One or more of the features that are needed to show you the maps functionality are not available in the web browser that you are using.
Please consider upgrading your browser to the latest version or installing a new browser.
More information about modern web browsers can be found at http://browsehappy.com/
Large variations in the predominance and severity of the various symptoms described here are observed according to the location, season, aggressiveness of the occurring bacterial strains and the cassava cultivars (Maraite, 1993).
Leaves show dark-green to blue, water-soaked, angular spots (1-4 mm in diameter), limited by veinlets and irregularly distributed on the lamina. With time they frequently extend and coalesce along the veins or the edges of the leaf; the central portion turns brown and the water-soaked part often becomes surrounded by a chlorotic halo. The lesions appear as translucent spots when viewed against the light. Under a magnifying glass, small droplets of exudate oozing from the central portion of the lesion are visible on the lower surface of the leaves. The droplets, which first glisten creamy-white and later yellow, are easily dissolved by rain or dew; on drying they form a thin scale. Under favourable conditions (young leaves, high soil and air humidities), water-soaked pinpoint spots develop, scattered around young angular spots. The surrounding part of the lamina turns light brown and within 2-3 days extensive areas of the leaflets become withered not only towards the tip or border of the leaflet, but also towards the base. The affected parts show light-brown and green zonations as if they had been superficially burnt. These necrotic areas are not translucent, no bacterial exudate is observed and bacteria are absent or present in only very limited amounts at the borders of the extending blight lesions. A severe attack leads to premature drying and shedding of the leaves.
Stem and Growing Point
Under conditions of high humidity, infection may spread through the vascular bundles from the leaflets to the petiole and twigs or stems, with the formation of black and dark-brown streaks as well as exudation drops along the pathway of progression. These parts may also become infected directly through wounds, which may be due to removal of leaves for consumption or insect punctures.
On the unlignified twig or stem, a dark-green to black water-soaked area develops around the infection point. Large gummy exudation drops appear some distance away from the infection point, in the axis of vascular bundles, and one or a small number of leaves, located on the same side, show a sudden loss of turgidity, followed by rapid wilting and shrivelling. Afterwards the base of the petiole collapses, but the dried leaves generally remain attached for some time. All leaves located above those showing the first symptoms wilt progressively. Finally the unlignified tip dies, appearing as a wick on the withered stem end, giving the 'candle' symptom, while new shoots grow out lower down the stem. As the infection progresses towards the base of the stem these shoots often also become wilted leading to plant dieback. In the infected shoots, xylem vessels are brownish.
Under the microscope the vessels appear obstructed by bacteria, tyloses and mucilaginous substances. Lytic pockets develop around the protoxylem. The spread of these pockets causes rupture of the xylem ring, development of lytic pockets in the phloem, and later rupture of the fibre ring in the cortical collenchyma. Externally the latter pockets become visible as dark-green water-soaked spots and small black streaks, corresponding to altered laticifers. These spots swell, rupture and extrude a sticky white-yellow gum. In fully lignified stems or branches only internal vascular browning is visible. Infection may spread more than 50 cm below any external visual symptom.
Only exceptionally does infection reach the roots in some very susceptible cultivars, whose swollen roots may show dry, rotted spots around the dead vascular strands (Lozano, 1986).
On the green capsules, water-soaked expanding spots can also be observed. Heavily infected seeds from such fruit may be deformed, with corrugation of the testa and necrotic areas on the cotyledons and endosperm.
Losses can be greatly reduced by a combination of measures taken within the perspective of IPM (Lozano, 1986).
In areas where cassava bacterial blight does not yet occur, great care must been taken in the introduction of germplasm. Vegetative propagated material must be introduced as meristem culture multiplied in vitro and certified disease-free. Botanical seed should originate from areas unfavourable for disease development, be heat-treated and planted in quarantine. Details can be found in the FAO/IBPGR technical guidelines for the safe movement of cassava germplasm (Frison and Feliu, 1991).
Cultural Control and Sanitary Methods
In areas where cassava bacterial blight is already widespread, disease incidence can be reduced by the use of clean planting material. Cuttings should be taken only from plantations that have been found to be free of the disease by inspections at the end of the rainy season. In cases of sporadic occurrence of the disease, great care must be taken in collecting cuttings only from healthy plants and from the most lignified portion of the stem, up to 1 m from the base, combined with visual inspection for the absence of vascular browning. Tools should be regularly disinfected using a bactericide.
Infected clones can be cleaned by rooting bacteria-free stem tips in conditions unfavourable for infection or by meristem cultures in vitro.
Crop rotation and fallowing proved very successful when the new crop was planted with uninfected cuttings. All infected plant debris and weeds on which epiphytic survival may occur should be removed and burned or incorporated into the soil. Rotation or fallowing should last at least one rainy season.
In some areas, planting towards the end of the rainy season instead of at the beginning will delay epidemic development during the growing period and so reduce yield loss. Intercropping cassava with maize or melon has been reported to reduce cassava bacterial blight significantly (Ene, 1977).
In potassium-deficient soils, increasing the potassium content of the leaves by fertilization tends to reduce disease severity (Odurukwe and Arene, 1980).
Soaking of infested botanical seed in hot water at 60°C for 20 min, followed by drying in shallow layers at 30°C overnight or at 50°C for 4 h, reduced the number of bacteria to less than the minimum detectable level without appreciably reducing germination (Persley, 1979a).
The FAO/IBPGR technical guidelines for the safe movement of cassava germplasm recommend visual inspection of the seeds, density selection, followed by treatment of the seeds by immersing them in water and heating in a microwave oven at full power until the water temperature reaches 73°C and then immediately pouring the water off. If a microwave oven is not available, a dry heat treatment for 2 weeks at 60°C is recommended (Frison and Feliu, 1991). A subsequent thiram dust treatment reduces seed re-infestation. Lozano and Nolt (1989) mentioned 77°C instead of 73°C for the microwave treatment.
Clear differences in host-plant resistance occur, especially with regard to stem infection and wilt; use of resistant genotypes is a major control strategy. Resistance to cassava bacterial blight appears to be due to several genes, mainly with additive effects but also to some extent with non-additive effects; resistance appears to be recessive to susceptibility (Hahn, 1979; Umemura and Kawano, 1983). A variation in aggressiveness, but no clear-cut pathogenic specialization, is observed among X. axonopodis pv. manihotis isolates from various countries, and also among those from a single country (Maraite et al., 1981; Alves and Takatsu, 1984). A strong genotype-environment interaction is often observed. Host-plant resistance is sustained by adequate fertilization.
Ninety-three varieties of M. esculenta were assessed by amplified fragment length polymorphisms (AFLPs) for genetic diversity and for resistance to X. axonopodis pv. manihotis. AFLP analysis was performed using two primer combinations, and a 79.2% level of polymorphism was found. The phenogram obtained showed between 74 and 96% genetic similarity among all cassava accessions analysed. The results demonstrate that resistance to X. axonopodis pv. manihotis is broadly distributed in cassava germplasm and that AFLP analysis is an effective and efficient means of providing quantitative estimates of genetic similarities among cassava accessions (Sanchez et al., 1999).
Foliar application of Pseudomonas fluorescens and P. putida has been shown significantly to reduce leaf infection by X. axonopodis pv. manihotis (Lozano, 1986). However, biological control has not yet gained practical acceptance.
Cassava bacterial blight is a major constraint on cassava cultivation and losses can be extremely severe after introduction of the pathogen, or possibly of more aggressive strains, in a region where highly susceptible cultivars are grown. In 1973, 1 year after the first report of cassava bacterial blight in Nigeria, estimated yield losses were 75% (Ezelio, 1977). Crop losses as high as 90-100% were observed in some parts of Uganda, 2 years after the disease was first recorded (Otim-Nape, 1980). In Zaire, the epidemics between 1971 and 1973 in the Kasaï and Bandundu provinces led to severe starvation, because of the importance of cassava roots and leaves as staple foods in these areas (Maraite and Meyer, 1975). In field experiments with X. axonopodis pv. manihotis-free and X. axonopodis pv. manihotis-infected stem cuttings, Otim-Nape (1983) observed a reduction in fresh tuber yield from 40.1 to 26.6 t/ha. By comparing the yield of susceptible clones to that of resistant ones under natural infection in Colombia during 1974-82, Umemura and Kawano (1983) observed an 18-92% yield reduction, depending on locality, planting time and degree of simultaneous infection by Elsinoë brasiliensis.
Under the selection pressure of severe cassava bacterial blight epidemics, the most susceptible clones are eliminated from the mixture generally planted by the smallholders, and overall severity decreases. Based on a CIAT survey of five major cassava-producing zones in Colombia, the estimated reduction in national production was, nevertheless, still 6.64% in 1973 (Lourido, 1974).