Xanthomonas axonopodis pv. phaseoli
(bean blight)

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Identity

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Preferred Scientific Name

• Xanthomonas axonopodis pv. phaseoli (Smith 1897) Vauterin et al. 1995

Preferred Common Name

• bean blight

Other Scientific Names

• Bacillus phaseoli Smith 1897
• Bacterium phaseoli (Smith 1897) Smith 1905
• Bacterium phaseoli var. fuscans (Burkholder) Okabe 1933
• Phytomonas phaseoli (Smith 1897) Bergey et al. 1923
• Phytomonas phaseoli var. fuscans Burkholder 1930
• Pseudomonas phaseoli (Smith) Smith 1901
• Pseudomonas phaseoli var. fuscans (Burkholder) Stapp 1935
• Xanthomonas campestris pv. phaseoli (Smith 1897) Dye 1978
• Xanthomonas campestris pv. phaseoli var. fuscans (Burkholder 1930) Starr & Burkholder 194
• Xanthomonas campestris pv. phaseoli var. indica Uppel et al.
• Xanthomonas fuscans (Burkholder) Burkholder 1959
• Xanthomonas phaseoli (ex Smith 1897) Gabriel at al. 1989
• Xanthomonas phaseoli var. fuscans (Burkholder) Starr & Burkholder 1942
• Xanthomonas phaseoli var. indica Uppal, Patel & Nikam 1946

International Common Names

• English: bacterial blight of bean; bacterial leaf pustule; common bacterial blight; common blight; fuscous blight of bean
• Spanish: mancha bacterial; quema bacteriana de las judias; quemaz bacterial commún; tizón común
• French: bactériose du haricot; brûlure bactérienne du haricot
• Portuguese: crestamento commun

Local Common Names

• Germany: Bacterielle brandfleckigkeit; Fettfleckenkrankheit
• India: sem ki jeewanik angmaari
• Italy: batteriosa del fagiola; nebbia batterica
• Japan: hayake-byo
• Turkey: fasulye adi yaprak yanikligi

EPPO code

• XANTPH (Xanthomonas axonopodis pv. phaseoli)

Taxonomic Tree

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• Domain: Bacteria
•     Phylum: Proteobacteria
•         Class: Gammaproteobacteria
•             Order: Xanthomonadales
•                 Family: Xanthomonadaceae
•                     Genus: Xanthomonas
•                         Species: Xanthomonas axonopodis pv. phaseoli

Notes on Taxonomy and Nomenclature

Top of page X. axonopodis pv. phaseoli was previously classified as a pathovar of X. campestris, which had been divided into 125 different pathovars, each characterized by a unique host range or disease (Bradbury, 1984). In the reclassification of Xanthomonas by Vauterin et al. (1995), Xanthomonas was divided into 20 genomic groups, and at least 32 former pathovars of X. campestris was transferred to X. axonopodis. X. campestris pv. phaseoli is now considered a pathovar of X. axonopodis and is classified as X. axonopodis pv. phaseoli.

X. axonopodis pv. phaseoli can be divided into three groups. X. axonopodis pv. phaseoli var. fuscans produces a diffusible brown pigment in culture that is enhanced by tyrosine (Goodwin and Sopher, 1994a), X. axonopodis pv. phaseoli var. indica produces a diffusible brown pigment in culture that is not enhanced by tyrosine (Bradbury, 1986) and X. axonopodis pv. phaseoli does not produce a brown pigment in culture. The brown pigment of X. axonopodis pv. phaseoli var. fuscans results from the secretion and oxidation of homogenistic acid, an intermediate in the tyrosine catabolic pathway (Goodwin and Sopher, 1994a). The fuscans variety is widespread and causes similar symptoms to X. axonopodis pv. phaseoli and was not considered to have any special taxonomic status (Bradbury, 1986). Common blight caused by the fuscans variety is known as fuscous blight of beans. There have been a number of reports indicating that the X. axonopodis pv. phaseoli var. fuscans isolates tend to be more pathogenic to beans, such as the demonstration that eight of the ten most aggressive isolates to Phaseolus vulgaris were the fuscous type (Opio et al., 1996). Several studies using RFLPs (Lazo et al., 1987), DNA-DNA homology (Hilderbrand et al., 1990), amplified DNA polymorphisms (Xue and Goodwin, 1993), RAPDs (Birch et al., 1997) and macrorestriction DNA polymorphisms (Chan and Goodwin, 1999) have consistently demonstrated that the fuscans strains are genetically distinct. It has been proposed that the fuscans variety should be considered a separate subspecies from those not producing a brown pigment in culture (Chan and Goodwin, 1999).

Description

Top of page X. axonopodis pv. phaseoli is a non-spore-forming, Gram-negative aerobic bacterium. It is rod-shaped with a single polar flagellum (Bradbury, 1986). Colonies are yellow, convex and slimy on glucose-containing media. The slimy appearance is due to the production of an extracellular polysaccharide, xanthan gum, on media containing glucose. The fuscans variety can be distinguished by the production of a dark-brown diffusible pigment in media containing tyrosine and certain other media. The non-fuscous strains can also produce low levels of diffusible brown pigments if high levels of tyrosine are added to the culture media (Goodwin and Sopher, 1994a).

See also Hayward and Waterston (1965a, b).

Distribution

Top of page See also CABI/EPPO (1998, No. 283).

Records for Eritrea and Bermuda cited in previous editions of the Compendium (IMI, 1996) were based on old references (Petri, 1932; Waterston, 1947) and no recent records could be found for these countries.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Last updated: 23 Apr 2020

Risk of Introduction

Top of page RISK CRITERIA CATEGORY

ECONOMIC IMPORTANCE High
DISTRIBUTION Worldwide
SEEDBORNE INCIDENCE High
SEED TRANSMITTED Yes
SEED TREATMENT Yes

OVERALL RISK Low


Notes on phytosanitary risk

The distribution of infected seed has already spread common blight throughout the world, and X. axonopodis pv. phaseoli is probably present almost everywhere that susceptible beans are grown.

Hosts/Species Affected

Top of page Many Phaseolus species have been reported as hosts of X. axonopodis pv. phaseoli. There are conflicting reports as to whether X. axonopodis pv. phaseoli is pathogenic to cowpeas (Vigna unguiculata ssp. unguiculata) (Gilbertson and Maxwell, 1992). X. axonopodis pv. phaseoli has been reported as naturally occurring on Calopogonium sp. and Pueraria sp. in Brunei, and on pea (Pisum sativum) in Myanmar (Bradbury, 1986). Races of X. axonopodis pv. phaseoli have been reported on Phaseolus acutifolius, P. calcaratus [Vigna umbellata] and P. aureus [Vigna radiata] (Bradbury, 1986). Opio et al. (1996) found eight races of X. axonopodis pv. phaseoli using P.acutifolius but only differences in aggressiveness were found to P. vulgaris. However, P. vulgaris genotypes have been reported to permit differentiation of races of X. axonopodis pv. phaseoli (Zapata, 1997). X. axonopodis pv. phaseoli, X. axonopodis pv. alfalfae, X. axonopodis pv. glycines and X. axonopodis pv. vignicola have all been reported to be pathogenic on common beans (Sabet, 1959) and there may be a continuum in host specificity among strains pathogenic to legumes.

Helianthus annuus, Lupinus polyphyllus, Phaseolus acutifolius and P. coccineus have been reported as hosts by artificial inoculation (Bradbury, 1986). Senna (Cassia) hirsuta and Digitaria scalarum are reported as symptomless hosts (Opio et al., 1996).

Host Plants and Other Plants Affected

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Growth Stages

Top of page Flowering stage, Fruiting stage, Seedling stage, Vegetative growing stage

Symptoms

Top of page 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).

List of Symptoms/Signs

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Biology and Ecology

Top of page Sources of Inoculum

X. axonopodis pv. phaseoli can survive in seed, infected plant debris and epiphytically on host and non-host plants (Saettler, 1991). Seed is particularly important in long-distance spread and for introducing X. axonopodis pv. phaseoli into new areas. Seed can also be important in long-term survival as X. axonopodis pv. phaseoli can remain viable in bean seeds for as long as 30 years (Trujillo and Saettler, 1980). Approximately 1000 to 10,000 bacteria per seed is the minimum needed to produce infected plants under field conditions (Weller and Saettler, 1980). Infection of flower buds and young pods can result in the transmission of X. axonopodis pv. phaseoli through the vascular system to the seed, leading to internal infection (Aggour et al., 1989). Plants grown from infected seed may have lesions of cotyledons, nodes or primary leaves which will then serve as sites for the spread of secondary infection. Seed may also become contaminated from affected plant residues during harvest.

Plant debris is probably more important as a source of inoculum in warmer climates where several susceptible crops can be planted in one year (Saettler, 1989). However, X. axonopodis pv. phaseoli populations will drop sharply in plant debris as other micro-organisms colonize and break down the material (Saettler, 1991). If infected bean debris is tilled into the soil it will greatly increase the rate of decay of the tissue and enhance the decline in X. axonopodis pv. phaseoli populations since it appears to be unable to survive for long in soil as free bacteria.

X. axonopodis pv. phaseoli can grow on the surface of both host and non-host plants (Cafati and Saettler, 1980). Growth on host-plant surfaces may provide a sizeable population with the potential to infect under appropriate conditions. The importance of epiphytic populations on non-host plants is not clear and Angeles-Ramos et al. (1991) found that weeds may not be not an important source of X. axonopodis pv. phaseoli inoculum because the pectolytic xanthomonads isolated from weeds were non-pathogenic to beans.

Transmission

X. axonopodis pv. phaseoli can be spread by planting infected seed: plants grown from infected seed usually show lesions on the cotyledon or primary leaves (Zaumeyer and Thomas, 1957). Bacteria in lesions, infected plant debris and epiphytic populations can be spread by splashing or wind-blown rain. Overhead irrigation can be very effective in secondary spread of the bacteria. Surface irrigation water may also spread the bacteria (Steadman et al., 1975).

X. axonopodis pv. phaseoli can also be disseminated on the bodies of insects, such as Diaprepes abbreviatus and Cerotoma ruficornis, which may also create wounds by feeding, thus producing favourable sites for infection (Kaiser and Vakili, 1978). Whiteflies (Bemisia tabaci), grasshoppers (Melanoplus sp.), Mexican bean beetles (Epilachna varivestris) and leaf miners have also been reported to transmit X. axonopodis pv. phaseoli (Zaumeyer and Thomas, 1957; Sabet and Ishag, 1969).

Infection

Infection occurs through natural openings and wounds. Severe epidemics can occur following storms with wind-blown rain, which can force the bacteria through openings, such as stomata, into the intercellular spaces. Wounds due to hail or insect feeding can create favourable sites for infection. Once inside the plant, X. axonopodis pv. phaseoli multiplies rapidly in the intercellular spaces and it can take as little as 10-14 days from initial infection until secondary spread occurs (Saettler, 1991). The optimal temperatures for disease development are 28-32°C (Saettler, 1989). Relatively high populations, 100,000 to 1,000,000 c.f.u./g of host tissue, are required before symptoms become visible (Gilbertson and Maxwell, 1992). Plants appear to be more susceptible in the reproductive stage than in the vegetative stage. As the bacterial population increases, it can ooze onto the leaf surface and be spread further by water. The polysaccharide covering of the bacteria helps to prevent desiccation (Wilson et al., 1965) and may assist the bacteria to attach to plant surfaces. The bacteria can also enter the vascular system of many varieties of beans and then spread systemically in the plant (Zaumeyer and Thomas, 1957). Wilting can result from vascular infection. Bacteria in the vascular system can also enter the developing pods and pass into the seeds (Aggour et al., 1989). Infection of the seed coats can also occur from pod infections.

Natural enemies

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Seedborne Aspects

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Incidence

X. axonopodis pv. phaseoli (Xap) and X. axonopodis pv. phaseoli var fuscans (Xapf) is extensively seedborne on Phaseolus spp. A survey of navy bean (P. vulgaris) seeds showed that approximately 35% had internal contamination with X. axonopodis pv. phaseoli (Saettler and Perry, 1972).  34 bean seed lots were collected in Paraná, Brazil from 1998 to 1999 and, when studied, 50% of the seedlots were infected with Xap with incidences ranging from 0.1 to 1.7% (Torres et al. 2009). Assays conducted on seed collected from naturally contaminated commercial fields in Serbia indicated presence of Xap in 20 of the 23 cultivars from which collections were made from (Popovic et al., 2010). Five out of seven seed samples collected in Egypt tested positive for the presence of Xap (Abd-Alla et al., 2010). Incidences of seed infection by X. axonopodis pv. phaseoli as high as 16.1%, with populations of the bacterium averaging between 100,000 and 1,000,000,000 c.f.u./100 seeds, were recorded in farmers commercial and research seeds in Africa (Opio et al., 1993). Approximately 1 in 10,000 seeds is capable of causing an outbreak of blight (Sutton and Wallen, 1970), or 1000 to 10,000 bacteria per seed is the minimum needed to produce infected plants under field conditions (Weller and Saettler, 1980).
Infection of flower buds and young pods can result in the transmission of X. axonopodis pv. phaseoli through the vascular system to the seed, leading to internal infection (Aggour et al., 1989). X. axonopodis pv. phaseoli is a systemic pathogen that penetrates the ovule through the funiculus. It enters the sutures of the pod from the vascular system of the pedicel and passes into the raphe leading into the seed coat. Bacteria also may enter though the micropyle (Burkholder, 1921; Zaumeyer, 1930). X. axonopodis pv. phaseoli is capable of long-term survival having been recovered from 15 year-old bean seeds (Schuster and Sayre, 1967).

Surface and internal populations of X. axonopodis pv. phaseoli were investigated on and in flower buds, flowers and pods of five susceptible (Pinto UI114, Cranberry Taylor Hort, Charlevoix, Black Magic and C20) and two resistant (Valley and I84100) Phaseolus vulgaris genotypes (Mabagala, 1997). Plants were grown in the field in Tanzania, and artificially inoculated at the seedling stage (18 day old). The pathogen was recovered in high numbers from flower buds, flowers, pods and seed of resistant and susceptible genotypes. Significant differences (P=0.05) in population levels of X. axonopodis pv. phaseoli between stages of reproductive tissue development were observed. Infected seed from resistant genotypes had no visible symptoms. It is suggested that these seeds may play an important role in the epidemiology of common bacterial blight disease because they are difficult to detect and may occur at low frequency in seed lots.

Effect on Seed Quality

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 (Zaumeyer, 1957). Infected seeds may also be symptomless (Yoshii, 1980).

Pathogen Transmission

Seed

Seeds are the primary source of inoculum for X. axonopodis pv. phaseoli. Plants grown from infected seeds frequently bear lesions on the cotyledons or primary nodes. These lesions enlarge and under humid conditions, slimy masses of bacteria accumulate on the leaf surface. These are then spread to healthy plants (Zaumeyer, 1957). Approximately 1000 to 10,000 bacteria per seed is the minimum needed to produce infected plants under field conditions (Weller and Saettler, 1980). A range of tolerances, ranging from 0 seeds infected in samples of 4000-45,000, are used in seed quality programmes in US seed companies to ensure that the pathogen is not transmitted by commercial seed lots (Maddox, 1997).

The most effective survival mechanism for Xap is to inhabit infected bean seed (Cafati & Saettler 1980a, Gilbertson et al., 1990; Arnaud-Santana et al., 1991; Opio et al., 1993), within which bacteria may survive for up to thirty six years (Allen et al., 1998).  Marques et al. (2005) indicated that the survival of seedborne X. axonopodis pv. phaseoli was reduced from 64 to 36-37% incidence during the first 6 months; however, seed stored at –18 and 5 ºC  maintained the contamination rate at 30 and 60 months, and  it was concluded that the optimum temperatures for storing seed is similar to conditions favourable for Xap longevity (Marques et al., 2005). Seed contamination may be internal or external (Saettler 1989; Allen et al., 1998) and even symptomless (Thomas & Graham, 1952; Weller and Saettler, 1980a), which has serious implications for seed certification schemes.  It has, however, been indicated that the development of X. axonopodis pv. phaseoli epidemics are depended on the level of horizontal resistance and climatic conditions rather than the population size of Xap in bean seeds (He, 2010). He (2010) found that Xap had a significant higher percentage of seed to seedling transmission than Xap. Although both variants reduced seedling emergence , Xapf was more severe and the incidence of typical CBB lesions were higher in seedlings infested with Xapf than Xap.

Other sources

Infected crop residues and other susceptible hosts are also sources of inoculum for X. axonopodis pv. phaseoli (Zaumeyer, 1957; Khlaif and Qadous, 1995). Conflicting reports exist on the ability of Xap to survive in infested soil and plant debris (Schuster & Coyne 1976; Saettler et al., 1986;  Gilbertson et al., 1990). Gilbertson et al. (1990) found Xap populations to overwinter in bean debris on no-tillage plots.  Non-pathogenic pectolytic strains of X. campestris were also consistently isolated.  Experiments conducted in the Dominican Republic indicated that Xap survived up to 7 months on infected debris on the soil surface, but not in buried debris after 30 days (Arnaud-Santana et al. 1991).  Xap survival studies conducted over ten years in Michigan indicated that infected crop debris is not the primary inoculum source for CBB (Saettler et al., 1986).  Infected bean debris may be more important as an inoculum source in tropical and sub-tropical than in temperate areas (Gilbertson et al., 1990).

Survival of Xap is greater under dry conditions (Schuster & Coyne 1977a) as bacteria decline rapidly under moist conditions (Allen et al. 1998).  Sabet & Ishag (1969) reported that Xap survived in press-dried bean leaves for more than 18 months in the laboratory, while Gilbertson et al. (1988) found Xap to remain viable in dry-leaf inoculum after 6 years.  The longer survival under laboratory conditions as opposed to that in the field could be attributed the presence of antagonists, such as protozoa, in the soil (Habte & Alexander 1975).

Xap also survives on weeds and other host plants (Cafati & Saettler 1980b; Angeles-Ramos et al., 1991; Opio et al., 1995).  Certain weed species may harbor the pathogen for up to 6 months (Opio et al. 1995).  Angeles-Ramos et al. (1991) isolated epiphytic, pectolytic Xanthomonads from symptomless weeds where pathogenic strains were isolated from within infected fields.  Epiphytic colonies survive on a wide range of plant species in the families Amaranthaceae, Commelinaceae, Compositae, Cruciferae, Gramineae, Oxalidaceae and Portulaceae in addition to various legumes (Allen et al., 1998).  Epiphytic Xap populations are important in the epidemiology of CBB on dry beans (Ishimaru et al., 1991) and are differentially affected in hosts of different genotypes (Cafati & Saettler 1980a).

Seed Treatments

Seed infection by X. axonopodis pv. phaseoli can be external or internal. 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).

The application of Rhizobium leguminosarum bv. phaseoli to common bean seeds reduced common bacterial blight severity and imnproved plant growth, both in field and greenhouse conditions (Osdaghi et al., 2011).

Under greenhouse conditions, bean seeds treated with a solution of tolylfluanid (1.20 g/L water) did not show any symptoms of infection until 30 days after sowing, and the overall prevelance of X. axonopodis pv. phaseoli was lower than in plants grown form untreated seeds (Lopes et al., 2008).

No methods are available to eradicate internal seed populations. However, external contamination may be controlled by streptomycin sulphate and sodium hypochlorite (Liang  et al. 1992).  Liang et al. (1992) investigated the potential of osmotic conditioning in reducing internal Xap populations from seeds, using polyethylene glycol (PEG) and glycerol as antibiotic carriers.  They found that tetracycline and chlorotetracycline in PEG solutions effectively reduced Xap, but were phytotoxic.  PEG solutions containing streptomycin reduced, but did not eradicate internal bacterial populations from naturally infected seeds with few phytotoxic effects. Tolylfluanid and Streptocycline were also reported as effective seed treatments (He, 2010).

Streptomycin is rapidly absorbed into bean stems and translocated to leaves but there is no indication that antibiotics are translocated downward through stems, trifoliate leaves or peduncle into the pod (Mitchell  et al. 1954).  Antibiotics should not be applied to leaves as resistant mutants may develop (Saettler 1989).  Development of resistance to chemicals (Romeiro et al. 1998), costs involved and efficacy limit use of chemical control which may be feasible under certain circumstances, such as seed production or as a component of an integrated control strategy (Allen et al., 1998).

Seed Health Tests

Selective medium (Mohan and Schaad, 1987; Higley et al., 1993)

- Soak seeds for 20 h in a solution of 0.85% NaCl and 0.01% Tween 20 (SST) at 5°C.
- Aliquots of the soak solution are spread on a semi-selective medium (M-SSM) developed by (Mabagala and Saettler, (1992).
- Bacterial colonies that develop are isolated and tested for pathogenicity by inoculation onto greenhouse-grown bean plants (cv. Yelloweye).

As indicated by Maddox (1997) samples sizes can vary greatly (4000-45,000 seeds) in routine seed quality tests for this pathogen.

Dome test (Venette et al., 1987)

In this test, bean seeds are soaked in water. The soaked bean infusion is then vacuum-infiltrated into pregerminated seeds of the same lot. Symptoms are then observed after seedlings are grown out at high humidity.

Phage (Kahveci and Maden, 1994)

High degrees of specificity and reliability for detection of seedborne X. axonopodis pv. phaseoli was claimed for 2 of 16 bacteriophages obtained from X. axonopodis pv. phaseoli.

Serology (Wong, 1991)

Immunoflourescence and ELISA methods have been described.

DNA hybridization (Audy et al., 1996)

X. axonopodis pv. phaseoli can be detected in bean seeds after DNA extraction of intact or crushed seed followed by a PCR assay using pathovar-specific primers (Audy et al., 1996). Another PCR assay has been developed that is specific to X. axonopodis pv. phaseoli var. fuscans and thus will not detect X. axonopodis pv. phaseoli (Toth et al., 1998).

Nondestructive assay (Higley et al., 1993)

Various non-destructive methods detected X. axonopodis pv. phaseoli in bean seeds.

Real-time PCR (He, 2010)

Real-time PCR offers a sensitive, reliable and fast approach to diagnosis of Xap and Xapf in seeds (He, 2010).  Assay specificity has been tested against DNA of several Xanthomonas species and pathovars of X. axonopodis. None of the closely related Xanthomonas strains were amplified using this PCR assay.

Plant Trade

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Plant parts not known to carry the pest in trade/transport
Bulbs/Tubers/Corms/Rhizomes
Flowers/Inflorescences/Cones/Calyx
Roots
Wood

Impact

Top of page 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).

Diagnosis

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Many different diagnostic methods have been developed for X. axonopodis pv. phaseoli and X. axonopodis pv. phaseoli var. fuscans (Xapf). Xap and Xapf can be easily isolated from CBB symptoms on leaves and pods using general isolation media (Schaad & Stall 1988).  On media such as sucrose peptone agar (SPA), colonies are circular, smooth and mucoid with a yellow pigment referred to as xanthomonadin.  Intensity of this yellow colour varies with medium used (Moffet & Croft 1983).  Isolation media containing tyrosine differentiates between Xap and Xapf in that the latter produces a brown diffusible pigment (Basu & Wallen 1967).  Goodwin & Sopher (1994) found this pigment to be produced due to secretion and subsequent oxidation of homogentisic acid rather than tyrosine activity.

Selective media are more effective for isolating specific bacteria from diseased material when selective at species level (Claflin, et al., 1987).  Examples of semi-selective media for X. axonopodis pv. phaseoli are MXP (Claflin et al., 1987), milk-tween agar (Goszczynska and Serfontein, 1998) and M-SSM (Mabagala and Saettler, 1992). Remeeus and Sheppard (2006) recommended the use of semi-selective media MT and XCP1 for the detection of Xanthomonas axonopodis pv. phaseoli. They indicated that although MT was not as effective than XCP1 a larger number of suspected and confirmed colonies of Xanthomonas axonopodis pv. phaseoli were found on MT versus XCP1.  A number of semi-selective media are, however, available to isolate Xap and Xapf (Kado & Heskett 1970, Schaad & White 1974, Trujillo & Saettler 1979, Claflin et al. 1987,  Dhanvantari & Brown 1993, Jackson & Moser 1994).

Apart from using selective media, techniques such as bacteriophage typing (Katznelson et al. 1954, Sutton & Wallen 1967), serology testing (Trujillo & Saettler 1979), host inoculation (Saettler 1971), ELISA (Wong 1991) and immunofluorescent staining  (Malin et al. 1983), can be used to detect and identify Xap and Xapf.  These techniques are time consuming and labourious.  More sensitive, rapid and specific detection of the pathogen is often needed.  This is particularly important when identification is complicated by epiphytic Xap strains (Gilbertson et al., 1989, Audey et al., 1994) that may confuse seed certification (Wong 1991, Audey et al. 1994).

Starch is frequently included in the medium to help detect X. axonopodis pv. phaseoli because it hydrolyses starch, an uncommon trait among bacteria. Various diagnostic physiological tests are available for use with pure cultures but a pathogenicity test is required for detection at the pathovar level (Sheppard et al., 1989). Detection with phages specific to X. axonopodis pv. phaseoli have also been attempted, but not all strains are susceptible to a particular phage and phages are usually not truly species-specific (Sheppard et al., 1989).

Immunosassays are available for X. axonopodis pv. phaseoli but most have not been sufficiently specific for accurate diagnosis. However, monoclonal antibodies are now available for X. axonopodis pv. phaseoli and have been used in immunofluorescence microscopy and an ELISA to detect it in seed (Wong, 1991). This monoclonal antibody appears to be highly specific to X. axonopodis pv. phaseoli and only cross-reacts with X. axonopodis pv. malvacearum (Wong, 1990).

Specific diagnosis of X. axonopodis pv. phaseoli was achieved with a DNA hybridization probe (Gilbertson et al., 1989). Based on this probe, another highly specific PCR probe, for Xap detection, was developed to detect as few as 10 colony forming units (CFU), using ethidium bromide-stained agarose gel (Audey et al. 1994).  Audey et al. (1996) developed a rapid, sensitive PCR assay for detection of seedborne Xap in large bean seed samples containing as few as one infected in 10 000 healthy seeds.  Birch et al. (1997) used RAPD-PCR to differentiate between Xap and Xapf.  Toth et al. (1998) used  primers which amplified a DNA fragment from all Xapf-isolates used, while no amplification products were obtained from Xap-isolates.  These primers, therefore, provide a rapid, improved method to differentiate between these two variants. More recent techniques used to differentiate Xap and Xapf include restriction fragment length polymorphism (RFLP) analyses (Chan et al., 1990; Gilbertson et al., 1991, Lazo et al., 1987), DNA-DNA hybridization (Hildebrand et al., 1990), pulse field gel electrophoresis (Chan et al., 1990) and rep-PCR (López et al., 2006; Mahuku, 2006; Mkandawire et al., 2004).

The pathogen can be readily isolated from symptomatic tissue (Dreo et al., 2003). A comparison of various extraction processes is given in He and Munkvold, 2012).

The method of identification issued by the International Seed Federation in 2006 is successfully used in Balaz et al. (2008). X. axonopodis pv. phaseoli was isolated from bean seeds and isolated on a semiselective media. ELISA and PCR can then be used to confirm the identity of resulting isolates. Milk Tween Agar (MTA) and Modifies Sucrose Peptone Agar (MSPA) are both suitable for isolation of P. savastanoi pv. phaseolicola.

The development and use of a PCR-based method for detection of X. axonopodis pv. phaseoli in pomegranate is described in Mondal et al. (2012).

Seed Health Tests

A sample, usually 1000 to 10,000 seeds, is washed in running water and then placed in a container to which a solution of phosphate-buffered saline or liquid semi-selective media is added. The samples are then incubated at room temperature for 2-3 hours. Longer incubation times can increase the number of saprophytic bacteria and reduce the number of aerobic xanthomonads. The solution, known as the seed-soak wash, is diluted and plated onto various culture media. The bacteria are then identified by physiological traits, phage tests, pathogenicity tests and/or immunoassays (Sheppard et al., 1989). The seed-soak wash can also be directly injected into susceptible plants or vacuum-infiltrated into pregerminated bean seeds, which are then observed for typical common blight symptoms (Venette et al., 1987; Sheppard et al., 1989).

A comparison of extraction methods showed that crushing seed in phosphate-buffered saline was more effective in releasing bacteria than soaking intact seeds (Maringoni et al., 1998). X. axonopodis pv. phaseoli can also be detected in seed after DNA extraction of intact or crushed seed followed by a PCR assay using specific primers (Audy et al., 1996). Results from studies conducted by He (2010) to assess the influence of different extraction steps on the sensitivity of Xap indicated that vacuum extraction and centrifugation of seed extracts increased sensitivity, and the highest sensitivity was obtained with the 3-hour vacuum extraction at room temperature followed by centrifugation.

For infected plant tissue other than seed, the material should be washed thoroughly in running water and dried. Surface sterilization may be necessary as a general hygiene precaution to avoid surface contaminants. The margin of a lesion is excised with a sterile blade and mixed with a small amount of sterile water or phosphate-buffered saline to allow the bacteria to diffuse out into the solution for 15-30 minutes. A sterile loop is then used to streak the solution onto agar media (Schaad and Stall, 1988).

Detection and Inspection

Top of page Because X. axonopodis pv. phaseoli is seedborne, considerable efforts have gone into detection. Visible symptoms are not reliable. Detection involves extraction of the bacteria from seeds, followed by identification of the bacteria by means of tests (see Diagnostic Methods). Bean seeds can be infected internally and externally (Sheppard et al., 1989).

Similarities to Other Species/Conditions

Top of page Xanthomonads that are non-pathogenic to beans have been isolated from bean debris and these isolates share many characteristics with X. axonopodis pv. phaseoli, including appearance in culture and growth on MXP, a semi-selective medium developed for the isolation of X. axonopodis pv. phaseoli (Gilbertson et al., 1990; Angeles-Ramos et al., 1991). These isolates differ from X. axonopodis pv. phaseoli in being pectolytic, but the only way to distinguish them accurately is by a pathogenicity test or a DNA-based assay (Gilbertson et al., 1989; Audy et al., 1996).

The symptoms of common blight can also be confused with those of chocolate spot of bean caused by Pseudomonas syringae pv. syringae.

Prevention and Control

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Due to the variable regulations around (de)registration of pesticides, your national list of registered pesticides or relevant authority should be consulted to determine which products are legally allowed for use in your country when considering chemical control. Pesticides should always be used in a lawful manner, consistent with the product's label.

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 Treatments

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 Methods

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.

Host-Plant Resistance

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).

Chemical Control

Chemical control may reduce leaf infection but usually has little improvement on yield. Copper compounds may be used (Weller and Saettler, 1976). Foliar antibiotic treatment can provide some control but is undesirable because it can result in antibiotic-resistant mutants of X. axonopodis pv. phaseoli.

References

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Abd-Alla MH; Bashandy SR; Schnell S, 2010. Occurrence of Xanthomonas axonopodis pv. phaseoli, the causal agent of common bacterial blight disease, on seeds of common bean (Phaseolus vulgaris L.) in Upper Egypt. Folia Microbiologica, 55(1):47-52. http://www.biomed.cas.cz/mbu/folia/

Aggour AR; Coyne DP; Vidaver AK; Eskridge KM, 1989. Transmission of the common blight pathogen in bean seed. Journal of the American Society for Horticultural Science, 114(6):1002-1008

Allen DJ; Buruchara RA; Smithson JB, 1998. Diseases of common bean [ed. by Allen, D. J. \Lenné, J. M.]. Wallingford, UK: CAB International, 179-235. [The pathology of food and pasture legumes.]

Angeles-Ramos R; Vidaver AK; Flynn P, 1991. Characterization of epiphytic Xanthomonas campestris pv. phaseoli and pectolytic xanthomonads recovered from symptomless weeds in the Dominican Republic. Phytopathology, 81(6):677-681

Ariyarathne HM; Coyne DP; Jung G; Skroch PW; Vidaver AK; Steadman JR; Miklas PN; Bassett MJ, 1999. Molecular mapping of disease resistance genes for halo blight, common bacterial blight, and bean common mosaic virus in a segregating population of common bean. Journal of the American Society for Horticultural Science, 124(6):654-662; 43 ref.

Arnaud-Santana E; Pena-Matos E; Coyne DP; Vidaver AK, 1991. Longevity of Xanthomonas campestris pv. phaseoli in naturally infested dry bean (Phaseolus vulgaris) debris. Plant Disease, 75(9):952-953.

Audy P; Braat CE; Saindon G; Huang HC; Laroche A, 1996. A rapid and sensitive PCR-based assay for concurrent detection of bacteria causing common and halo blights in bean seeds. Phytopathology, 86(4):361-366; 33 ref.

Audy P; Laroche A; Saindon G; Huang HC; Gilbertson RL, 1994. Detection of the bean common blight bacteria, Xanthomonas campestris pv. phaseoli and X. c. phaseoli var. fuscans, using the polymerase chain reaction. Phytopathology, 84(10):1185-1192

BASU PK; WALLEN VR, 1967. Factors affecting virulence and pigment production of Xanthomonas phaseoli var. fuscans. Canadian Journal of Botany, 45(12):2367-2374.

Beaver J, 1999. Advances in Caribbean Andean bean breeding. Agronomia Mesoamericana, 10(1):77-81; 25 ref.

Beaver JS; Steadman JR; Coyne DP, 1992. Field reaction of landrace components of red mottled beans to common bacterial blight. HortScience, 27(1):50-51

Beaver JS; Zapata M; Miklas PN, 1999. Registration of PR9443-4 dry bean germplasm resistant to bean golden mosaic, common bacterial blight, and rust. Crop Science, 39(4):1262; 2 ref.

Birch PRJ; Hyman LJ; Taylor R; Opio AF; Bragard C; Toth IK, 1997. RAPD PCR-based differentiation of Xanthomonas campestris pv. phaseoli and Xanthomonas campestris pv. phaseoli var. fuscans. European Journal of Plant Pathology, 103(9):809-814; 23 ref.

Bradbury JF, 1984. Xanthomonas Dowson 1939. In: Bergey's Manual of Systematic Bacteriology. Baltimore, USA: Williams and Wilkins, 199-210.

Bradbury JF, 1986. Guide to Plant Pathogenic Bacteria. Wallingford, UK: CAB International.

Brooks F, 2002. List of Plant Diseases in American Samoa 2002. Land Grant Technical Report No. 44. Pago Pago, American Samoa: American Samoa Community College Land Grant Program.

Burkholder WH, 1921. The bacterial blight of bean: as systemic disease. Phytopathology, 11:61-69.

CABI/EPPO, 1998. Distribution maps of quarantine pests for Europe (edited by Smith IM, Charles LMF). Wallingford, UK: CAB International, xviii + 768 pp.

CABI/EPPO, 2007. Xanthomonas axonopodis pv. phaseoli. Distribution Maps of Plant Diseases, No. 401. Wallingford, UK: CAB International.

Cafati CR; Saettler AW, 1980. Effect of host on multiplication and distribution of bean common blight bacteria. Phytopathology, 70(7):675-679.

Cafati CR; Saettler AW, 1980. Transmission of Xanthomonas phaseoli in seed of resistant and susceptible Phaseolus genotypes. Phytopathology, 70(7):638-640.

Cafati CR; Spttler AW, 1980. Role of nonhost species as alternate inoculum sources of Xanthomonas phaseoli. Plant Disease (formerly Plant Disease Reporter), 64(2):194-196

Chan JWYF; Goodwin PH, 1996. Pulsed-field electrophoresis to determine chromosome sizes and macrorestriction DNA polymorphisms of Xanthomonas campestris pv. phaseoli. Personal communication. Department of Environmental Biology, University of Guelph, Guelph, Ontario N1G 2W1, Canada.

Chan JWYF; Goodwin PH, 1999. Differentiation of Xanthomonas campestris pv. phaseoli from Xanthomonas campestris pv. phaseoli var. fuscans by PFGE and RFLP. European Journal of Plant Pathology, 105(9):867-878; 45 ref.

Chen HongYu; Xu XinXin; Duan CanXing; Wang ShuMin; Zhu ZhenDong, 2012. Identification of pathogens causing common bacterial blight on common bean (Phaseolus vulgaris L.). Scientia Agricultura Sinica, 45(13):2618-2627. http://www.ChinaAgriSci.com

Claflin LE; Vidaver AK; Sasser M, 1987. MXP, a semi-selective medium for Xanthomonas campestris pv. phaseoli. Phytopathology, 77(5):730-734

Coyne DP; Shuster ML; Hill; K, 1973. Genetic control of reaction to common blight bacterium in bean (Phaseolus vulgaris) as influenced by plant age and bacterial multiplication. Journal of the American Society of Horticultural Science, 98:94-99.

Dhanvantari BN; Brown RJ, 1993. YSSM-XP medium for Xanthomonas campestris pv. phaseoli. Canadian Journal of Plant Pathology, 15(3):168-174.

Díaz Plaza R; Téliz Ortiz D; Munoz OA, 1991. Effect of diseases on bean grown under rainfed conditions at Mixteca poblana. Revista Mexicana de Fitopatología, 9(1):21-30; 20 ref.

Díaz Plaza R; Téliz Ortiz D; Munoz Orozco A, 1991. Interaction between drought and some bean pathogens. Revista Mexicana de Fitopatología, 9(2):121-125; 16 ref.

Dreo T; Demsar T; Ravnikar M, 2003. Quarantine of Xanthomonas campestris pv. phaseoli in beans. (Karantenska bakterija Xanthomonas campestris pv. phaseoli na fizolu.) In: Zbornik predavanj in referatov 6. Slovenskega Posvetovanje o Varstvu Rastlin, Zrece, Slovenije, 4-6 marec 2003. Ljubljana, Slovenia: Drustvo za varstvo rastlin Slovenije, 123-127.

EPPO, 2014. PQR database. Paris, France: European and Mediterranean Plant Protection Organization. http://www.eppo.int/DATABASES/pqr/pqr.htm

Faria JC de; Melo PE de, 1989. Inoculation of common beans with Xanthomonas campestris pv. phaseoli under field conditions. Pesquisa Agropecuaria Brasileira, 24(8):987-990

Flores-Revilla C; Osada-Kawasoc S; Teliz-Ortiz D; Torre-Almarez R de la, 1993. Control alternatives of several bean (Phaseolus vulgaris L.) diseases in Huejotzingo, Puebla, Mexico. Revista Mexicana de Fitopatologia, 11:64-68.

Garcfa-Espinosa R, 1997. Breeding for horizontal resistance in bean: an example from Mexico. Biotechnology and Development Monitor, No. 33:5.

Gilbertson RL; Maxwell DP, 1992. Common bacterial blight of bean. Plant diseases of international importance. Volume II. Diseases of vegetables and oil seed crops. [edited by Chaube, H.S.; Kumar, J.; Mukhopadhyay, A.N.; Singh, U.S.] Englewood Cliffs, New Jersey, USA; Prentice Hall, Inc., 18-39

Gilbertson RL; Maxwell DP; Hagedorn DJ; Leong SA, 1989. Development and application of a plasmid DNA probe for detection of bacteria causing common bacterial blight of bean. Phytopathology, 79(5):518-525

Gilbertson RL; Otoya MM; Pastor-Corrales MA; Maxwell DP, 1991. Genetic diversity in common blight bacteria is revealed by clonal repetitive DNA sequences, 34:37-38.

Gilbertson RL; Rand RE; Carlson E; Hagedorn DJ, 1988. The use of dry-leaf inoculum for establishment of common bacterial blight of beans. Plant Disease, 72(5):385-389.

Gilbertson RL; Rand RE; Hagedorn DJ, 1990. Survival of Xanthomonas campestris pv. phaseoli and pectolytic strains of X. campestris in bean debris. Plant Disease, 74(4):322-327

Girard JC, 1991. Phytobacteriology of market vegetable cultivars. Rapport Annuel - CIRAD Reunion Saint Denis, France; CIRAD, 74-75

Girma T; Negatu D, 1995. Haricot bean: its importance, production and research in Ethiopia. Breeding for disease resistance with emphasis on durability. Proceedings of a regional workshop for eastern, central and southern Africa, held at Njoro, Kenya, October 2-6, 1994 [edited by Danial, D. L.] Wageningen, Netherlands; Landbouwuniversiteit Wageningen (Wageningen Agricultural University), 245-250

Goodwin PH; Sopher CR, 1994. Brown pigmentation of Xanthomonas campestris pv. phaseoli associated with homogentisic acid, 40:28-34.

Goodwin PH; Sopher CR, 1994. Brown pigmentation of Xanthomonas campestris pv. phaseoli associated with homogentisic acid. Canadian Journal of Microbiology, 40:28-34.

Goodwin PH; Sopher CR, 1994. Water stress in leaves of Phaseolus vulgaris infected with Xanthomonas campestris pv. phaseoli. Journal of Phytopathology, 140(3):219-226

Goodwin PH; Sopher CR; Michaels TE, 1995. Multiplication of Xanthomonas campestris pv. phaseoli and intercellular enzyme activities in resistant and susceptible beans. Journal of Phytopathology, 143(1):11-15

Goszczynska T; Serfontein JJ, 1998. Milk-Tween agar, a semiselective medium for isolation and differentiation of Pseudomonas syringae pv. syringae, Pseudomonas syringae pv. phaseolicola and Xanthomonas axonopodis pv. phaseoli. Journal of Microbiological Methods, 32(1):65-72; 27 ref.

Grondeau C; Samson R, 1994. A review of thermotherapy to free plant materials from pathogens, especially seeds from bacteria. Critical Reviews in Plant Sciences, 13(1):57-75

Habte M; Alexander M, 1975. Protozoa as agents responsible for the decline of Xanthomonas campestris in soil. Applied Microbiology, 29(2):159-164.

Hayward AC; Waterson JM, 1965. Xanthomonas phaseoli var. fuscans. CMI Descriptions of Pathogenic Fungi and Bacteria, No. 49. Wallingford, UK: CAB International.

He Y, 2010. Improved seed health tests for Xanthomonas axonopodis pv. phaseoli in common bean. Ames, USA: Iowa State University.

He Y; Munkvold GP, 2012. Comparison of extraction procedures for detection of Xanthomonas axonopodis pv. phaseoli in common bean seed. Plant Pathology, 61(5):837-843. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-3059.2011.02586.x/full

Higley PM; McGee DC; Burris JS, 1993. Development of methodology for non-destructive assay of bacteria, fungi and viruses in seeds of large-seeded field crops. Seed Science and Technology, 21(2):399-409; 13 ref.

Hildebrand DC; Palleroni NJ; Schroth MN, 1990. Deoxyribonucleic acid relatedness of 24 xanthomonad strains representing 23 Xanthomonas campestris pathovars and Xanthomonas fragarip. Journal of Applied Bacteriology, 68(3):263-269

IPPC, 2008. First outbreak of Xanthomonas axonopodis pv. phaseoli in the Czech Republic. IPPC Official Pest Report, No. CZ-6/1. Rome, Italy: FAO. https://www.ippc.int/IPP/En/default.jsp

Irigoyen ED; Garbagnoli C, 1997. Common bacteriosis in bean (Xanthomonas campestris pv. phaseoli [E.F. Smith] Dowson): detection, infection and transmission through seeds. Fitopatologi^acute~a, 32(3):166-172; 30 ref.

Ito MF; Valarini PJ; Patrfcio FRA; Sugimori MH, 1997. Detection of Xanthomonas campestris pv. phaseoli and fungi in bean seeds produced in Sao Paulo State. Summa Phytopathologica, 23(2):118-121; 20 ref.

Jackson LE; Moser PE, 1994. Development of a medium for isolation and differentiation of three bacterial plant pathogens, 37:23-24.

Jung G; Coyne DP; Skroch PW; Nienhuis J; Arnaud-Santana E; Bokosi J; Ariyarathne HM; Steadman JR; Beaver JS; Kaeppler SM, 1996. Molecular markers associated with plant architecture and resistance to common blight, web blight, and rust in common beans. Journal of the American Society for Horticultural Science, 121(5):794-803; 39 ref.

Kado CI; Heskett MG, 1970. Selective media for isolation of Agrobacterium, Corynebacterium, Erwinia, Pseudomonas and Xanthomonas, 60:969-976.

Kahveci E; Maden S, 1994. Detection of Xanthomonas campestris pv. phaseoli and Pseudomonas syringae pv. phaseolicola by bacteriophages. Journal of Turkish Phytopathology, 23(2):79-85

Kaiser WJ; Vakili NG, 1978. Insect transmission of pathogenic xanthomonads to bean and cowpea in Puerto Rico. Phytopathology, 68(7):1057-1063

KATZNELSON H; SUTTON MD; BAYLEY ST, 1954. The use of baeteriophage of Xanthomonas phaseoli in detecting infection in Beans, with observations on its growth and morphology. Canadian Journal of Microbiology, 11:22-29 pp.

Khlaif HM; Qadous NS, 1995. Common blight of beans in the Jordan Valley: sources of inoculum. Dirasat. Series B, Pure and Applied Sciences, 22(3):717-728; 13 ref.

Kikoka LP; Katunzi AL; Teri JM, 1989. Evaluation of effect of cropping systems on bean diseases and yield. Proceedings: Integrated Pest Management in Tropical and Subtropical Cropping Systems '89, vol. 3. February 8-15, 1989, Bad Durkheim, Germany Frankfurt am Main, Germany; DLG Verlag GmbH, 853-858

Kishun R, 1988. Loss in yield of French beans affected with common blight. Advances in research on plant pathogenic bacteria. Based on the proceedings of the National Symposium on Phytobacteriology held at the University of Madras, Madras, India during March 14-15, 1986 [edited by Gnanamanickam, S.S.; Mahadevan, A.] New Delhi, India; Today & Tomorrow's Printers & Publishers, 29-31

Lazo GR; Roffey R; Gabriel DW, 1987. Pathovars of Xanthomonas campestris are distinguishable by restriction fragment-length polymorphism. International Journal of Systematic Bacteriology, 37(3):214-221

Liang LZ; Halloin JM; Saettler AW, 1992. Use of polyethylene glycol and glycerol as carriers of antibiotics for reduction of Xanthomonas campestris pv. phaseoli in navy bean seeds. Plant Disease, 76(9):875-879

Lopes LP; Alves PFR; Zandoná C; Nunes MP; Mehta YR, 2008. A semi-selective medium to detect Xanthomonas axonopodis pv. phaseoli in bean seeds and its eradication through seed treatment with tolylfluanid. (Meio semi-seletivo para detectar Xanthomonas axonopodis pv. phaseoli em sementes de feijoeiro e sua erradicação através do tratamento de sementes com o fungicida tolylfluanid.) Summa Phytopathologica, 34(3):287-288. http://www.scielo.br/pdf/sp/v34n3/20.pdf

López R; Asensio C; Gilbertson RL, 2006. Phenotypic and genetic diversity in strains of common blight bacteria (Xanthomonas campestris pv. phaseoli and X. campestris pv. phaseoli var. fuscans) in a secondary center of diversity of the common bean host suggests multiple introduction events. Phytopathology, 96(11):1204-1213.

Mabagala RB, 1997. The effect of populations of Xanthomonas campestris pv. phaseoli in bean reproductive tissues on seed infection of resistant and susceptible bean genotypes. European Journal of Plant Pathology, 103(2):175-181; 15 ref.

Mabagala RB; Saettler AW, 1992. An improved semiselective medium for recovery of Xanthomonas campestris pv. phaseoli. Plant Disease, 76(5):443-446

Maddox DA, 1996. Regulatory Needs for Standardized Seed Health Tests. In: McGee DC, ed. Plant Pathogens and the Worldwide Movement of Seeds. St. Paul, MN, USA: APS Press, 81-92.

Mahuku GS; Jara C; Henriquez MA; Castellanos G; Cuasquer J, 2006. Genotypic characterization of the common bean bacterial blight pathogens, Xanthomonas axonopodis pv. phaseoli and Xanthomonas axonopodis pv. phaseoli var. fuscans by rep-PCR and PCR-RFLP of the ribosomal genes. Journal of Phytopathology, 154(1):35-44. http://www.blackwell-synergy.com/servlet/useragent?func=showIssues&code=jph

Makini FW, 1995. Bean production and constraints in Kenya with emphasis on diseases. Breeding for disease resistance with emphasis on durability. Proceedings of a regional workshop for eastern, central and southern Africa, held at Njoro, Kenya, October 2-6, 1994 [edited by Danial, D. L.] Wageningen, Netherlands; Landbouwuniversiteit Wageningen (Wageningen Agricultural University), 104-109

Malin EM; Roth DA; Belden EL, 1983. Indirect immunofluorescent staining for detection and identification of Xanthomonas campestris pv. phaseoli in naturally infected bean seed, 67:645-647.

Maringoni AC; Kimati H; Kurozawa C, 1998. Comparison between two extraction methods of Xanthomonas campestris pv. phaseoli from bean seeds. Pesquisa Agropecua^acute~ria Brasileira, 33(5):659-664; 41 ref.

Marques ASdos A; Guimarães PM; Santos JPdos; Vieira TM, 2005. Survival and viability of Xanthomonas axonopodis pv. phaseoli associated with bean seeds stored under controlled conditions. (Sobrevivência e viabilidade de Xanthomonas axonopodis pv. phaseoli em sementes de feijão armazenadas sob condições controladas.) Fitopatologia Brasileira, 30(5):527-531. http://www.scielo.br/pdf/fb/v30n5/26152.pdf

Mayek-Perez N; Pedroza-Flores JA; Villareal-Garcia LA; Valdez-Lozano CGS, 1995. Genetic and envirtonmental factors related to temporal dynamics and diseases effects on dry beans (Phaseolus vulgaris L.) at Marin, Nuevo Leon, Mexico. Revista Mexicana de Fitopatologia, 13:1-9.

Miklas PN; Johnson E; Stone V; Beaver JS; Montoya C; Zapata M, 1996. Selective mapping of QTL conditioning disease resistance in common bean. Crop Science, 36(5):1344-1351; 37 ref.

Miklas PN; Zapata M; Beaver JS; Grafton KF, 1999. Registration of four dry bean germplasms resistant to common bacterial blight: ICB-3, ICB-6, ICB-8, and ICB-10. Crop Science, 39(2):594; 3 ref.

MITCHELL JW, 1954. Absorption and translocation of streptomycin by bean plants and its effect on the halo and common blight organisms. Phytopathology, 44(1):25-30.

Mkandawire ABC; Mabagala RB; Guzmán P; Gepts P; Gilbertson RL, 2004. Genetic diversity and pathogenic variation of common blight bacteria (Xanthomonas campestris pv. phaseoli and X. campestris pv. phaseoli var. fuscans) suggests pathogen coevolution with the common bean. Phytopathology, 94(6):593-603.

Moffet ML; Croft BJ, 1983. Xanthomonas. In: Plant bacterial diseases: A diagnostic guide [ed. by Fahy, P. C. \Persley, G. J.]., Australia: Academic Press, 189-228.

Mohan SK; Schaad NW, 1987. An improved agar plating assay for detecting Pseudomonas syringae pv. syringae and P. s. pv. phaseolicola in contaminated bean seed. Phytopathology, 77(10):1390-1395

Molouba F; Guimier C; Berthier C; Guenard M; Olivier V; Baril C; Horvais A, 2001. Detection of bean seed-borne pathogens by PCR. Acta Horticulturae, No. 546:603-607; 11 ref.

Mondal KK, 2004. Integrated management strategies for fuscous blight and floury leaf spot of rajmash. Indian Phytopathology, 57(2):135-139.

Mondal KK; Rajendran TP; Phaneendra C; Mani C; Jyotsana Sharma; Richa Shukla; Pooja; Geeta Verma; Kumar R; Singh D; Kumar A; Saxena AK; Jain RK, 2012. The reliable and rapid polymerase chain reaction (PCR) diagnosis for Xanthomonas axonopodis pv. punicae in pomegranate. African Journal of Microbiology Research, 6(30):5950-5956. http://www.academicjournals.org/ajmr/PDF/Pdf2012/9August/Mondal%20et%20al.pdf

Morßn Medina F; Barrales Domfnguez JS, 1990. Bean collections, their behaviour and flowering habits under rainy season conditions. Revista Chapingo, 15(71-72):68-72; 7 ref.

Naumann K; Karl H, 1985. On two bacterial plant diseases recorded for the first time in the GDR in leguminous crops. Nachrichtenblatt fur den Pflanzenschutz in der DDR, 39(12):244-246

Ohlander LJR, 1980. Research on haricot bean (Phaseolus vulgaris L.) production in Ethiopia 1972-1976. Rapport, Institutionen for Vaxtodling, Sveriges Lantbruksuniversitet, No. 82:305 pp.

Opio AF; Allen DJ; Teri JM, 1995. The role of weeds and non-host crops in the survival of Xanthomonas campestris pv. phaseoli in Uganda, 38:166-167.

Opio AF; Teri JM; Allen DJ, 1993. Studies on seed transmission of Xanthomonas campestris pv. phaseoli in common beans in Uganda. African Crop Science Journal, 1(1):59-67

Opio F; Male-Kayiwa S, 1995. The status of bean breeding in Uganda. Breeding for disease resistance with emphasis on durability. Proceedings of a regional workshop for eastern, central and southern Africa, held at Njoro, Kenya, October 2-6, 1994 [edited by Danial, D. L.] Wageningen, Netherlands; Landbouwuniversiteit Wageningen (Wageningen Agricultural University), 110-113

Osdaghi E, 2014. Occurrence of common bacterial blight on mungbean (Vigna radiata) in Iran caused by Xanthomonas axonopodis pv. phaseoli. New Disease Reports, 30:9. http://www.ndrs.org.uk/article.php?id=030009

Osdaghi E; Shams-Bakhsh M; Alizadeh A; Lak MR; Maleki HH, 2011. Induction of resistance in common bean by Rhizobium leguminosarum bv. phaseoli and decrease of common bacterial blight. Phytopathologia Mediterranea, 50(1):45-54. http://www.fupress.com/pm/

Osdaghi E; Zademohamad AA, 2016. Phaseolus lunatus, a new host of Xanthomonas axonopodis pv. phaseoli in Iran. Journal of Phytopathology, 164(1):56-60. http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1439-0434

Park SO; Coyne DP; Dursun A; Jung G, 1998. Identifying randomly amplified polymorphic DNA (RAPD) markers linked to major genes for common bacterial blight resistance in tepary bean. Journal of the American Society for Horticultural Science, 123(2):278-282; 36 ref.

Pazos V; Hevesi M, 1975. Common blight of beans. Rev. Cenic. Cienc. Biol., 6(2):291-294

Pedroza SA; Téliz OD; Torre ARde la; Campbell CL, 1994. Varieties and cultural practices as management tools for multiple diseases on beans (Phaseolus vulgaris L.) in Puebla, Mexico. Revista Mexicana de Fitopatología, 12(2):146-154; 19 ref.

Pedroza-Sandoval A, 1994. Response of French bean varieties to seed treatment and use of organic and chemical fertilizers in controlling the main bean diseases in the Comarca Lagunera. Revista Mexicana de Fitopatología, 12(1):63-67; 9 ref.

Petri L, 1931. Rassegna dei casi fitopatologici osservatii nel 1930. Boll. R. Staz. Patol. Vegt., 11:1-50.

Popovic T; Balaz J; Nikolic Z; Starovic M; Gavrilovic V; Aleksic G; Vasic M; Zivkovic S, 2010. Detection and identification of Xanthomonas axonopodis pv. phaseoli on bean seed collected in Serbia. African Journal of Agricultural Research, 5(19):2730-2736. http://www.academicjournals.org/ajar/PDF/pdf%202010/4%20Oct/Popovic%20et%20al.pdf

Rajappan K; Ramaraj B; Natarajan S, 2000. Field evaluation of fungicides and neem formulations against bacterial blight of Frenchbean. Indian Phytopathology, 53(3):303-304.

Remeeus PM; Sheppard JW, 2006. Proposal for a new method for detecting Xanthomonas axonopodis pv.phaseoli on bean seeds, 3:1-11. [ISTA Method Validation Reports.]

Reynolds KL; Laurence JA, 1988. Effects of hydrogen fluoride on growth, common blight development, and the accumulation of fluoride in field-grown red kidney beans. Phytopathology, 78(9):1168-1173

Reynolds KL; Zanelli M; Laurence JA, 1987. Effects of sulfur dioxide exposure on the development of common blight in field-grown red kidney beans. Phytopathology, 77(2):331-334

Rheenen HA van; Hasselbach OE; Muigai SGS, 1981. The effect of growing beans together with maize on the incidence of bean diseases and pests. Netherlands Journal of Plant Pathology, 87(5):193-199

Romeiro Rda S; Moura AB; Oliveira JRde; Silva HSA; Barbosa LS; Soares FMP; Peres F, 1998. Evidences of constitutive multiple resistance to antibiotics in some plant pathogenic bacteria. (Evidências de resistência múltip constitutiva a antibióticos em algumas bactérias fitopatogênicas.) Summa Phytopathologica, 24(3/4):220-225.

Sabet KA, 1959. Studies on the bacterial diseases of Sudan crops. III. On the occurrence, host range and taxonomy of the bacteria causing leaf blight diseases of certain leguminous plants. Annals of Applied Biology, 47:318.

Sabet KA; Ishag F, 1969. Studies on the bacterial diseases of Sudan crops, VIII: survival and dissemination of Xanthomonas phaseoli (E.F. Sm.) Dowson. Annals of Applied Biology, 64:65-74.

Sabet KA; Ishag F; Khalil O, 1969. Studies on the bacterial diseases of Sudan crops. VII. New records. Annals of Applied Biology, 63:357-369.

Saettler AE, 1989. Common bacterial blight. In: Schwartz H, Pastor-Corrales MA, eds. Bean production problems in the tropics. Cali, Columbia: CIAT, 261-283.

SAETTLER AW, 1971. Seedling injection as an aid in identifying Bean blight bacteria. Plant Disease Reporter, 55(8):703-706.

Saettler AW, 1991. Common bacterial blight. In: Hall R, ed. Compendium of Bean Diseases. St. Paul, USA: APS Press, 29-30.

Saettler AW; Cafati R; Weller DM, 1986. Nonoverwintering of Xanthomonas bean blight bacteria in Michigan. Plant Disease, 70(4):285-287.

Saettler AW; Perry SK, 1972. Seed-transmitted bacterial diseases in Michigan Navy (pea) beans, Phaseolus vulgaris. Plant Disease Reporter, 56:378-381.

Santana EA; Coyne DP; Beaver JS; Zaiter HZ, 1993. Effect of photoperiod and temperature on common blight disease of common beans (Phaseolus vulgaris L.). Euphytica, 66(3):211-216

Schaad NW, 1988. Laboratory guide for identification of plant pathogenic bacteria. Laboratory guide for identification of plant pathogenic bacteria., Ed. 2:vii + 164 pp.; many ref.

Schaad NW; White WC, 1974. A selective medium for soil isolation and enumeration of Xanthomonas campestris. Phytopathology, 64(6):876-880.

Schuster ML; Coyne DP, 1976. Survival mechanisms of phytopathogenic bacteria, 12:199-221.

Schuster ML; Coyne DP, 1977. Survival of plant parasitic bacteria of plants grown in tropics with emphasis on beans (Phaseolus vulgaris). Fitopatologia Brasileria, 2(2):117-130.

Schuster ML; Coyne DP; Behre T; Leyna G, 1983. Sources of Phaseolus species resistance and leaf and pod differential reactions to common blight. HortScience, 18(6):901-903

Schuster ML; Coyne DP; Hoff B, 1973. Comparative virulence of Xanthomonas phaseoli strains from Uganda, Colombia, and Nebraska. Plant Disease Reporter, 57(1):74-75

Schuster ML; Sayre RM, 1967. A coryneform bacterium induces purple coloured seed and leaf hypertrophy of Phaseolus vulgaris and other Leguminosae. Phytopathology, 57:1064-1067.

Scott ME; Michaels TE, 1992. Xanthomonas resistance of Phaseolus interspecific cross selections confirmed by field performance. HortScience, 27(4):348-350

Sheppard JW, 1983. Historical perspectives of the production of disease-free seed, control and management of bacterial blights of beans in Canada. Seed Science and Technology, 11:885-891.

Sheppard JW; Roth DA; Saettler AW, 1989. Detection of Xanthomonas campestris pv. phaseoli. In: Saettler AW, Schaad NW, Roth DA, eds. Detection of bacteria in seed and other planting material. St. Paul, USA: APS Press, 17-29.

Steadman JR; Maier CR; Schwartz HF; Kerr ED, 1975. Pollution of surface irrigation waters by plant pathogenic organisms. Water Resources Bulletin, American Water Resources Association, 11(4):796-805

SUTTON MD; WALLEN VR, 1970. Epidemiological and ecological relations of Xanthomonas phaseoli and X. phaseoli var. Tuscans on beans in southwestern Ontario, 1961-1968. Canadian Journal of Botany, 48:1329-34.

Sutton MD; Wallen VR, 1970. Epidemiological and ecological relations of Xanthomonas phaseoli and Xanthomonas phaseoli var. fuscans on beans in southwestern Ontario, 1961-1968. Canadian Journal of Botany, 48:1329-1334.

Tar'an B; Michaels TE; Pauls KP, 1998. Stability of the association of molecular markers with common bacterial blight resistance in common bean (Phaseolus vulgaris L.). Plant Breeding, 117(6):553-558; 20 ref.

Tebaldi ND; Souza RM; Machado JC, 2007. Detection of Xanthomonas axonopodis pv. phaseoli in seeds of common bean on semi-selective medium. (Detecção de Xanthomonas axonopodis pv. phaseoli em sementes de feijão em meio de cultura semi seletivo.) Fitopatologia Brasileira, 32(1):56-58. http://www.scielo.br/pdf/fb/v32n1/08.pdf

Thomas CV; Waines JG, 1984. Fertile backcross and allotetraploid plants from crosses between tepary beans and common beans. Journal of Heredity, 75:93-98.

THOMAS WD; GRAHAM RW, 1952. Bacteria in apparently healthy Pinto Beans (a phytopathological note.). Phytopathology, 42(4):214 p.

Torres JP; Silva Jr TAF; Maringoni AC, 2010. Detection of Xanthomonas axonopodis pv. Phaseli in common beans from the state of Paraná (Brazil). Detection of Xanthomonas axonopodis pv. Phaseli in common beans, 35:136-139.

Toth IK; Hyman LJ; Taylor R; Birch PRJ, 1998. PCR-based detection of Xanthomonas campestris pv. phaseoli var. fuscans in plant material and its differentiation from X. c. pv. phaseoli. Journal of Applied Microbiology, 85(2):327-336; 38 ref.

Trujillo GE; Saettler AW, 1979. A combined semi-selective medium and serology test for the detection of Xanthomonas blight bacteria in bean seed. Journal of Seed Technology, 4(2):35-41.

Trujillo GE; Saettler AW, 1980. A liquid semi-selective medium for Xanthomonas phaseoli and X. phaseoli var. fuscans. Michigan State University Agricultural Experiment Station Research Report, 411:8.

Tsvetkov D; Donev Ts, 1984. Testing of antibiotics against Xanthomonas phaseoli (Smith) Dowson on bean. Gradinarska i Lozarska Nauka, 21(7):65-70

Tu JC, 1999. Relationship between disease severity and yield loss of navy bean caused by bacterial blight (Xanthomonas phaseoli). Mededelingen - Faculteit Landbouwkundige en Toegepaste Biologische Wetenschappen, Universiteit Gent, 64(3b):637-642; 14 ref.

Tun S, 1970. Plant protection in Burma. Beitrage zur tropischen und subtropischen landwirtschaft und tropenveternarmedzin, 8:287-294.

Urrea CA; Miklas PN; Beaver JS, 1999. Inheritance of resistance to common bacterial blight in four tepary bean lines. Journal of the American Society for Horticultural Science, 124(1):24-27; 25 ref.

Valarini PJ; Galvao JAH; Oliveira Dde A, 1996. Xanthomonas campestris pv. phaseoli: importance of seed inoculum in the epidemiology of common bacterial blight of French bean. Fitopatologia Brasileira, 21(2):261-267; 29 ref.

Vauterin L; Hoste B; Kersters K; Swings J, 1995. Reclassification of Xanthomonas. International Journal of Systematic Bacteriology, 45(3):472-489

Venette JR; Lamppa RS; Albaugh DA; Nayes JB, 1987. Presumptive procedure (dome test) for detection of seedborne bacterial pathogens in dry beans. Plant Disease, 71(11):984-990

Wallen VR; Jackson HR, 1975. Model for yield loss determination of bacterial blight of field beans utilizing aerial infrared photography combined with field plot studies. Phytopathology, 65(9):942-948

Waterston JM, 1947. The fungi of Bermuda. Bull. Dep. Agric. Bermuda, 23, 305 pp.

Watson DRW, 1970. Bean common blight and fuscous blight in New Zealand. Plant Disease Reporter, 54:1068-1072.

Webster DM; Temple SR; Galvez G, 1983. Expression of resistance to Xanthomonas campestris pv. phaseoli in Phaseolus vulgaris under tropical conditions. Plant Disease, 67(4):394-396

Weller DM; Spttler AW, 1976. Chemical control of common and fuscous bacterial blights in Michigan Navy (pea) beans. Plant Disease Reporter, 60(9):793-797

Weller DM; Spttler AW, 1980. Colonization and distribution of Xanthomonas phaseoli and Xanthomonas phaseoli var. fuscans in field-grown navy beans. Phytopathology, 70(6):500-506

Wilson HA; Lilly VG; Leach JG, 1965. Bacterial polysaccharides, IV: longevity of Xanthomonas phaseoli and Serratia marcescens in bacterial exudates. Phytopathology, 55:1135-1138.

Wong WC, 1990. Production of monoclonal antibodies to Pseudomonas syringae pv. phaseolicola and Xanthomonas campestris pv. phaseoli. Letters in Applied Microbiology, 10(6):241-244

Wong WC, 1991. Methods for recovery and immunodetection of Xanthomonas campestris pv. phaseoli in navy bean seed. Journal of Applied Bacteriology, 71(2):124-129

Xue BG; Goodwin PH, 1994. Amplified DNA polymorphisms of putative two-component regulatory genes of several Xanthomonas campestris pathovars. Canadian Journal of Plant Pathology, 16(1):1-7

Yoshii K, 1980. Common and fuscous blights. In: Schwartz HF, Galvez GE, eds. Bean Production Problems: Disease, Insect, Soil and Climatic Constraints of Phaseolus vulgaris. Cali, Columbia: CIAT, 157-172.

Yoshii K; Galvez GE; Alvarez-Ayala G, 1976. Estimation of yield losses in beans caused by common blight. Proceedings of the American Phytopathological Society, 3:298-299.

Young JM; Saddler GS; Takikawa Y; Boer SHde; Vauterin L; Gardan L; Gvozdyak RI; Stead DE, 1996. Names of plant pathogenic bacteria 1864-1995. Review of Plant Pathology, 75(9):721-763; 10 pp. of ref.

Yu ZH; Stall RE; Vallejos CE, 1998. Detection of genes for resistance to common bacterial blight of beans. Crop Science, 38(5):1290-1296; 36 ref.

Zapata M, 1997. Identification of Xanthomonas campestris pv. phaseoli races in Phaseolus vulgaris leaves. Agronomia Mesoamericana, 8(1):44-52; 52 ref.

Zapata M, 1998. Hypersensitive reaction of tepary bean upon inoculation with the common bean blight pathogen. Journal of Agriculture of the University of Puerto Rico, 81(3/4):181-190; 9 ref.

Zapata M; Freytag GF; Wilkinson RE, 1985. Evaluation for bacterial blight resistance in beans. Phytopathology, 75(9):1032-1039

Zaumeyer WJ, 1930. The bacterial blight of beans caused by Bacterium phaseoli. USDA Technical Bulletin, No. 186, 36 pp.

Zaumeyer WJ; Thomas HR, 1957. A monographic study of bean diseases and methods for their control. United States Department of Agricultural Technical Bulletin, 868.

Distribution References

Beaver J S, Steadman J R, Coyne D P, 1992. Field reaction of landrace components of red mottled beans to common bacterial blight. HortScience. 27 (1), 50-51.

Bradbury J F, 1986. Guide to plant pathogenic bacteria. Farnham Royal, Slough, UK: CAB International. xviii + 332pp.

Brooks F, 2002. List of Plant Diseases in American Samoa 2002. In: Land Grant Technical Report No. 44, Pago Pago, American Samoa, American Samoa Community College Land Grant Program.

CABI, EPPO, 2007. Xanthomonas axonopodis pv. phaseoli. [Distribution map]. In: Distribution Maps of Plant Diseases, Wallingford, UK: CABI. Map 401 (Edition 4).

CABI, Undated. CABI Compendium: Status as determined by CABI editor. Wallingford, UK: CABI

Chen HongYu, Xu XinXin, Duan CanXing, Wang ShuMin, Zhu ZhenDong, 2012. Identification of pathogens causing common bacterial blight on common bean (Phaseolus vulgaris L.). Scientia Agricultura Sinica. 45 (13), 2618-2627. http://www.ChinaAgriSci.com

EPPO, 2014. EPPO Global database (available online). Paris, France: EPPO. https://gd.eppo.int/

EPPO, 2020. EPPO Global database. In: EPPO Global database, Paris, France: EPPO.

Girard J C, 1991. Rapport Annuel - CIRAD Réunion. Saint Denis, France: CIRAD. 74-75.

IPPC, 2008. First outbreak of Xanthomonas axonopodis pv. phaseoli in the Czech Republic. In: IPPC Official Pest Report, Rome, Italy: FAO. https://www.ippc.int/IPP/En/default.jsp

Mondal K K, 2004. Integrated management strategies for fuscous blight and floury leaf spot of rajmash. Indian Phytopathology. 57 (2), 135-139.

Naumann K, Karl H, 1985. On two bacterial plant diseases recorded for the first time in the GDR in leguminous crops. (Über zwei erstmalig in der DDR festgestellte bakterielle Pflanzenkrankheiten in Leguminosenbeständen.). Nachrichtenblatt für den Pflanzenschutz in der DDR. 39 (12), 244-246.

NPPO of the Netherlands, 2013. Pest status of harmful organisms in the Netherlands., Wageningen, Netherlands:

Osdaghi E, 2014. Occurrence of common bacterial blight on mungbean (Vigna radiata) in Iran caused by Xanthomonas axonopodis pv. phaseoli. New Disease Reports. 9. http://www.ndrs.org.uk/article.php?id=030009 DOI:10.5197/j.2044-0588.2014.030.009

Osdaghi E, Zademohamad A A, 2016. Phaseolus lunatus, a new host of Xanthomonas axonopodis pv. phaseoli in Iran. Journal of Phytopathology. 164 (1), 56-60. http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1439-0434 DOI:10.1111/jph.12379

Pazos V, Hevesi M, 1975. Common blight of beans. Rev. Cenic. Cienc. Biol. 6 (2), 291-294.

Rajappan K, Ramaraj B, Natarajan S, 2000. Field evaluation of fungicides and neem formulations against bacterial blight of Frenchbean. Indian Phytopathology. 53 (3), 303-304.

TUN S, 1970. Plant protection in Burma. Beitrage zur tropischen Landwirtschaft und Veterinarmedizin. 8 (4), 287-294.

WATSON D R W, 1970. Bean common blight and fuscous blight in New Zealand. Plant Disease Reporter. 54 (12), 1068-1072.

Distribution Maps

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