Xanthomonas axonopodis pv. vasculorum (sugarcane gumming disease)
- Taxonomic Tree
- Notes on Taxonomy and Nomenclature
- Distribution Table
- Risk of Introduction
- Hosts/Species Affected
- Host Plants and Other Plants Affected
- Growth Stages
- List of Symptoms/Signs
- Biology and Ecology
- Pathway Vectors
- Plant Trade
- Wood Packaging
- Detection and Inspection
- Similarities to Other Species/Conditions
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Xanthomonas axonopodis pv. vasculorum (Cobb 1894) Vauterin et al. 1995
Preferred Common Name
- sugarcane gumming disease
Other Scientific Names
- Bacillus vasculorum Cobb 1893
- Bacterium vasculorum (Cobb) Migula 1900
- Phytomonas vasculara (Cobb) Bergey
- Phytomonas vasculorum (Cobb) Bergey et al. 1923
- Pseudomonas vasculorum (Cobb) Smith 1901
- Xanthomonas axonopodis subsp. vasculorum
- Xanthomonas campestris pv. vasculorum (Cobb 1894) Dye 1978
- Xanthomonas campestris subsp. vasculorum
- Xanthomonas vasculorum (Cobb) Dowson 1939
International Common Names
- English: bacterial leaf streak of corn; gumming disease of sugar cane; gummosis
- Spanish: gomosis de la caña
- French: gommose
Local Common Names
- Germany: Cobb'sche Krankheit: Zuckerrohr; Gummikrankheit: Zuckerrohr; Schleimkrankheit: Zuckerrohr
- XANTVA (Xanthomonas axonopodis pv. vasculorum)
Taxonomic TreeTop of page
- Domain: Bacteria
- Phylum: Proteobacteria
- Class: Gammaproteobacteria
- Order: Xanthomonadales
- Family: Xanthomonadaceae
- Genus: Xanthomonas
- Species: Xanthomonas axonopodis pv. vasculorum
Notes on Taxonomy and NomenclatureTop of page
Xanthomonas campestris is a species established on the basis of a common phenotype, and divided into more than 125 pathovars on the basis of pathogenicity to one or more host plants (Dye et al., 1980). A reclassification of Xanthomonas was recently proposed by Vauterin et al. (1995). The previously described species Xanthomonas campestris was divided into 16 DNA homology groups. The groups A and B of Vauterin et al. (1992), which appeared similar to the groups identified by Stead (1989) and Péros et al. (1994), were reclassified as X. axonopodis pv. vasculorum and X. vasicola pv. vasculorum, respectively. Strains isolated from sugarcane have characteristic symptoms of gumming. The current preferred name for this species is X. axonopodis pv. vasculorum.
DescriptionTop of page
X. axonopodis pv. vasculorum is aerobic, Gram-negative, a capsulate rod, approximately 0.4-0.5 x 1-1.5 µm. It occurs singly, in pairs or short chains and is motile with one polar flagellum. Cells are non-spore forming and surrounded by xanthan gum. The colonies on nutrient agar are smooth, glistening, round, yellow and butyrous. On medium with carbohydrate, copious mucoid growth usually develops (Bradbury, 1973).
DistributionTop of page
X. axonopodis pv. vasculorum is currently not observed in several areas where it was widely reported in the past (Australia, Fiji, Central America and the Caribbean). It may be that the local conditions and use of resistant cultivars have combined to eradicate the pathogen in these regions (Bradbury, 1973). Gumming is a problem only in Mauritius and Reunion where resistance to the pathogen is still an objective in breeding programmes.
Distribution TableTop of page
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.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|India||Absent, unreliable record||Ricaud et al., 1983; Bradbury, 1986; EPPO, 2014|
|Indonesia||Absent, unreliable record||EPPO, 2014|
|Ghana||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Madagascar||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Malawi||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Mauritius||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Mozambique||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Réunion||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|South Africa||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Swaziland||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Zimbabwe||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Mexico||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|USA||Present||Present based on regional distribution.|
|-Colorado||Present||Jackson-Ziems et al., 2016||bacterial leaf streak of corn|
|-Illinois||Present||Jackson-Ziems et al., 2016||bacterial leaf streak of corn|
|-Iowa||Present||Jackson-Ziems et al., 2016||bacterial leaf streak of corn|
|-Kansas||Present||Jackson-Ziems et al., 2016||bacterial leaf streak of corn|
|-Nebraska||Present||Jackson-Ziems et al., 2016||bacterial leaf streak of corn|
Central America and Caribbean
|Antigua and Barbuda||Present||CABI and EPPO, 1999; EPPO, 2014|
|Barbados||Absent, formerly present||CABI and EPPO, 1999; EPPO, 2014|
|Belize||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Cuba||Present||CABI and EPPO, 1999; EPPO, 2014|
|Dominica||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Dominican Republic||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Guadeloupe||Present||CABI and EPPO, 1999; EPPO, 2014|
|Jamaica||Present||CABI and EPPO, 1999; EPPO, 2014|
|Martinique||Present||CABI and EPPO, 1999; EPPO, 2014|
|Panama||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Puerto Rico||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Saint Kitts and Nevis||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Saint Lucia||Absent, formerly present||CABI and EPPO, 1999; EPPO, 2014|
|Saint Vincent and the Grenadines||Absent, formerly present||CABI and EPPO, 1999; EPPO, 2014|
|Trinidad and Tobago||Present||CABI and EPPO, 1999; EPPO, 2014|
|Argentina||Restricted distribution||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|Brazil||Absent, formerly present||188*||Bradbury, 1986; Ricaud and Autrey, 1989; CABI and EPPO, 1999; EPPO, 2014|
|-Pernambuco||Absent, formerly present||EPPO, 2014|
|Colombia||Present||Bradbury, 1986; CABI and EPPO, 1999; EPPO, 2014|
|French Guiana||Present||Bradbury, 1986; EPPO, 2014|
|Portugal||Absent, unreliable record||EPPO, 2014|
|-Madeira||Absent, unreliable record||EPPO, 2014|
|Australia||Absent, formerly present||CABI and EPPO, 1999; EPPO, 2014|
|-New South Wales||Absent, formerly present||Ricaud and Autrey, 1989; CABI and EPPO, 1999; EPPO, 2014|
|-Queensland||Eradicated||Ricaud and Autrey, 1989; CABI and EPPO, 1999; EPPO, 2014|
|Fiji||Absent, formerly present||Bradbury, 1986; Ricaud and Autrey, 1989; CABI and EPPO, 1999; EPPO, 2014|
|Papua New Guinea||Present||CABI and EPPO, 1999; EPPO, 2014|
Risk of IntroductionTop of page
There are quarantine restrictions on X. axonopodis pv. vasculorum in the Mascareigne islands. The neighbouring East African countries are anxious to exclude new strains from the Mascareignes (Bradbury, 1973).
Hosts/Species AffectedTop of page
Natural infection of X. axonopodis pv. vasculorum appears to be restricted to sugarcane (Saccharum spp.), maize (Zea mays), Guatemala grass (Tripsacum laxum), broom bamboo (Thysanolaena latifolia) and three palms, hurricane palm (Dictyosperma album), royal palm (Roystonea regia) and nut palm (Areca catechu). The following plants were infected after artificial inoculation: tall bamboo (Bambusa vulgaris), para grass (Bracharia mutica), coconut palm (Cocos nucifera), Job's tears (Coix lachryma-jobi), guinea grass (Panicum maximum), elephant grass (Pennisetum purpureum), Johnson grass (Sorghum halepense), sweet sorghum (Sorghum arundinaceum) and sorghum (S. bicolor) (Hughes, 1939; Orian, 1941).
Sugarcane appears to be the most susceptible host, infection of other host plants being induced under conditions of high inoculum potential (Ricaud and Autrey, 1989). In addition, comparison of strains isolated from sugarcane or from other hosts indicated that different xanthomonads are implicated (Péros et al., 1994; Dookun et al., 2000).
Host Plants and Other Plants AffectedTop of page
|Areca catechu (betelnut palm)||Arecaceae||Wild host|
|Bambusa vulgaris (common bamboo)||Poaceae||Wild host|
|Cocos nucifera (coconut)||Arecaceae||Wild host|
|Coix lacryma-jobi (Job's-tears)||Poaceae||Wild host|
|Megathyrsus maximus (Guinea grass)||Poaceae||Wild host|
|Panicum miliaceum (millet)||Poaceae||Wild host|
|Pennisetum purpureum (elephant grass)||Poaceae||Wild host|
|Roystonea regia (cuban royal palm)||Arecaceae||Other|
|Saccharum officinarum (sugarcane)||Poaceae||Main|
|Sorghum bicolor (sorghum)||Poaceae||Wild host|
|Sorghum halepense (Johnson grass)||Poaceae||Wild host|
|Sorghum sudanense (Sudan grass)||Poaceae||Wild host|
|Thysanolaena latifolia (Asian broom grass)||Poaceae||Wild host|
|Zea mays (maize)||Poaceae||Other|
Growth StagesTop of page Vegetative growing stage
SymptomsTop of page There are two distinct phases: the foliar stage and the systemic stage. On leaves, streaks 3-6 mm wide arise from the leaf margin and develop along the vascular bundles towards the base. Streaks are yellow to orange with red flecks, becoming necrotic and grey with age. The necrosis may involve large areas of leaf. A few short streaks are observed in resistant cultivars or when environmental conditions are not favourable for the disease.
On highly susceptible cultivars and when conditions are favourable, the bacterium progresses down the lamina and the sheath, and infects the stalk. The systemic stage of the disease is characterized by a reddish discoloration of the vascular bundles at the nodes, and by a bacterial slime. Gum pockets are formed and the slime exudes from the cut surface of the stalks. Stalk deformation and knife-cut lesions due to transverse splits in young elongating tissue can also be observed. When conditions are not favourable for cane growth, the formation of the gum pockets near the apex and in the leaf spindle results in the death of the growing point. Another characteristic of the systemic stage of the disease is the partial or total chlorosis of new leaves in mature canes. Chlorosis can also occur in young ratoons as a result of transmission by contaminated leaves.
List of Symptoms/SignsTop of page
|Leaves / abnormal colours|
|Leaves / necrotic areas|
|Stems / internal discoloration|
|Stems / internal red necrosis|
|Stems / ooze|
Biology and EcologyTop of page
The introduction of X. axonopodis pv. vasculorum into new areas is a result of planting diseased cuttings. The pathogen is spread from plant to plant by wind-driven rains. High levels of humidity and warm temperatures are needed for the exudation of inoculum from infected leaves as well as for the entry of the pathogen into new leaves wounded by the shearing action of their saw-tooth edges and the wind. Transmission is also achieved by cane knifes when young shoots are cut above their growing point (Ricaud, 1969). This latter mode of transmission appears responsible for the white chlorosis observed in young ratoon crops. Agricultural tools, workers, animals and flies may also carry the inoculum, but these modes of transmission are not considered as significant.
The violent wind and rain during cyclones are ideal conditions for infection. High temperature during the growing season favours the disease. Epidemics are particularly severe when late cyclones immediately precede the early start of a dry and cool maturing season (Ricaud and Autrey, 1989). These latter conditions appear very favourable to the systemic infection as they lower the plant resistance.
Plant TradeTop of page
|Plant parts liable to carry the pest in trade/transport||Pest stages||Borne internally||Borne externally||Visibility of pest or symptoms|
|Bulbs/Tubers/Corms/Rhizomes||Yes||Pest or symptoms usually invisible|
|Leaves||Yes||Pest or symptoms usually visible to the naked eye|
|Roots||Yes||Pest or symptoms usually invisible|
|Seedlings/Micropropagated plants||Yes||Pest or symptoms usually invisible|
|Stems (above ground)/Shoots/Trunks/Branches||Yes||Yes||Pest or symptoms usually visible to the naked eye|
|Wood||Yes||Pest or symptoms usually visible to the naked eye|
|Plant parts not known to carry the pest in trade/transport|
|Fruits (inc. pods)|
|Growing medium accompanying plants|
|True seeds (inc. grain)|
Wood PackagingTop of page
|Wood Packaging liable to carry the pest in trade/transport||Timber type||Used as packing|
|Wood Packaging not known to carry the pest in trade/transport|
|Loose wood packing material|
|Processed or treated wood|
|Solid wood packing material with bark|
|Solid wood packing material without bark|
ImpactTop of page
In the past, gumming was a major disease of sugarcane in Australia, Mauritius and Reunion. Severe epidemics occurred in Australia where reductions of 30-40% in cane tonnage and 9-17% in sugar content were reported between 1893 and 1899 (North, 1935). In the 1890s, heavy losses were also observed in Mauritius and susceptible cultivars were abandoned. Besides the losses in the field, gumming causes problems in the milling process, resulting in a lower sugar recovery.
The economic importance of the disease decreased when the susceptible noble canes were replaced by inter-specific hybrids in the 1930s (Ricaud and Autrey, 1989). This led to the eradication of the pathogen from Australia, Fiji, Brazil and the West Indies. In the Mascareigne islands, there has been evidence of some losses in the hybrids, especially when the cultivars are susceptible to the systemic infection (Ricaud, 1969). During the 1980-1981 epidemic, sugar yields from systemically infected stalks of cv. M377/56 were found to be 19.5% lower than from stalks with foliar streaks only (Ricaud and Autrey, 1989). A decrease in sugar yield of up 45% was reported in cv. M377/56 after inoculation in field trials (Autrey et al., 1986).
In the Mascareigne islands, the need to include resistance to gumming in breeding schemes and the replacement of cultivars which show susceptibility, increases the economic impact of this pathogen. For instance, in Réunion the popular cultivar R397 represented 60% of sugarcane production in 1958, but was then abandoned following a severe epidemic of X. axonopodis pv. vasculorum.
DiagnosisTop of page
X. axonopodis pv. vasculorum may be isolated from leaf blade portions showing the streak symptoms. After surface sterilization, streak portions may be shredded in a drop of sterile water. The resulting suspension is then spread into plates containing yeast extract peptone glucose agar (YPGA) or Wilbrink's agar. The development of pale yellow mucoid colonies within 3-4 days is characteristic of X. axonopodis pv. vasculorum.
According to Hayward (1962) and Bradbury (1973) the bacterium liquefies gelatin, hydrolyses starch, does not reduce nitrate to nitrite, produces ammonia and H2S but not indole, and turns litmus milk alkaline. On synthetic media or media low in peptone, it produces acid aerobically without gas from arabinose, cellobiose, fructose, galactose, glucose, glycerol, mannose, sucrose and xylose, but not from adonitol, dulcitol, alpha-methyl-glucoside, maltose, mannitol, inulin, rhamnose, salicin and sorbitol. The use of lactose and raffinose varies among the isolates. Salts of acetic, citric, lactic, malic, propionic and succinic acids can be used as carbon sources, but not those of benzoic, gluconic, oxalic and tartaric acids. Asparigine is not used as a carbon and nitrogen source simultaneously. The tests are positive for Simmon's citrate, catalase and lipase, and negative for Christensen's urease, Kovacs oxidase and tyrosinase. The bacterium hydrolysed aesculin, but not sodium hippurate. There are conflicting results for hydrolysis of pectate gel. Péros et al. (1994) indicated that the bacterium is not able to use L-fucose and hydrolyse casein only weakly. The tolerance for NaCl ranges from 3-5%. The maximum temperature for growth is 37-39°C (optimum 28°C and minimum 5°C). The thermal death point is 50°C according to Bradbury (1973), but some isolates have been found still viable at 65°C (Ricaud and Autrey, 1989).
Specific antisera have been produced in Taiwan (Wu et al., 1977), Mauritius (Anon., 1983; Dookun et al., 1996) and in Réunion. The immunofluorescence method has been proved useful for the diagnosis of the pathogen. X. axonopodis pv. vasculorum may also be characterized by gas chromatography of fatty acid methyl esters (Stead, 1989; Vauterin et al., 1992; Péros et al., 1994; Dookun et al., 2000) or DNA analysis (Saumtally and Autrey, 1990; Qhobela and Claflin, 1992; Vauterin et al., 1992; Péros et al., 1994).
Much heterogeneity exists in the population of the gumming bacterium. In Mauritius and Réunion island, where gumming disease is still a problem, three races named race 1, race 2 and race 3 or three types (A, B and C) are described (Ricaud and Autrey, 1989; Péros et al., 1994). Quobela and Claflin (1992) compared Eastern and South African strains of the gumming bacterium using RFLP and confirmed two distinct geographical groups. Vauterin et al. (1995) recognized two major groups on the basis of DNA-DNA hybridization analysis. On the other hand, when comparing a wider range of isolates using DNA-based techniques and fatty acid profiling, five groups of the pathogen were described (Saumtally and Dookun, 2000; Dookun et al., 2000) and a renaming of some of the groups proposed.
Detection and InspectionTop of page Microscopic examination of a leaf portion mounted in water will reveal a profuse concentric exudation of bacteria and slime from the cut end of vascular bundles. The systemic stage can be easily recognized by the presence of gum pockets and the exudation of slime from the cut surface of infected stalks.
Similarities to Other Species/ConditionsTop of page
Foliar streaks of gumming may be confused with those of leaf scald (Xanthomonas albilineans) and sugarcane chlorotic streak. The leaf chlorosis in young ratoon is indistinguishable from that of leaf scald. In South Africa and Zimbabwe, stalks with systemic infection may show red stripes which look like those induced by Acidovorax avenae subsp. avenae.
Prevention and ControlTop of page
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.
The degree of cultivar susceptibility is often revealed during an epidemic. Then, the planting of highly susceptible cultivars is prohibited and their replacement is undertaken. The speed of the cultivar replacement depends on the availability of resistant cultivars with acceptable yield. The breeding schemes in Mauritius and Réunion include the resistance to gumming as an important objective.
Resistance to foliar infection and tolerance to systemic infection appear independently controlled genetically (North, 1935; Ricaud, 1969). In areas where there is a risk of epidemics, the planting of cultivars with foliar susceptibility should be avoided. When environmental conditions are conducive to epidemics, such cultivars facilitate the increase in inoculum pressure and the selection of strains with higher pathogenicity. The losses encountered during an epidemic are directly related to the tolerance to systemic infection.
Interspecific hybridization has been very successful in the control of many sugarcane diseases and gumming has been eradicated from areas where resistant cultivars have been grown. Resistance to the disease appears governed by a few major genes rather than a polygenic system (Stevenson, 1965). This could explain the resistance failure of some cultivars after the appearance of new pathogenic strains (Antoine and Pérombelon, 1965; Ricaud and Sullivan, 1974). Evidence of variation in X. axonopodis pv. vasculorum has accumulated over the years from different parts of the world (Ricaud and Autrey, 1989). Phenotypic differences between the eastern and southern African strains were observed by Hayward (1962) and confirmed at the DNA and membrane protein levels by Qhobela and Claflin (1992). Phenotypic and pathogenic differences were also recorded in Mauritius and in Réunion. It has been suggested that three races of the pathogen have been involved in the epidemics observed in Mauritius (Anon, 1983). However, the inoculation of the putative differential cultivars in controlled conditions revealed that the different morphological types of strains varied in aggressiveness, not in virulence (Péros, 1988). The variability of the pathogen requires the evaluation of resistance of new genotypes of sugarcane against all prevailing strains.
The screening method developed by North (1935) in Australia is still used in Mauritius. Test varieties are planted between rows of a susceptible cultivar, which is inoculated. The disease spreads from the inoculated plants and the natural infection of the test varieties is rated during peak infection in the maturing season. Replication of the resistance tests permit accurate assessment of the behaviour of the promising varieties. However, the field trials are space and time consuming and need environmental conditions favourable for the disease to spread. Other methods have been investigated to complement the field trials and for a more rapid screening. Inoculation of detached leaves was found reliable but laborious (Anon., 1973). The inoculation of potted plants in the greenhouse was performed and gave results in accordance with field behaviour (Girard and Péros, 1987). Péros and Lombard (1992) induced the development of the disease in plantlets inoculated in vitro. However, the weak expression of the foliar symptoms appeared to limit the use of the in vitro test.
The rapid spread of X. axonopodis pv. vasculorum from infection foci limits the use of control methods based on sanitation (Ricaud and Autrey, 1989). Sanitation control includes: the use of seed cane from fields without systemic infection; the eradication of volunteer stools of susceptible cultivars and alternative hosts when replanting; and disinfection of knives and harvesters to avoid mechanical spread. Thermotherapy, which is used to control other pathogens of sugarcane, can also be used. However, the treatment (50°C for 30 minutes, and 2-3 hours the next day at the same temperature) will not completely cure the planting material. Disease-free plantlets can be produced by tissue culture techniques.
ReferencesTop of page
Anon., 1973. Annual Report 1972. Mauritius: Mauritius Sugar Industry Research Institute.
Anon., 1983. Annual Report 1982. Mauritius: Mauritius Sugar Industry Research Institute.
Antoine R; PTrombelon M, 1965. Canes diseases: 2. gumming disease. In: Annual Report 1964. Mauritius: Mauritius Sugar Industry Research Institute.
Autrey LJC; Dhayan S; Sullivan S, 1986. Effect of race three of gumming disease pathogen on growth and yield in two sugar cane varieties. Proceedings of the International Society of Sugar Cane Technologists, 19:420-428.
Dookun A; Autrey LJC; Jones P, 1996. Monoclonal antibodies specific to race 1 of Xanthomonas campestris pv. vasculorum, causal agent of gumming disease of sugarcane. Proceedings of the International Society of Sugar Cane Technologists, 22:380-389.
Dookun A; Stead DE; Autrey LJC, 2000. Variation among strains of Xanthomonas campestris pv. vasculorum from Mauritius and other countries based on fatty acid analysis. Systematic and Applied Microbiology, 23(1):148-155; 17 ref.
Dye DW; Bradbury JF; Goto M; Hayward AC; Lelliott RA; Schroth MN, 1980. International standards for naming pathovars of phytopathogenic bacteria and a list of pathovar names and pathotype strains. Review of Plant Pathology, 59(4):153-168
EPPO, 2014. PQR database. Paris, France: European and Mediterranean Plant Protection Organization. http://www.eppo.int/DATABASES/pqr/pqr.htm
Girard JC; JP PTros, 1987. Une mTthode d'Tvaluation en serre de la rTsistance de la canne à sucre à la gommose. L'Agronomie Tropicale, 42:126-130.
Hayward AC, 1962. Studies on bacterial pathogens of sugarcane. 1. Differentiation of isolates of Xanthomonas vasculorum with notes on an undescribed Xanthomonas sp. from sugar cane in Natal and Trinidad. Mauritius Sugar Industry Research Institute, Occasional Paper, 13:1-12.
Hughes CG, 1939. Alternate hosts of Bacterium vasculorum, the causal agent of gumming disease of sugar cane. Bureau of the Sugar Experiment Station, Queensland, Technical Communication 1939 No. 3.
Jackson-Ziems T; Korus K; Adesemoye T; Meter Jvan, 2016. Bacterial Leaf Streak of Corn Confirmed in Nebraska, Other Corn Belt States. Cropwatch. Institute of Agriculture and Natural Resources. Lincoln, USA: University of Nebraska-Lincoln. http://cropwatch. Cropwatch. Institute of Agriculture and Natural Resources. Lincoln, USA: University of Nebraska-Lincoln. http://cropwatch.unl.edu/2016/bacterial-leaf-streak-corn-confirmed-nebraska
North DS, 1935. The gumming disease of the sugar cane, its dissemination and control. Agricultural Report No. 10. Sydney, Australia: Colonial Refining Co. Ltd.
Orian G, 1941. Hosts of the sugar cane disease organism. Revue Agricole et SucriFre de l'Ile Maurice, 20:19-58.
Peros JP, 1988. Variability in colony type and pathogenicity of the causal agent of sugarcane gumming Xanthomonas campestris pv. vasculorum (Cobb) Dye. Zeitschrift fur Pflanzenkrankheiten und Pflanzenschutz, 95(6):591-598
Peros JP; Girard JC; Lombard H; Janse JD; Berthier Y, 1994. Variability of Xanthomonas campestris pv. vasculorum from sugarcane and other Gramineae in Reunion Island. Characterization of a different xanthomonad. Journal of Phytopathology, 142(3-4):177-188
Peros JP; Lombard H, 1992. In vitro evaluation of sugarcane resistance to gumming disease and of Xanthomonas campestris pv. vasculorum aggressiveness. Plant Cell, Tissue and Organ Culture, 29(2):145-151
Qhobela M; Claflin LE, 1992. Eastern and southern African strains of Xanthomonas campestris pv. vasculorum are distinguishable by restriction fragment length polymorphism of DNA and polyacrylamide gel electrophoresis of membrane proteins. Plant Pathology, 41(2):113-121
Ricaud C, 1969. Investigation on the systemic infection of gumming disease. Proceedings of the International Society of Sugar Cane Technologists, 13:1159-1169.
Ricaud C; Autrey LJC, 1989. Gumming disease. In: Ricaud C, Egan BT, Gillaspie AG Jr,. Hugues CG, eds. Diseases of sugarcane. Major diseases. Amsterdam, The Netherlands: Elsevier, 21-38.
Ricaud C; Bailey RA; Egan BT; Gillaspie AG Jr; Matsuoda S, 1983. Sugarcane diseases and their world distribution. Proceedings of the International Society of Sugar Cane Technologists, 18:27-68.
Ricaud C; Sullivan S, 1974. Further evidence of population shift in the gumming disease pathogen in Mauritius. Proceedings of the International Society of Sugar Cane Technologists, 17:42-44.
Rott P; Girard JC, 2000. Sugar cane producing countries/locations and their diseases. In: Rott P, Bailey RA, Comstock JC, Croft BJ, Saumtally AS, eds. A Guide to Sugar Cane Diseases. CIRAD and ISSCT, 323-336.
Saumtally S; Dookun A, 2000. Gumming. In: Rott P, Bailey RA, Comstock JC, Croft BJ, Saumtally AS, eds. A Guide to Sugar Cane Diseases. CIRAD and ISSCT, 32-37.
Stevenson GC, 1965. Genetics of breeding of sugar cane. London, UK: Longmans, Green and Co. Ltd.
Vauterin L; Yang P; Hoste B; Pot B; Swings J; Kersters K, 1992. Taxonomy of xanthomonads from cereals and grasses based on SDS-PAGE of proteins, fatty acid analysis and DNA hybridization. Journal of General Microbiology, 138(7):1467-1477
Distribution MapsTop of page
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