf spot.

6. Brown Spot The brown water soaked lesions appear on leaves. The spots may coalesce and form larger, brown patches. The lesions are mostly found on basal portion of leaves but may also appear on leaf sheaths and stem. The causal fungus, Physoderma maydis belongs to family Physodermaceae, order Chytridiales of the sub-division Mastigomycotina. The sporangia are brown in colour and are air born and release zoospores. Zoospores attach to leaf and cause infection. The fungus is an obligate parasite. Field sanitation can control the disease.

7. Helminthosporium Leaf Spots These leafspots are caused by five species of Helminthosporium; H. turcicum; H. maydis; H. carbonum; H. rostratum and H. sativum and all these species are found in India. The first three species cause severe diseases. The genus Helminthosporium was converted to Drechslera and finally has been placed to genus Bipolaris. These diseases are also called as leaf blights and Northern leaf blight in America.

Fig.14. Stalk rot of maize Fig15. Maydis leaf Fig.16. Turcicum caused by Rhizoctonia blight of maize Leaf Blight of maize solani f sp.sasakii

8. Maydis Leaf Spot The disease is caused by Drechslera (= Bipolaris) maydis (Nisik) Subram. & Jain) and the perfect stage or teliomorph is Cochliobolus heterostrophus (Drechsler) Drechsler. The symptoms appear as large number of minute to large spots of 3.75 cm long and 1.75 cm in width on leaves (Fig.15). The lesions are oval and zonated. These lesions coalesce and leaves may show brown coloured stripes. The growth of affected plants is stopped and devoid of cob formation. The infection takes place by the inoculum which survives as mycelium or conidia on leaf debris in soil. The conidia develop on conidiophores under favourable conditions of temperature over 35 C and high humidity. The control measures as applicable with turcica leafspots are also applicable with maydis leaf spot disease. The resistant hybrid such as Ganga white-2 and composite maize like Vijay etc. have been developed in India.

9. Turcica Leaf Spot or Leaf Blight The disease symptoms appear as boat shaped, light grey or brown lesions on lower leaves and also on the upper leaves. In severe infections, all the leaves are affected and infected plants look like cold injury (Fig 16). The cobs are small and poorly filled. The disease predisposes the plants for bacterial stolk rot. The perfect stage of the pathogen Bipolaris turcicum is Trichometasphaeria turcica (Pass.) Luttrell. The fungus develops conidia on the

conidiophores which are geniculated and each conidium has 3 – 8 septa and is slightly curved. The conidia reach to the host through wind and cause infection through bipolar germination on free water on leaf and at a temperatue from 18 -27 C. They can cause leafspot symptoms within 7 – 12 days. The perfect stage, T. turcica forms the perithecia in which Asci and ascospores are enclosed. The control measures are use of certified disease free seeds, crop rotation and use of resistant cultivars.

Diseases of Sorghum

1. Sorghum Smuts There are seven smut diseases but only four are found in India. The causal fungi belong to the family Ustilaginaceae, order Ustilaginales and sub-division Basidiomycotina. The damage is confined mostly to the heads or penicles, reducing both the grain yield and forage value.

(i)Covered Smut or Grain Smut of Sorghum This smut is caused by Sporisorium sorghi (Link) Clint (syn: Sphacelotheca sorghi). The smut is more common where farmers use untreated seed. Seeds in a smutted head are converted into dark brown powdery masses of teliospores or chlamydospores. The smut spores are covered with a tough grayish white or brown membrane. This membrane is ruptured during harvesting and threshing and the spores are attached to the healthy grains where they remain attached till the seed is sown next year. The smut sori are smooth, oval or cylindrical or may be white, gray or brown. When the infested seeds are sown, the teliospores which are 4-7µ in diameter germinate alongwith the seed and a four celled promycelium bearing lateral sporidia is formed. The sporidia germinate and infect the developing seedling. Sometimes the teliospores germinate directly by producing germ tubes. The fungal mycelium grows systemically along with the plant but does not show any disease symptom until heading. While heading, the teliospores are formed and the whole seed is converted into smut sori covered with a membrane. During threshing time the membrane ruptured and the teliospores are fallen down on soil and also adhere to healthy seeds. The teliospores on soil normally do not cause any infection to seedlings. The optimum temperature for disease development is 25 C and the infection decreases at temperatures between 35-40 C. Several physiologic races of covered smut are known worldwide. (ii)Loose Smut of Sorghum This disease is caused by the fungus Sporisorium cruenta (syno: Sphacelotheca cruenta (Kuhn) Potter.). All seeds in an infected panicle are smutted. Some kernels are transformed into leafy structures and are escaped of infectiom. The seeds are converted into 2.5 cm long, pointed smut sori which are surrounded by thin gray membrane. This membrane is usually ruptured at the time when panicle emerges from the boot. Infected panicles emerge earlier than healthy ones. The smut sori contain dark brown to black teliospores which are blown away by wind leaving a long, black pointed conical and curved structure (columella) in the centre. Some of the teliospores (6-10µ in diameter) adhere to the surface of healthy kernels on near by plants and carry with the seed. The affected plants are stunted with unusual excessive tillering and have thin stalks as compared to healthy plants.

When infested seeds are sown, the teliospores germinate along with the seed through a thick four celled promycelium bearing lateral sporidia. The sporidia germinate and infect the seedling. The infection occurs at a temperature 20-25 C with a wide range of humidity. The

fungus grows systemically with the plant without showing any visible symptoms. The symptoms appear only when the head emerges. The normal seeds are replaced by long, black and pointed smut galls or sori. Teliospores in soil are not important for infection. The major difference between covered and loose smuts is that the plants affected by loose smut are stunted, have thin stalks and heads emerge earlier than healthy plants and also abundant tillering was observed with loose smut infection.

(iii)Head Smut of Sorghum Head smut is caused by Sporisorium holci-sorghi (syn: Sphacelotheca reiliana (Kuhn) Clinton). This fungus attacks both sorghum and corn but both the hosts are attacked by different physiological races. Smutted plants have week root systems and are more susceptible to stalk rot and root rot fungi.

Infection first appears even when the heads are still in boot. The heads are completely converted into a large smut galls covered by a thick whitish membrane. The membrane ruptured before the heads are emerged and dark brown to black teliospores are exposed. The teliospores are intermingled with a network of long, thin, dark broom like filaments of vascular tissue. The heads are totally smutted with characteristic “witches broom” (many small, rolled leaves coming out from heads of suckers at the nodes). The affected plants remain dwarfed or stunted. The teliospores are blown off by wind or rain to the soil and plant debris and survive there till the next crop is sown. The parts of the panicle left out from infection show sterility and proliferation of individual florets. Occasionally smut galls may develop on leaves and stem of sweet sorghum.

When sorghum seeds are sown the teliospores (9-14µ in diameter) which are already in the soil germinate along with the seed producing a four celled branched promycelium that bears sporidia terminally near the septa. The poridia sprout by producing yeast-like secondary sporidia or may germinate directly by producing a germtube that penetrates meristematic tissue of seedlings. The sporidia germinate faster at a temperature of 27-31 C in moist soil. The infection of seedlings can also takes place by teliospores already adhere to seed during the last season. The healthy soil thus can be infected through seed infection. Apparently, seed infection is not important in causing infection.

(iv) Long Smut of Sorghum The disease is caused by Tolyposporium ehrenbergii (Kuhn) Pat. The spores are covered into a solid ball. The surface of spores is echinulated. The spores germinate by the formation of promycelium. Numerous sporidia are formed singly or in chains. The spores are soil borne. The sporidia produced by soil borne spores are wind borne and reach to buds and initiate a systemic mycelium which later expresses in the head. The ovary is converted into smut sorus. The primary inoculum may be introduced from alternate hosts. Since the infection is airborne, control is difficult.

Control of Sorghum Smuts Covered and loose smuts are easily controlled by seed treatment with a protectant fungicide. Since physiological races of the three smuts can hybridize with one another, it is extremely difficult to develop highly resistant or immune hybrids, varieties or cultivars. However, resistant varieties have been developed for example in India SPV 104, 115, 102, 245 etc have been found resistant against covered smut in Maharashtra. Some sweet sorghum varieties are resistant to Head smut. Other seed treatments like soaking seed in Formalin (0.5%) or copper

sulphate 0.5-3.0 % solution for 10-15 minutes, seed dressing with mercurial fungicides like Agrosan GN (1:500) are effective to control smuts.

Other measures like collection and burning of smutted heads before the spores are scattered, crop rotation and deep ploughing during summer months are useful to avoid damage by sorghum smuts. Solar heat treatment was recommended in India by Asthana, 1946. During summer months seeds are kept in ordinary water for 4 -10 hours during night and then dry them for 10-12 hours in the sun. The method was found effective in Uttar Pradesh.

2. Grain Mold of Sorghum About 40 genera of fungi are detected in moldy sorghum grains and some of them produce mycotoxins. Fusarium species are more prevalent in mold affected sorghum. Fusarium thapsimum appears to be the most prevalent fungus associated with sorghum grain mold. However, the disease varies from region to region and depends on sowing dates, relative humidity and temperature. Earlier sowings had the highest incidence of the grain mold when temperarure ranges from 20 to 24 C.

The grain mold can be controlled with proper storage to avoid fungal growth. The moisture contents below 14 % or more and a temperature of 5-8 C are ideal for storage. The storage should be kept free from insects and mites. Quick drying of seeds and keep them in storage bins with good aeration systems also useful for protection against grain mold. It has been recently shown that agents like hydrated sodium calcium aluminosilicate bind the mycotoxins, making the grains safe for consumption.

3. Anthracnose of Sorghum The disease is caused by the fungus Colletotrichum graminicola (Cess) Wilson. It causes damage to foliage and stems of sorghum. On susceptible hybrids stem holding the head (peduncle) shows sunken areas with distinct margins. If infected stem is cut lengthwise invasion of soft pith tissue visible as brick red discoloration would be seen. The peduncle infection inhibits the flow of water and nutrients to the grains resulting poor grain development. The fungus also invades individual grain and small branches of the panicle causing severe losses to the yield.

The lesions also develop on leaves as small, elliptical to circular usually less than 3/8 inch in diameter. The spots have circular straw coloured centre with wide margins which may be reddish to black purple. The spots may coalesce to form larger areas of infected tissue. The pathogen lives saprophytically on crop residue. Towards maturity of the plants black acervuli appear on the stems, leaves and sometimes on spikes of infected heads. The fungus survives as mycelium on crop residue and is a major problem where reduced tillage is practiced for minimizing loss of soil or water.

The fungus produces one celled, ovoid, cylindrical and sometimes curved colorless conidia in acervuli. The conidia are pink in colour. The acervuli are subepidermal and break out through the surface of plant tissue. The infection is favoured by high temperature and humidity. The conidia are spread by splashing rain, insect and tools etc. The sporidia germinate directly in the presence of water and invade host tissues. The mycelium spread within the plant inter and intracellularly and cause disease symptoms on stem and leaves.

The use of resistant hybrids and good management of crop residue are effective control measures.

Diseases of Bajra (Pearl Millet) 1. Downy Mildew or Green Ear Disease of Bajra This is one of the serious diseases of bajra (Pennisetum typhoides) and found in all bajra growing countries. The disease is known to occur in all bajra growing states of India especially in water stagnated areas. The yield loss in bajra hybrids has been reported upto 30 per cent.

Symptoms: The disease symptoms begin as chlorosis of basal leaves. Older leaves show more chlorosis than younger leaves. Infected plants look weak, stunted and light yellow in colour. As the disease advances, the leaves show chlorotic stripes parallel to leaf veins. The chlorotic areas develop abundant white asexual sporangia on the lower leaf surface and can be observed as whitish growth in the morning. The floral parts are transformed into leafy structure and the whole ear looks like a bunch of leaves and this stage is normally called as green ear (Fig.17). There is either no grain formation in infected ears or lower half of the ear transformed into leafy structures and upper half develops normal grain. Although the ear size remains as that of healthy ears but in some cultivars the ear size is reduced and the complete ear is turned into leafy structures (Fig 17). The affected plants may develop excessive tillers and give bushy appearance as the internodes become short.

Fig.17. Symptoms of Green ear disease of Bajra on Plant and inflorescence

Pathogen: The causal pathogen is Sclerospora graminicola (Sacc.) Schroet which belongs to family Peronosporaceae, order peronospores and class Oomycetes of Eumycota. The pathogen produces asexual sporangia on sporangiophores during the night under moderate temperature of 20C and high humidity. There is no sporulation below 70% relative humidity. Sporangia are broadly elliptical and papillate. The sporangia germinate in the presence of free water and liberate 1-12 zoospores on the leaves. Sporangia generally do not remain viable after the day break. Zoospores encyst and germinate through germtube. The oospores are formed as sexual spores when the crop is near maturity. They are thick walled, spherical, brownish yallow and 22-25µm in diameter. The oospores can survive from 8 months to 13 years under laboratory condition.

Disease Cycle: The disease is principally soil-borne but evidence of its seed-borne nature is also available. The oospores which remain viable in soil or on infected debris germinate when the crop is sown and are the source of primary infection. The spores germinate through the germtube and cause infection by penetrating root hairs of the developing seedlings. The mycelium of the fungus become systemic and grow along with the plants and cause symptoms on leaves and ears and also develop asexual spores (sporangiospores) on the lower surface of the leaves. The spores are spread through rain, wind or insects to the near by healthy plants causing the secondary spread of the disease.

Control: The use of certified seed, eradication of infected plants, crop rotation for at least five years and seed treatment with fungicides like metalaxil and spray with fungicides (0.05 – 0.01% ridomil) are effective to manage the disease. However, the best control is to grow resistant hybrids, variety or cultivars which are now available for different regions in India. For example, variety HB-1 is highly resistant to the disease.

2. Ergot Disease of Bajra This is the most important disease of bajra hybrids. The form in which the pathogen overwinters is called a sclerotium and this small structure is normally referred as “ergot”.

Symptoms: The disease occurs at the time of flowering. Small droplets of cream to pink mucilage droplets of “honey dew” ooze out from ergot infected florets on bajra panicles. A few to many such spikelets may be found in a group, which darken with age, and after 12-15 days , these droplets dry and harden , and dark brown to black sclerotia develop in place of seeds on the panicles (Fig 18). The sclerotia are larger than seeds and are irregular in shape measuring about 0.5 to 1 cm in length and 1 to 2 mm in diameter.

Pathogen: The causal pathogen is Claviceps fusiformis Loveless = Clavicep microciphala (Walter) Tul. in the family Erysiphaceae, order Clavicipitales of the sub-division Ascomycotina. The pathogen attacks the ovary and grows profusely producing hyphal mass which forms the sclerotium. These hyphae develop small conidiophores on which conidia are produced. The conidia are hyaline, one celled, lunate and measure 13-25 X 3-6 micron. The honey dew droplets in the affected ears are full on conidia. Conidia may also produce secondary conidia after germination. When the sclerotium bodies are cut open, the central portion will show the white hyphal strands. The Sclerotia germinate following rain and form 1-16 fleshy stipes which are 6-20mm long. The asci develop on these stripes. Each ascus is apical, globular, capitulate, light to dark brown with numerous perithecial projections. Asci are interspersed with paraphyses. Ascospores emerge through ostioles. Thread-like ascospores are hyaline, septate and measure 100-1700 X 0.5-0.7µm. The Ascospores infect the emerged stigmas before pollination. The infection is favoured with a relative humidity of more than 80% and temperature 20 – 30C. The sclerotia contain ergotoxin, which when consumed in excessive quantities is toxic to animal life.

Fig .18: Symptoms of Ergot disease of Bajar on panicles

Disease Cycle: The fungus spreads from plant to plant through conidia. The honey dew having conidia attracts insects, which help in the the spread of the pathogen. The sclerotia help the pathogen to perpetuate from season to season.. They remain in soil or plant debris and germinate during the crop season. After germination they produce Asci. The ascospores from ascus can cause infection of spike and produce the conidial stage. The honey dew

contains millions of asexual conidia which are dispersed by insects. Alkaloids and lipids accumulate in the sclerotium. When the mature sclerotium drops to the ground, it remains dormant until proper conditions trigger its germination.

Control: Since the pathogen is air borne, affecting the spike only at the time of flowering, it is difficult to control. Early sowing of crop, crop rotation, use of certified seed or seed treatment with fungicides and sanitation are the methods for management of ergot disease. For small quantity of seed, the ergot can be removed by a putting seeds in 10% salted water and collect the sclerotia which will float over the water. Resistant hybrids are available and should be used for effective control of the disease.

Diseases of Sugarcane 1. Red Rot of Sugarcane Red rot of sugarcane was first recorded from java in 1883 and in Indian subcontinent by Barber and later by Butler in 1906.

Symptoms: The symptoms of red rot first appear on the midrib of leaves as red bright lesions with ash grey centre. Near harvesting of the crop (September-October onwards) the leaves show drooping and colour change of upper leaves. Initially, third or fourth leaf from the top show withering and finally the whole crown droop and withers.The withering of leaves progresses downwards as the disease advances. In severe cases, pith of canes dries up and canes shriveled loosing their weight. If such canes are split open, reddish colour areas can be seen giving an alcoholic smell which develops due to fermentation of sugar. The size of lesions and reddish areas depend on the variety.

Pathogen: The disease is caused by the pathogen Colletotrichum falcatum Went. which belong to the order Melanconiales of Deuteromycotina. The perfect stage is Physalossora tucumanensis Speg. = Glomerella tucumanensis Van Arx and muller.

Disease Cycle: The pathogen develops fruiting bodies on rind, usually just below or above nodes. The spores can survive in soil for a long time. The pathogen produces conidia in acervuli which are colorless, one celled, ovoid, cylindrical and sometimes falcate or sickle shaped, granular and guttulate measuring 16-48 X 4-8µm. The acervulus is ovoid, subepidermal measuring 70- 300 µm long and has bristle-like structure on it. The acervuli break out trough, the surface of plant tissues and the conidia are exposed and spread through splashing rain, insects or tool etc. The conidia germinate in presence of water on leaves and penetrate the host directly and form chlamydospores inside the host tissues. The chlamydospores survive in soil and infect sugarcane plants when conditions are favourable. The disease perpetuates from year to year through soil, decaying leaves and planting the diseased setts or through the diseased canes lying in the field. The ratoon crop helps in multiplication and penetration of fungus.

Control: The cultivation of disease resistant varieties is the best control of the disease. In India, several genotypes such as COLK 8102, COLK 7810 etc. and clones such as CO 86249, CO 81011 etc. are resistant to red rot of sugarcane. Other measures like crop rotation, use of disease free seed setts or treating them with fungicides and collection and burning of affected parts after harvesting are also useful for managing the disease. Ratoon crop should not be taken if first crop is found infected. The common control in practice is hot air treatment with

54C temperature for 10 hours and hot water treatment at 50C for two hous. This facility has been created for farmers at the site of sugar Factories in India.

2. Smut of Sugacane The smut of sugarcane commonly known as whip smut is found in many sugarcane growing countries including India. The disease appears to move from wild canes to improved varieties.

Symptoms: The disease show a whip-like black shoot at the apex of diseased plants which may be several feet in length and curved. The smut powder covered with a thin silvery membrane is attached to the whip. The membrane is ruptured and a thick mass of millions of smut spores is scattered by wind. In case of systemic infection, the nodes or eyes produce lateral shoots on affected plants which may also develop whip but if the infection is localized, main shoot may not develop the whip. The smut masses are present in several layers on whips.

Pathogen: The causal pathogen is Ustilago scitaminea Syd. Which belongs to family Ustilaginaceae, order Uatilaginales of the sub-division of Basidiomycotina. The smut spores are spherical, punctuate walled, light brown in colour about 5-10 µ in diameter. Under moist condition, the spores germinate and form a septate promycelium. The sporidia develop from each cell of the septa which are elongated and develop infection threads after their germination. Sometimes the sporidia form more sporidia in chain. The spore germinates at a temperature of 25-40 C with a relative humidity of 100%.

Disease Cycle: The sugarcane crop is available in the field throughout the year. The spores from the whip blown by wind are deposited on the junction of leaves and leaf sheaths of healthy plants and create infection at the nodal region. The infection occurs through germinating shoot on the host tissue or through the injuries made by insects. The disease perpetuates by planting diseased seed setts or through spores brought by wind on to the buds or through ratoon crops

Control: To remove smutted whips, avoid ratoon crop, disinfection of seed setts such as dipping in 1% formalin solution for 5 minutes covering with moist cloth for two hours, avoiding use of susceptible varieties and hot water treatment at 55-60C for 10 minutes before planting are suitable methods for control of sugarcane smut. However, use of resistant varieties already known in CO series like CO 1148, CO 7108 etc. developed in India is the best control of the disease.

3. Wilt Disease of Sugarcane Wilt is a destructive disease of sugarcane in India. It is also reported from the Philippines, South Africa and West Indies.

Symptoms: The symptoms appear as yellowing and withering of the top when sugarcane crop is near harvesting. The affected canes rapidly dry and become light and hollow. A few leaf joint may show reddening when split open. The pith becomes hollow. The main and adventitious roots may show red colouration and die. Gum may appear in lumen of the vessels, intercellular spaces and in the cells near vessels.

Pathogen: The disease is caused by Cephalosporium sacchari Butler of Deuteromycotina. The conidiophores are septate, vertically branched and with pointed tips measuring 6-30x3-

4µ Conidia develop in succession at the tips and are hyaline, ovoid, oblong ellipsoid and measure 4-12 X 1-3µ. The fungus has three strains based on the difference in mycelium colour and size of conidia. However, it has now been found that fungi, Acremonium fulcatum and Fusarium moniliforme are also associated with sugarcane wilt.

Disease Cycle: The pathogen survives in vascular tissues of apparently healthy canes for longer periods. If such canes are used for seed setts they function as the source of inoculum. The healthy plants are infected through injuries from this inoculum. More wilt was observed when canes are infected with red rot disease. The fungus causes disease symptoms when the crop is near harvesting. Control: Use of disease free setts, destruction of diseased plants and use of resistant varieties like CO 356, CO 1158 etc are the methods for wilt control in sugarcane

Diseases of Groundnut 1. Early and Late Leaf Spots of Groundnut The disease is commonly called as tikka disease. It is caused by two fungi, Cercosporidium personatum (Cercospora personata) and Cercospora arachidicola. Both the pathogen can occur on the same leaf. C. personatum appears first about 30 days earlier than C. arachidicola when the plants are one or two months old and causes early spots. The C. arachidicola appears late in the season and causes late leaf spots. C. personatum is more damaging than the other as its rate of development is fast and may cause severe epidemics.

Symptoms: The lesions developed by the two pathogens differ in shape, size, and colour. Both leaves and stems may show the lesions caused by the two fungi. The disease symptoms first appear on the upper surface of leaves as pale areas.The spots caused by C. personata are small, circular 1-6 mm in diameter and dark brown to black in colour. The spots are not surrounded by a yellow halo, a characteristic of the spots caused by C. arachidicola. The lower surface of the halo is dark black. The spots caused by C. arachidicola are circular to irregular in shape measuring 1-10 mm in diameter. The spots may coalesce at later stages covering more leaf surface. They are surrounded by a yellow halo. The necrotic areas on the upper surface of leaf are reddish brown to black and light brown on the lower surface.

Pathogens: Cercosporidium personatum (Berk. & Curt) Deighton (prfect stage: Mycosphaerella berkeleyii W.A. Jankins) and Cercospora arachidicola Hori (perfect stage: M. arachidicola W.A. Jankins = C. arachidis Deighton). Both the pathogens belong to the order Hyphomycetales in the division Eumycota. Cercosporidium personatum: The mycelium is septste and intercellular. The haustoria are found in pellisade and mesophyll cells.The conidiophores develop on dense, oval, brown to black stroma measuring 20-30µm.They emerge rupturing the epidermis and are olive brown, unbranched and geniculate measuring 24-54 X 5-8µm. Conidia develop on conidiophores are cylindrical, light coloured and measure 18-60 X 6-11µm with 1-7 septa. The perfect stage M. berkeleyii belongs to Ascomycotina in which perithesia are ascostromata which develop asci.The asci contain two celled eight ascospores of 15-35µm in size. Cercospora arachidicola: The mycelium first intercellular but later become intracellular. No haustoria are found. Conidiophores are similar to C. personatum but differ in size, 15-45 X 3- 5µm.Stromata are light to dark brown measuring 25-100µm in diameter. Sporidia are hyaline

or pale yellow, septate with truncate base and subacute tips. The ascospores of M. arachidicola are slightly curved, hyaline and two celled measuring 11 X 3.6µm. The two fungi can be differentiated at the time of conidia formation. In C. arachidicola conidia usually develop on the upper surface of the leaf but rarely on the lower surface. They are not formed in concentric rings but the conidia of C. personatum are restricted to the lower surface and the conidiophores develop in cocentric spots.

Disease Cycle: The healthy plants initially infected by the the conidia lying in soil or in plant debris or in contaminated seed or shells. A period of high humidity for three days is essential for maximum infection by both the pathogens. Secondary spread occurs through the conidia brought by wind or insects from the lesions formed on leaves of infected plants. The affected leaves fall down on the soil and cause infection in the next season.

Control: To remove plant debris, self sown plants of groundnut, crop rotation, mixed cropping with arhar, early sowing and use of early maturing varieties, seed treatment and spray with suitable fungicides like Benlate are useful to avoid infection to the crop. Resistant varieties should always be sown like VIR-3, ICGS -10 etc.

2. Sclerotium Stem Rot of Groundnut The disorder is caused by the pathogen, Sclerotium (Corticium) rolfsii Sacc. The pathogen causes disease to numerous crops worldwide including groundnut.

Symptoms: The symptoms of the disease appear as sudden wilting of a branch which is completely or partially in contact with the soil. The leaves turn brown and wilt. White coating of mycelium is formed near the soil level. A white mycelium web spreads over the soil and the basal canopy of the plant. Infection of pegs takes place independent of stem or together with it. Lesions on developing pegs can retard pod development. Infected pods are usually rotted. Entire plant may be killed later.

Pathogen: The pathogen, Sclerotium rolfsii Sacc. produces sclerotia of mustard seed size which appear on the infected areas. The sclerotia fell dawn in soil where they remain overseason and act as inoculum to cause disease the following season.

Disease Cycle: The pathogen is soil-borne and attacks the basal portion of stem and roots, causing sudden wilting and/or rotting of the stem tissues

Control: The cultivation in an infected field with an inversion plough significantly reduce infection of groundnuts by this fungus and also improve the quality of the produce. Lower plant density increase the incidence of the disease in an infected field, and is therefore not considered to be a viable form of cultural control. Difenoconazole with biological antagonist, Trichoderma harzianum has been identified to reduce the inoculum in the soil. Crop rotation and use of resistant varieties should be adopted.

3. Seedling Rot of Groundnut This disease is caused by Rhizopus species and highly damaging to crop at early stages of plant growth. Symptoms: The disease causes decay of pre-emerged seedlings. Seedlings are reduced to dark brown or black spongy mass of rotten tissues covered with a mat of mycelium. The grey black spores are produced on the mycelium.

Pathogen: The pathogens causing disease are Rhizopus arrhizus and R. oryzae and R. stolonifer.These fungi belong to the family Mucoraceae of class zygomycetes of sub- division Zygomycotina. The pathogens produce two morphologically similar gametes which come in contact and the point of contact dissolve resulting to plasmogamy. Control: Removal of crop debris, deep ploughing, harvesting at normal maturity, and to avoid deep sowing and use of damaged seeds are useful to avoid infection to the crop. Seed treatment with fungicides like thiram, captan etc. is important for the control of disease. 4. Seedling Blight of Groundnut Symptoms: Rolling of the hypocotyle and seedling blight are the major symptoms. The tissues of the cotyledonary nodes are rotted. Whole collar region becomes shredded and dark brown. Lesions may develop on stem below soil in severe cases. Dead and dry branches can be easily detached from the disintegrated collar region. Pathogen and Disease Cycle: The disease is caused by Aspergillus niger and A. pulverulentus which belong to family Eurotiaceae in subdivision Ascomycotina. The mycelium of the fungi is septate. Both sexual and asexual reproduction is found. The asexual spores are the conidia. The conidia are globose and unicellular and spread by wind and cause infection to healthy plants. The female and male gametes are formed on the mycelium and form ascus which contains ascospores. The cleistothecium develops at a later stage and the ascospores are lying within it. The ascospores are released by rupturing the wall of the cleistothecium and spread by wind to healthy plants where they germinate and cause infection. Control: A variety J-11 has been found resistant to the disease which should be used. Deep planting of seed must be discouraged. Other methods like destruction of plant debris, deep ploughing, to avoid mechanical damage and crop rotation with gram or wheat are useful to avoid infection. Seed treatment with fungicides like captan @ 3g/kg or spray with mancozeb @ 3g/litre of water when the disease is first noticed are helpful to avoid damage by the disease.

Diseases of Sunflower 1. Sclerotinia Stalk Rot Sclerotinia has an extremely wide host range infecting about 370 species of plants. Sunflower crop is more commonly damaged by stalk rot. Sclerotinia is also a pathogen of common home garden vegetables and flowers. Symptoms: The symptoms appear on the stalk as a brownish to grey water socked lesion, most commonly at or near the leaf node. A canker develops around the stalk, and the decayed tissues have a wet pulpy appearance. The stalk falls at the point of decay and tissue above canker die. The dense mycelium and sclerotia develop in and outside the stalk when the weather is wet. Finally affected tissues become bleached and have a shredded appearance. Stalk decay may move both to upper and lower portion of the stalk upto the base and head. Sometimes the fungus decays the petiole, reaches to stem and causes rot. Pathogen: The causal organism is Sclerotinia sclerotiorum (Lib.) de bary. The pathogen belongs to family Aganomycetaceae, order Aganomycetales and sub-division Deuteromycotina. The pathogen produces hard, black coloured sclerotia which are of different shapes and size. The sclerotia survive in the soil for several years. They germinate and produce either a white mycelium or a mushroom –like structure called as apothecia. The apothecia are tan to brown

measuring about 1/8 to ¼ inch in diameter. They produce ascospores which can infect the plants. The ascospores are spread by wind from one sunflower field to another. During dry periods the ascospores can survive for two to three weeks only. Disease Cycle: During high soil moisture for at least two weeks the sclerotia germinate to form apothecia. The apothecia produce ascospores continuously for a week or more depending on moisture. The ascospores are carried to sunflower plants by wind. Apothecia are produced abundantly in crop of dense canopies and which are frequently irrigated. Ascospores germinate on a film of water on senescing plant tissue in the soil before infecting the plant. They may also infect the host through wound caused by insect etc. The pathogen can infect the seed and remains on the seed coat in the form of mycelium. However, the spread of the fungus through seed is not important. The leaf infection can lead to stalk rot. Control: The control measures of Sclerotinia stalk rot of sunflower are not to plant on infested soil and to prevent the build up of sclerotia in soils either by monitoring of crop for disease incidence or through crop rotation. At present, no resistance is apparently available but some hybrids show difference in susceptibility. Chemical control is not satisfactory.

2. Alternaria Blight of Sunflower Alternaria blight is a major disease of sunflower in humid areas of India and many other countries where sunflower is grown as oil seed crop. The yield loss may be from 15-90% and oil loss from 20-30 %. Symptoms: The symptoms of the disease appear as dark brown spots on the leaves. These spots are irregular in shape and size with dark border and grey centre.The spots on young plants have a yellow halo. The spots may coalesce and the leaf withers. On stem, the lesions appear as dark flecks which enlarge to form long and narrow lesions. The stem lesions are randomly distributed and often coalesce to form large black areas resulting breakage of the stem. Pathogen: The disease is caused by Alternaria helianthi (Hansf.) Tubaki and Nishihara. The pathogen belongs to family Dematiaceae, order Moniliales and sub-division Deuteromycotina. The conidiophores are cylindrical, scattered, gemiculate and septate. The conidia are ellipsoid, slightly curved with transverse and longitudinal septa and 40-110 x 13- 28µ in size. The conidia are not produced in chain. Disease Cycle: The pathogen overwinters on diseased stalk and can be seed borne but rarely. Seedling blight caused by Alternaria may develop when sunflower plants emerge in humid condition in infested soil. Plants at maturing stage are more susceptible than the young plants. Safflower and cocklebur serve as alternate host of A. helianthi. The disease development is favoured by 25 – 27 C temperature and atleat of 12 hours wet foliage. Moisture for longer periods can cause severe disease. Control: Satisfactory control measures include crop rotation and chopping and burying of infected plants. Fungicidal sprays and seed treatment with captan significantly reduce the infection. The disease is controlled by spraying 0.2% Dithane M-45 any other copper fungicide on the 30th, 40th and 50th days.

Diseases of Mustard 1. Alternaria Blight of Mustard Alternaria species attack several plant species in cruciferae family and two species, A. brassicae and A. brassicicola attack to them. Loss to mustard yield has been estimated upto 35 per cent. Symptoms: The symptoms caused by A. brassicicola appear as dark coloured circular lesions on the leaf. Concentric rings may also form in the lesions. The spots may be linear on stem, petioles and pods. Similar spots are also caused by A. brassicae except that these spots are smaller and lighter in colour. When too many spots are formed on leaves, they die prematurely indirectly affecting the yield. Pathogen: Alternaria brassicicola (Schw.) Wiltshire and Alternaria brassicae (Berk.) Sacc. are the causal pathogens. The conidiophores of A. brassicicola are septate, olive green and branched measuring 5 – 7.5 X 35 – 45µ. Conidia are linear; develop in chains of 8 – 10 and measure 11 – 17 X 50 – 75µ on maturity. In A. brassicae, the conidiophores arise in fascicles. The conidia borne singly or in short chains and are dark, obclavate, muriform and measure 125 – 225 X 16 – 18µ. . Disease Cycle: In temperate regions, these pathogens are seed borne but in tropical regions seed borne inoculum does not play any role. Spores and mycelium in plant debris serve as major means of perpetuation especially in tropical regions. Conidia are abundantly formed in humid weather and disseminated by wind and cause infection to mustard even from other cruciferous plants. After infection, the fungi become subcuticular in leaves and subsequently develop conidia which are dispersed and cause infection to healthy crop plants. Control: Seed treatment is required in temperate regions only but not in tropics. Foliar sprays with chemicals like Dithane M-45 and other copper fungicides have been found very effective to control the disease. 2. White Rust of Mustard (Crucifers) White rust infects a large number of cruciferous plants both wild and cultivated species. In India, mustard and other Brassica species, turnip, radish, Eruca sativa and several weeds are found infected with white rust fungus. Seed crop suffers heavily due to infection of the fungus to floral parts causing deformity. Symptoms: The pathogen causes both local and systemic infection and symptoms may appear to all plant parts except roots. In case of local infection, white pustules are irregularly formed on leaves and stems (Fig.19). These pustules may merge together to form larger pustules. The host epidermis is ruptured showing white powder of spores. When fungus becomes systemic it causes deformities to stem and floral parts. Due to hyperplasia and hypertrophy of tissues, the axis of the inflorescence and flower stalk become thickened, floral parts become swollen and green to violet in colour (Fig.20). The petals look like sepals and stamens become leafy. The carpels may be open and ovules and pollen grains atrophied causing sterility to ovary. The swollen parts carry the oospores of the fungus. In case of early infection whole plant may remain dwarfed and only small leaves will develop. Swelling on stem may be restricted to some portion or may spread to whole stem. The stem and floral axis may twist showing a zigzag appearance and lateral shoots may appear on the stem. Pathogen: The causal pathogen is Albugo candida (Lev.) Kuntze also known as Cystopus candidus Lev. The pathogen belongs to family Albuginaceae, order Peronosporales and sub- division Mastigomycotina of Eumycota. The pathogen is an obligate parasite. The mycelium develops intercellularly with knob shaped haustoria. The sporangiophores develop from the

Fig.19: Symptoms of white rust on leaf and stem of Fig. 20:Influorescence symptoms Mustard caused by white rust of crucifers

mycelium and produce sporangia in basipetal succession in chains. A gelatinous pad is formed between the sporangia which swell during the presence of moisture thus helps in disintegration and freeing the sporangia. The sporangia germinate and produce zoospores in water. The zoospores swim in water with the help of flagella and later become round and encysted and go for hibernation. Under favourable conditions (optimum temperature 10 C and maximum 25 C) the encysted zoospores germinate by producing germtube and infect the host through stomata and form new mycelium. Sexual organs are formed from the mycelium within intercellular spaces of systemically invaded tissues.The oogonium is globose, terminal or intercalary and is clearly defined into a periplasm and a single central oospere. The antheridium also develops near the oogonium and at the point of their contact, the wall become thin and a papilla of the oogonium protrudes into the anthridium but disappears soon. The fertilization tube from the antheridium enters into the oosphere passing through the thin wall. The nuclei of both antheridium and oosphere undergo two mitotic divisions and form a granular body known as coenocentrum in the oosphere. A single female functional nucleus is attached at a point near it. The fertilization tube penetrates the coenocentrum and finally discharge a single male nucleus which fuges with the female nucleus and thus fertilization takes place resulting the formation of oospore. The oospore is formed by the development of a thick and tuberculate wall around the oosphere. The fuged nucleus of oospores undergoes several mitotic and one meotic division and thus forms about 30 nuclei. These oospores germinate and produce zoospores for further infection to the healthy plants. Disease Cycle: The pathogen perpetuates through oospores lying in the soil or on plant debris. Weed hosts also serve as a source of primary inoculum. Secondary spread takes place by means of sporangia and zoospores. Moist and cool weathers favour the development of the disease. Control: Early sowing is useful to avoid floral malformation. Other measures like clean cultivation, destruction of plant residue and crop rotation are also useful to avoid disease in the crop. If required, fungicides such as Dithane M -45 @ 0.2% etc. should be sprayed. Resistant varieties like Kranti, TM-20, RN-510, MDYR-2029, NPJ-81, PAB-2001 and PAB- 2002 etc. should be sown. 3. Downy Mildew of Mustard The disease is commonly found on mustard and damage plants at early stages of growth and also to inflorescence at later stages. The disease can cause a loss upto 37-47 % with a mixed infection with white rust in pod yield and upto 17-32 % in seed yield of Brassica juncea.

Symptoms: Pulpish brown spots are formed underside the leaf. The upper surface above the lesions show tan to yellow colouration. The cottony growth of the fungus appears on the

undersurface of the lesions. In systemically infected plants symptoms appear similar to white rust except that the deformities are more on stem but flower parts donot show deformities except enlargement and twisting of ovary. The stalks are abruptly bent and flower buds are atrophied.

Pathogen: The causal pathogen is Peronospora parasitica (Pers.) ex Fr. and belongs to family Peronosporaceae, order Peronosporales and sub-division Mastigomycotina. The pathogen is an obligate parasite and the mycelium is intercellular with branched haustoria. The numerous branched conidiophores emerge through the stomata on the lower surface of leaves. The conidiophores are dichotomously branched 6-8 times at the tip. A single conidium is formed on each tip of the branch and is oval, ellipsoidal and hyaline, and measure 24-27 X 15-20µ.The conidia fall of and germinate through a lateral germtube. Sexual organs develop late in the season. The oogonium is spherical and fertilized by a single antheridium. The oospores are globose measuring 26-43µ in diameter and are enclosed in a crest-like fold and appear pale yellow in colour and germinate by a germ tube. More conidia develop at 13 C than 18 C. Disease Cycle: The pathogen perpetuates in soil through oospores. The seeds may also carry the infection of oospores as a contamination. Wild hosts also serve the source of primary inoculum. Secondary spread is through conidia.

Control: Cultural practices like crop rotation avoiding cruciferous plants, eradication of weed hosts, deep summer ploughing and destruction of crop residue are important. Spraying with fungicides like Dithan Z-78 (0.3%), Blitox-50 (0.3%) etc. is useful to control the disease. In India at Pantnagar mustard varieties YRT-3 and TMV-2 were found resistant to downy mildew pathogen.

4. Sclerotinia Stem Rot of Mustard Indian mustard (B. juncea) is the major oil seed crop in India. The losses caused by the disease in seed depend on the time of disease appearance. Maximum losses upto 92.32 % were recorded in seed yield when the plants were infected at the age of 70 days. Symptoms: First symptoms of stem rot appear in the field 65-70 days after sowing. Diseased plants can be identified by sudden drooping of leaves and finally drying of plants. Lodged stems come in contact of soil and develop watery lesions with snowy white mycelium and black, irregularly shaped sclerotia. Pathogen: The causal pathogen is Sclerotinia sclerotiorum (Lib.) de Bary and belongs to family Aganomycetaceae, order aganomycetales and sub-division Deuteromycotina. The pathogen infects about 400 other plant species. Disease Cycle: The primary survival structure of the fungus is sclerotium. A sclerotium is a hard resting structure consisting of a light coloured interior portion called as medulla and an exterior black protective covering called the rind. The rind contains melanin which is highly resistant to degradation. The medulla consists of fungal cells rich in glucans and proteins. The sclerotia can come to the fresh crop by wind from infected fields, remains in plant debris, through contamination or irrigation. The sclerotia are also carried by seed or contaminated soil. The disease cycle starts from sclerotia in the soil. They germinate by carpogenic germination which results in the production of a small mushroom-like structure called as apothecium. The apothecium produces ascospores which are wind transported to healthy plants. The sclerotia may also germinated directly producing mycelium on certain hosts.

Control: The pathogen is soil borne and the sclerotia can survive in soil for several years, crop rotation of non-host crops of atleast 4-5 years may be helpful. Use of certified seeds, avoid excessive irrigation, sowing in rows with wider row spacing and destruction and burning of crop debris are important to avoid stem rot disease. Chemical controls are most effective when combined with cultural control strategies and are usually not necessary if sound cultural practices are followed. In India, genotypes ZYR-6, PCR-10, cutlass etc. were found resistant.

5. Bacterial Rot of Mustard Little is known about the disease and its life cycle, but presumably the pathogen gets entry into the plant through natural openings or wounds. Symptoms: The disease can be easily recognized by its foul odor. Affected plants are soft and mushy. The water soaked lesions develop on pods that become necrotic and dry with time. The disease appears in high humidity and when high doses of fertilizer (nitrogen) is applied to the crop. Pathogen: The disease is caused by a bacterium, Pseudomonas syringae pv maculicola. The bacterium belongs to family Pseudomonadaceae, class Proreobacteria and division Gracilicute of Prokaryotae. Disease Cycle: The pathogen enters the host through injuries caused by insects etc. or through the natural openings. Splashing water, equipments and aerosols disseminate the bacterium. Control: Management strategies like crop rotation by non-hosts, removal of plant debris, weed control in and around fields and furrow irrigation with pathogen free sources of water such as tube wells, avoiding excessive irrigation and high fertilizer doses are useful to manage the disease. Copper bactericides may provide suppression of the disease if applied preventively and regularly.

Diseases of Pigeonpea 1. Wilt of Pigeonpea The disease is most destructive to pigeonpea throughout India and several African countries. The plant mortality upto 50% has been observed with severe infection of wilt. Symptoms: The main symptoms are wilting of seedlings and adult plants. The wilting starts gradually showing yellowing and dying of leaves following by wilting of whole infected plant (Fig 21). However, sometimes wilting is sudden. The affected plants can be seen in patches in the field and can be easily recognized. The tissues of root and stem at the base show black streaks, which can be easily observed by removing the bark. The branches arising from discoloured parts show the wilting symptoms first. The wilting may be partial as the branches on one side will show wilting while on the other side they remain healthy. The wilting is due to blockage of water conducting tissues by fungal mycelium and by the production of toxins by the fungus within host and also around the roots in the soil. Pathogen: The causal pathogen is Fusarium udum Butler.The perfect stage of the fungus has been reported as Gibberella indica. The pathogen is restricted to vascular tissues. The mycelium is septate, hyaline, and both inter and intracellular. The fungal hyphae produces three types of spores within the host tissues; microconidia, macroconidia and chlamydospores. The micoconidia are minute, elliptical, curved, and unicellular with one or two septa and measure 5-15 X 2-4 µ. The macroconidia are long, curved, pointed at the tips

with 3-4 septa and measure 15-50 X 3-5 µ. Chlamydospores are oval, single or in chains, terminal or intercalary and remain in the soil for long time. Disease Cycle: The wilt pathogen is soil borne. The pathogen survives in soil as a saprophyte on dead host roots and other plant parts. The pathogen spores can also survive for long time. Under favourable conditions, the spores germinate with a germ tube which penetrates the fine rootlets. The fungus may move to larger roots if they got injury. The affected roots become black and shriveled. The disease is favoured at a temperature of 17-29 C. The main infection is through soil only and secondary infection by conidia on above ground parts is rare. The infected plants develop spores which fell down on the soil and function as inoculum for the next crop. Control: The disease is manageable by cultural practices like crop rotation, field sanitation, deep ploughing during summer, mixed cropping with sorghum, amendment of soil with oil cakes, trace elements such as zinc and manganese, growing green manure crops in the rotation. Growing of resistant varieties is the best control. Varieties like Pusa 992, AL 1430, METH 121, BSMR 853 etc. have been found resistant to wilt of pigeonpea in India.

Fig.21: Symptoms of wilt of Arahar Fig.22: Symptoms of Phytophthora blight of Arahar

2. Phytophthora Blight of Pigeonpea The disease was first reported from the fields at Indian Agricultural Research Institute by Williams et al, 1968. The disease commonly occurs in fields having heavy soil and poor drainage. Symptoms: Affected plants show as water soaked brown to dark lesions on the leaves which become necrotic afterward. The lesions on stem and petiole are somewhat brown and sunken. The lesions enlarge in size and girdle the stem resulting drying of branches and foliage. The seedlings die suddenly due to infection (Fig 22). No symptoms are found on root system. Branches and petioles lead to desiccation. In severe cases, the whole foliage becomes blighted. Infected stem can easily break by the wind. In advanced stages, the stem is commonly swollen into cankerous structures near the lesions. The seedlings are highly prone to this infection and dry plants are common during rainy season. The disease is serious when continuous rains occur or there is water logging in the field. Such conditions can create epidemic of the disease. Pathogen: The disease is caused by Phytophthora drechsleri Tucker f. sp. cajani Disease Cycle: The pathogen survives in soil and on infected plant debris. Cloudy weather and drizzling rain with temperature of 25 C favour infection. Low lying area where water stagnates and close spacing encourage blight build up. Warm and humid weathers after infection result in rapid development of disease.

Control: The disease can be managed by avoiding the sowing in fields with heavy soil with poor drainage system, selection of disease-free fields, soil solarization or summer ploughing and wide row interspacing are good cultural practices for disease control. Other measures are to treat the seed with ridomil or metalaxyl (0.3 g per kg of seeds) and two sprays of metalaxil at 15 days interval starting from 15 days after germination and use of resistant varieties and cultivation of pigeonpea on ridges.

3. Sterility Mosaic Disease of Pigeonpea Sterility mosaic is the most damaging disease of pigeonpea endemic in Indian subcontinent. About 90% of pigeonpea is grown in India and Nepal. The losses caused by the disease in India and Nepal are more than USD 300 million per annum. Symptoms: The plants infected with sterility mosaic remain stunted. The leaves show mosaic symptoms and the symptoms may develop on all the leaves of infected plants. The flowering is partially or completely stopped and a few flowers which develop are sterile. Infection by the pathogen in plants when they are less than 45 days old results in 95-100 % losses, while older plants suffer 26-97 % losses. Pathogen: A previously undescribed virus, pigeonpea sterility mosaic (PPSMV), shows properties similar to viruses in the genus Tenuivirus. However, all tenuiviruses are phloem limited, are transmitted by planthoppers and infects plants only in family Poaceae, thus ruling out PPSMV as a tenuivirus. In ultrastructural studies of PPSMV infected tissues showed 100 – 150 nm quasispherical-membrane bound bodies (MBBs) and fibrous inclusions. The filamentous virus-like particles (VLPs) of PPSMV resemble the nucleoprotein particles of tomato spotted wilt virus (TSWV), but PPSMV VLPs are slightly larger than those of TSWV and is not serologically related to maize stripe tenuivirus and peanut bud necrosis tospovirus. The sterility mosaic causal agent is transmitted by the arthropod mite vector – Aceria cajani an eriophyid mite. PPSMV and High plains virus share some common properties: transmission by eriophyid mite A. cajani, 4-7 similar sized MBBs and similar morphology. Similar MBBs have been detected in plants infected with fig mosaic, wheat spot moaic etc. which are also infected by eriophyid mite, suggesting that these viruses may constitute a new virus genus. Disease Cycle: The sterility mosaic thrives readily in crops under irrigation or near irrigated fields. Such crops remain at risk of early infection. The virus and the vector mite both survives on self sown plants during off season and when the crop is sown the virus infection takes place through the vector. The secondary infection takes place from primarily infected plants in the crop by the mite vector. Management: Cultivation of disease resistant varieties is the most viable way to manage this virus disease of pigeonpea. The broad based resistant genotypes are rare in the pigeonpea gene pool but a related wild species, Cajanus scarabaeoides (synonym C. indicus ) has high level of resistance. Eradication of self sown plants in and around pigeon pea fields is very helpful to manage sterility mosaic.

Diseases of Soybean 1. Rhizoctinia Blight of Soybean This disease is distributed throughout India but more severe in Madhya Pradesh and Uttranchal. The disease may cause yield loss upto 35 %. The causal fungus infects all plant parts, root, lower stem of seedlings as well as mature plant, stem, leaves, petioles and pods.

Symptoms: Initially the disease appears on lower leaves as water soaked lesions which are later turned as greyish brown to reddish brown and finally turn dark brown. Subsequently, the affected leaves get blighted and in severe cases the whole crop looks blighted. During flowering time the root of affected plants show brown to dark brown discoloration of cortical region. The root tissues may also be lignified. A reddish brown canker may encircle the stem at the base and drooping of leaves is also common. Under high humidity the fungal mycelium can be observed on leaves and in between closely spaced plants. Oval to elongated spots appear on stem, petiole and pods. Dark brown sclerotia are formed on leaves and petioles. The disease also affects the seedlings causing stunting and also pre emergence mortility. Seeds on infected plants may show irregularly shaped tan or light brown sunken lesions. Pathogen: The disease is caused by Rhizoctinia solani Kuhn. The perfect stage of the pathogen is Thanatephorus cucumeris. The mycelium of the causal fungus produces branches at right angle of the main hypha, slightly constricted at the main junction and have a cross wall near the junction. The pathogen produces sclerotia – like tufts of short, broad cells that function as chlamydospores, or the tufts develop into sclerotia. The basidia of the perfect stage develop on a membranous layer of mycelium and have four strigmata, each bearing one basidiospore. Disease Cycle: The pathogen is seed, soil and air borne. Inoculum in the seed or soil causes infection and is responsible for pre and post emergence mortality. Inoculum may be splashed out and infects the stem and leaves of the older plants and spread from leaf to leaf and plant to plant by contact. The parts detached from infected plants serve as secondary inoculum. Rain or free moisture on plant surface with warm (24-32 C) and humid weather will cause severe infection. Control: Control of Rhizoctinia diseases is difficult but measures like avoiding thick population, seed treatment with fungicides like captan @ 3-4g/kg, spray of carbendazim etc. and use of moderately resistant / tolerant varieties like PK 262, 416, SL-295 etc. and mulching are helpful to avoid losses due to this disease.

2. Pod Blight and Seed Rot of Soybean It is commonly found in India in the states of Madhya Pradesh, Uttaranchal, Punjab, Himachal Pradesh and Rajasthan. Symptoms: The disease symptoms may be observed on any part of infected plant. The infected seeds are cracked badly, shrivel and remain covered with dirty white mycelium. Bright red to brown lesions are also produced on cotyledons which may result in seedling blight. Seedlings emerging from infected seeds have seed coat attached to cotyledons which may also result to seedling blight. Later in the season, adult plants develop black speck sized pycnidia which are linearly arranged on infected petiole or abscised leaves, broken branches, stem and pods. Under favourable conditions such as warm and humid climate, premature death of branches, shedding of leaves, and undeveloped podes are the common symptoms. Pod blight results in mouldy and light seeds. Leaf infection is rare and latent infection is common. Pathogen: Diaporthe phaseolorum (Cke, and Ell.) Sacc. var. sojae (Lehman) and Phomosis longicolla are two major pathogens involved with pod blight disease while other species, D. phaseolorum var. caulivora is commonly associated with seed rot. In India, only D. phaeolorum var sojae is known to occur. Disease Cycle: The pathogens are seed and soil borne. The fungus overseasons as mycelium in host debris and in infected seed. Pycnidia and/or perithecia are produced on plant debris.

The dormant mycelium, conidia from pycnidia and ascospores from perithecia cause the primary infection and develop the lesions. The conidia produced by pycnidia in these lesions are spread by splashed rains and cause secondary infection. Infection in the pods leads to seed infection and decay. Control: The infection can be minimized by ploughing down crop residue, use of healthy seeds, crop rotation, seed treatment with fungicides like thiram + carbendazim (2:1) @ 3g/kg, spray with benomyl @ 0.1%, adequate potash in the field and to grow moderately resistant vars. Like Bragg, HIMSO 1563, NRC 37 PK 262, JS 80-21 etc.

3. Seedling Blight in Soybean Seedling blight in soybean is caused by several pathogens such as Phytophthora sojae, Rhizoctonia solani, Fusarium oxysporum or F. solani. These fungal pathogens are soil borne. R. solani infection has already been covered under Rhizoctinia blight.

(i). Phytophthora Seedling Blight Symptoms: If the plants are killed at seedling stage, the disease is called seedling blight. Diseased plants may stand alone or in small circular groups particularly at low spots in the field or may be seen throughout the plantings. Dead seedlings are visible on the ground. Infected plants that die before true leaf stage will have a rotted appearance. Infected seedlings have a grey green colour which later turns to brown. A few days later the infected plants die. The roots are rotted. Infected plants have a brown discoloration extending from root tips to the stem. Warm condition is favourable for Phytophthora infection whereas, soybean planted in cold wet soil infection by Pythium spp. is more common. The symptoms caused by both the fungi are very similar. Pathogen: Over 39 races of the pathogen Phytophthora sojae cause seedling blight. The pathogen produces structures called oospores which enable the pathogen to survive in soil or on crop residue. Disease Cycle: The oospores present on crop debris or in soil germinate and produce sporangia. The sporangia release zoospores which enter in soybean root tips and cause infection. The oospore may survive in the soil for several years and thus the inoculum is always there in a contaminated field. Control: The measures like application of less manure and fertilizer before planting, crop rotation, seed treatment use of fungicides and to grow resistant varieties are useful to avoid seedling blight.

(ii) Fusarium Seedling Blight Symptoms: The disease is most common on seedlings and young plants. Fusarium seedling blight is frequently found in combination with Rhyzoctinia blight or soybean cyst nematode. Damage from the Fusarium may be more severe when it occurs in combination with other diseases or stresses. Pathogen: The disease is caused by either Fusarium oxysporum or F. solani. Disease Cycle: These two pathogens can persist in the soil and colonize on various plant residues and survive as chlamydospores or mycelium. The infection is favoured by herbicide injury, deep planting, poor seed quality, hail damage, mechanical injuries, poor fertility and other factors that delay germination and emergence favour the development of Fusarium seedling blight. The infection initially comes from the soil inoculum.

Control: Measures like use of good quality seeds minimize or avoid stress which delay germination and seed treatment with fungicides are useful to manage the disease. 4. Bacterial Pustule Pustule has been reported in most soybean growing areas of the world where warm and humid weather prevails during crop season. The disease may cause premature defoliation, which may decrease yield by reducing seed size and number of grains.

Symptoms: Early symptoms are minute, pale green spots with elevated centres on both surfaces of leaves. Later, a small raised, light coloured pustule develops in the centre of lesions on the lower surface of leaves. Lesions are often associated with main leaf veins. The spots vary in size from specks to large, irregular mottled brown areas. Leaves become ragged when dead areas are torn away by wind. Severe disease often results in defoliation. Pathogen: The bacterium, Xanthomonas axonopodis pv. Glycines is the causal pathogen. Colonies on beaf infusion agar are pale yellow, become deep yellow with age and are small, circular, and smooth, with an entire margin. Disease Cycle: The pathogen overseasons in seeds, in crop residue, and in the rhizosphere of roots. Strains can infect common bean and cowpea. The pathogen spreads through splashing water or wind blown rain and during operation when foliage is wet. The pathogen can enter the plant through natural openings and wounds. Warm weather and frequent showers promote the development of this disease. Control: Use of resistant cultivars, crop rotation, tillage, limit cultivation to times when the foliage is dry and use of copper fungicides are the effective control measures. 5. Soybean Mosaic Disease The disease is occurring all over the soybean growing areas of the world including India. The disease can reduce the yield from 50-90% depending on age of plant and time of infection and affects seed germination, nitrogen fixation and oil contents. Symptoms: The affected soybean plants show rugocity, dark vein banding and light green interveinal areas, stunting, leaf curling, and seed coat mottling, male sterility, frower deformation, less pubescent, necrosis some times necrotic lesions, systemic necrosis and bud blight Pathogen: Soybean mosaic virus (SMV) is the causal pathogen. SMV is filamentous; flexuous rod shaped with a clear modal length of 650-700 nm or 760 nm , 15-18 nm wide. The pathogen belongs to potyvirrus group in family potyviridae. Virions contain 5.3% nucleic acid and 94.7% protein. The genome consists of single stranded RNA of the size of 10.4 kb. The genome is unipartite. The SMV is mechanically transmissible by sap inoculation to hosts, like Chenopodium album, C. quinoa, Cyamopsis tetragonoloba where SMV produces local lesions and systemic symptoms on hosts like Phaseolus vulgaris, Glycine max etc. SMV can also be detected in ELISA and PCR systems of diagnosis. Sixteen species of aphids such as Acyrthosiphon pisuii, Ahis fabae and Myzus persicae are the vectos which transmit the virus nonpersistently. Disease Cycle: The pathogen is internally seed borne and initial infection comes from infected seeds and secondary spread occurs through aphid vectors at a faster rate. Seeds are means of long distance transport and survival from one season to another. The virus is also pollen transmitted. Several plant species in families, Chenopodiaceae, Leguminosae, Scrofulariaceae and Solanaceae are susceptible to the soybean mosaic virus (SMV) and may serve the source of inoculum for transmission by aphids to soybean crop.

Management: Presowing soil application of phorate @ 10kg/ha, avoid monoculture of varieties, clean cultivation, and foliar sprays of insecticides for aphid control and use of moderately resistant varieties like JS71-05, Punjab-1, MACS 58 and PK 416 etc. are the methods for SMV management.

Diseases of Gram 1. Wilt Disease The disease has been reported from India and Burma and is widely distributed in Indo- gangetic plains of India. Symptoms: The affected plants show drooping and their sudden death is very common. The leaves of affected plants turn yellow and fall off prematurely. Collar region of affected plants show necrosis and discolouration. Wilting can occur in seedlings and adult plants as well. Initially petioles and rachis alongwith leaflets show drooping and within 2-3 days drooping of entire plant takes place (Fig. 23).The affected plants can be pulled out more easily than healthy plants as most of the lateral roots of infected plants become weak.Transverse sections of basal region show discolouration of vascular tissues and the fungal hyphae.

Fig .23: A Wilted plant of Gram Pathogen: The disease is caused by Fusarium oxysporum Schlecht, emend.Snyd. & Hans. f. sp. ciceri (Padwick) Snyd. & Hans. The pathogen belongs to family Tuberculariaceae, order Moniliales and sub-division Deuteromycotina. The mycelium is inter and intracellular and found abundantly in vascular tissues. The pathogen produces micro and macroconidia. Macroconidia are sickle shaped, septate and hyaline and measure 25-40 x 3-4µ, while microconidia are elliptical, have one or two septa and measure 4-6 x 2-4µ. Disease Cycle: The pathogen is a facultative parasite and survives for a long time on plant debris in soil especially on host roots which are left in the soil after harvesting. The pathogen may produce resting spores known as chlamydospores that can survive under adverse conditions. As soon as next crop is sown the chlamydospores become active and infect plants. The disease may also be carried to new areas by contamination of seeds by chlamydospores in the hylum region of the seed. Pigeonpea, pea and lentil are symptomless carriers of the pathogen. Control: The control is difficult as the pathogen survives in soil for long period. However, cultural practices like date of sowing (crop period from November to February) and supplement of high organic matter will reduce the disease. Seed-borne inoculum can be eradicated by treated seed with a mixture of 30% benomyl and 30 % thiram.

2. Ascochyta Blight of Gram The disease occurs in North-western part of Uttar Pradesh, Punjab and Hariyana in severe form. The disease is also found in Pakistan, countries bordering Mediterranean sea and parts of eastern Europe. Symptoms: Brown, circular spots with brownish red margin appear on leaves and pods of affected plants (Fig 24). On petioles and stem the spots are elongated in shape. The spots on leaves coalesce turning the leaf completely brown. On green pods, the circular lesions have dark margin where black dot like bodies appear known as pycnidia. The pycnidia are arranged in concentric circles. The elongated lesions on stem and petioles also bear black dots and may girdle the stem. The parts above the lesions droop and wilt. If the stem is girdled at the base the whole plant will show wilting. During wet weather the disease spread very fast and may cover the whole field.

Fig.24. Symptoms of Ascochyta Pathogen: Ascochyta rabiei (Pass.) Labrousse is the causal pathogen. The pathogen belongs to family Sphaeropsidaceae in Deuteromycotina. The perfect stage of the fungus is Didymella rabiei (Kov.) Von Arx. The mycelium of the pathogen is septate. The pycnidia develop on stem, leaves and seed pods are dark brown, globose and measure 140-200µ. Conidia are formed within pycnidium and remain viable for long period of time. The pycnidia absorb water, swell and release conidia. Several strains of the pathogen are known. Disease Cycle: The pathogen survives on plant debris left in the field and also on seeds which serve the source of primary inoculum. Further spread of the pathogen is through conidia which are disseminated by splashing rain, by insects, contact of healthy and diseased leaves and by the movement of man and animals. The disease spread fast at a temperature of 22-26 C and wet weather. Control: The disease can be managed by sound cultural practices like removal of plant debris from the field, crop rotation, deep sowing, mixed cropping with wheat and deep ploughing during summer and seed treatment with organomercuriales (Agallol, Agrosan etc.). Spraying fungicides like Zineb, captan etc.ia also helpful. Use of resistant varieties is the best control.

3. Grey Mould of Gram Grey mould is a major yield reducer of gram in India, Nepal , Bangladesh and Australia. Symptoms: The disease attacks the base of the stem and collar region of young plants, where a soft rot develops and then becomes covered with a fluffy grey mould. Infected plants wither and dye. Leaf infection causes comparatively less yield loss. When disease appears in severe form the crop is totally lost. Seeds are also infected and they become white due to infection decreasing the market value of the produce. Crop losses are very high during wet season.

Pathogen: The disease is caused by the pathogen, Botrytis cinerea Pers. Ex. Fr. Which belongs to Deuteromycotina. Disease Cycle: The pathogen survives in seed and crop residue and in soil. The plants can be infected at any stage of their growth. Infected seeds are the primary source of inoculum. Infected plants develop masses of spores which are air borne and spread the pathogen rapidly. Once the infection is established, conditions under the canopy are ideal for spreading the disease. Control: The control options include use of less susceptible varieties, lower seed rate, plant thinning and delayed sowing and need based foliar sprays with fungicides, crop rotation and seed treatment with fungicides.

Diseases of Lentil 1. Rust of Lentil The rust is a common disease of lentil in North India and cause heavy damage to the crop. Symptoms: The disease symptoms are necrosis and deformity of stem and affected plants often die. Yellowish powdery pustules are developed on leaves, stem and petioles and even on pods. These yellow spots have aecia in round and elongated clusters. Uredopustules develop on both side of leaves, petiole and stem as powdery light brown pustules. Dark brown or black teliospores also develop in the same sorus at later stages.They mostly develop on stem and petioles. Later the aecidia and pycnidia develop. It is autoceous rust. Pathogen: The causal pathogen is Uromyces fabae (Pers.) de Bary. The pathogen belongs to Basidiomycotina. Aeciospores developed in aecia are round to elliptical, yellowish in colour and measure 14-22 micron. Uredospores are round to ovate, light brown and measure 20-30 x 18-26µ in size. Teliospores are subglobose to ovate, brown in colour and measure 25-38 x 18-27µ. Disease Cycle: The dissemination of lentil rust pathogen takes place by aeciospores which form secondary aecia after infection of leaves. The secondary aecia are formed at a temperature of 17-22 C but at 25 C the infection causes development of uredia. The aeciospores and probably the uredospores do not survive during off season. The teliospores can withstand the summer heat and hence the lentil rust perpetuates in its telial stage in the left over diseased plants trash or on seed as external contaminant and infects the new crop in the next season. Aeciospores from lentil have also been found to infect pea and Vicia faba and Lathyrus. However, another species of Uromyces, U. pisi (Pers) Wint. is a heteroceous rust and commonly occur on cultivated pea. The aecial stage of this pathogen develops on Euphorbia cyparissias L. This rust is not common in India. Control: Destruction of diseased plant trash after harvest, crop rotation, and seed treatment with fungicides are the effective control measures. 2. Wilt of Lentil The disease is common in India on lentil crop. Symtoms: Like other Fusarium wilts, the infected plants may wither and die. Leaves may show yellow to brown discoloration and finally drop off. Necrosis and discoloration on collar region is visible and most of the lateral roots are destroyed due to infection.

Pathogen: The disease is caused by the pathogen, Fusarium oxysporum Orthoceros var. lentidis. It belongs to family Tuberculariaceae, order Moniliales and sub-division Deuteromycotina. The pathogen is present both inter and intracellularly in vascular bundles of the host and produces macro and microconidia overthere. Disease Cycle: The pathogen is a facultative parasite and lives saprophytically on organic matter in the soil. When the crop is harvested, the roots remain in soil and pathogen survives on these roots for several years. The pathogen may produce chlamydospores which may face adverse soil conditions and become active and infect plants when next crop is sown. Control: The pathogen is soil borne. Crop rotation with resistant crops and soil amendments with organic matter can reduce the chances of infection. Growing resistant varieties is the best control.

Diseases of Cotton 1. Anthracnose of Cotton The disease is found in most of the cotton growing areas of the world. Symptoms: All the aboveground parts of the plant are infected and plants can be infected at any stage of their growth.The cotyledons and primary leaves show small reddish circular spots. The lesions at the collar region girdle the stem resulting death of young seedlings. The stem of the mature plants can also be attacked resulting split and shredding of bark. On bolls, water soaked, circular, sunken and reddish brown lesions develop which may cover most of the bolls including the bracts. The lesions later turn to black with red margins. The lint become yellow to brown, rot and transformed into brittle fibres. Seeds are also infected and shrevelled discolored and brown in colour. Affected bolls are smaller in size. Pathogen: The causal pathogens are: Colletotrichum capsici (Syd.) Butl. & Bisby ( C. indicum Dast) and C. gossypii Southw. The pathogens belong to family Melanconiaceae, order Melanconiales and sub-division Deuteromycotina. Perfect stage of C. gossypii is Glomerella gossypii (Southw.) of the Ascomycotina. In most of the Indian parts the disease is caused by C. capsici but in Maharashtra it is caused by C. gossypii. Numerous acervuli are produced on affected parts. The conidia are falcate, hyaline, thin walled and single celled produced on conidiophores arising out from the mycelium. The conidia of C. gossypii measure 18-25 x 3.5-5µ where as conidia of C. gossypii are 11-20 x 4-9µ in size. Disease Cycle: The pathogens are seed borne and survive in seed for about a year and are the primary source of inoculum.Two common weeds namely Aristolochia bractiata and Hibiscus diversifolius are also susceptible to C. capsici and can also be a source of primary inoculum.Secondary spread takes place by air and soil borne conidia. The disease spread rapidly during wet weather. Control: Seed treatment with conc. Sulfuric acid or fungicides and to use seeds of over one year old for sowings are important for eliminating seed infection. Boll infection can be checked by spraying calcium cyanamide @ 30kg/ha to reduce humidity. Removal of collateral hosts and spraying of plants with 1% Bordeaux mixture or other fungicides can check the infection.

2. Vascular Wilt of Cotton The disease is common in cotton fields in heavy soil with a soil temperature between 20-30 C during crop season. Due to unfavourable soil temperature the disease is not found in loamy and sandy loam soils. Symptoms: Yellowing and browning of cotyledons and formation of a brown ring on the petiole are the first symptoms of the disease. The affected seedlings are collapsed due to infection. In mature plants, symptoms appear as turgidity of leaves followed by wilting and drooping starting from older leaves upwards and finally involving of branches and whole plant. The stem of seedlings becomes dark as against partial discoloration of stem of mature plants. The discoloration confined only one side of the stem. The black streaks can be observed on stem upto roots after peeling the bark. The plants with minor infection may recover but remain stunted and unproductive. A discolored ring can be seen in transverse sections of infected stem and roots. Vascular tissues are filled up with a gummy substance which contains the fungal hyphae. Pathogen: The causal pathogen is Fusarium Oxysporum f. vasinfectum (Atk.) Synder & Hansen. The pathogen belongs to family Tuberculariaceae, ordes Moniliales and sub-division Deuteromycotina. The mycelium is inter or intracellular and plug the xylem partially or wholly. Both micro and macroconidia are formed which produce mycelium after germination. The pathogen also produces chlamydospores. Disease Cycle: The pathogen can survive in soil for many years. It is also seed borne. The primary infection takes place by hyphae or chlamydospores available in soil or through seed. After infection the fungus reaches to xylem and multiplies fast. The vessels are plugged causing wilting of plants due to non-availability of nutrients. Secondary spread takes place through conidia which are disseminated by wind, water and insects. Control: Cultural practices like deep ploughing during summer, application of high doses of farm yard manure, increased doses of potash and soil amendment with zinc and treatment of seeds with fungicides can reduce the infection. The indigenous cotton, Gossypium arboretum and G. herbaceum are susceptible but some varieties of G. hirsutum and G. barbadence introduced from America and Egypt are immune. Varieties like Jayadhar, Jarila, Vijay, Pratap, Varun and B.D.S. are wilt resistant.

3. Bacterial Blight, Angular Leaf Spot or Black Arm Disease This is the most serious disorder of cotton crop and is found in most of the cotton growing countries. The disease is widely distributed in India.

Symptoms: Minute water soaked areas develop on the under surface of cotyledons of germinating seed. The lesions increase in size, and form black to brown patches causing the cotyledons to dry and wither. If the disease appears on seedlings they also wither and die. The water soaked lesions are also developed on both sides of leaves, increase in size and turn dark brown to black anular spots alongwith veinlets (Fig. 25). The lesions increase in size and cover larger areas of leaf resulting death of leaf. The infection can spread upto petioles causing them to collapse. Lesions on stem, petiole and fruiting branches are elongated, sunken and dark brown to sooty black in colour. The affected stems show cracking and girdling and can be easily broken by wind. Similar symptoms appear on bolls which can fall down prematurely.The bacterium passes through fibres and infects the seed externally or may reach the interior of seed.

Pathogen: The bacterium Xanthomonas campestris pv. Malvacearum (Smith) Dye. is the causal organism of the disease. The pathogen is rod shaped 0.3-o.6 x 1.3-2.7µ in size. It is non-spore forming, encapsulated, gram-negative and motile by a polar flagellum. Several races of the bacterium are known to occur but race-10 is widely distributed in India. Disease Cycle: The pathogen may survive in dead leaves for 17 years and in dry or wet soil for 8 days at 21-30 C. The main source of primary inoculum is contaminated seeds. On germination of seeds the pathogen infects cotyledons where it maintains the resident population on first and second leaf but not on third leaf. Under favourable conditions (high humidity and a temperature of 28-30 C) the inoculum from this source spread to new leaves and further spread continues. The infection may also come from infected bolls, leaves and twigs lying on soil. Secondary spread is through splashing rains and dew and spread very fast at 35 C and high humidity.

Fig.25. Seedling of Cotton showing symptoms of bacterila blight Control:Removal and destruction of plant debris, deep ploughing, pre-sowing irrigation, crop rotation, late sowing, early thinning, good tillage, and addition of potash are recommended to reduce initial infection. Seed treatment with conc. Sulfuric acid can eliminate external inoculum from seed. For iternal inoculum, treatment with antibiotics like streptomycin is essential. Hot water treatment at 56 C for 10 minutes is also recommended. Secondary spread can be checked by spraying copper fungicides (0.2-0.3 %). Five to six fortnightly sprays starting from the time when crop is 5-6 weeks old depending on severity of the disease. Resistant varieties have been developed such as HC-9, BJA-592, P-14, T-12, 102 B and Riba B-50 etc. which should be sown. In Hirsutum group resistant cultivars, 70 IH – 480/2, 70IH- 480/3, 70 IH-280/9, K 4005, Badnawar-13-1007, Khandwa-2, DHY-286, M-937-CTO-421 have been reported.

Diseases of Potato 1. Early Blight of Potato The disease is world-wide in distribution wherever potato is cultivated. The disease affects young crop and may cause yield loss upto 40% if not contained.The disease appears both in tropical and temperate regions. Symptoms: Small pale brown spots first appear on leaves. Lowest leaves are attacked first followed to upper parts of the plant. Concentric rings on leaves surrounded by chlorotic areas are the characteristic symptom of the disease. In dry weather spots become hard and leaves are curled but in humid weather big rotted patches are formed and leaves may fall down.

Similar patches are developed on stem resulting in the whole plant to collapse. The rotting may reach upto the tuber. Affected plants develop less and smaller size tubers. Pathogen: Fungus Alternaria solani (Ell. & Martin) Jones and Grout is the causal pathogen. The pathogen belongs to family Dematiaceae, order Hyphomycetales and sub-division Deuteromycotina. The conidiophores of the pathogen emerge through stomata from the spots and bear conidia. The conidia are beaked, muriform with 5-10 transverse septa alongwith a few longitudinal septa. Conidia germinate within 35-45 minutes at 28-30C. Other hosts of pathogen are tomato, chillies, Atropha belladonna, Cymphomandra betacea, Hyascymus albus, H. niger and Nicotiana alata. Disease Cycle: The mycelium of the pathogen remains viable on dry infected leaves for 10- 12 months. Conidia are also viable upto 17 months at room temperature. Initial infection therefore takes places either by mycelium or conidia surviving in soil on dead plant debris. Contamination of seed tubers with conidia or mycelium may be another source of primary inoculum. The infection starts from lower most leaves and further spread of the disease takes place from the conidia formed on these leaves. The conidia are disseminated by water, wind and insects. Under favourable conditions of rains followed by warm and dry weather the disease spreads very rapidly. Control: Destruction of plant debris after harvest and use of certified seed are important measures to avoid infection. Regular sprays with fungicides at an interval of 10-21 days depending on severity of the disease should be done. Fungicide Dithane Z-78 @ 2lb/100 gallons of water gives best result. Other fungicides like Dithane M-45 (0.2%), Blitox-50 (0.25%), Captan (0.2%) etc.have also been recommended for disease control. Resistant varieties like Kufri Navin (for hills), Kufri Sinduri and Kufri Jivan (for planes) should be used.

2. Late Blight of Potato The famous Irish famine of 1845-46 was due to failure of potato crop by a disease which was later identified as late blight of potato. In this famine, millions of people died due to starvation as potato was staple food of Irish people. Several epiphytotics have been reported due to late blight in different parts of the world. In India, the disease is found in all the potato growing areas. The disease also occurs on tomato. Symptoms: The disease usually appear late in the season than early blight. Brownish black areas develop on leaves which can cover the whole leaf surface. The disease spreads very fast when high humidity is there and cover the whole leaf within 1-4 days. The disease can cover all the leaves and stem of the infected plant and sometimes the whole crop is blighted. The tubers can also be infected while in soil or during harvesting or in storage.Most of the tubers of infected plants are rotted showing brown to purple discoloration on the skin of tubers. Moist atmosphere is suitable for wet rot and dry weather causes dry rot. Pathogen: The pathogen, Phytophthora infestans (Mont) de Bary is the causal pathogen of the disease. The pathogen belongs to family Pythiaceae, order Peronosporales and sub- division Mastigomycotina. The mycelium is endophytic and intercellular. Sporangiophores develop from the mycelium and come out through stomata or lenticels of tubers. Sporangia are pear shaped and papillate and develop at the tips of sporangiophores.The sporangia germinate and form secondary sporangia which produce zoospores upon germination. The zoospores are biflagellate and cause infection to the host. Sexual reproduction is not known. Several physiologic races are known in the pathogen.

Disease Cycle: Four factors have been suggested for development of epiphytotics by the disease: (i) night temperature below dew point for at least four hours (ii) minimum temperature of around 10C (iii) Clouds on the next day and (iv) Rain fall during the next 24 h at least 0.1mm. Primary infection most likely comes through seed tubers particularly under Indian conditions. The mycelium from contaminated tubers grows upward in the stem and cause sporulationon small dwarfed shoots. Infection of foliage takes place from the spores produced in primary lesions. The sporangia are spread through wind, water and leaf eating insects to the healthy crops in the region. The spores are washed out to the soil from affected leaves and infect tubers. The tubers also got contaminated when come in contact of infected leaves during harvesting or in contact with infected tubers in the storage. Control: Use of certified seeds, sanitation, delayed harvesting, storage in cool, dry and well aerated stores are the major precautions to avoid infection.Spraying of crops with fungicides starting well ahead of disease appearance time can provide good control. Dithiocabamates (Zineb, Maneb etc) are more widely used to control the disease. Spray with Dithane Z-78 and Dithane M-45 @ 2-2.5 kg/ 1000 litre of water / ha have been recommended. Early sprays of Bordeaux mixture (4:4:50) and late spays at an interval of 15-21 days with Bordeaux mixture (6:6:50) should be given. Late blight resistant varieties have been developed by Central Potato Research Institute, Shimla for different regions of India as given below: North-western plains: Kufri Jeevan, Kufri Alankar, Kufri Navtal, Kufri Badshah and Kufri Swarna. North-eastern region: Kufri Naveen, Kufri Khasigaro, Kufri Himalini, and Kufri Sherpa Shimla hills: Kufri Jeevan, Kufri Jyoti and Kufri Muthu Nilgiri hills: Kufri Naveen and Kufri Moti. Some high yielding hybrids were also found resistant to late blight of potato.

3. Black Scurf or Rhizoctonia Stem Canker The disease is found world-wide and causes qualitative damage as it affects the maket value of infected tubers both for table and seed purposes. Symptoms: The main phases of the disease are the stem canker and blight phase and the black scurf phase. The emerging tips of sprouting tubers are affected by the fungus which may be killed before emergence. Most of the emerging seedlings from the buds are killed in this way. The plants coming out from left over buds are stunted with yellowish hills. On growing plants, cankers are developed which inhibit flow of carbohydrates resulting their accumulation in the tips causing stunting, rosetting and purple colouration of affected plants. Aerial tubers develop in the axis of branches and petioles. In the black scurf phase, a superficial black crust on the skin of tubers can be seen. This crust is due to formation of sclerotia of the fungus. In India, black scurf is more common than stem canker. Pathogen: The causal pathogen is Rhizoctonia solani Kuhn. of Deuteromycotina. The basidial stage is Thanatephorus cucumeris (Frank.) Donk. The mycelium develops superficial scab-like and black sclerotia. Each sclerotium is accompanied by a superficial, dark coloured, short celled, abundantly branched stout mycelium. No other spores are produced in asexual stage of the fungus. Basidial stage is mostly saprophytic. The basidia are formed on dead leaves or stem parts lying near the ground. The basidia produce thin walled basidiospores; in turn they can produce secondary basidiospores by repetition on germination. Several srains of the pathogen are known to occur.

Disease Cycle: The pathogen survives in soil or on seed tubers as sclerotia. Sclerotia germinate at an optimum temperature of 23C. The basidiospores germinate at optimum temperature of 21-25C. The optimum temperature for infection is 18C. Soil moisture is secondary to soil temperature for development of soil canker. Disease develops more in sandy soil. The primary inoculum comes from soil or infected tubers and further spread is through newly developed sclerotia. Control: This is a polyphagus pathogen with a large host range. The pathogen can survive in soil or on tubers for long time.The sanitation and seed treatment are therefore important to control the pathogen. Soil treatment with PCNB 20-30 kg/ha or soil amendment with neem or margose cake 25 quantal/ha or with saw dust at the same rate followed by the application of 120 kg nitrogen / ha at the time of planting are effective measures for black scurf control. Resistant varieties should be grown.

4. Common Scab of Potato The disease is widely distributed in cool and hilly places. The disease decreases the maket value of tubers due to rough skin. Symptoms: Superficial or deep seated lesions are formed on the skin of tubers. The areas of lesions become rough and are raised over the skin. The lesions have darker corky tissues of different shape and size. Sometimes the lesions join together covering the complete surface of the skin. Pathogen: The causal pathogen of the disease is a bacterium, Streptomyces scabies (Thaxter) Waksman and Henrici. The spores are smooth walled and cylindrical measuring 0.8-1.0 x 1.2-1.5µ in size. Disease Cycle: The pathogen survives in soil and get distributed through movement of soil by wind and cultural operations but main distribution is through contaminated seed tubers. Infection occurs through newly formed unsuberized lenticels, stomata, wounds and may be directly through the cuticle when skin is thin. The pathogen develops in dead cells and causes the development of lesions. The pathogen is most active in dry soil, and hence the disease can be suppressed by irrigation. Optimum infection takes place at 20-22 0C. Control: Use of healthy seed tubers, seed treatment with mercurial fungicides like agalol-6 and aretan etc. by dipping for 5 min in 0.25% solution are useful for elimination of disease. Crop rotation, growing of legume crops before potato planting and application of 20-30 kg / ha of PCNB (Brassicol) will reduce common scab.

5. Bacterial Brown Rot or Wilt Disease of Potato The disease commonly occurs in tropical and sub-tropical regions. The disease is known to occur in India for a long time and locally known as ‘bangle’ or ‘bangdi’ due to a brown ring formation in infected tubers. The wilt disease pathogen also affects chilli, tomato, egg plant and several wild hosts. It also affects other cultivated plants like caster, groundnut, banana and ginger. Symptoms: Diagnostic symptoms are wilting, stunting and yellowing of plants and browning of xylem. A brown ring is formed within tuber due to discoloration of vascular bundles. In severe cases, eye buds become black and if infected tubers are cut, grayish white bacterial ooze comes out of the vascular bundles. Pathogen: The disease is caused by a bacterium, Pseudomonas solanacearum (Smith) Smith. The bacterium is rod- shaped, motile and gram-negative type.

Disease Cycle: The pathogen survives in soil, infected tubers and alternate cultivated and wild hosts. Soil is a potential source of primary inoculum. Infected and surface contaminated potato tubers also serve the source of primary inoculum. The pathogen invades the potato by way of stolons and also spread by contaminated knife while cutting tubers for sowing. In Nilgiri hills the bacterium may survive on potato crop grown throughout the year. Control: Use of healthy seed tubers, treatment of seed tubers with streptocycline (0.02%) for 30 min after giving 5mm deep cut, sanitation and crop rotation are the general precautions recommended against the disease. 6. Virus Diseases of Potato Potato is host of several groups of viruses viz; tobamoviruses, potyviruses, tymoviruses, potexvirus, nepoviruses, luteoviruses, carlaviruses, mop top furovirsuses, potato-T virus, potato yellow dwarf, nucleorhabdoviruses, potato yellow mosaic bigeminivirus and several others. In India, two diseases, potato virus Y and leaf roll are of common occurrence and damaging in potato crop. Recently, a geminivirus which appears to be a strain of tomato leaf curl geminivirus has been found in an alarming proportion in potato varieties.

7. Potato Y Virus (PVY) The disease caused by PVY show mild to severe mottling, or streaks with veinal necrosis on leaves of infected potato plants. However, severity of the disease depends on the cultivar and the strain of the virus. PVY infects large number of plant species naturally such as tomato and Nicotiana spp. Plant species in nine families were found susceptible under experimental conditions. Pathogen: The potatovirus Y pathogen belongs to family potyviridae. The virus particles (virions) are filamentous and flexuous with a modal length of 684-730 nm and 11 nm wide. Virions contain 5.4-6.4 % nucleic acid. The genome is single stranded (ssRNA), linear and unipartite. The virus is transmitted by several aphid vectors and Myzus persicae is the most efficient vector which transmits the virus in a non-persistent way. The virus is also transmitted by mechnical inoculations and also by grafting. Disease Cycle: Potato plants as “ground keepers” are reservoir host of PVY. The pathogen also survives on several solanaceous hosts, thus the inoculum remains throughout the year on one crop or the other and also on weed hosts. The pathogen from the reservoirs reaches to potato crop by aphid vectors. Control: Growing potato crop in aphid free period which is from October to mid-January in Northern plains of India Destroying haulms of seed potato crop in January when aphid population starts to build in. A technique known as “seed plot technique” should be strictly followed for raising seed potato. Use of certified seed and growing of resistant varieties are very important to manage the virus.

8. Potato Leaf Roll Virus (PLRV) Symptoms: Reddening of leaf margins and tips of leaves, leaf rolling, usually leaflets rolled upwards and starts from lower and oldest leaves are the major symptoms of the disease on leaves of potato caused by PLRV (Fig.26). Affected plants remain stunted and yield of tubers is greatly reduced. Tomato and some solanaceous plants are natural hosts of PLRV. Experimental host range is wide. Pathogen: Potato leaf roll virus is the causal pathogen and belongs to luteovirus group. The virions are isometric, 24 nm in diameter and have 30 % nucleic acid and 70 % proteins. The

genome is ssRNA, linear and unipartite. The most efficient and impotant vector of PLRV is Myzus persicae which transmits the virus in persistent manner. The virus is also transmitted by grafting.

Fig.26. Potato leaf roll disease Disease Cycle: The primary inoculum comes through infected tubers used as seed and also from natural hosts. Further spread of the PLRV takes place by insect vector. Control: The control measures are same as mentioned for potato virus Y. Since the virus is transmitted in persistent manner, use of insecticides to control the vector population may be effective especially in seed crop.

Diseases of Tomato 1. Early Blight of Tomato This is common disease of tomato occurring all over India and other tomato growing countries. The disease is caused by the fungus Alternaria solani ( Ell.& Mart.) Jones &Grout. The pathogen attacks the foliage causing characteristic leaf spots and blight. The disease symptoms, life cycle and control measures are given under early blight of potato.

2. Wilt of Tomato The disease is found throughout the world and is serious where tomato crop is grown in the same field continuously. Symptoms: Clearing of the leaf veins and chlorosis are the initial symptoms of the disease. Petioles and leaves of affected plants droop and wilt (Fig. 27). In severe cases black discoloration of vascular tissues can be seen if the roots and stem are split open. Pathogen: Fusarium oxysporum f. lycopersici (Sacc.) Snyder & Hansen is the causal pathogen of the disease.The pathogen belongs to family Tuberculariaceae, order Moniliales and sub-division Deuteromycotina. The pathogen hyphae are found in the vascular tissues and are inter and intracellular. The pathogen produces both macro and microconidia. Disease Cycle: The pathogen remains saprophytically in soil and attack the root region when crop is planted in field or plants are raised in nurseries. After the infection the pathogen moves upwards and multiply rapidly in vascular bundles causing interference with upward movement of the nutrients which causes wilting of plants. Probably factors like plugging of vascular tissues, action of phytotoxins and pectic and cellulotic enzymes acting together cause the wilting of plants.

Fig.27. Wilt of Tomato caused by Fig .28. Late blight of Tomato Fusarium oxysporum F.lycopersici Control: Since the pathogen is soil borne, control is difficult. The best control of the disease is to grow exotic varieties such as Rutgers, Kanora and Roma etc. which have been reported to have resistance. 3. Late Blight of Tomato The disease is caused by Phytophthora infestance (Mont.) de Bary. The disease occurs in some parts of North India particularly in hills and also in Karnataka state. The symptoms are same as has been described under late blight of potato (Fig. 28). Some species of Solanum and Lycopersicon are the collateral host of the pathogen. Certain species and varieties of tomato are resistant to late blight. The disease is controlled by timely spraying of fungicides such as zineb, nabam, maneb etc.

4. Root Knot Disease of Tomato and Brinjal Root knot disease is found in most of the countries on various vegetable crops such as potato, tomato, brinjal, chili, okra, bhendi, cucurbit etc. The losses caused by this disease are from 20-75 % in tomato and 17-81 % in brinjal. Symptoms: The affected tomato and brinjal plants show unthrifty development and stunted growth if the infection occurs during early stages of plant growth. Leaves become yellowish green to yellow and sometimes show scorching along the margins. The roots show galls of various sizes and shapes (Fig.29). Presence of root galls is the most characteristic symptom of the disease. Pathogen: The disease is caused by the nematode pathogens of the genus Meloidogyne. The common species are M. incognita, M. javanica, M. arenaria which commonly attack tomato and other vegetables. The male nematodes are vermiform and 1.2 to 1.5 mm x 30-36µm in size. The females are pear shaped and measure 0.15 – 0.25 mm wide at the base. Upto 600 eggs are laid by each female. Disease Cycle: A large number of females are found in the root galls which survive in the soil on plant debris. The second stage larvae are liberated in the soil. Sandy light soil is best for their movement. These larvae can be killed at higher temperature of 40-50 C and excess of soil moisture. The larvae are attracted by root exudates and thus come in contact of the roots. They gathered in a mass around roots and cause infection by penetrating roots of healthy plants. The male and female nematodes develop depending on the number of larvae per unit area of the host tissues. If they are more crowded mostly male develops but if only few larvae are there then females will develop. The reproduction is mostly parthenogenetic. A temperature of 25-28 C is best for infection and gall formation by nematodes.

Fig.29. Root galls caused by root-knot nematode (Meloidogyne spp.) Control: Cultural practices such as crop rotation, fallow soil, sanitation, deep ploughing during summer, soil solarization and flooding of soil are important to avoid infection by the nematodes. The organic soil amendment such as addition of neem cake, karanje cake @ 25 quantals / ha reduced the root knot incidence. The use of soil fumigation with nematocides is the best method of control but these chemicals are highly toxic and expensive. Resistant varieties such as SL-120, Nimetex, Y-220, PAU-1(7-3-1-4), Hissar Lalit etc. for tomato and Vijay, black beauty, T-3, S-149 etc. for brinjal should be used. Transgenic plants and biological control are promising and may be exploited for nematode control in future.

5. Damping Off of Tomato, Tobacco and Crucifer Vegetables Damping off is a common disease of nurseries of tomato, tobacco and vegetables. The disease is found world wide. Symptoms: The young seedlings are killed before they emerge or the seeds failed to germinate. Young seedlings can be attacked at any time during germination. The infection spreads very fast killing the invaded tissues resulting death of seedlings. This is known as ‘pre-emergence damping off. Next is the ‘post emergence phase’ in which seedling can be killed at any time of their growth till the stem becomes hard enough to resist invasion. Usually roots or stem at or below ground level are attacked. Infected tissues become water soaked. The infection spreads and basal part of the stem become thinner than rest of the stem and fall down on the ground. The infection in seedlings continues till they are completely dead. The disease usually radiates from the point of infection to nearby plants and dead seedlings can be seen in large areas of nursery beds. Pathogen: The damping off is caused by several fungal pathogens but most common are Pythium spp.such as P. debaryanum Hesse, P. aphanidermatum (Eds.) Fitz., P. ultimum Trow and P. arrhenomanes Drechsler. Several othe fungi and bacteria can also cause similar symptoms such Phytophthora, Sclerotinia, Fusarium, Rhizoctonia etc. Pythium produces white mycelium on which sporangia are developed. The sporangia either germinate directly by germ tube or by producing a balloon like secondary sporangium known as vesicle. In this vesicle over 100 zoospores are formed and they swim after their release and then rounded off to form a cyst. The zoospores create new infection after germination. The sexual stage develops as oogonia and antheridia. The oogonium after fertilization develops thick wall and known as oospore. The oospores can survive in adverse conditions and this is the resting stage. The oospores germinate in the same way as sporangia. Disease Cycle: The pathogen is soil borne. Spore germ tube directly penetrates the seed or young seedlings when comes in contact. Proteolytic enzymes break the protoplast and in some cases the cell wall is disintegrated by cellulolytic enzymes causing death of seeds or

young seedlings. The disease is more serious in poorly aerated and poorly drained soil. As the infection progresses the sporangia begin to appear, followed by sexual spores inside or outside of host tissues. The movement of infection is very fast and can quickly rot even the fleshy vegetables or fruits in the field, in storage, in transit and even in market when healthy and infected fruits come in contact. Control: Sterilization of soil by steam or dry heat will control damping off in nurseries. Use of seed protectants such as blitox-50 (soaking seeds in 0.20 % solution) for tobacco seeds, Agrosan-GN or agrosan (seed dressing @ 0.3% by seed weight) for tomato seeds and mercuric chloride (1: 1000 solution dipping for 5 min.) for cucumber seeds is important for disease control. Soil treatment of nurseries by formalin ( 1 : 50) drenching or spraying several days before nursery planting is important. Nursery beds should be raised with light soil having good proportion of sand with high nitrogen dose. The seeds should be sown thin and only light irrigation at frequent intervals shoud be given. Spraying of seedlings with fungicides like metalaxil, captan etc. would be required if soil is heavily infested with the fungus and was wet for long time. 6. Virus Diseases of Tomato Tomato plants are susceptible by large number of virus diseases such as leaf curl, black ring, bushy stunt, golden mosaic, mild mottle, mosaics, yellow leaf curl etc. Tomato spotted wilt, mosaic, leaf curl and a cucumovirus are important for India. (i)Tomato Yellow Leaf Curl Symptoms: The affected tomato plants remain stunted with chlorotic and puckered leaves. Curling of leaves with bright yellow colour is the characteristic symptoms of the disease. Pathogen: The causal virus is a geminivirus and belongs to family geminiviridae. The virons are geminate, 20 nm in diameter and 30 nm. In length.The genome is single stranded DNA, circular and distributed in both the particles. Virions are found in phloem. The virus is transmitted by an insect vector, Bemisia tabaci, a whitefly in a persistent manner. The virus is also transmitted mechanically and by grafting. Several plant species in family solanaceae, leguminoceae and malvaceae are susceptible to virus infection. Disease Cycle: The disease spreads through white fly vector when the crops are overlapping or from symptomless plants like Malva parviflora. Control: Control of white fly vector by safe chemicals or to grow crop in vector-free period are the only preventive measures at present. (ii)Tomato Indian Leaf Curl The disease is present in tomato throughout India and is a major threat to tomato production. Symptoms: Affected plants remain stunted, with small chlorotic puckered leaves (Fig.30). Affected plants look bushy in the field and hardly bear any fruit. The mild or severe symptoms of the disease depend on the variety and strainof the causal virus. Pathogen: The causal virus is a geminivirus and belongs to family geminiviridae. The virus has large number of hosts in several plant families. The virions are geminate (Fig 30), 20 x 30 nm in size. The particles are found in phloem parenchyma and in nuclei. The genome of the virus is single stranded DNA, circular and in two parts known as DNA-A and DNA-B. The virus is transmitted by white fly, Bemisia tabaci in a persistent manner. Disease Cycle: Both virus and its vector have very wide host range. The inoculum is present throughout the year either on cultivated crops or on weeds. The virus is not seed borne. The inoculum already present on other hosts is brought to the new crop by insect vector

Control: Control of vector by insecticides, trap plants and yellow mulches and use of less susceptible varieties are the only management practices at present.

Fig.30. Tomato leaf curl and Gemini virus particles associated with the disease (iii) Tomato Spotted Wilt Tomato spotted wilt virus has been reported from most of the countries infecting one crop or another. The virus has been reported on potato, sunflower, groundnut, tobacco etc. In India, the virus is known to infect sunflower, groundnut and several plants of family leguminoceae. However, there is no authentic report on tomato. Symptoms: Necrotic or chlorotic local lesions, systemic wilting, necrotic spotting, streaking, mosaic, mottling, malformation of leaves, vein yellowing, ringspots, line patterns and colour breaking of flowers are the variety of symptoms found on various hosts. Pathogen: The causal virus is tomato spotted wilt virus which belongs to Tospovirus group in family Bunyaviridae. The virus is transmitted by several species of Thrips and Frankliniella. T. tabaci is the major vector and the virus is transmitted in a persistent manner. The virus multiplies in vector and has a transovarial transmission. It is also transmitted mechanically and by grafting. The virus particles are isometric, enveloped, 85 nm in diameter. Virions contain 5% nucleic acid, 70% protein and 20% lipid and 5% carbohydrate. The genome of the virus is ssRNA. The virions are distributed in all parts of infected plants. Disease Cycle: The inoculum survives throughout the year on one host or the other from where it reaches the healthy plants by thrip vector. The inoculum is also present in thrips and they can infect the plant without fresh acquisition on infected plants. Control: Control of insect vectors and development of virus resistant transgenics are the main methods to control tomato spotted wilt virus. (iv)Tomato Mosaic The disease has a very wide host range and is found throughout the world. Symptoms: Systemic leaf mosaic with leaf narrowing are the main symptoms of the mosaic disease. Pathogen: The causal virus is tomato mosaic virus which belongs to tobamovirus group.The virus particle are rod shaped, usually straight with a modal length of 300 nm and width 18 nm. Virions contain 5% nucleic acid and 95% protein. The genome is unipartite and is ssRNA. The virus does not have a vector but is transmitted by mechanical inoculations, grafting, and by contact of diseased and healthy plants. It is transmitted externally seed infection.

Disease Cycle: The primary inoculum comes via seed and then spread by contact. Infection normally occurs during transplanting. Control: Seed treatment with sodium hypochloride or any other chemical to remove external inoculum from seed and use of resistant cultivars are the only measures to manage the disease. (v)Cucumovirus Infecting Tomato Symptoms: Severe leaf malformation, leaf mottling, leaf reduction sometimes showing shoe sting symptoms (Fig.31),dwarfing and malformed fruits are the main symptoms of the virus on tomato. Pathogen: The cucumovirus is a member of family Bromoviridae and has a very wide host range. Virions are isometric (Fig.31), 29nm in diameter. The genome is ssRNA divided in several parts. There is non-genomic nucleic acid in the virions known as satellite RNA. The virus is transmitted by several species of aphids including Myzus persicae in a non-persistent manner. It is also transmitted by mechanical inoculations and in seeds of a weed, Stellaria media.

Fig. 31: Cucumo virus infected tomato plants Disease Cycle: The virus spreads in healthy crop by the aphid vectors from the inoculum present either on crop plants or in weed host. Control: Control of aphid vectors and use of virus resistant transgenic plants are the options to manage the disease.

Diseases of Brinjal 1. Phomosis Blight, Leaf Spot and Fruit Rot The disease was first reported from Gujarat in 1914 and later to other parts of India. The causal pathogen causes seedling blight, leaf spots and fruit rot. Symptoms: The nursery plants show damping off when plants are infected at seedling stage. Infected leaves show circular spots of cinnamon-buff colour with irregular blackish margin. Lesions may also develop on petioles and stem. The affected portion of the plant is blighted. On fruits, minute, sunken, dull and dusky spots appear first which coalesce later converting in rotten areas. Severely affected fruits show rotting of the entire flesh. Pathogen: The disease is caused by Phomosis vexans. Numerous pycnidia are developed on the affected portion of the fruit coat. The fungus is specific pathogen of brinjal.

Disease Cycle: The pathogen survives in soil on affected plant debris and also externally seed-borne. When the seeds or seedling are planted in infested soil, the organism become active and infects the plants.

Control: Field sanitation and seed treatment with fungicides are important control measures. Treating the seeds with 0.1% mercuric chloride or other organomercuric fungicides can eliminate fungal infection. In nurseries and fields, spraying with 1% Bordeaux mixture helps in protecting plants from infection.

2. Bacterial Blight of Brinjal The disease is found only in tropical and sub-tropical regions. In India, the disease has been reported from West Bengal. The pathogen also attacks several solanaceous crops such as potato, tomato and chillies and other cultivated plants which include castor, groundnut, banana, ginger and many wild plants. The disease is often associated with nematode infestation. Symptoms: The most characteristic symptoms are wilting and stunting. The stem at the base becomes dark brown and constrict leading to wilting of plants.Sudden wilting and drooping of leaves occur when the infection is severe. Pathogen: The disease is caused by the bacterium, Pseudomonas solanacearum (Smith) Smith. Three races of the pathogen have been reported and race-1 causes infection to solanaceous plants. Details of the pathogen have been mentioned under Bacterial wilt of potato. Disease Cycle: The pathogen survives in soil or on alternate or cultivated or wild hosts. Soil is a potential source of primary infection. The disease destroys tomato, brinjal and chilli crops every year. Control: Okra-cowpea-maize rotation reduces the infection by the bacterium. Foliar application of agrimycin-100, chloramphenicol, or streptomycin sulphate are effective at 100ppm but prior to infection.Rain or irrigation water should not be allowed to flow from diseased to healthy fields.

Diseases of Chilli 1. Anthracnose of Chilli This is one of the worst diseases of chilli found in several countries including India. Symptoms: Symptoms of the disease mostly appear on ripened fruits, hence the disease is also called ripe fruit rot. Usually circular and sunken spots with black margin appear on fruits (Fig.32). These spots enlarge and form concentric markings with dark fructifications representing the fungus acervuli. The fruits with many spots drop off prematurely. The fungus can also attack fruit stalk and stem causing die-back symptoms. Pathogen: The causal pathogen is Colletotrichum capsici (Syd.) Butl. & Bisby. The pathogen belongs to family Melanconiaceae, order Melanconiales and sub-division Deuteromycotina. The pathogen remains localized on fruit surface and produce acervuli. The acervuli have hymenial layer with short conidiophores which bear conidia. The conidia are hyaline and falcate and measure 11-24 x 4-5.5µ and contain oil globules. The conidia cause infection upon germination.

Disease Cycle: The pathogen is externally seed borne which is the potential source of primary inoculum. Secondary spread is through conidia which are disseminated by splashing rain. Control: Seed treatment with organomercuriales and foliar sprays with copper fungicides at fortnightly intervals starting from the time of first infection are the best control measures to contain the disease.

Fig .32 Anthracnose disease of Chilli Fig.33 Mosaic disease of Chilli

2. Mosaic Disease of Chilli Symptoms: The leaves of affected plants show systemic dark green to yellow mosaic or mottling with or without deformation of leaves, stunting and extremely deformed (Fig.33).The affected plants developed only a few deformed fruits. Pathogen: The associated pathogens are two different viruses. The filamentous particles belong to potato virus Y and the spherical ones to cucumber mosaic virus. The virus (es) are transmitted mechanically and also by aphid vectors and infect Capsicum annum, C. fruitescens, Nicotiana tabacum, N. glutinosa, mustard and radish etc. causing variable symptoms. The details of pathogens have been described under potato virus Y and cucumber mosaic diseases. Disease Cycle: The inoculum of pathogens remain throughout the year on overlapping crops and on various hosts from where the viruses infect new crop plants by insect vectors Control: Best control is use of resistant cultivars and control of insect vectors. Application of NPK reduced the incidence of the disease. However, maximum disease reduction was obtained with the application of DAP + MOP + rogor. Early planting and growing nurseries under insect free conditions are also helpful. 3. Virus Diseases of Chilli In India, the most important disease of chilli caused by virus is yellow mosaic disease which causes a yield loss of 65-75%. It is a complex disease and eight viruses have been identified to be associated with the disease in Karnataka and four in Punjab. The most common ones are potato virus Y, pepper vein banding virus, pepper veinal mottle virus, tobacco etch virus, tobacco mosaic virus, tobacco leaf curl virus and cucumber mosaic virus. Among them potato virus Y and cucumber mosaic virus are of common occurrence and cause mosaic disease either in combination or singly. Sometimes leaf curl caused by geminivirus also appears in severe form. This has been described under tomato leaf curl disease.

Diseases of Vegetable Crucufers 1. Black Rot of Crucifers The disease is found throughout the world and most members of crucifer family are sceptible to black rot. Symptoms: Infected young seedlings show dwarfing, one sided growth and their leaves droop. In the field, leaves of affected plants show V- shaped chlorotic blotches at leaf margins which move towards the mid-ribs of the leaves turning the veins black within chlorotic areas. This blackening advances towards the stem from where it moves upwards and downwards to other leaves and shoots. Infected leaves may fall prematurely one after the other. In cross sections of stem and petioles, vascular tissues show blackening and slime deposits having bacterial population. Cauliflower and cabbage heads, fleshy roots of turnip and radish are also affected and become discoloured. Invaded tissues may be attacked by soft rot bacteria giving repulsive odor. Pathogen: The bacterium Xanthomonas campestris pv. Campestris is the causal pathogen. Disease Cycle: The pathogen survives on plant debris and on or in the seed. When the crop is sown, the bacteria infect the cotyledons or young leaves through stomata, hydathodes, and wound. The bacteria then move intercelullularly and finally reach the open ends of vessels. The pathogen multiplies in the vessels and spread throughout the plant reaching upto the seed. The xylem disintegrates at places and bacteria spread to neighbouring parenchyma cells and kill them. The pathogen spread by splashing rains, winds and farm equipments to other leaves and infect them. Control: Use of pathogen-free seeds, seed treatment with hot water (50C for 30 min) and tetracycline or streptomycin will eliminate bacteria from seed. Sprays with copper fungicides at 10 days intervals help in reducing the disease incidence. 2. Downy Mildew of Crucifers Downy mildew is common on cruciferous plants when young and cause significant damage. During late infection, it infects to influorescence and cause sterility. Symptoms: The symptoms appear as purplish brown spots on the lower side of leaves. Above these lesions on upper surface of leaf tan to yellow patches can be seen. The cottony growth of the mycelium can be seen on lower side of leaves. On the stem, deformities as swellings appear which may be small to several inches long. The young ovary becomes elongated and twisted. Often, the floral buds show atrophy and sepals, petals and stamens shrink. Pathogen: The fungus, Peronospora parasitica (Pers.) ex Fr. is the causal pathogen. However, the pathogen occurring on Brassica campestris has been named as P. brassicae by Gaumann. The pathogen is an obligate parasite. Numerous erect and branched conidiophores are developed from intercellular mycelium and emerge out through the stomata on the underside of the leaves. The conidiophores have dichotomous branching six to eight times on their tips. A single conidium is developed at the tip of each branch. The conidia readily fall off and germinate by germ tube. Oospores are formed in the floral organs late in the season. Disease Cycle: The pathogen survives in soil as oospores. Seeds also carry oospores through contaminating trash. Wild hosts can also serve as the source of primary inoculum. Secondary spread of the disease is through conidia. Control: Crop rotation avoiding cruciferous plants, deep ploughing during summer, and eradication of weed hosts are important cultural practices. Spraying fungicides like Dithane Z- 78 (0.3%), Dithane M-45 (0.1-0.3%) Ridomil (0.1%) etc. are recommended to control the

disease. Resistant varieties should be grown. Mustard varieties YRT-3 and TMV-2 and yellow sarson type-6 are resistant to the fungus.

Diseases of Cucurbits 1. Fusarium Wilt of Cucurbits This is an important disease of cucurbits and found throughout the world and several species of Fusarium are known to cause the diseases in plants of family cucurbitaceae. Symptoms: In young seedlings, cotyledons are dropped and weather due to wilt disease. Older plants wilt suddenly and vascular bundles at the collar region show brown discoloration. Pathogen: The fungus, Fusaium oxysporum Schl. is the causal pathogen. The pathogen belongs to family Tuberculariaceae, order Moniliales and sub-division Deuteromycotina. The pathogen produces both macro and microconidia. The conidia germinate and produce hyphae and mycelium. Disease Cycle: This wilt is a soil borne disease. Inoculum increases more rapidly in sandy soils than in clay, silty or loam. The inoculum can reach to high level after just two successive crops. The fungus available in soil penetrates the root system through injury. After infection the fungus multiplies and moves to xylem vessels which are later plugged by the pathogen mycelium. The blocking of xylem vessels intrupts the movement of nutrients resulting wilting of plants. Control: Crop rotation with resistant crops to fungus is viable methods of overcoming the disease. Soil drenching with fungicides like carbendazim etc. can reduce the inoculum. Soil solarization for 2-4 weeks by using impermeable plastics after amending the soil with ammonium sulphate is a good method to control the disease. Growing resistant varieties is the best method. 2. Downy Mildew of Cucurbits This is an important disease of vegetable cucurbits such as sponge gourd, ridge gourd, bottle gourd, bitter gourd, snake gourd, pumpkin and cucumber etc. Symptoms: Leaves first show mosaic like mottling. The pale green areas are separated by dark green islands. Soon the angular yellow coloured spots restricted along veins develop on the upper surface of leaves. Below the spots on the lower side of leaf purplish downy growth appears. The affected leaves die quickly. Usually middle leaves are infected first followed by other leaves. Only a few small fruits with poor taste develop on diseased plants. Pathogen: The fungus Pseudoperonospora cubensis (Berkeley & Curtis) Tostowzew is the causal pathogen. The pathogen is an obligate parasite. The sporangiophores in a group of 1-5 arise from the intercellular mycelium. Sporangia develop on the branches of sporangiophores usually during night and are dispersed during morning hours. The sporangia produce zoospores upon germination which cause the infection to plants. Oospore formation is not common in this species of fungus but has been reported from Madhya Pradesh, Punjab and Rajasthan. Disease Cycle: The pathogen infects large number of wild hosts from where the primary inoculum comes to cultivated crops. In areas where oospores are formed, the primary infection may be through them. The disease in the field spread through sporangia which are disseminated by splashing rains and beetles.

Control: Spraying of fungicides, zineb, mancozeb and tricop-50 has been recommended to control the disease. Removal of infected vines and eradication of wild cucurbits from near the vegetable growing areas are economic control measures in view of the cash value of the crop. 3. Powdery Mildew of Cucurbits This is a serious disease of cucurbits especially on pumpkins and bottle gourd. Symptoms: White to dirty grey powdery spots appears on leaves and stem. These spots enlarge in size and can cover the whole surface of the host. Leaves are fall down during severe infection. Fruits on affected plants are smaller in size. Humid condition favours the fast development of disease. Pathogen: Two fungi, Erysiphe cichoracearum D.C. and Sphaerotheca fuliginea (Schlecht.) Poll. have been reported as pathogens of powdery mildew of cucurbits. The size of conidia of E. cichoracearum varied according to physiologic races and Cleistothecia are not common. The number of ascospores is usually two, rarely three in each ascus. S. fuliginea is known to cause powdery mildew of cucurbits in India. The perithecia are formed from September to February and each perithecium has one ascus. Disease Cycle: Perithecia develop on left over cucurbits in isolated areas may serve as a source of primary inoculum. The conidia from wild cucurbits may be another source of primary inoculum. The conidia are dispersed by wind or insects and infect the plant through epidermal cells of the host. Control: Field sanitation and dusting with 200-mesh sulphur @ 25-30 kg / ha is quite effective to control the disease. Sprays with other fungicides like calexin (0.1 or 0.05 %), copper sulphate and karathane are also effective. Resistant varieties of each crop should be grown. 4. Cucumber Mosaic The disease is world-wide in distribution. Naturally the disease occurs in cucumber and many cucurbits, tomato and spinach. Symptoms: The leaves of affected plants show mosaic, severe chlorosis, green blisters and reduction and narrowing of leaves (Fig. 34). The plants remain stunted and bear deformed fruits.

Fig.34. Cucumber mosaic disease symptoms and virus particles associated with this disease. Pathogen: The disease is caused by a virus of cucumovirus group in the family Bromoviridae. The virus particles are isometric, 29 mm in diameter. Genome of the virus is single stranded RNA and consists of 18% RNA and 82% protein. The virus is transmitted by large number of aphid species such as Myzus persicae, Aphis craccivora etc. in a nonpersistent way. It is transmitted through seeds of 19 plant species.

Disease Cycle: The virus inoculum is present throughout the year on one crop or the other or on weeds from where it is brought to new crop by insect vectors. Contaminated seed is another source of primary inoculum. Control: Control of cucumber mosaic virus is difficult. However, virus resistant cultivars or transgenic plants can give protection from the virus. Growing cucumber in polyhouses is advantageous as the crop remain free from virus resulting in more yield and quality of fruits.

Diseases of Pea 1. Powdery Mildew of Peas The disease is of world-wide occurrence on pea. Usually the disease appear late in the season during the pods formation. Symptoms: The disease symptoms appear on leaves as white powdery patches but soon other parts of the plant such as stem, pods etc. also show the symptoms. At advanced stages all aerial parts of the plant are covered with white powder. The white powder consists of the fungus mycelium and spores. Necrosis of epidermal cells is common. Pathogen: The disease is caused by a pathogen, Erysiphe polygoni D.C. = E. pisi D.C. This fungal pathogen is an obligate parasite. The fungal mycelium is ectophytic. The conidiophores develop from the superficial hyphae and each conidiophore bears several spores in chain. The mature conidia are dispersed by wind. The conidia are elliptical, barrel- shaped and measure 25-35 x 13-16µ in size. Late in the season black coloured sexual spores, the Cleistothecia are formed. Each cleistothecium contains 2-8 asci and each ascus has 3-8 ascospores. The Cleistothecia are also formed on plant debris left in the soil. Disease Cycle: The Cleistothecia persist in the soil till next season of the crop. Under favourable conditions, the cleistothecial wall disintegrates and ascospores are released. The ascospores first infect the lower most leaves near the soil of the new crop. Once the infection is established, secondary spread takes place by the conidia. Available information on survival of the fungus suggests that the fungal mycelium may also survive in the pea seeds. Control: Field sanitation, early sowing, seed disinfection by hot water treatment or seed dresser fungicides are precautionary measures to avoid infection. Chemical control using 200 mesh sulphur dust @ 25-30 kg / ha, o.1% bavistin, 0.2-0.25% kerathane etc. is effective. Use of resistant varieties like T-10, T-56, P-185, P-383, NDVP-4, Arka Ajit, DP-53, DMR-9, Pusa Panna etc. is the best method of control. 2. Rust of Peas Two species of Uromyces occur on cultivated pea I. Uromyces pisi (Pers.) Wint. Which are heteroceous rust having its aecial stage on Euphorbia cyparissias L. II. Uromyces fabae (Pers.) de Bary is autoceous rust and occurring on pea and lentil in India. U. pisi is not common in India. Symptoms: Small, oval and light to brown coloured pustules develop on both sides of leaves. The pustules slowly cover the whole surface of leaves. Affected leaves wither and fall off prematurely. The pustules on the leaves contain uredosori. The dark brown teliosori are developed both on leaves and stem near maturation of the crop. The aecia and pycnidia also develop on pea. The morphological characters of aecia and pycnia are similar to Puccinia graminis tritici except in size and colour etc.

Pathogen: The causal pathogen is a fungus, Uromyces fabae (Pers.) de Bary which belongs to family Pucciniaceae, order Uredinales and sub-division Basidiomycotina. The pathogen produces aecia on stem and petioles which are mixed with spermagonia. The aeciospores are elliptical and yellow brown in colour measuring 14-22µ in diameter. The uredial stage is repeated several times during crop season. Urediospores are spiny, light brown, elliptical and measure 20–30 x 18–26µ. The teliospores are thick walled and measure 25-38 x 18-27µ. They are single celled, ovate and pedicillate and produce four celled basidia upon germination. Disease Cycle: The pathogen completes its life cycle on pea but other hosts such as broadbean, lentil, sweet pea, and lathyrus also carry infection as uredial and telial stages of the fungus and can serve as a source of primary inoculum to pea crop. Further spead of the disease takes place by means of uredospores. Control: Economic control of this disease is difficult except to use resistant varieties,

Diseases of Beans 1. Bean Blight The desease is known to occur in several countries including India. Symptoms: First symptoms appear as small circular spots with dark green centre surrounded by reddish margin. The spots coalesce and form large necrotic patches and cause blightening. The fruiting bodies, pycnidia of the fungus appear in large numbers in the form of small, light brown, pin head-like bodies on the necrotic spots. Both young and old leaves are susceptible to infection and severely affected plants are completely deformed. The spots also develop on pods. Pathogen: The disease was identified to be caused by the fungus, Foma jolyana Priozy and Morg. The genera Phyllostricta, Phoma and Ascochyta are closely related. The pycnidia are formed on leaves. Conidia are formed within pycnidia from inner cells. The conidia can remain viable in pycnidium for long time. Disease Cycle: The pathogen’s pycnidia survive in soil on plant debris and also on seed. Mycelium may also survive on seed coat. The soil borne and seed borne inoculum acts as primary source of infection. Further spread of the disease occur through conidia which are disseminated by splash rains, insects or by contact of leaves. Control: Removal and destruction of plant debris, seed treatment with thiram and captan and four sprays of topsin-M (0.1%), or mancozeb (0.25%) at 10 days interval starting from the onset of disease are very effective measures to control the disease. Use of resistant cultivars is the best control. 2. Anthracnose of Beans This is the major disease of beans in many parts of the world. In addition to beans, the disease also affects cowpea and mungbean etc. Symptoms: On cotyledons, dark brown, sunken spots appear first followed by necrosis of veins and adjoining tissues of young leaves. Mature leaves show angular and brown coloured lesions adjacent to veins. Similar spots with purple border develop on stem and pods. Mature seeds from infected pods also show brown shades and seedlings develop from such seed show typical lesions on cotyledons.

Pathogen: The disease is caused by the pathogen, Colletotrichum lindemuthianum ( Sacc. & Magn.) Scriber. The perfect stage of the pathogen is Glomerella lindemuthianum (Sacc. & Magn.) Shear.The conidial stage develops on stromata beneath the cuticle. The cuticle is ruptured and conidia are released. The conidia are formed singly on the stromatoid masses in acervuli. The conidia form 1-4 germtube during their germination. The perfect stage has only been reported in cultures. Disease Cycle: The causal pathogen is soil and seed borne. In soil, it survives on disease debris. In seeds, the pathogen survives till the seeds are viable.The primary inoculum usually comes from seeds. The pathogen grows on cotyledons from where it spreads to other parts of the plant. The spores are embaded in gelatinous mass and water is required for their release. Usually they are washed down by rains or dew to stem or new leaves. Movement of insect or wild animals or man also helps in dissemination. Cool and rainy weather is conductive for epidemic of the disease. Control: Use of disease-free seed, removal of plant debris, crop rotation, weed control, enough spacing between plants are good cultural practices for disease control. Fungicides like captan, zineb @ 2 kg / ha should be sprayed if the disease is severe. Vita vax and agrosan GN have bben recommended for seed treatment. 3. Virus Diseases of Beans Beans are affected by several virus diseases which are originally reported on them or they are the host of viruses infecting other crops. The most damaging virus diseases in India are: bean common mosaic, southern bean mosaic virus, urdbean leaf crinkle virus and mungbean yellow mosaic virus. (i)Bean Common Mosaic Symptoms: The main symptoms are mosaic with vein banding, the dark green areas along main leaf veins. Sometimes accompanied by leaf malformation such as curling or blisters on leaves. Pathogen: The causal virus has filamentous particles measuring 750 nm in length and belongs to potyvirus group of viruses. The virus is transmitted non-persistently by several aphid species but Aphid fabae and Myzus persicae are the major vectors. It is highly transmitted through seeds of beans or other hosts like urdbean, mungbean etc. The virus infects several legumes, tobacco and other plant species. Disease Cycle: Primary inoculum comes through infected seeds or from nearby infected crops. Further spread is through vectors. Control: Use of virus-free seed and cultivation of resistant varieties are the effective control measures.

(ii) Southern Bean Mosaic Symptoms: Chlorotic spots, systemic vein clearing or vein banding, mosaic, leaf distortion and stunting of affected plants are the main symptoms of the disease. Pathogen: The causal virus particles are isometric, 28 nm in diameter and belong to sobemovirus group. The particles contain 21 % nucleic acid and 79 % protein. The viral genome is ssRNA. The virus is transmitted by beetles such as Epilachna variestis in semipersistent manner. It is also transmitted by mechanical inoculation, grafting and by seed and pollen.

Disease Cycle: Primary inoculum comes through seeds or from other crops infected by the virus through vector. Further spread of the pathogen takes place through beetle vector or by pollen. Control: Same as with bean common mosaic disease. (iii)Urdbean Leaf Crincle Disease Symptoms: Leaf rugocity, crinkling and distortion of leaves are the major symptoms. The leaves on infected plants are bigger than normal and more vegetative growth was also seen in some varieties. The disease also attacks mungbean, cowpea, pigeon pea and tepari bean. Pathogen: The particles of the causal virus are isometric, 25-30 nm in diameter. Genome of the virus is ssRNA and unipartite. The virus is transmitted by mechnical inoculations, by beetles and via seeds. Disease Cycle: Primary inoculum of the pathogen comes through infected seeds and further spread is by beetle vector, Henosepilachna dodecastigma. (iv) Mungbean Yellow Mosic This is the most serious disease and is found on many legumes and weeds. There is almost a total loss to yield of mung bean crop if it is infected at an early stage. Symptoms: The symptoms of the disease as yellow spots on the leaves can be seen when the crop is about one month old. The symptoms of the disease are so conspicuous that infected plants can be identified from a distance. Severe yellow mosaic and mottling of leaves are the major symptoms (Fig.35). The virus become systemic and all leaves of infected plants show yellow mosaic. Number and size of the podes is greatly reduced. Seeds are smaller in size and shriveled. Pathogen: The causal virus is a geminivirus recently named as genus Begomovirus. The virus is transmitted only by whitefly vector, Bemisia tabci and not by sap inoculations. The Thailand strain of the virus is mechanically transmitted. The geminate particles measure 30 x18 nm and have ssDNA as their genome. The virus has a wide host range which includes legumes and weeds.

100 nm Fig.35: Mung bean yellow mosaic disease, its vector and virus particle Disease Cycle: The primary inoculum comes from other infected legumes or weeds through whitefly. Once the infection is established in the crop the disease spread very fast by whitefly vector and cover the complete field within few weeks.

Control: The control of the disease is very difficult because both pathogen as well as vector have wide host range. The only means of control is by the use of resistant cultivars. Urdbean varieties T-9, UPU-1, Pat-19, 26, 30 and 35 are fairly resistant. In mungbean, Pant 1,2,3, T-1 and T-44 are resistant , In soybean, PK-416, 472, 1024, 1029, 1042, Pusa 37, SL-295, SL-525 etc. are resistant to yellow mosaic infection.

Diseases of Mango 1. Mango Malformation The disease was recorded in India in 1910 and presently wide spread in North Indian states. The disease is also found in Pakistan and Egypt. Symptom: The dease appear in two phases, the vegetative malformation and floral malformation. The vegetative phase is more common in young trees. The main symptoms are excessive vegetative branches of limited growth, swollen and with short internodes and give a look of rosette. In older trees, similar symptoms also develop but the growth of swollen axillary buds do not impair but persist and crowded at nodes sometimes form girdle. All such branches develop floral malformation. Malformed flowers are bigger than normal flowers and only a few of them are hermaphrodite. Malformed panicles have more flowers but do not bear fruits. Some light type panicles which are compact bear fruits. The bracts of malformed flowers are larger and give a leafy appearance. Pathogen: Several biotic and abiotic factors are reported to cause mango malformation such as physiological disorder, Eryophyid mite and virus. It is now established that the disease is caused by a fungal pathogen, Fusarium moniliforme var. subglutinans. Probably Eryophyid mite acts as a vector of the Pathogen. Disease Cycle: It has not been fully understood. Spread through vegetative propagation and by unkown means from tree to tree is possible. Control: Except pruning of twigs having malformed flowers no other control method is known.

2. Powdery Mildew of Mango This is one of the worst diseases of mango which affects almost all commercial varieties of mango. The severity depends on climatic conditions. The low temperature of 18-20C and relative humidity of 70-80 % favour the fast spread of the disease. The losses upto 70-80 % may occur on individual trees when infection is severe. Symptoms: The appearance of whitish to greyish powdery growth on tender leaves and influorescence are the main symptoms of the disease. Most of the floral axis, tender leaves and young twigs of a tree are infected as the disease progresses. Infected floral parts may drop off prematurely. The axis becomes dry showing die-back symptoms. The fruit setting is very poor and premature fruit drop is very common. Pathogen: Oidium mangiferae Berth. is the causal pathogen of mango powdery mildew. The mycelium is hyaline and produces conidiophores on which conidia are formed. Disease Cycle: The pathogen spreads from tree to tree by conidia. The pathogen survives in soil as Cleistothecia on infected plant debris and ascospores attack the lower most leaves. Further spread takes place by conidia.

Control: The disease is controlled by giving two preventive sprays of wettable sulphur once before the flowers open and second after the fruit set. Dusting with 200 mesh sulphur powder can also check the disease. Orchard sanitation is important to avoid infection. 3. Bacterial Blight of Mango The disease is known to occur in India and a similar disease was reported from South Africa. Symptoms: Initially small, water soaked lesions develop on leaf blade.The lesions start from the leaf tip and slowly cover most of the leaf surface, petioles, fruits and tender stem. The lesions are rough and slightly raised due to heavy exudates of the bacteria. Most of the infected leaves are drop down. On fruits, the lesions are first water soaked and later turn black.The fruit skin may be cracked and badly affected fruits are dropped. Pathogen: The causal bacterium is Xanthomonas campestris pv. Mangiferaeindicae (Patel et. al., Robbs et al.).The bacterium is rod shaped measuring 0.36 – 0..54 x 0.45-1.44µ in size. The bacterium is gram-negative and has a single polar flagellum. The bacterial cells are either single or in chaines and are motile. Disease Cycle: The blight bacterium is a phyllopane and remains in the orchard throughout the year. It infects the new trees through injury mostly caused by insect feeding such as weevils, bugs and leaf Webbers. These insects also carry the bacterial cells on their legs and mouth parts and thus transmit the pathogen mechanically. Control: Seedling certification, inspection and orchard sanitation are important measures to contain the disease. Three sprays of streptocycline (100 ppm) or agrimycin-100 (3000 ppm) should be sprayed after first visual symptoms at 10 days interval. Monthly sprays of bavistin (1000 ppm) or copper oxychloride (3000 ppm) were also found effective.

Diseases of Apple 1. Apple Scab This is the most serious disease of apple throughout the world where apple is grown. The disease was first reported from Sweden as early as 1819. In India, the disease was first reported from Kashmir velley in 1935 on a popular variety of apple “Ambri”. Since then it has been found in most groves of apple in the country. The losses caused by the disease had been very heavy and are both types, qualitative and quantitative. The affected fruits have lower market value. Symptoms: The symptoms appear during spring on young leaves and flower buds. Then the infection moves to fruits, parts of flowers and even young shoots. Light or olive green irregular spots develop on both surfaces of leaves. The spots are mostly circular and tissues around them are thicker and sometimes raised. On fruits, early spots develop near calyx but stalk end lesions appear later. The size of spots depends on the variety and time of infection of fruit development. The spots are initially dull but later turn to black. Splitting of fruit skin on spot area is common with early infection. Corky layers with deep cracks are often seen on mature fruits. Affected fruits are malformed. The bark of twigs can split at the point of spots and give a silvery grey look. The lesions can develop on fruits even in storage. Pathogen: Apple scab is caused by the fungal pathogen, Venturia inaequalis (Cke.) Wist which belong to family Venturiaceae, order Pleosporales and the sub-order Ascomycotina. The imperfect or conidial stage is Spilocaea pomi Fr. Ex Fr. The mycelial strands develop on leaves and fruits between epidermis and cuticle. In dead leaves, mycelium is a saprophyte where it grows and form ascostroma. The conidiophores

develop from the hyphal strands or from the compact stroma. The conidiophores bear conidia which are ovate and lanceolate and measure 12-22 x 6-9µ. Perfect stage of the pathogen develops on fallen leaves where ascospores are formed. Disease Cycle: The scab pathogen has two stages in its life cycle, the saprophytic stage which is found on dead leaves and where the pathogen overwinters. The parasitic stage is the second stage in which the pathogen completes its parasitic life cycle on living parts of the plants such as on leaves, flower, twigs and fruits. Ascospores developed on dead leaves are the primary souerce of infection. They infect young leaves and buds during spring. Secondary spread of the disease is by conidia developed after the primary infection sets in. Weather conditions are very important for the development and release of ascospores and formation of conidial cycle. The optimum temperature for ascospore maturation is about 20C. Rains favour ejection of ascospores. The ascospores germinate and cause infection at a temperature of 10-22C and free water or 90% relative humidity. Control: The forecasting systems to warn possible time of disease appearance have been developed based on: I. ascospores ready to mature II. Ascospores release is expected III. Ascospores release has taken place and IV. Infection period has occurred. These informations are collected from the fungal stages on dead leaves. It is therefore important to collect and burn the fallen leaves. Spray of 5% urea in the autumn before leaf fall and 2% urea before bud burst is used. Post harvest spray with 0.4% benlate or other fungicides will reduce perithecia formation on fallen leaves. Spray schedules have been developed for different apple growing regions. For example, in Himachal Pradesh following schedule of fungicide sprays has been developed: First spray of difolton @ 300g / 100L water or other benzimidazole during March-April. Second spray of dithane M-45 @200g / 100L water or captan @200g / 100L water during April-May. One to three sprays of dithane M-45 @ 250g / 100L water at post blossom stage during summer at 10-15 days interval. 2. Powdery Mildew of Apple The disease causes severe losses to apple nurseries and orchard trees throughout the apple growing regions of the world. Pear and Quince are also susceptible to powdery mildew disease. Symptoms: A white powder is seen on leaves and young shoots of plants. Affected leaves are narrower and longer than healthy leaves.. Later, the leaves curl from margins and become brown coloured. Infected buds die; fruits are reduced in size, deformed with a rough skin. Pathogen: Podosphaera leucotricha Ellis & Ever is the causal pathogen of the disease. The pathogen belongs to family Erysiphaceae of the sub-division Ascomycotina. Aerial conidiophores arise from the mycelium on leaves and shoots. Each conidiophore develops conidia in chain which are of 25-30 x 10-12µ in size.The Cleistothecia are embaded in the mycelium. Each cleistothecium contain a single ascus which borns ascus. Disease Cycle: Cleistothecia play little role in the perennation of the pathogen. The primary source of inoculum is the resting mycelium or encapsulated haustoria in the buds. When such buds sprout in next season, large number of conidia are formed which are wind borne and serve as secondary inoculum. Conidia germinate at a temperature of 19-25 C and penetrate the leaf at high humidity.

Control: Dusting the trees with sulphur can control the disease. Prunning of affected shoots and spraying with fungicides like bavistin (0.05%) or morocid (0.1%) or kerathane help to protect from infection. 3. Stem Black of Apple The disease has been reported from Kumaun hills. The disease affects twigs and stem. The symptoms are seen as black streaks on stem starting from pruned end. Affected stem shows cracking followed by engirdling of stem and killing the tissues. The disease is common on thick mature stem than on young ones. The disease is caused by the fungus Coniothecium chomatosporum Corda. The disease can be controlled by applying fungicidal paste to pruned ends.

4. Stem Brown of Apple Symptoms: The disease usually starts from wounds caused by pruning and then moves downwards to twigs and stems causing dieback symptoms.The bark becomes loose due to infection and become papery brown and peels off exposing the dark brown stem. Horizontal and vertical cracks develop on stem. The infection is more on mature stems than young branches. Pathogen: The fungus, Botryosphaeria ribis Cross & Dugg. is the causal pathogen. Pycnidia and perithecia are formed on dead twigs and stems from where the spores of the pathogen reach to the cut ends or wounds and get entry to the plant. Control: Sanitary measures and to apply fungicidal paste to cut wounds may avoid infection.

5. Pink Disease of Apple The disease is wide spread in many apple growing countries and also known as dieback, pink canker, or twig blight. Symptoms: Canker, blight and dieback symptoms are seen on trunk, stem and twigs. Infection mostly starts from the forks of thick branches proceeding upwards and downwards. The lesions are sunken, dull brown with cobweb-like growth. The mycelium remains superficial and transforms into pinkish encrustations during rainy season. Disease causes wilting of shoots and drying up of branches. Pathogen: The disease is caused by the fungal pathogen, Corticium salmonicalor Berk. & Br. ( Synonym : Botryobasidium salmonicolor (Berk. & Br.) Venkatnarayan; Pellicularia salmonicolor (Berk. & Br.) Dast.). The perfect stage is Necator decretus Mass. The pink conidia are produced on the surface of infected branches and stem. Disease Cycle: The pathogen persists season to season through dormant mycelium inside the bark and the cankerous tissues. Control: Removal of affected branches and applying fungicide paste to cut ends/wounds is important preventive measures.

6. Fire Blight of Apple The disease was first recorded In United states as early as 1780 and often appears in epiphytotic form. The disease is also known to occur in India but is not of much economic importance as now. Symptoms: The blossoms become brown and then black showing a brunt appearance, hence the disease is called as fire blight. Droplets of amber coloured exudates having masses of bacterial cells appear on the pedicels. The disease also attack leaves and spur. Late in the season, cankers develop on branches and twigs.These cankers can engirdle the branches and

trunk and may cause collar blight. . A greyish brown liquid exudes from the canker. Early infection of influorescence can cause complete loss to the crop. But if the infection sets in after fruit set, brown circular lesions develop on unripe fruits which may drop prematurely. Pathogen: The bacterium, Erwinia amylovora (Burrill) Bergey et. al., is the causal pathogen of the disease Disease Cycle: The sugary exudates having large number of bacterial cells attract flies, bees and ants which carry the bacteria from place to place from infected to healthy trees. The disease spread like a wild fire during flowering season. In the off season bacterium survives in cankers on stem. When inflourescence appear, the ants carry the infection from sugary exudates coming out from cankers on infected plants. Secondary spread takes place by honey bees while visiting infected flowers and then to healthy flowers. Control: Prunning of affected trees during off season and applying 0.1% Bordeaux mixture can control the disease. Spraying of 100 ppm of streptomycin sulphate in 1% glycerine during pre-blossoming and blossoming time gives effective control of the disease.

7. Collar Rot of Apples Collar rot disease is present in all the apple growing region of the world. In India, this disease was reported in 1960. Symptoms: Affected trees are typically unthrifty showing poor terminal growth and are stunted. Foliage is sparse and chlorotic and develops purple discoloration in the autumn. Fruits tend to be small and colour prematurely. Affected trees declined over the years. However, trees may decline suddenly in excessive wet autumn and spring. Crown and collar portion of the plants show brown necrotic areas on the phloem and the cambium. The necrosis may extend upto 1m above the trunk but not much below the graft union. Pathogen: Several Phytophthora species have been reported as the cause of the disease from different regions. In India, major pathogen of the disease is Phytophthora cactorum ( Lebert and Cohn)Schroter, although other Phytophthora species such as P. cambivora, P. citricola, P. syringae and Pythium ultimum were also found associated with collar rot symptoms..The pathogen is semi-auatic, soil borne, homothallic with a complex life cycle consisting of an asexual phase in which motile zoospores are produced from sporangia and a sexual phase resulting in the formation of oospores. Disease Cycle: The pathogen can survive in soil where a soil temperature remains 12-20C and pH 5-6. It survives as chlamydospores in the plant debris or soil and may colonize fallen apple fruits on the orchard floor. Mainly infection of stem occurs through mycelium penetration at the ground line but zoospore infection is also common. Oospores usually serve as a source of primary inoculum. Secondary spreads takes place through zoospores. Control:Planting in well drained soil, water management and high graft union are most important for reducing the incidence of collar rot. Clonal rootstocks, M-2, M-4, MM-110, MM-114, MM-115 and crab apple are resistant under Indian conditions. Fungicides, mancozeb and copper oxychloride are usually effective in soil drench. Irrigation mixed with Ridomil MZ (0.2%) at 1.5 ft radius soil around the tree trunk and outside portion of basin with Bavistin (0.1%) can eradicate the infection. Fosetyl-aluminium application as foliar spray completely controlled the disease. Isolates of Trichoderma and Gleocladium species identified as potential biocontrol agent for the contro of collar rot disease of apple.

Diseases of Papaya 1. Stem or Foot Rot of Papaya This disease is wide spread in papaya plantations of India, Sri Lanka, Hawaii and South Africa.Under favourable conditions of high rain fall and high temperature, the whole plantation is wiped out within one season. Symptoms: Initially, water-soaked patches appear on the stem at ground level. These lesions enlarge and girdle the entire base of the stem and finally rot it. The terminal leaves wilt and fall off prematurely. The fruits if there are also fall down. The affected plants died within a short period due to rotting of stem and roots. The tissues below the bark give a honeycomb appearance. The plants can die at any stage of their growth. Pathogen: The disease is caused by Pythium aphanidermatum (Eds.) Fitz. However, in Hawaii, Phytophthora parasitica is also known to be associated with this disease. The mycelium is intercellular with branched hyphae. The entire thallus is full of oospores, oogonia and antheridia both within host tissues and its surface. The sporangia are 500 x 20µ in size and upon germination form a bladder-like vesicle having 30-40 zoospores. The oospores are formed after fertilization of sexual structures. They germinate and cause infection. Disease Cycle: The pathogen is soil borne. The oospores are formed on the papaya residue in soil. The pathogen can survive on dead organic matters as saprophyte and causes infection when suitable host is grown in such soil. The secondary spread takes place by zoospores. Control: Planting in well drained soil, uprooted and burnt of infected plants and avoid planting on the same place are the best cultural practices for disease management. Chemical control is also possible at early stages of infection by removing infected tissues and applies the fungicidal paste. Soil drenching and spraying the stem with 6:6:50 Bordeaux mixture or 0.2% Esso fungicide-406 or captan may reduce the incidence of the disease.

2. Papaya Viruses Papaya is infected by three important viruses viz; papaya mosaic, papaya ringspot and papaya leaf curl. Papaya mosaic is caused by a potexvirus and has not been found in India. The other two are commonly found in papaya plantations. (i)Papaya Ringspot (PRSV) Synonyms: papaya distortion mosaic, papaya leaf distortion, papaw distortion ringspot and papaw mosaic. Symptoms: Mottling and malformation of leaves, ringspot and shoe sting effect of leaves and streaking or rings on fruits, stem and petioles are the main symptoms of the disease (Fig 36). Cucurbita pepo, C. melo, Chenopodium amaranticolor, C. quinoa are the experimental host of the virus.

Fig.36. Papaya mosaic symptoms on plant and fruit and potyvirus particles associated with it

Pathogen: The causal virus particles are filamentous with a modal length of 760-800 nm with a width of 12 nm. The virus belongs to potyvirus (potyviridae) group. The genome of the virus is ssRNA, unipartite and 12 kb in size. The virus has two strains; PRSV -W that infects watermelon but not to papaya and PRSV-P strain which infects both papaya and cucurbits. The virus is transmitted by aphid vectors, Myzus persicae and Aphis gossypii in a non-persistent manner. A protein, the helper component is required for virus transmission. It is also transmitted by mechanical inoculations. Disease Cycle: The virus survives on papaya plants in the field from where it infects healthy papaya by aphid vectors. The aphids that have fed on infected plants when feed on healthy plants the virus is transmitted by feeding process. Control: Avoiding vectors, removing source of inoculum are the measures for management of the disease. No variety of papaya is resistant and hence growing virus-resistant transgenics, if available is the best method of disease control.

(iii) Papaya Leaf Curl The disease is common on papaya in India but the incidence is less as compared to PRSV. The affected plants do not bear any fruit causing heavy loss to the farmers. Symptoms: The most characteristic symptoms are severe curling, crinkling and distortion and rugocity of leaves and reduction of leaf lamina in size (Fig.37). Leaves become leathery and inverted cup shaped and veins are highly thickened. The petioles are twisted in a zig-zag manner. The growth of affected plants is reduced and affected leaves appear as a bunch of leaves at the top. Affected plants do not bear any fruit.

Fig. 37: Papaya leaf curl disease Pathogen: The causal virus particles are geminate and the virus belongs to family Geminiviridae. The genome of the virus is single stranded DNA and divides into two parts, DNA-A and DNA-B. The virus is transmitted by whitefly, Bemisia tabaci and also by graft inoculations. Disease Cycle: The virus is not seed borne. The inoculum survives on papaya in nature or may be on other plants like tobacco, tomato, and several weed hosts. From these sources, the virus infects papaya by the whitefly vector. Affected plants never recover from the disease and hence are a perennial source of inoculum. Control: Affected plants must be uprooted and destroyed. The vector may be kept under control. No source of resistance is available.

Diseases of Citrus 1. Anthrcnose Disease of Citrus There are three anthracnose diseases of citrus caused by Colletotrichum species: I. post- bloom fruit drop II. Lime anthracnose and III. Post-harvest anthracnose.

(i)Post-Bloom Fruit Drop (Pfd) Symptoms: Water soaked lesions developed on petals which eventually become pink and then orange brown. Petals become dry and hard but remain attached to the flower. The fruitlets abscis at the base of the ovary. Fruit setting is stopped. Leaves around the affected flourescence are small, chlorotic, twisted with enlarged veins. Pathogen: The disease is caused by the fungal pathogen, Colletotrichum acutatum J.H. Simmonds. The conidia of the pathogen are fusiform and developed in acervuli on the surface of petals. Conidia germinate and produce appresoria. Disease Cycle: The pathogen survives on buttons, leaves and twigs. When the first flowers of the next bloom open the appresoria are stimulated to germinate and form hyphae with a few conidia. The conidia are dispersed by splashing rains to new flowers, completing the cycle. In adjacent plantings, fungus moves by bees or other insects when they visit new flowers. Long distance spread occurs through transportation of infected petals by equipments or vehicles in harvesting sacks. Control: Avoid overhead irrigation, removal of declining trees before bloom, wider tree spacing are important to avoud PDF. Fungicide sprays during bloom such as benomyl or a combination of benomyl and ferbam and captafol are very effective.

(ii)Lime Anthracnose Mexican lime or kagzi lime is the only known host of the disease. Symptoms: The disease affects flowers, young leaves, shoots and fruits. Infected fruitlets are dropped. In severe cases, leaves become totally blighted and drop causing shoot-tip dieback.Under favourable conditions, necrotic lesions are formed on leaves and fruits. Fruit lesions are larger and deeper than leaves. Pathogen: This disease is caused by the pathogen, Colletotrichum acutatum = Gloeosporium limetticola Clausen. Disease Cycle: The acervuli of this strain of pathogen are produced on all infected parts: leaves, twigs, flowers and fruits. Therefore, the inoculum is more readily available than PDF strain which makes acervuli only on petals. Control: The disease is difficult to control because of the constant emergence of new leaves and frequent flowering and the large amount of inoculum produced on infected tissues. Fungicides such as mancozeb and captafol are effective but must be applied frequently.

(iii) Post-Harvest Anthracnose of Citrus The disease appears only on fruits that are injured by pests, chemical injury, or held too long in storage. Symptoms: Brown to black lesions are formed on fruit rind. The fruits become soft. As the decay progresses a soft rot occus. Pathogen: The disease is caused by Colletotrichum gloeosporoides (Penz.) Penz. Sacc. In Penz.

Teleomorph: Glomerella singulata (Stoneman) Spauld & H. Schrenk. The acervuli of the pathogen are superficial. The conidia are broadly oval and contain one or two oil drops. The conidia germinate and produce an appresorium which contains distinct collar. Disease Cycle: The conidia develop abundantly on dead twigs and are spread by rains. Ascospores are air borne and travel long distances. After the conidia germinate, fungus remains quieacent as ungerminated appresoria. Further infection takes place when appresoria germinate on new host. Control: Good cultural practices and proper handling of fruits to avoid injury and washing after harvest will reduce the disease. Post-harvest treatment with thiabendazol and storage of fruits below 10C will help to control the disease. 2. Citrus Canker There is a distinct form of citrus canker bacterial disease. The disease is found in one or other form in all the citrus growing countries. Asiatic form of canker is most widely distributed. The disease is serious where warm temperature and rain fall are frequent during shoot emergence and development of young fruits. In general, Mexican lime and trifoliate orange are more susceptible, sour orange, lemons and sweet oranges are moderately susceptible and mandarins are moderaly resistant. Symptoms: Circular, pin-point, raised lesions appear on leaves which may increase in size with time. The leaf minor (Phyllocnistis citrella) can greatly increase the number of lesions. On fruits, the lesions can vary in size.The lesions can develop on both surfaces of leaves and become corky with raised margins and sunken centre. Lesions on fruit and stem are upto 1 mm deep and are superficial similar to leaves (Fig.38). A yellow halo with water soaked margin around the lesions on leaves is the most characteristic symptoms of the disease. The halo disappears in older lesions.

Fig 38: Citrus cancer symptoms on leaves and fruit Pathogen: The disease is caused by the bacterium, Xanthomonas campestris pv. citri (Hasse) Dye (Syn. X. citri (Hasse) Dowson and X. axonopodis pv. citri (Hasse) Vaut. It is a rod shaped, gram-negative bacterium with a single polar flagellum. Disease Cycle: The pathogen survives in lesions on leaves, stems and fruits. It can also survive for several years on woody branches. The bacteria ooze out from the lesions when free moisture is on them and can be dispersed to infect new growth. Wind driven rains are the main dispersal agent and bacterium penetrates through stomata or through injuries made by insects or during tree operations. The bacteria remain alive in lesions on leaves and fruits until they drop down. Control: No planting material should be allowed from canker having regions. Nursery and orchard infections quarantines and on-site burning are important to avoid the spread of bacterium. Control of leaf minor and frequent sprays of copper are helpful to check the

canker infection. In sandy areas, vegetable growing between plant rows may be helpful to avoid wind injury by wind blown sand. 3. Citrus Decline Citrus decline is common in citrus plantations of India. The disease is most commonly known as citrus die-back. Symptoms: Severity of symptoms may vary with season, cultivar, age of tree and nutritional status of the affected tree. Symptoms first appear on one branch with a chlorotic leaf patterns similar to zinc or iron deficiency. Irregular blotches or mottling sometimes with yellowing of leaf veins or of entire leaf are prominent. There is leaf fall of heavily infected branches and the leaf-less branches start dying from the top downward because they are attacked by several fungi. The affected trees are stunted and have sparse growth. Such trees bear lopsided fruits which are bitter in taste and have abortive seeds. Finally such trees are declined. This type of decline is known as slow decline. However, sometimes the affected tree shows wilting symptoms for a few weeks and then decline or dead. Such decline is known as sudden decline (Fig.39)

Fig 39: Decline of citrus trees Causes: The disease has been reported to be caused by several abiotic factors such as nutritional deficiency, soil and physiological disorders, poor management of orchards etc. but the possible cause of the disorder in India has been reported due to greening bacterium followed by infection by several fungi such as Colletotrichum gloeosporoides, Diplodia natalensis, Curvularia tuberculata and Fusarium species. However, recent investigations revealed that a few viruses and virus-like diseases, some of them were not known earlier are also involved with citrus decline complex. These diseases including citrus greening are described in this chapter. 4. Citrus Greening Bacterial Disease The greening disease is now known as “Haunglongbing” as this disease was first reported by this name from China. Until 1970, the disease was considered to be of viral origin but now it is known to be caused by a phloem limited fastidious (uncultured) bacterium “Candidus liberibacter spicies” belonging to the alpha-proteobacterial sub-division. It seriously affects production of citrus in Asia, South East Asia, Indian sub-continent, Peninsula and Africa. Recently, it has been reported from North and South America. Symptoms: The symptoms of the disease are somewhat similar to dieback described above. Leaf mottling is the characteristic symptom of the disease. Fruits on affected trees are poorly coloured. Pathogen: Two forms of bacterium causing greening disease are known; the Asiatic form and the African form. Asian form bacterium is Candidus liberibacter asiaticus and the African form is Candidus liberibacter africanus. In electron microscopy the bacterium looks

pleomorphic bodies of various sizes in the sieve tubes of phloem tissues of infected leaves (midribs). The bacterium in Asian countries is transmitted by a psyllid vector, Diaphorina citri and African bacterium is transmitted by another psyllid, Trioza erytreae. The disease is also transmitted by grafting and dodder, Cuscuta campestris from citrus to periwinkle (Catharanthus roseus). The dodder transmission can be used for disease diagnosis. African greening show symptoms at cool temperature (20C) but the Asian form can show symptoms at both cool and warm conditions (35C). Disease Cycle: The inoculum of the bacterium is available on infected citrus trees from where the vector can carry the infection to healthy plants. Control: Control of vector population, reduction of inoculum sources by pruning affected branches or by eradication of affected trees, use of disease-free budwood for propagation and if possible use of disease or vector-free areas for nurseries are the important preventive methods. 5. Citrus Tristeza Virus Disease (CTV) Citrus tristeza is most devastating disease and citrus industry in several countries was wiped out due to this virus. The disease probably originated in Asia from where it is spread throughout the world through movement of infected planting material. The disease is responsible for quick decline in certain stock-scion combination. Symptoms: Stunting, stem pitting, chlorosis of leaves and reduced fruit size are common symptoms (Fig.40). Sweet orange trees grafted on sour orange root stock are commonly declined. Leaf cupping and vein clearing symptoms are observed on indicator hosts, Kagzi lime and Citrus excelsa. Symptom severity is highly variable between CTV isolates. CTV infects most citrus species, cultivars, and intergeneric hybrids. The only non-rutaceous host is Passiflora species. Pathogen: Citrus tristeza virus belongs to closterovirus group. CTV has flexuous particles of 2000 nm length. The virus is transmitted by several aphid vectors but Toxoptera citricidus is the most efficient vector. It is graft and mechanically transmitted by stem slash inoculation. CTV genome is positive sense single stranded RNA.

Fig. 40: Stem pitting symptoms due to Fig 41. Symptoms of Indian Citrus Citrus tristeza virus ringspot on Citrus leaves

Disease Cycle: CTV is spread by movement of infected planting material and by aphid vectors from the inoculum present in orchard trees. Control: Prevention by quarantine to new areas, and budwood certification are important to check the losses caused by CTV. CTV tolerant root stocks such as trifoliate orange or its hybrids should be used. Cross protection using immunization of plants by mild strain is

important method to control CTV. Shoot-tip grafting and thermotherapy are other methods of eliminating CTV. 6. Indian Citrus Ringspot Disease The disease commonly occurs on Kinnow mandarin and sweet oranges in India. This disease is a major constraint in citrus production in the country and restricted to India so far. Symptoms: The leaves of affected trees show rings of various sizes. These rings have yellow border and dark green centre (Fig.41)These rings enlarge in size and may cover the whole leaf surface. Infected leaves fall off prematurely. Affected trees show die-back symptoms at later stages of their growth commonly after first or second harvest. On inoculated Mosambi plants, vein clearing or flecking symptoms develop on young leaves. These symptoms survive till maturation of leaves. The mature leaves show ringspot symptoms. Pathogen: The disease is caused by a filamentous virus having a modal length of 650 nm. The virus belongs to genus Mandrivirus of family Flexiviridae. The virus genome is ssRNA. The virus is named as Indian citrus ringspot virus (ICRSV). ICRSV is transmitted by grafting and also by mechanical inoculations from citrus to herbaceous hosts. Disease Cycle: The virus spreads through vegetative propagation when infected budwood are used. No vector spread is known. Control: Use of healthy planting material is the only method of control currently available. 7. Citrus Yellow Mosaic The disease is found on satgudi and Mosambi sweet oranges in South India and in Maharashtra. An incidence of the disease upto 70% was observed on Satgudi in Andhra Pradesh. Symptoms: The most characteristic symptom of the disease is yellow mosaic on leaves of infected trees (Fig.42). The trees are systematically infected.The trees over 10 years of age show decline. Most of the commercial cultivars are susceptible to virus infection. Temperature does not appear to effect the symptom development.

Fig.42. Symptom and virus particles of Citrus yellow mosaic disease Pathogen: The causal virus has bacilliform particles measuring 130 x 30 nm in size. The genome of the virus is double stranded DNA and the virus belongs to Badnavirus group. The virus is named as citrus yellow mosaic badnavirus (CYMBV). The vector of the virus is a mealybug, Planococcus citri. The virus is also transmitted by grafted. Disease Cycle: The primary spread of the virus is through the use of infected budwood for propagation. Secondary spread may be by the mealybug vector but the spread by the vector is comparatively low. Control: Use of healthy planting material and control of mealy bug from citrus and neighbouring crops such as sugarcane are the methods to control the disease.

8. Citrus Exocortis Disease This is the disease of rootstocks used for citrus propagation and found throughout the world. Symptoms: Bark scaling, tree stunting, and stem blotching of trifoliate orange, sweet lime, Rangpur lime and some citrons and lemons are the main symptoms of the disease (Fig.43). The disease is apparently symptomless unless grafted on sensitive rootstocks.

Fig. 43: Bark scaling symptoms on rootstock due to exocortis disease Pathogen: The disease is caused by a viroid pathogen known as citrus exocortis viroid (CEVd). It is an infectious, circular, single stranded RNA of about 371 nucleotides which are highly base pared, forming a stable rod-like structure. CEVd is graft and mechanically transmitted disease. It is also transmitted through contaminated operational tools. Seed and vector transmission has not been confirmed. CEVd can be detected most reliably by grafting on Etrog citron which will show epinasty of leaves. Disease Cycle: Dissemination of the pathogen occurs through propagation of symptomless, CEVd –infected budwood. Further spread takes place through contaminated tools used for orchard operation. Control: Use of CEVd-free budwood and avoiding of spread by treatment of tools with sterilant like sodium hypochlorite (1%) are the methods to control the disease.

Diseases of Peach and Pear 1. Peach Leaf Curl The disease is found worldwide and is a serious disease of peach. Symptoms: Parts of peach and nectarine leaves are swollen, distorted and curl downwards. Affected leaves first appear reddish, then turn yellow, also flowers, fruits abd current year’s twigs may be affected. In plums, the disease first appears as small white blisters on the fruit. The disease can be very severe in wet humid regions where bud brust can be delayed for 2-7 weeks. Pathogen: The disease is caused by the pathogen, Taphrina deformans (Berk.) Tul. which belongs to the sub-division Ascomycotina. The pathogen has a yeast-like phase on host surfaces and a parasitic phase inside the vegetative growth and fruit. Intercellular growth of the pathogen causes cell division and cell enlargement (hyperplasia and hypertrophy) that result in thickened, curl to convoluted or blistered leaves, shoots or fruits. Disease Cycle: The conidia survive the off-season within the infected host tissues and become active in the next season to cause infection. The ascospores are formed on freshly infected tissues and are the chief source of secondary infection. They multiply by budding

and the resultant conidia germinate to infect the host tissue or remain dormant in the off season. Control: One spray of lime sulphur before bud break and second spray in the fall are effective to eliminate the disease. Spray with 0.3% fytolon or blitox-50 (0.25%) also gives protection from the disease. 2. Brown Rot of Peach The disease causes great loss due to decay of fruits in the orchard, in transit, in the market and prior to consumption. The disease is widely distributed in peach plantations throughout the world. Infected flowers wilt and turn brown due to brown rot. Infected fruits develop circular light brown spots that rapidly extend to decay the flesh. Spurs on peach trees may be blighted near harvest following fungal invasion from infected fruits including shriveled mummies ones. The fungus forms small cankers on non-bearing shoots. The disease is caused by the fungus, Sclerotinia fructicola (G. Wint.) Rehm. The teliomorph is Monilinia fructicola (G. Wint.) Honey. The conidia and ascospores develop on mummified fruits and pedicels. Conidia are formed in chains on infected tissue. The inoculum remains available on infected trees from where the infection spreads to healthy plants. No control measures are known.

3. Peach Scab The disease is economically important in regions of high rain fall, high humidity and warm temperatures between bloom and harvest usually rare in semi-arid peach producing regions. Symptoms: Circular, olivaceous to black, velvety spots are produced on fruits and twigs, less frequently on leaves. Lesions of fruit coalesce followed by cracking of fruits. These lesions reduce the appearance, quality and market value of fruits. Lesions on shoots and twigs are slightly raised, circular to oval becoming brown with slightly raised purple margins later in the season. Pathogen: The disease is caused by the fungus. Anamorph: Cladosporium carpophilum Thum = Fusicladium carpophilum (Thum.) Qudem. Teleomorph: Venturia carpophila (Thum.) Quedem. Disease Cycle: The pathogen overwinters in lesions on twigs with conidial production which begins when shucks covering the fruit split. Control: To develop planting material through tissue culture is the best control of the disease.

Diseases of Guava 1. Wilt of Guava Guava wilt is a common disease in India. Symptoms: The symptoms appear as browning and wilting of leaves, discoloration of the stem and death of branches on one side. The infection may girdle the entire stem resulting wilting of the whole plant. The leaves may fall off and trees usually collapsed within a year or earlier depending on the intensity of infection. When the stem is cut open vascular tissues will show dark colour extending upto the cambium region. The fungus normally present in tissues of the stem near ground level. Pathogens: The disease is caused by fungi, Fusarium oxysporum f. psidii and Cephalosprium species. Wilt associated with pathogens, F. solani and Macrophomina phaseoli bring about gradual decline and death of undernourished 1-5 yr old guava trees in West Bengal. A disease

brought about by the wound parasite, Myxosporium psidii, causes the death of many guava trees, especially in summer, throughout Taiwan. Disease Cycle: The pathogens are soil borne. The fungus may invade the trunk and roots through tunnels bored by the larvae of Coelosterna beetles. Control: No effective control is known.

2. Stem Canker of Guava Symptoms: The disease is found in some parts of India. The symptoms appear as cracks and lesions on the stem. The stem tissues are killed by the pathogen resulting wilting of branches due to lack of transportation of nutrients. Pathogen: Canker disease is caused by the fungus, Physalospora psidii Stevens and Pierce. The perithecia of the pathogen are formed on the infected tissue. Disease Cycle: The pathogen remains inside the infected tissues beneath the bark and becomes active whenever weather conditions are favourable. The pathogen spreads from plant to plant by air-borne spores. Control: The infected branches should be cut and destroyed. The cut ends should be pasted with fungicidal paste. Prunned ends should be painted with fungicidal paste such as Bordeaux paste. Insecticidal sprays after pruning will help in preventing the disease. 3. Guava Anthracnose Anthracnose disease is caused by the pathogen,Colletotrichum gloeosporioides.The pathogen attacks the fruits usually during rainy season. The lesions of the disease appear on fruits. In field conditions, the development of lesions was greater on punctured guavas than on uninjured or sand injured ones, both in rainy and winter seasons. Disease incidence increased as inoculum density increased from 101 to 106 conidia/ml. The optimum temperature for severe infection was 30 C and high humidity is essential for infection. The control of the disease is the same as with other Anthracnose diseases described earlier.

Disease of Grapes 1. Powdery Mildew Under favourable conditions, powdery mildew appears in epidemic form in vine plantations in India. Symptoms: All stages of plant growth are susceptible to infection. The symptoms appear as white powdery patches on affected parts. All above ground parts including fruits, leaves, stem, tendrils and flowers are susceptible to infection. Both surfaces of leaves and other plant parts show powdery pustules. The pustules subsequently become grey and finally dark coloured. Affected leaves become malformed and colourless. Affected plants remain dwarfed and give wilting appearance. The stem turn brown and infected berries become malformed and rarely ripe. There is no fruiting if the infection occurs early. Pathogen: The causal pathogen is a fungus, Uncinula necator (Schw.) Bur. The mycelium of the fungus is superficial and gives rise to conidiophores. Each conidiophore bears 3-4 conidia in chain measuring 25-30 x 15-17µ. The conidia are disseminated by wind. In India, perfect stage is not known but it is formed in other countries. The perfect stage of the pathogen produces Cleistothecia and each cleistothecium carries asci and ascospores.

Disease Cycle: In countries where Cleistothecia are formed, inoculum is carried by cleistothecia from season to season. The pathogen is favoured by warm temperature with enough humidity and cloudy overcast weather. Conidia are borne by wind and cause infection from plant to plant. Control: Cultural practices like pruning after shedding of leaves, thinning out and cutting back of laterals and removal and destruction of diseased parts are helpful for healthy grapevine cultivation. The disease can be controlled by sulphur (300-mesh) dusting. The first dusting needs to be given when new shoots are 3-6” long, second spray before blossoming and the last at 40-50 days later. New fungicides, bayleton and kerathane are highly effective against powdery mildew of grapes. 2. Downy Mildew of Grapes It is a historical disease as it brought several epidemics in France badly affecting the wine industry. The disease could not be controlled till Professor Millardet of Bordeaux University made an accidental discovery of Borsdeaux mixture in 1885. The disease is now known to occur in all wet grapevine growing regions of the world. Symptoms: The symptoms are more pronounced on leaves, young shoots and immature fruits than other aerial parts of the plant. Initially, irregular yellow spots are formed on upper surface of leaves. On the ventral surface, below the spots, downy growth of the fungus can be seen. Later, the spots become necrotic and the spots become brown and lower surface of the leaves become dirty grey. Dirty spots coalse and form larger necrotic areas. Shoots become hypertrophied. The affected bunch of fruits is destroyed. Pathogen: The fungus, Plasmopara viticola (B. and C.) Berl. & de T. is the causal pathogen of the disease. The mycelium is intercellular and produces conidiophores during night in high humidity conditions. Conidiophores emerge directly from the cuticle of leaf and from lenticels of young berries. The branching of conidiophores is at right angle to the main axis and at regular intervals.From the tip of each branch 2-3 sterigmata arise and bear lemon- shaped sporangia. The sporangia produce zoospores after germination. Each zoospore has two flagella at the apex. Oospores are produced in tissues adjacent to midribs of leaves. The oospores germinate and produce sporangia. Disease Cycle: The pathogen is an obligate parasite and survives in active phase on evergreen grapevine. The main source of survival is oospores which survive on leaves and shoots lying on the ground. The oospores germinate under favourable conditions and infect lower leaves of the plant. Then the sporangia are formed which soon detached from leaves by wind causing infection to new plants. Water is another source of their dispersal. The germ tube of sporangium forms zoospores which enter the host through stoma and lenticels. Control: Proper sanitation, suitable spacing, removal of leaves at ground level are important to avoid infection. Fungicides are effective. Zineb or maneb (0.2%) , captan (0.2-0.5%), Bordeaux mixture 4:4:50 are commonly used. Among the new fungicides ridomil is very effective to control downy mildew infection. The following spray schedule has been developed. • Immediately after pruning. • Three to four weeks after pruning. • Before buds are open. • After setting of berries. • During growth of shoots.

The resistant varieties are Amber, Queen, Champion, Cardinal, Champa and red Sultana.

Diseases of Sapota (Achras sapota L.) Sapota commonly known as ‘chiku’ is a very popular fruit crop in India. Only a few diseases of sapota are known in the country. A leaf spot disease caused by fungus, Phavophleospora indica Chinnappa is known to occur on sapota in South India but the sooty mold disease is economically more important. Sooty Mold This ectoparasitic disease is most common on sapota which hampers the tree growth. The pathogen which causes sooty mould is non-pathogenic and develops as saprophyte on the “honey dews”secreted by the insects on leaves and twigs of host plant. The insects commonly secret honey dews are scale insects, aphids and whiteflies. The honey dew attracts the fungus, which multiplies rapidly, covering the leaf surface. The foliage becomes black which affects the photosynthesis and thereby interfere in the normal growth of the plant. The sooty mold pathogen can also multiply on fruits making them unfit for market. The disease is caused by fungus, Capnodium species. The disease may be controlled by spraying of insecticides to control insects followed by spraying of a starch solution which dries up and comes out in flakes alongwith the mold. Another spray of insecticide would help in eradicating the insects, thereby avoiding another onset of sooty mold fungus.

Diseases of Ber (Ziziphus mauritiana Lam., Ziziphus jujube L.) The tree is most commonly affected by a parasitic vine (Cuscuta spp.). Powdery mildew (Oidium sp.) causes defoliation and fruit drop. Sooty mold (Cladosporium zizyphi) casuses leaves to fall. Leaf spots are caused by Cercospora spp. and Isariopsis indica var. zizyphi. Leaf rust is caused by Phakospora zizyphivulgaris, ranges from mild to severe on all commercial cultivars in Punjab. A witches’ broom disease caused by phytoplasma was reported from Pune. Fruits on the tree are attacked by Alternaria chartarum, Aspergillus nanus, A. parasiticus, Helminthosporium atroolivaceum, Phoma hessarensis and Stemphyliomma valparadisiacum. Twigs and branches may be affected by Entypella zizyphi, Hyphoxylon hypomiltum, and Petillaria atrata. In storage, fruits may be attacked by fungi, Alternaria brassicicola, Phoma spp., Curvularia lunata, Cladosporium herbarum. Fruit rots are caused by Fusarium spp., Nigrospora oryzae, Epicoccum nigrum, and Glomerella cingulata.

Diseases of Custard Apple (Anona squamosa L., A. reticulate l ) This common fruit is grown all over India. The trees are affected by a few fungal diseases. 1. Leaf Spot Symptoms: Water soaked lesions mostly angular in shape are developed on leaves. The lesions are dark brown to greyish and vary in size. Single leaf may have over 100 lesions. The lesions dry off and wither resulting in a scorched appearance of the affected leaf. The fruits may also be infected in severe cases.

Pathogen: The fungus, Cercospora anonae Muller & Chupp. is the causal organism. The pathogen belongs to family Dematiaceae, order Moniliales, and sub-division Deuteromycotina. Disease Cycle: The pathogen perpetuates only through the conidial stage. The pathogen survives in the host tissues all the year around and thus inoculum is also available for new infections. Control: The fungicidal sprays can be given in advanced cases. Another leaf spot is caused by Pleosphaeropsis anonae Chona & Munjal 2. Root Rot The disease is caused by Diplodia natalensis Evans. The pathogen is a soil inhabitant, attacking the roots and spreading upwards to the basal portion of the stem causing the wilting of plants. When the disease appears in one or two plants in the plantation, the area of such trees must be isolated, and plants should be cut and destroyed. Other plants can be replaced by a protective cover on the trunk with Bordeaux paste and also drenching the soil around the stem with Bordeaux mixture.

3. Fruit Rot The pathogen attacks the young leaves, stem, influorescence and fruits. The affected fruits develop black spots and the skin becomes discoloured.The fruit pulp below the spots becomes hard and decay at ripening. The affected fruits may drop off prematurely. Severely spotted fruits have low market value.The disease spreads rapidly during rainy season. The disease is caused by Glomerella cingulata (Stonem) Spauld & Schrenk which is the perfect stage of Colletotrichum gloeosporioides Penzing. The disease can be managed by avoiding overcrowded planting and giving preventive sprays with Bordeaux mixture. Dipping mature fruits in hot water at 51 C for 15 min saves them from damage during storage. 4. Pink Disease Pink disease of custard apple is caused by the fungus, Pellicularia salmonicolor ( BERk. & Br.) Dastur. A pinkish powdery coating on the stem appears as initial symptom of the disease. Later, the girdling of stem happens. The pink colour is due to the conidia produce on the stem surface. Affected shoots show wilting, shredding of leaves and finally the braches dry up. In some cases, the fungus may produce the pustules which are of orange red colour and are arranged in rows along the stem. The pathogen persists from season to season through dormant mycelium inside the bark and cankerous tissues. The disease may be checked by cutting and removing the affected branches. Cut wounds may be protected with fungicidal paste.

Diseases of Coconut Palm Coconut Cadang-Cadang Disease The disease causes heavy losses to the coconut palm industry in the Philippines. It is not found in India so far. Symptoms: The initial symptoms are the rounding of nut shape; and appearance of fine, translucent, bright yellow spots on leaves. Influorescence then become necrotic, nut

production decline, and finally stopped. General chlorosis and death of the crown are the advanced symptoms. Eight to ten years are taken between the appearance of first symptoms and death of the palm. Pathogen: The disease is caused by a viroid pathogen which belongs to potato spindle tuber viroid group. The viroid has 287-302 nucleotides. No mechanism of its natural spread is known. A low rate of seed transmission was observed and pollen transmission is suspected. The pathogen is experimentally transmitted by high pressure injection into the shoot of germinating nuts. Disease Cycle: The inoculum remains in infected trees from where it may go by unknown agents or spreading by contaminated seed or operational tools. Control: The infection can be avoided by using sterile operational tools. No resistance has been found. 2. Phytoplasmal Diseases of Coconut Palm Three important diseases of phytoplasmal origin have been repoted. In India, rootwilt and tatipaka are commonly found. (i)Root Wilt or Kerala Wilt Symptoms: The symptoms of the disease normally appear when the plants are about 30 months old. The most characteristic symptom is bending of leaflets called as ‘flexidity’. In older palms, yellowing and marginal necrosis of the older leaves also develops (Fig. 44). Parts of affected palms show degeneration of phloem, disorganized tracheal elements and tylosis in the metaxylem. They eventually rot. The disease is not lethal but productivity is significantly reduced.

Fig. 44: Coconut root wilt disease. Pathogen: The disease is now known to be caused by a phytoplasma, a mollecute, formerly known as Mycoplasma-like Organism (MLO). The pathogen has pleomorphic bodies which can only be viewed in electron microscope. These organisms are limited to the sieve tubes of the phloem tissues. The root wilt phytoplasma is transmitted by insect vectors, Stephanitis typica-a lace-bug but Proutista moesta is the efficient vector. Disease Cycle: The inoculum is available in the infected plants from where the pathogen spreads to new plants. Control: Tetracycline therapy gives temporary remission of disease symptoms but no control of the pathogen.Movement of planting material from infested areas to new areas should be avoided.

(ii)Tatipaka Disease Reduction in number and size of leaves, fasciation, light green leaves and chlorotic spots on leaves are the main symptoms of the disease. Abnormal bending of fronds, tapering of stem and production of small sized influorescence bearing atrophied empty nuts can also occur.

The disease is caused by a phytoplasma but no vector or other means of spread are known. The disease can be controlled as mentioned under root wilt. 3. Bud Rot and Fruit Rot Fungal Diseases of Coconut These diseases are prevalent in most of the coconut growing countries. Symptoms Bud Rot: The initial symptoms are chlorosis and collapse of the youngest leaves. The buds rot and spear leaves withers of the infected plants. Successive leaves turn yellow and die resulting death of central fonds and only outer fringe remains with green fonds. Eventually the whole palm dies. Fruit Rot: Two to five months old nuts are attacked. Symptoms begin as water-soaked lesions near the perienth. The lesions turn brown and become irregular in shape. They spread into the husk and may reach the endosperm. Premature nuts may fall any time. The pathogen can also infect the influorescence. Pathogen: Phytophthora palmivora (Butler) Butler Sensu lato is the causal pathogen of these diseases but now P.arecae is also regarded to be a part of this complex.The pathogen has a wide host range in different countries but in India, the additional host is Borassus flabellifer. The pathogen belongs to family Pythiaceae, order Peronosporales and sub-division Dueteromycotina. The sexual and asexual stages of Phytophthora spp. have been mentioned in earlier chapters. Disease Cycle: The pathogen is most active during wet weather. Spores are dispersed by rain splash and through air currents. Palms may be predisposed by damage or adverse growing conditions. Resistant chlamydospores can survive in soil and coconut debris including nut tissues. Nuts may be infected internally. Control: When the infection starts to the outer leaves, these leaves alongwith older ones should be shaved off and remaing central shoots and the entire crown must be sprayed with one per cent Bordeaux mixture or any other suitable fungicides. In endemic areas, spraying more than once is essential. Planting material should move in the form of embryo and pollen. Nuts should be partially de-husked and treated with a fungicide before planting to avoid the possibility of seed transmission.

Management of Plant Diseases through Host Resistance Selection and breeding of plants with genetic resistance to parasites is one of the most effective methods of disease control. Once the plant has been bred, and seed multiplied, no further measures are required. However, resistance is not always durable owing to the loss of effective avirulence genes by the parasite. Breeding for durable resistance could become a reality if we knew the nature of genes that conferred this character. Plant has many genetically determined components/factors known as resistance and susceptible factors. The parasite is known to have many genetically determined components which are known as virulence or pathogenecity factors. If these facors are matched with susceptible factors of the host, the reaction is known as compatable. But when virulence or pathogenicity factors are not matched with susceptiblilty factors of the host, the reaction is incompatible. Similarly, where virulence factors are matched with resistance factors in the host, the reaction is compatible. But when virulence factors are not matched by resistance factors in the host, the reaction is incompatible. Currently, it is thought that such genes encode products which

recognize essential fitness components of the parasite. Consequently, parasites that have lost their avirulence/fitness genes are unable to cause disease even in susceptible hosts.

To obtain the desired variety through selection we must have: ¾ Resistant lines or biotypes in the population we are working with. ¾ The technique for screening the varieties for resistance must be reliable. ¾ The selected variety should combine other desirable properties, including better agronomic qualities. ¾ The variety must be tested under optimum conditions for resistance to the disease.

World-wide search for genetic material in different crop plants has been going on and extensive collections of germplasm are available at many institutions. These include wild and cultivated plants carrying resistant genes for various plant pathogens. Selection of resistance sources/lines and mating them with susceptible but commercially good types produces off springs, some of which possess desirable agronomic qualities as well as resistance to the disease. The process of developing varieties is time consuming. The offsprings and their progenies are to be carefully screened and tested in a number of places in different agroclimatic zones under conditions most favourable for disease development.

During the association of plants with parasites, a basic compatibility evolved which is likely multigenic on the part of both host and parasite. However, it may easily be upset by single gene changes either in host or parasite. The pathogens are constantly changing, evolving new varieties or races of their species of their pathogens. While new races are evolved, many of which may be more virulent and aggressive pathogens than the parents. While newer crop varieties are evolved to manage the diseases, newer races of the older pathogens arise to attack the newer varieties. Hence, it is never ending struggle for scientists to go on evolving newer crop varieties not only to secure better agronomic qualities and increase production but to combat new or more virulent pathogens.

Eriksson in 1884 showed that cereal rust pathogen, Puccinia graminis consists of different races which differ in their pathogenicity but can not be differentiated morphologically. For example, some of them could attack to wheat but not to other cereals such as oat and rye. Stakman later showed necrotic or hypersensitive reaction which a pathogen causes to its host. Biffen in 1905 reported that resistance of two wheat varieties and their progeny was inherited in a mendelian fashion.. Stakman established that the races can be identified by infecting a set of host differential varieties. This work helped to determine the presence or appearance of new physiologic races.

There are two types of generic resistance to pathogens in plants i.e. monogenic and polygenic. While monogenic characters are stable over a wide range of conditions, polygenic resistance is highly variable and is influenced by environmental conditions. Polygenic resistance is also influenced by host nutrition, while monogenic resistance is completely stable. Repeated selections through breeding or resistance in a crop result in accumulation of more genes for resistance in new varieties, which is the case in most of the varieties of crop plants which are widely cultivated over the world. Another finding is that in a crop variety there may be a gene which may inhibit completely or partially the explanation of resistance to a disease. Similarly an inhibitor gene may suppress the expression of susceptibility in some varieties. It has been shown that resistance in some varieties may fluctuate within certain limits. If the pathogen is capable of producing many races, the monogenic resistance in the host may break and the host may become susceptible to one or more of the newer races of the

pathogen. This is what happens in wheat varieties which breakdown for infection by newer rust races. If large number of genes for resistance is accumulated in one variety, by repeated breeding or selection, then the possibilities of its continued resistance to most races of rust are better.

Host resistance may be inherited as a qualitative or quantitative character, and its expression is influenced by environments. In polygenic avirulent gene combination in the pathogen, vulnerability of host may endure.

The work on genetics of disease resistance and susceptibility could not progressed till Flor in 1946 while working on flax rust caused by Malampsora lini showed that for each gene for resistance in the host, there was a corresponding gene for avirulence in the pathogen and for each gene for virulence in the pathogen there was a gene for susceptibility in the the host plant. This relationship is popularly known as ‘gene for gene hypothesis’. This classical work made it clear to understand the relationship of plants and their parasites in a generic sence. Flor also established the inheritance of virulence in M. lini and found that avirulence was dominant. The generic relationship may be stated as: for each gene determing resistance on the part of the host there is a comlementary gene determining avirulence on the part of the pathogen. Gabriel and Rolfe in 1990 pointed out that the virulence is not necessarily a single gene trait and that where it is oligogenic, the interaction may be gene for gene pathway rather gene for gene.

Temperature and genetic background can have significant effects on the expression of resistance gene. For example, the gene Sr6 which is resistant to races of stem rust of wheat Puccinia graminis tritici that have a corresponding avirulence gene, P6 is temperature sensitive. At 15 C, Sr6 is effective, developing only a fleck but it is ineffective at 24C giving a medium sized uredial pustule. Resistance genes generally give protection for a few years and then fail owing to change in the corresponding avirulence gene in the pathogen. It has also been shown that a gene which conferred durable resistance interacts with a parasite gene that contributed significantly to the parasite fitness.

The presence of inhibitor genes interfere with the interaction of the products of resistance and avirulence genes and thus block the recognition phenomenon which leads to the resistant reaction. Inhibitor genes may also be temperature dependent.

Advances have also been made in the genetics of pathogenicity and virulence factors. These have proved the importance of toxins and cell wall degrading enzymes. Studies have confirmed that the pathogens that are able to avoid or degrade such resistance factors as saponins and phytoalexins being virulent and those that are unable to do so being avirulent.

Venderplank in 1963 suggested that the resistance is of two types; one known as vertical resistance which is controlled by a few “major” resistance genes. This resistance is effective against one or few races of the pathogen, and the other known as horizontal resistance which is determined by many “minor” resistant genes and is weaker but effective against all races of a pathogen. Some pathogen genes for virulence and even more genes for avirulence have been isolated and the sequences and products such as enzymes, toxin, inhibitors, growth regulators etc. of many of the genes have been studied. The resistance in plants may be cytoplasmic resistance or morphological or mature plant resistance.

(i)Cytoplasmic Resistance This type of resistance is more common in improved varieties of wheat. When a resistant variety is exposed to uredospores or aeciospores, the spores germinate and form appresoria in the same fashion as on susceptible varieties. In the resistant variety, only a few stomata may permit entry of the infection hypha while in the susceptible variety many infection hyphae will succeed. After penetration, a susceptible variety will permit the germ tube to form sub- stomal vesicle, subsequent mycelia and haustoria which will ultimately enable the pathogen to develop a pustule. However, in the resistant variety, the protoplasmic contact will inhibit the pathogen. A small haustorium may be formed but the further development of the pathogen will cease due to death of the haustorium mother cell. This type of resistance is based upon the interaction of protoplasts of the host and the pathogen. For every gene in the rust pathogen that controls its virulence, there is a corresponding gene in the host that control its resistance. These genes control the production of specific enzymes and other proteins.

Some parasites have evolved several ways to establish physiological contact with their host plants. At the prepenetration stage they may respond to chemotaxis or the compounds diffusing from their host. Alternatively, the response may be thigmotropic as in the development of infection structures by rust fungi. Thereafter, the cuticle and cell wall may be pentrated by mechanical force, an array of enzymes or a mixture of the two.

The importance of cutinases and pectinases has been established in some host-parasite interactions both by classical biochemical studies and by molecular techniques. Other enzymes which may be of importance to the pathogenicity or virulence of plant parasites are cellulases and proteases. Lignin is often a prominent constituent of plant cell walls and play significant role to avoid infection.

The toxins are heterogenous group of compounds and are deleterious to the normal functioning of plants. The primary lesions caused by toxins have been elucidated in a few cases. The most important role of toxins is to impair the defence responces of the plant. The hypersensitive reaction is the first response of a plant to an incompatible parasite. Infected cells die rapidly and in doing so they trigger a range of defence reactions that confers increased resistance to tissues close to the site of infection. This is known as local acquired resistance. But if the signal is systemic then it is called systemic acquired resistance (SAR). Salicylic acid, a relative of aspirin and some other substances have been recognized which trigger SAR genes. SAR increases the synthesis of pathogenesis related proteins (PR proteins). Several PR proteins are now known to have chitinase and glucanase activity. The synthesis of low molecular weight compounds, the phytoalexins are triggered by components of the parasite as well as the plant and termed as biotic elicitor. They are also triggered by a range of physical and chemical treatments and they are referred as abiotic elicitor. Phytoalexins play key role in resistance.

Other defence responses include lignification, suberization, the synthesis of hydroxyproline- rich glycoproteins, the formation of papillae and the deposition of callose.

Many symptoms caused by plant diseases by biotrophic parasites are considered either by degradation of enzymes or toxins or by hormonal imbalance due to infection. Enhanced concentration of auxins and cytokinins can cause symptoms like hypertrophy and local increase in cytokinin concentration caused by parasites can give rise to green islands resulting in redirection of nutrients. Stunting of infected plants has been attributed to reduced concentration of gibberlins or enhanced concentration of ascorbic acid. Ethylene can give

effect to epinasty, abscission of organs, chlorosis and necrosis as well as the promotion of certain difence responses. (ii)Morphological or Mature Plant Resiatance A given variety may be susceptible to a given set of races but highly resistance to some races when the plants have matured. The resistance increases with the age of plants. The resistance based upon the relative amount of the thick walled collenchyma developed in different varieties at maturity of plants. The collenchyma is not invaded by rust pathogens. The resiatance of a plant to the disease is greatly influenced by environment including host nutrition, and by the environment-physiologic race complex.

Acquired resistance can be exploited to give good control of disease. In particular, cross protection has been used with some virus diseases with encouraging results. More information would be required in order to build up a complete picture of such defence mechanisms so that the protection they give may be logically exploited. During recent years lot of work on the genetics of resistance of wheat rusts has been done which is summarized below: Genetics of Resistance to Rusts in India Identification of sources of resistance in leaf rust (P. recondata) Seedling Resistance: A series of nearly 45 leaf rust loci with allelic series at some loci for reaction to P. recondata have been described. Among the leaf rust resistance genes, Lr9, Lr19, Lr 24, Lr 25, Lr.28, Lr 29, Lr 32, Lr 39, Lr 40, Lr 41, Lr 42, Lr 43 Lr 44 and Lr 45 are effective against all the pathogenic variability present in the country. Adult Plant Resistance (APR): Lines carrying known single gene for APR showed field resistance with Lr 22a and Lr 34. Lr 22a derived from Triticum tauschii. It also showed excellent resistance under field condition in a line Tc + Lr 22a. Lr 34 showed resistance to highly virulent and prevalent pathotypes.

Lr 35 from T. speltoides/ T. monococcum and Lr 37 from T. ventricosum were effective in adult plants. Lr 37 confers slow rusting. Identification of Novel Resistance: Near isogenic lines for seedling resistance genes Lr 14b, Lr 14ab and Lr 30 in ‘Thatcher’ background identified additional plant resistance gene(s). The wheat rye translocation chromosome (IB/IR) which carries Lr 26 has been the most widely exploited source of rust resistance in the development of wheat cultivars. Using these combinations, selection 212 was developed. These genes are effective to all highly virulent and prevalent pathotypes of leaf and stem rusts. Kundan is slow ruster wheat. Stem Rust (P. graminis tritici): The stem rust resistance (Sr) genes identified are Sr 24, Sr 25, Sr 26, Sr 27, Sr 31, Sr 32 and a combination of sr 36+9b and Sr 36+9c. In order to exploit the stem rust resistance genes of significant potential Sr 24, Sr 26, Sr 31, Sr 32, Sr 36+9e and SrAgi have been introgressed into variety Kalyan sona. Stripe Rust Resistance: Yellow rust genes Yr 5 and Yr 10 are available in European population. Yr 5 has been matched by virulent races in India. More details on genetic analysis of wheat cultivars resistant to wheat rusts in India are given on chapter of wheat rusts.

Molecular Apptoach to Disease Resistance Since 1980, great emphasis was given on determining the molecule and the ‘genetic connection’ of any substance involved in disease development. Already the number, location, size, sequence and function of most or all genes of many viruses are known in detail. Many of these genes have been transferred into the plants and such plants showed resistance. Similar transfers have been done with a few bacterial and fungal genes coding for certain pathogenesis-related proteins. In 1941, Beadle showed that one gene codes for one enzyme. In the following year Flor described the gene for gene concept.

Studies on bacterium Agrobacterium tumefaciens showed that the T-DNA of its Ti plasmid contains several genes, two of which code for growth regulators and were responsible for developing tumors by the infected cells.It was later demonstrated that the two genes could be removed and replaced with one or more genes from other organisms such as plants, other bacteria, viruses and even animals, genes that could be transferred into and translated by the plant cells.This discovery made it possible to transfer foreign genes into plants at will and combind with tissue culture whole plant can be developed from single cell. Now several methods are available to introduce foreign DNA into plant cells. Some bacterial and fungal genes, coding for enzymes that breakdown the cell wall of the pathogen, have been engineered into plants which provided resistance against these pathogens.

A molecule in the cell wall of Phytophthora megasperma found to act as elicitor of the defence response in its soybean host. The elicitors interact as a receptor molecule on the plant cells. Almost subsequently the avirulence gene was isolated from Pseudomonas syringae pv. Glycinea. These discoveries helped in our understanding of pathogen virulence and plant disease resistance. Hypersensitive response protein (hrp) genes affect the transport of proteins of pathogenic bacteria into plant cells.

In 1986, Beachy and his team developed virus resistant transgenic tobacco plant by introducing the coat protein gene of TMV. The resistance in such transformed transgenic plant is known as pathogen derived resistance. Plants transformed with the genes that code for chitinase showed resistance to the disease caused by fungi that contain chitin in their cell wall. Tobacco plants transformed with the gene stilbene synthetase, the enzyme that synthesizes a phytoalexin showed disease resistance. The first fungal avirulence gene (avr 9) was isolated from Cladosporium fulvum and first plant resistance gene (Hm-1) was isolated from corn. Hm-1 operates by producing a protein that detoxifies the host-selective toxin of the pathogen Cochliobolus carbonum. Later many plant resistance genes were isolated. All these genes shared leucine-rich repeat in the protein they coded for.

Plant pathogens produce proteins that actively suppress the defence reaction of their host plants. In addition, the avirulence proteins of some pathogens contain signals that allow these proteins not only to be introduced into plant cells, most likely through the hrp protein system, but also to move into and function into plant nucleus.

A new type of defence against pathogens is through ‘RNA-silencing’ i.e. of regulating genes based on targeting and degrading sequence specific RNAs. RNA silencing can be induced experimentally and targeting to a single specific gene or to a family of related genes. This discovery will play an important role in engineering resistance into plants. The complete sequence of the genome of organisms will help to locate, identify, compare isolates and manipulate the genes for pathogenicity in the pathogens and of resistance in their host plants,

as well as introduction of them into specific locations of the plant genome where they would be most effective.

Genomes of the experimental plant, Arabidopsis thaliana, several plant viruses and viroids, bacteria, Ralstonia solanacearum and Xylella fastidiosa, fungus, Phanerochaete chrysosporium and nematode, Caenorhabditis elegans and several other pathogenic fungi like Magnaporthe grisea, Ustilago maydis, Cochliobolus heterostrophus, Botrytis cinarea, Fusarium graminearum, Phytophthora infestans etc. have been completely sequenced. Several resistance genes have already been identified, isolated, transferred into susceptible host plants and such transformed plants showed resistance.

It is hoped that Molecular Plant Pathology will provide cultivars that can resist disease in the presence of pathogen, without the need to use any pesticide.

Suggested Readings 1. Agrios, G.N. 2005. Plant Pathology Vth edn. Academic Press, New York. 2. Brunt, A.A., Crabtree, K., Dallwitz, M.J., Gibbs, A.J., Watson, L. and Zurcher, E.J. (eds) (1996 onward) Plant Viruses on Line: description and lists from the VIDE database. http://biology.anu.edu.au/groups/mes/vide/ 3. Dasgupta, MK. 1998. Phytonematology. Naya Prakash, Naya Udyog, Bidhan Sarai, Kolkata, India. 4. Gupta, VK and Sharma, Satish, K. (eds.) 2000. Diseases of Fruit Crops. Kalyani Publishers, New Delhi. 5. Johnson, R. and Jellis, GJ (eds.) 1993. Breeding for Disease Resistance. Kluwer, Hingham, Massachusetts. 6. Joshi, L.M., Singh, D.V., and Srivastava, K.D. 1986. Problem and progress of wheat pathology in South Asia. Malhotra Publishing House, New Delhi 7. Mehrotra, RS. 2003. Plant Pathology. Tata McGraw Hill, New Delhi. 8. Rangaswami, G. 1998. Diseases of crop plants in India,3rd Edn. Prentice-hall of India, New Delhi. 9. Raychaudhuri, SP, and Verma Jeev, P. (eds) 1984-1990. Vol. I. Diseases of Cereals, Vol.II. Diseases of Fruits, Vol.III. Review of Tropical Plant Pathology (Vegetable Diseases, Vol IV. Diseases of Plantation Crops and Forest Trees Vol. V. Diseases of Fibre and Oil Seed Crops. Today & Tomorrow Printers and Publishers, New Delhi. 10. Singh, R.P. et. al. 2006. The wheat rusts.htpp://www.fao.org/docrep/2006/y4011e/y4011eog.htm 11. Singh, R.S. 1998. Plant diseases, 7th Edn. Oxford & IBH Pub. Co. Pvt. Ltd. New Delhi 12. Singh, U.S., Mukhopadhyay, A.N., Kumar, J. and Chaube, H.S. 1992. Plant diseases of International importance, Vol 1-4, Prentice Hall, Eaglewood cliffs, New Jersey. 13. Smith, K.M. 1972. A text book of plant virus diseases. Academic Press, New York. 14. Timmer, L.W., Garnsey, S.M. and Graham, J.H. 2000. Compendium of citrus diseases 2nd edn. APS Press, St. Paul, MN. 15. Vanderplank, JE. 1984. Disease Resistance in Plants. 2nd Edn. Academic Press, Orlando, Florida.