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X. axonopodis pv. phaseoli produces similar symptoms on leaves, pods, stems and seeds. Small water-soaked spots are the first symptoms observed on leaves and appear within 4 to 10 days of infection. These spots enlarge and the centre turns necrotic and brown. Areas around the lesion may become flaccid (Goodwin and Sopher, 1994b). The lesion is surrounded by a narrow band of bright yellow tissue. However, yellowed tissue is occasionally absent.
Stem infection is less common. It begins as a water-soaked spot, which becomes a reddish-brown lesion, usually without chlorosis. Stem girdling may develop at the cotyledonary node. The bacteria can invade the xylem, and wilting may occur if sufficient bacterial numbers develop in the xylem.
Pod lesions begin as water-soaked spots which become sunken and dark to red brown. Under humid conditions, a yellowish bacterial ooze will develop from the lesion.
Severely infected seed may be shrivelled and show poor germination or produce weakened plants. On white-seeded varieties, yellow or brown spots may appear on the seed coat, particularly near the hilum area. On dark-seeded varieties, this discoloration is not visible. Infected seeds may also be symptomless (Yoshii, 1980).
Use of Disease-Free Seed
Approximately 1 in 10,000 seeds is capable of causing an outbreak of blight (Sutton and Wallen, 1970). A survey of navy bean (Phaseolus vulgaris) seeds showed that approximately 35% had internal contamination with X. axonopodis pv. phaseoli (Saettler and Perry, 1972). The level of infected seed will vary depending on the level of common blight occurring during seed production.
Use of disease-free seed with a strict seed certification programme is important to reduce the amount of initial inoculum. Beans for seed production should be grown in an isolated area separated from production fields and should be inspected for common blight. Growing beans in irrigated desert areas greatly reduces the chances of spread by splashing rain, and in the USA and Canada, bean seed is grown in areas such as Idaho where bacterial blights are minimal and field inspections are strict (Sheppard, 1983). Seed should be tested for internal infection as the presence of symptoms is not a reliable indicator of infection (Sheppard et al., 1989). Seed may also be treated with bactericides, such as streptomycin or sodium hypochlorite, to eliminate surface contamination by X. axonopodis pv. phaseoli (Liang et al., 1992). Treating seed may reduce disease levels in a subsequent crop but should not form the basis of quarantine measures.
For further information on seed health tests, see Diagnostic Methods.
Seed infection by X. axonopodis pv. phaseoli can be external or internal. Thermotherapy is widely applied for the control of seedborne bacteria (Gondreau and Samson, 1994). Both hot water and dry heat have been successful in treating bean seeds for X. axonopodis pv. phaseoli (Gondreau and Samson, 1994). This involves either incubating for 20 minutes in 52°C water or 23-32 hours in 60°C dry air at 45-55% RH. The latter treatment does not appear to affect seed viability. Treatment with an antibiotic such as streptomycin may be used to control external contamination with X. axonopodis pv. phaseoli, and streptomycin in polyethylene glycol may reduce, but not eliminate, internal populations of X. axonopodis pv. phaseoli (Liang et al., 1992).
Cultural practices are important in controlling common blight. Eliminating weeds, volunteer beans and other potential hosts of X. axonopodis pv. phaseoli will reduce disease incidence. Good weed control will not only remove potential sources of epiphytic X. axonopodis pv. phaseoli populations, but will also improve aeration around the crop so that the plants dry faster, thus reducing the chances for bacterial spread and infection. X. axonopodis pv. phaseoli is readily spread by water, and walking or working in the field while plants are wet will splash the bacteria and create wounds. Plants should be allowed to dry before allowing workers or machinery to enter. Eliminating infected plant debris is very important, particularly in tropical regions (Saettler, 1991). A rotation of at least 2 years between bean crops will give time for the X. axonopodis pv. phaseoli population to decline in the debris. Deep ploughing will also encourage the breakdown of infected plant debris and reduce the population of X. axonopodis pv. phaseoli (Gilbertson et al., 1990). Another option is to burn the crop debris to eliminate infected plant material. The incidence of X. axonopodis pv. phaseoli can also be reduced if beans are grown with maize rather than in a monoculture (Van Rheenen et al., 1981). The maize appears to provide a physical barrier to the movement of X. axonopodis pv. phaseoli between bean plants.
There are no reports of high resistance to X. axonopodis pv. phaseoli in P. vulgaris. However, many lines of P. vulgaris show some resistance to X. axonopodis pv. phaseoli and these varieties may be planted if available. Increased resistance can be developed by selecting for horizontal rather than vertical resistance (Garcia-Espinosa, 1997). Partial resistance to X. axonopodis pv. phaseoli in P. vulgaris has been linked to delayed flowering under long photoperiods (Coyne et al., 1973). P. acutifolius is highly resistant to X. axonopodis pv. phaseoli and partial resistance has been transferred from this genotype to P. vulgaris (Goodwin et al., 1995). There are also several other reports of resistance transferred from P. acutifolius to P. vulgaris (Thomas and Waines, 1984; Park et al., 1998; Yu et al., 1998). Resistance in P. acutifolius is controlled by one or two dominant genes and is related to the hypersensitive response (Zapata, 1998; Urrea et al., 1999). In addition, crosses between P. coccineus and P. vulgaris also showed resistance to X. axonopodis pv. phaseoli (Zapata et al., 1985; Yu et al., 1998). A number of P. vulgaris lines with varying levels of resistance to X. axonopodis pv. phaseoli have been registered (for example, Beaver et al., 1999; Miklas et al., 1999).
A number of molecular markers have been developed for resistance genes to X. axonopodis pv. phaseoli. A growing number of DNA markers, particularly RAPDs, have been found to be linked to common blight resistance genes and are being used in marker assisted selection (Jung et al., 1996; Miklas et al., 1996; Park et al., 1998; Tar'-an et al., 1998; Yu et al., 1998; Ariyarathne et al., 1999).
Several factors should be taken into consideration in evaluating resistance to X. axonopodis pv. phaseoli. Not all plant parts react similarly and the level of resistance to X. axonopodis pv. phaseoli has been found to be different in foliage and pods, each of which are determined by different genes (Schuster et al., 1983). Variation in the virulence of X. axonopodis pv. phaseoli has been observed frequently and isolates from tropical regions appear to be more virulent than those from temperate areas (Schuster et al., 1973). Environmental conditions can also affect resistance. Some cultivars which are moderately resistant in temperate regions become susceptible in the tropics, probably because of their poor adaptation to tropical growing conditions (Webster et al., 1983). Common blight is more severe under the higher temperatures and shorter photoperiods, which are found in subtropical and tropical areas (Arnaud Santana et al., 1993).
Due to the variable regulations around (de-)registration of pesticides, we are for the moment not including any specific chemical control recommendations. For further information, we recommend you visit the following resources:
Common blight can cause significant losses in beans in tropical, subtropical and temperate climates. Its wide distribution, capacity to reduce yield and difficult control in addition to the fact that it uses seeds as a means of dispersal and survival make X. axonopodis pv. phaseoli one of the most economically important pathogens affecting beans worldwide (Irigoyen and Garbagnoli, 1997).
Greater damage is more likely when early plant infection occurs. This is due to premature defoliation, which reduced the photosynthetic area available, interferes with translocation and reduces seed number and size. Lesions on seed and pods reduces quality. In the USA, crops with pods having 4% blemishes caused by blight are substandard and may not be harvested for seed, resulting in substantial economic losses. In 1983 in Uganda, there was a bacterial blight outbreak at the main seed multiplication site. This caused the operation to be abandoned and delayed the release of seed to farmers (Allen and Lenne, 1998).
This disease is most severe in tropical conditions, where it favours the high temperature and rainfall. In Colombia, a yield loss of 22% was reported for naturally infected fields and 45% for inoculated fields (Yoshi et al., 1976), while in north-western Argentina, it is one of the main diseases of Phaseolus vulgaris (Irigoyen and Garbagnoli, 1997).
In Mexico in 1988, X. axonopodis pv. phaseoli was found at a frequency of 37% in two locations. An inverse correlation was found between disease incidence and yield; disease incidence and severity were shown to increase after rain (Diaz-Plaza et al., 1991). In another trial in Mexico, the occurrence of bean common blight was associated with late flowering of P. vulgaris (Moran-Medina and Barrales-Dominguez, 1990). In field trials conducted during 1989-90 in Mexico, X. axonopodis pv. phaseoli was again found to be one of the most important diseases (Flores-Revilla et al., 1993). In the spring-summer and summer-autumn seasons of 1991, common blight had the highest incidence, severity and relative increase rate when compared with Macrophomina phaseolina and bean common mosaic virus in two experiments. It increased in incidence and severity with increases in temperature and rainfall (Mayek-Perez et al., 1995). In a separate set of trials in 1990 and 1991, disease severity was 53% and severity was 20%. Bacterial blight severity was negatively correlated with yield (Pedrosa et al., 1994). X. axonopodis pv. phaseoli severity has been shown to decrease under drought conditions in Mexico (Diaz-Plaza et al., 1991).
In Colombia, yield losses of 22 and 45% were estimated from natural and artificial infection, respectively. Studies in the 1980s showed yield losses of 20-47% (Allen and Lenne, 1998).
In the Caribbean, X. axonopodis pv. phaseoli is reported as frequently limiting bean yield (Beaver, 1999).
In Ethiopia, P. vulgaris is the most important legume crop and over 300,000 ha are grown annually by smallholders. Average yields vary between 500 to 1000 kg/ha, the reasons for the low productivity being abiotic and biotic factors; X. axonopodis pv. phaseoli is considered to be a major disease (Ohlander, 1980; Girna et al., 1994). In Kenya, X. axonopodis pv. phaseoli is again a constraint to bean production. Percentage crop losses of between 10 and 75% have been reported (Makini and Danial, 1994). Intercropping bean with maize was shown to reduce the severity of common bacterial blight during 1987-88 in Tanzania (Kiroka et al., 1989).
In Uganda, P. vulgaris is also the most important legume crop. Production is low, varying between 400 and 700 kg/ha, attributed to biotic and abiotic constraints. X. axonopodis pv. phaseoli is widespread and can cause considerable decreases in yields along with several other diseases (Opio et al., 1994). Recent losses are estimated at 40%. Work in Uganda has also shown that for each 1% increase in the incidence of common blight during reproductive growth there is a yield loss of 3.5-11.5 kg/ha, depending on the season (Allen and Lenne, 1998).
Major losses have also occurred in temperate climates. In southern Ontario, Canada, a yield loss of 38% was recorded in 1971-72. Yield losses of bean crops in 1968, 1970 and 1972 were 762,000, 1,256,000 and 217,000 kg, respectively (Wallen and Jackson, 1975). In white pea bean lines from a P. vulgaris/P. acutifolia cross, susceptible lines showed an average yield loss of 25% when disease free and inoculated plots in Ontario were compared. Resistant lines recorded little or no yield loss. The most severely infected lines tended to have the greatest loss in yield (Scott and Michaels, 1992). In Michigan, USA, a 1976 outbreak of common blight affected 75% of a 263 000 ha bean crop causing an estimated yield loss of 10-20% (Allen and Lenne, 1998).
Experimental studies have also reported on the losses due to this disease and the factors that can affect disease severity or incidence. Disease intensity and yield loss (green pods) varied from 4 to 71 and 1 to 84%, respectively, for two P. vulgaris cultivars infected with X. axonopodis pv. phaseoli at different growth stages. Early inoculation resulted in greater losses (Kishun et al., 1988).
Treatment of P. vulgaris plants with antibiotics at the beginning of anthesis was shown to reduce seed infection by X. axonopodis pv. phaseoli and increased yield by 14.4% (Tsvetkov and Donev, 1984). Increasing cumulative sulfur dioxide concentrations resulted in a significant decrease in the rate of lesion appearance. However, while the sulfur dioxide effectively inhibited disease development, it also led to a reduction in yield (Reynolds et al., 1987).
Results from laboratory, greenhouse and field experiments with seed from two cultivars of P. vulgaris inoculated with X. axonopodis pv. phaseoli showed that the inoculum could be localized on the seed surface or internally. A high degree of seed transmission of the pathogen was recorded. Seedling emergence was not affected up to a frequency of 10% infected seeds, but infection levels of 5% or more reduced crop yield (Valarini et al., 1996).
Inoculation of P. vulgaris with X. axonopodis pv. phaseoli by sandblast injury in the field resulted in 26-28% blight of leaves compared with 8-16% under natural infections. However, disease incidence and severity were low, and were not correlated with yield in this experiment (de Fario and de Melo, 1989).
The effect of hydrogen fluoride (HF) on field-grown beans spray-inoculated with an antibiotic-resistant strain of X. axonopodis pv. phaseoli was assessed. Final disease severity was not affected by exposure to HF, but the apparent infection rate increased with an increase in concentration of HF. In 1984, bean yield was not affected by HF, but in 1985 yield decreased with an increase in foliar tissue fluoride concentration (Reynolds and Laurence, 1988).