Friday, 6 September 2019

Wheat Disease

Wheat Disease

Wheat Disease

Black chaff of Wheat

Pathogen: Xanthomonas translucens pv. translucens (Jones et al.) Vauterin et al.

Synonyms: Xanthomonas campestris pv. translucens (Jones et al.) Dye

X. campestris pv. cerealis (Hagborg) Dye
X. campestris pv. hordei (Hagborg) Dye
X. campestris pv. secalis (Reddy et al.) Dye
X. campestris pv. undulosa (Smith et al.) Dye

Common names: Black chaff, leaf streak, bacterial stripe, or bacterial blight of cereals and grasses

Symptoms
Infected leaves show narrow, water-soaked streaks (yellowish in barley and triticale), necrotic at the enter with a rust-colored margin (in wheat). On young leaves, generally, small, water-soaked leaf spots appear that later develop into longitudinal yellow to brown streaks (Smith, 1917; El Baby and udolph, 1989; Duveiller and Maraite, 1993b). Leaves may wilt. In wet weather, small droplets of yellowish bacterial slime can be observed on the lesions (Jones et al., 1917) (Photo 2.1).

Symptoms of bacterial leaf streak on wheat.


PHOTO 2.1 Symptoms of bacterial leaf streak on wheat. (Courtesy of Mary Burrows, Montana State

University, Bozeman, MT, Bugwood. org.)

Symptoms ften develop in the middle of the leaf, where dew remains longer in the morning. Seedlings hardly show any symptoms. Glumes and seeds show “black chaff” symptoms, with purple-black discoloration of the surface. Symptoms take 10–14 days to appear. Streaks are more usual on triticale than n wheat. Culms, leaves, rachis, glumes, and awns may become infected, and symptoms on wheat
have been reported to vary with the environment, variety, disease severity, and interaction with fungi Bamberg, 1936; Boosalis, 1952). On the stem, brown to black stripes may be formed. On the chaff of
many hosts, water-soaked spots are formed that later develop into brown to black spots. Ears may show brown discoloration and distortion. Seeds may be black and shriveled. The heavily infected crops show water-soaked to yellow-brown streaks, wilting, and complete necrosis of leaves.

X. translucens pv. translucens has ice-nucleating activity (Kim et al., 1987) and may therefore be associated with frost injury (Sands and Fourrest, 1989). Dissemination of the bacterium may in turn e favored by this injury, since symptoms tend to appear after periods of subfreezing temperatures. however, ice nucleation is not a necessary condition for the induction of an epidemic (Duveiller
et al., 1991).

Strains of X. translucens pv. translucens have been found to be host specific, and the original format speciales, later pathovars, were defined in this way: hordei (= translucens) on barley, secalis on rye, and undulosa on wheat and triticale. pv. cerealis had a relatively wide host range. Duveiller 1989) noted that recent isolates from wheat, rye, and triticale were not host specific. The fact that pecific and nonspecific strains can be found tends to support the use of a broad concept of the pathovar (Paul and Smith, 1989).

Host
Primary host: barley (Hordeum vulgare), rye (Secale cereale), wheat (Triticum spp.), and triticale
(Triticum × secale).
Secondary host: Bromus spp., Phalaris spp., Elymus repens, and on other Poaceae by inoculation.

Geographical Distribution
EPPO region: Belgium (found but not established), Bulgaria (Koleva, 1981; but the bacterium is now declared absent), France (found but not established), Israel, Libya, Morocco, Romania, Russia (southern, Caucasus), Spain (single outbreak; Noval, 1989), Sweden (found but not established), Syria (Mamluk et al., 1990), Tunisia, Turkey (Demir and Ustun, 1992), Ukraine.

Asia: Azerbaijan, China (Henan, Xinjiang), Georgia, India (Delhi), Iran (Alizadeh and Rahimian, 1989), Israel, Japan, Kazakhstan, Malaysia (Sabah), Pakistan, Russia (Siberia), Syria, Turkey, Yemen.
Africa: Ethiopia, Kenya, Libya, Madagascar, Morocco, Senegal (probably a misidentification, since record is on rice), South Africa, Tanzania, Tunisia, Zambia.

North America: Canada (Alberta, Manitoba, New Brunswick, Quebec, Saskatchewan), Mexico, the United States (Arkansas, Colorado, Illinois, Indiana, Iowa, Kansas, Michigan, Minnesota, Mississippi, Missouri, Nebraska, North Carolina, North Dakota, Ohio, Oklahoma, South Dakota, Texas, Utah, Virginia, Washington, Wisconsin).South America: Argentina, Bolivia, Brazil (Mato Grosso do Sul, ParanĂ ), Paraguay, Peru, Uruguay. Oceania: Australia (New South Wales).

Disease Cycle
X. translucens pv. translucens is a seed-borne pathogen. The transmission rate is very low but causes serious outbreaks in the field under suitable conditions. The pathogen is disseminated by seed on a large scale (Sands and Fourest, 1989). On a local scale, bacteria are transmitted by rain, dew, and contact between plants (Boosalis, 1952). Aphids trapped in sticky exudates may carry the bacterium and transmit it to wheat and barley, thus enabling long-distance dissemination (Boosalis, 1952). Milus and Mirlohi (1995) concluded that other means of overwintering were insignificant by comparison with survival on the seed.

X. translucens pv. translucens is a true parenchymatous pathogen. Intercellular invasion occurs after entry through stomata. The spread from a single plant can affect up to 30 m 2 during a growing season. However, movement in space is usually more limited. Infection cycles can be as short as 10 days (Hall et al., 1981). Bacteria may survive in seeds longer than 63 months (Forster and Schaad, 1990). However, recovery is greatly decreased after some months of storage. Survival in the field does not only depend on the infection of host plants, as epiphytic populations may survive on nonhost species as well (Timmer et al., 1987). Moreover, bacteria may overwinter on perennial hosts or on crop debris in the soil (Boosalis, 1952; Mehta, 1986a). The disease cycle of black chaff of wheat is illustrated in Figure 2.1.

 Disease cycle of black chaff of wheat caused by X. translucens PV. translucent.
FIGURE 2.1 Disease cycle of black chaff of wheat caused by X. translucens PV. translucent.

Outbreaks of the disease are sporadic and more frequent on breeder’s plots. They are prevalent during wet seasons. Inoculation experiments (Sands et al., 1986) show that plants are most readily infected under wet conditions (rain or sprinkler irrigation). However, the importance of dew, rainfall, or irrigation has not yet been documented, and it is not certain whether free water is needed. The bacterium tolerates a wide range of temperatures (15°C–30°C) (Duveiller et al., 1991), its optimal temperature being around 22°C. The pathogen grows best when relative humidity is high. The disease is favored by warm, moist conditions (26%–30%), especially at heading.

Economic Impact
Little quantitative information is available on losses caused by this disease (Duveiller, 1994a). Direct yield losses have been evaluated from 10% or less up to 40%. Duveiller and Marmite (1993a) have developed a system for forecasting losses from infection levels earlier in the season. Further Duveiller (1994b) has proposed a disease assessment key. The pathogen may also cause sterility of wheat spikes (Forster and Schaad, 1988). Finally, high infection levels may lead to a 10%–30% decrease in kernel weight (Shane et al., 1987). Both durum and bread wheat can be severely affected, while triticale and barley are less frequently affected. There seems to be little information on this disease on rye.

Control Measures
No known control measures exist for the disease in the field (Duveiller, 1994a). Chemical control focuses on seed treatments. Organomercurial seed treatments were used in the past and were mostly considered effective. The recent resurgence of the disease has been linked to the withdrawal of this group of pesticides. Duveiller (1994a), however, queries this and attributes the recent developments to other causes: cultivation of cereals in new areas, favorable conditions for the disease, susceptible cultivars, and so on. Various other treatments are now applied to seed lots to eliminate bacteria, especially cupric acetate (Schaad et al., 1981), formalin (Duveiller, 1989), and guazatine (Mehta, 1986b), but these treatments are phytotoxic. Pantene 30 was 95% effective, without phytotoxicity. An alternative treatment is a dry heat at 72°C for 7 days, as proposed by Fourest et al. (1990), but the effectiveness of this treatment remains to be confirmed.

Resistant cultivars are available for many cereals and the level of resistance depends on the cereal involved (Milus and Mirlohi, 1994). In the absence of any really effective seed treatment, control should center on pathogen-free seed certification (Duveiller, 1994a). The use of healthy seeds through seed certification programs (and eventually by decontamination with acidic cupric acetate, but this is not 100% effective) and of varieties with low susceptibility or high resistance is the only way to prevent or control diseases caused by X. translucens.

Basal Glume rot of Wheat

Basal Glume rot of Wheat


Pathogen: Pseudomonas syringae pv. atrofaciens (McCulloch) Young, Dye and Wilkie
Synonyms: Pseudomonas atrofaciens and Phytomonas atrofaciens 
Bacterium atrofaciens McClloch
Ph. atrofaciens (McCulloch) Bergey et al.
P. atrofaciens (McCulloch) Stevens

Common names: Basal glume rot, basal bacteriosis of wheat

Symptoms
Infected leaves have small, dark, water-soaked spots. The spots eventually elongate and become yellow, then necrotic as the tissue dies. Symptoms occur during wet weather, particularly at heading time. The main symptom is a brown, discolored area at the base of the glumes (Photo 2.2) that over at the kernel. This discoloration is darker on the inside than on the outside of the glume. usually only one-third of the glume is discolored but sometimes the entire glume may be affected. frequently, the only sign of the disease is a dark line at the attachment of the glume to the spike. severely diseased spikelets are slightly dwarfed and lighter in color than healthy ones. The base f a diseased kernel has a brown to black discoloration.

Host
Wheat, barley, oats, rye.

Geographical Distribution
Australia, Bulgaria, Canada, former Czechoslovakia, Morocco, New Zealand, Romania, Russia Siberia), South Africa, Ukraine, the United States, and Zimbabwe (CMI, 1982); reported as a new record on durum wheat in Syria (Mamluk et al., 1990).

Disease Cycle
Basal bacteriosis actively develops in cool and damp years, particularly during cold, damp spring. Its
distribution is promoted by low monthly average temperature (15°C–18°C) during the beginning of
heading till maturing, with increased air humidity (60%–65% and more) and excessive precipitations
just before grain ripening. The optimum temperature for basal bacteriosis development is 23°C–25°C.
P. syringae PV. atrofaciens survives epiphytically on seed or in infested soil residue. This bacterium
is disseminated with dust particles by wind and becomes entrapped in the water in grooves and small spaces of the spikelets. It is also disseminated by insects and splashing water. It multiplies near glume
joints in the presence of moisture but remains dormant when conditions are dry.

 Field symptoms of bacterial infection on wheat glumes.
PHOTO 2.2 Field symptoms of bacterial infection on wheat glumes. (Courtesy of Mary Burrows, Montana State University, Bozeman, MT, Bugwood.org.)

Economic Impact
In nature, the pathogen of basal bacteriosis of wheat also attacks rye, barley, and oats. Depending on the zone of wheat cultivation and weather conditions favorable for bacteriosis development, this disease can infect 10%–80% of ears of wheat plants during epiphytotic. In the Central Black Earth Region, basal bacteriosis severity ranges from 1% to 50% (at development 0.3%–25.3%), depending on a variety of spring wheat and conditions of cultivation; some varieties of winter wheat in Voronezh and Lipetsk regions can be infected up to 72%. In the Krasnodar Region, about 36% of plants are affected by this disease with the severity of 50%–100%.

Control Measures
• Seed should be thoroughly cleaned and treated with a seed-protectant fungicide.
• Rotate wheat/barley with resistant crops, such as legumes.
• Destroy residue.
• Other control measures include optimal agriculture, maintenance of crop rotation, cultivation of relatively resistant varieties, careful removal of plant residues, separating seeds from shrunken grains, pesticide treatment of seeds before sowing, and treatment of plants by pesticides during the vegetation period.

Bacterial leaf Blight of Wheat

Bacterial leaf Blight of Wheat


Pathogen: Pseudomonas syringae pv. syringae van Hall

Synonyms: P. syringae

Common names: Bacterial blotch disease

Symptoms
Bacterial leaf blight develops on the uppermost leaves after plants reach the boot stage. Initially, small, water-soaked lesions appear and may expand and coalesce into irregular streaks or blotches within 2–3 days under cool, wet conditions. Lesions turn from grayish-green to tan or white as tissues become necrotic. Ears and glumes may occasionally be infected, resulting in tan to brown necrotic spots with distinct margins.

Host
The pathogen has a very wide host range. Commonly attacked hosts are apple (Malus spp.), apricot (Prunus armeniaca), kidney bean (Phaseolus vulgaris), European bird cherry (Prunus padus), hawthorn (Crataegus spp.), lilac (Syringa vulgaris), orange (Citrus sinensis), peach (Prunus persica), plum (Prunus domestica and Japanese plum), poplar (Populus spp.), sweet cherry (Prunus avium), sour cherry (Prunus cerasus), and wheat (Triticum aestivum). Some host specialization has been reported (Little et al., 1998). P. s. pv. syringae can also cause stem canker and dieback in conifers (Pinus radiata; see Dick, 1985).

Control Measures
Hot-water treatment of seed at 53°C for 30 min and seed treatment with phytobactiomycin, quinoline, falisan, and carboxin are reported to be effective (Koleva, 1981).

YelloW ear rot of Wheat

YelloW ear rot of Wheat

Pathogen: Rathayibacter tritici (ex Hutchinson) Zgurskaya et al. (1993).
Synonyms: Clavibacter tritici (Carlson and Vidaver 1982) Davis et al.
Corynebacterium tritici
Common names: Yellow ear rot of wheat, bacterial rot of wheat ears, tundu disease

Symptoms
The “tundu” disease is characterized by the twisting of the stem, distortion of the gearhead, and rotting of the spikelets with a profuse oozing liquid from the affected tissues. Hence, the name of the disease is yellow ear rot. The ooze contains masses of the bacterial cell and the nematode Anguina tritici. The nematode alone causes wrinkling, twisting, and various other distortions of the leaves and stems. Infected plants are shorter and thicker than healthy plants. In the distorted gearheads, dark galls are found in place of kernels (Singh et al., 1959; Gupta, 1966; Midha, 1969). When the bacterium is associated with the nematode, the disease symptoms are intensified at the flowering stage and the yellow ear rot sets in. Due to the combined action of the nematode and the bacterium, the gearhead becomes chaffy and the kernels are replaced by dark nematode galls, which are also contaminated with the bacterium. The disease is severe during the rainy season.

The infected plants produce more tillers than do healthy ones. Another interesting feature is the early emergence of ears in nematode-infected plants, which is about 30–40 days earlier than in the healthy ones. Suryanarayana and Mukhopadhyaya (1971) observed that kernels are modified into galls and bear a superficial resemblance to normal kernels. The number of nematode larvae per gall may vary from 80 to 32,000.

Host
Wheat, Agrostis avenacea, and Polypogon monspeliensis

Geographical Distribution
It was first reported in Punjab in 1917. The disease also occurs in Egypt, China, Australia, Cyprus, and Canada. Similar diseases occur on a number of grasses in many European countries.

Disease Cycle
The disease starts from seeds contaminated with the nematode galls. When such contaminated seeds are sown in the field, they absorb moisture from the soil. The larvae escape from the galls and short climb up the young wheat plants. The nematodes have a tendency to seek the tender growing points of the plants where they remain as ectoparasites. After the plant's flower, the nematodes enter the floral parts and form galls in the ovaries. While within the galls, sexual differentiation occurs, copulation takes place, and the female lays eggs, up to 2000 in number. The eggs hatch into larvae under favorable conditions and become active parasites. Once the nematode enters the tissue of the ovary, the bacterium becomes active and causes rotting. The yellow ooze coming out of the rotting gearhead provides the inoculum for the secondary spread of the disease, which is favored by wind and rain. The nematode probably functions as a vector, transporting the bacterium to the otherwise inaccessible meristematic regions of the host. The nematode secretes some substance in the presence of which the bacterium can cause the disease. Chand (1967) observed that the bacterium C. tritici survived in soil debris under laboratory conditions for about 7 months and concluded that the diseased debris probably does not take any part in primary infection because of the limited survival of the bacterium in the soil.

Mathur and Ahmad (1964) reported that bacteria remained viable for at least 5 years in the galls of Anguina tritici. The nematode galls are reported to remain in the soil for 20 years or more and perhaps the bacterium can survive inside the gall for a fairly long time. Midha et al. (1971) have shown that the galls serve as nutrient sources to the bacterium. Pathak and Swarup (1984) have shown that the bacterium does not survive in the free state in the soil, nor do the nematodes separately carry the bacterium on their bodies. Nematode galls show the presence of bacterium in up to 40%–50% of cases, and it is believed that the main sources of survival of the pathogen are the nematode galls.

Control Measures
The sowing of gall-free seeds in noninfested soil will help to reduce the incidence of disease. The seeds can be freed from galls by being floated in brine, at 160 g of sodium chloride per liter of water. Wheat, barley, oats, or other susceptible crops should not be sown in infested soil. Solar heat during May and June in the northern wheat belt of India can be utilized for destroying galls and nematodes. Infected plants should be carefully taken out and burnt. Seeds for sowing purposes should be taken from disease-free areas only.

Bacterial mosaic of Wheat

Bacterial mosaic of Wheat


Pathogen: Clavibacter michiganensis subsp. tessellarius

Synonyms: C. m. subsp. michiganensis and C. m. subsp. nebraskensis

Symptoms
The disease is characterized by small, yellow lesions with undefined margins. The lesions are more or less distributed uniformly over the whole leaf. Individual lesions may resemble the hypersensitive reaction of rust. Water soaking and bacterial oozing from lesions are not observed.

Geographical Distribution
Illinois (Chang et al., 1990), Alaska, Iowa, the United States, and Canada

Disease Cycle
C. michiganensis subsp. tessellarius is seed borne (McBeath and Adelman, 1986; McBeath et al., 1988).

Economic Impact
The economic significance of this disease is unknown (Carlson and Vidaver, 1982a). However, since the disease can destroy flag leaves in severely infected plants, it may cause significant losses (McBeath, 1993).

Control Measures
Control methods include discarding of contaminated seed and using varieties that are resistant to the disease. There seems to be a wide range of host response to the disease among spring wheat genotypes, indicating that genetic improvement to achieve disease resistance trait is possible.

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