Puccinia kuehnii (orange rust)
- Summary of Invasiveness
- Taxonomic Tree
- Notes on Taxonomy and Nomenclature
- Distribution Table
- History of Introduction and Spread
- Risk of Introduction
- Hosts/Species Affected
- Growth Stages
- List of Symptoms/Signs
- Biology and Ecology
- Natural enemies
- Means of Movement and Dispersal
- Plant Trade
- Wood Packaging
- Impact Summary
- Environmental Impact
- Impact: Biodiversity
- Social Impact
- 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
- Puccinia kuehnii (W. Krüger) E.J. Butler 1914
Preferred Common Name
- orange rust
Other Scientific Names
- Uromyces kuehnii W. Krüger 1890
International Common Names
- English: rust: sugarcane; sugarcane leaf rust; sugarcane rust
- Spanish: roya de la cana; roya de la cana de azucar
- French: rouille de la canne a sucre
Local Common Names
- Germany: Rost: Zuckerrohr
- PUCCKU (Puccinia kuehnii)
Summary of InvasivenessTop of page P. kuehnii is easily spread by wind and wind-blown rain. The recent detection and severe incidence of the disease in central Queensland crops (latitude 20°S) was followed by spread to latitudes 16.5 to 24.0°S within 12 months. This indicates the rapid capability of the pathogen to spread. With a large area planted to a susceptible cultivar, the disease quickly established itself and became endemic in the areas to which it spread. The disease caused large losses in commercial sugarcane crops and losses as high as 35-40% have been reported (Magarey et al., 2003; Staier et al., 2003). The epiphytotic caused severe financial hardship to both sugarcane farmers and the factories processing the sugarcane crop. Financial losses have been put at Aus$200 million with the losses in Australia in the 2000-harvested crop recognized as the largest single season losses caused by a disease in the history of the Australian sugarcane industry (Magarey et al., 2002b).
Taxonomic TreeTop of page
- Domain: Eukaryota
- Kingdom: Fungi
- Phylum: Basidiomycota
- Subphylum: Pucciniomycotina
- Class: Pucciniomycetes
- Order: Pucciniales
- Family: Pucciniaceae
- Genus: Puccinia
- Species: Puccinia kuehnii
Notes on Taxonomy and NomenclatureTop of page The fungus was originally described as Uromyces kuehnii (Krüger, 1890). The name was changed to Uredo kuehnii (Wakker and Went, 1898), then reclassified as Puccinia kuehnii (Butler, 1918). Puccinia melanocephala Syd. & P. Syd. is a closely related species.
DescriptionTop of page The following description is based on descriptions and reports by Butler (1918), Laundon and Waterson (1964a, b), Cummins (1971) and Ryan and Egan (1989).
The uredinia are amphigenous, sometimes only hypophyllous, usually orange to yellowish-brown but sometimes cinnamon-brown when older, linear, up to 1.5 mm long. Paraphyses are usually inconspicuous and peripheral, cylindrical to capitate, up to 45 µm long, thin-walled (1-2 µm) and hyaline to pale brown. Urediniospores are mostly obovoid or pyriform, sometimes ellipsoidal, very variable in size, 25-57 x 17-34 µm, with walls golden to orange or cinnamon-brown, 1-2 µm thick laterally, but usually with a pronounced apical thickening to 5 µm or more, and with four or five equatorial germ pores. The spores are moderately echinulate, the spines being 3-4 µm apart, not clustered at the pore caps and not regularly placed.
Telia are hypophyllous, small, blackish, linear and rarely present; only Butler (1918) seems to have found them. Paraphyses are similar to those in uredinia. The teliospores are oblong to clavate, rounded at the apex, two-celled and not constricted at the septa, with pale-yellow walls not thickened apically, 25-40 x 10-18 µm, and borne on short, hyaline pedicels. Spermogonia and aecia are unknown. Other descriptions of morphology are provided by Mordue (1985), Fang et al. (1986) and Coutinho et al. (1991).
DistributionTop of page The disease is limited to the Asia-Oceania region (Egan, 1981; Koike, 1986; Ryan and Egan, 1989; Suma and Pais, 1996), the pathogen most probably originating in those countries comprising the centre of diversity for Saccharum species. It should be noted that older reports of the disease in Africa and South America were incorrect because there was confusion with brown (common) rust caused by Puccinia melanocephala (Bailey, 1979; Egan, 1979; Liu and Bernard, 1979; Ricaud and Autrey, 1979; Ryan and Egan, 1989). In countries in Asia-Oceania, it is not difficult to find the disease on one of its hosts during seasons favouring pathogen colonization.
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|
|China||Present||Ryan and Egan, 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|-Hong Kong||Present||CABI/EPPO, 2015|
|India||Present||Ryan and Egan, 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|-Andaman and Nicobar Islands||Present||EPPO, 2014; CABI/EPPO, 2015|
|-Andhra Pradesh||Present||CABI/EPPO, 2015|
|-Indian Punjab||Present||CABI/EPPO, 2015|
|-Tamil Nadu||Present||CABI/EPPO, 2015|
|-Uttar Pradesh||Present||CABI/EPPO, 2015|
|Indonesia||Widespread||Ryan and Egan, 1989; EPPO, 2014; CABI/EPPO, 2015|
|-Irian Jaya||Present||Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|-Java||Present||Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|-Kalimantan||Present||EPPO, 2014; CABI/EPPO, 2015|
|-Moluccas||Present||EPPO, 2014; CABI/EPPO, 2015|
|-Nusa Tenggara||Present||CABI/EPPO, 2015|
|-Sulawesi||Present||EPPO, 2014; CABI/EPPO, 2015|
|-Sumatra||Present||Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Japan||Present||Ryan and Egan, 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|-Honshu||Present||EPPO, 2014; CABI/EPPO, 2015|
|-Ryukyu Archipelago||Present||EPPO, 2014; CABI/EPPO, 2015|
|Malaysia||Present||Ryan and Egan, 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|-Peninsular Malaysia||Present||EPPO, 2014; CABI/EPPO, 2015|
|-Sabah||Present||EPPO, 2014; CABI/EPPO, 2015|
|Myanmar||Present||Ricaud et al., 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Pakistan||Present||Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Philippines||Present||Ryan and Egan, 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Sri Lanka||Present||Ricaud et al., 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Taiwan||Present||Ricaud et al., 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Thailand||Present||Ricaud et al., 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Vietnam||Present||Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Cameroon||Restricted distribution||EPPO, 2014; CABI/EPPO, 2015|
|Côte d'Ivoire||Restricted distribution||EPPO, 2014; CABI/EPPO, 2015|
|Mauritius||Absent, invalid record||CABI/EPPO, 2015|
|Mozambique||Absent, invalid record||CABI/EPPO, 2015|
|South Africa||Absent, invalid record||EPPO, 2014; CABI/EPPO, 2015|
|Mexico||Restricted distribution||Flores et al., 2009; NAPPO, 2010; EPPO, 2014; CABI/EPPO, 2015|
|USA||Restricted distribution||EPPO, 2014; CABI/EPPO, 2015|
|-Florida||Widespread||Comstock et al., 2008; EPPO, 2014; CABI/EPPO, 2015|
|-Louisiana||Present, few occurrences||Grisham et al., 2013; CABI/EPPO, 2015|
Central America and Caribbean
|Costa Rica||Present||Chavarría et al., 2009; EPPO, 2014; CABI/EPPO, 2015|
|Cuba||Restricted distribution||EPPO, 2014; CABI/EPPO, 2015|
|Dominican Republic||Restricted distribution||Briggs et al., 2014; EPPO, 2014; CABI/EPPO, 2015|
|El Salvador||Restricted distribution||Flores et al., 2009; EPPO, 2014; CABI/EPPO, 2015|
|Guatemala||Restricted distribution||Ovalle et al., 2008; EPPO, 2014; CABI/EPPO, 2015|
|Jamaica||Present||EPPO, 2014; CABI/EPPO, 2015|
|Nicaragua||Present||Chavarría et al., 2009; EPPO, 2014; CABI/EPPO, 2015|
|Panama||Restricted distribution||Flores et al., 2009; EPPO, 2014; CABI/EPPO, 2015|
|Brazil||Restricted distribution||IPPC, 2010; EPPO, 2014; CABI/EPPO, 2015|
|-Espirito Santo||Present||EPPO, 2014; CABI/EPPO, 2015|
|-Goias||Restricted distribution||EPPO, 2014; CABI/EPPO, 2015|
|-Mato Grosso||Restricted distribution||EPPO, 2014; CABI/EPPO, 2015|
|-Mato Grosso do Sul||Present||EPPO, 2014; CABI/EPPO, 2015|
|-Minas Gerais||Present||EPPO, 2014; CABI/EPPO, 2015|
|-Parana||Present||EPPO, 2014; CABI/EPPO, 2015|
|-Pernambuco||Present||Chaves et al., 2013; CABI/EPPO, 2015|
|-Rio de Janeiro||Present||EPPO, 2014; CABI/EPPO, 2015|
|-Rio Grande do Norte||Restricted distribution||EPPO, 2014; CABI/EPPO, 2015|
|-Sao Paulo||Present||EPPO, 2014; CABI/EPPO, 2015|
|Colombia||Restricted distribution||Cadavid et al., 2012; CABI/EPPO, 2015|
|Ecuador||Restricted distribution||EPPO, 2014; Garcés et al., 2014; CABI/EPPO, 2015|
|Guyana||Present||Briggs et al., 2018|
|American Samoa||Present||Brooks, 2002; CABI/EPPO, 2015|
|Australia||Restricted distribution||Ryan and Egan, 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|-Australian Northern Territory||Restricted distribution||CABI/EPPO, 2015|
|-New South Wales||Restricted distribution||Ryan and Egan, 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|-Queensland||Restricted distribution||Ryan and Egan, 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Cook Islands||Present||CABI/EPPO, 2015|
|Fiji||Present||Ricaud et al., 1989; Ryan and Egan, 1989; EPPO, 2014; CABI/EPPO, 2015|
|French Polynesia||Present||CABI/EPPO, 2015|
|Guam||Present||Ryan and Egan, 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Micronesia, Federated states of||Present||EPPO, 2014; CABI/EPPO, 2015|
|New Caledonia||Present||Ricaud et al., 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Papua New Guinea||Present||Ryan and Egan, 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Samoa||Present||Ryan and Egan, 1989; Magarey, 2000; EPPO, 2014; CABI/EPPO, 2015|
|Solomon Islands||Present||Ricaud et al., 1989; Magarey, 2000; CABI/EPPO, 2015|
History of Introduction and SpreadTop of page There is little information on the introduction of the pathogen to the locations in which it occurs. It could reasonably be assumed that P. kuehnii may be indigenous to the countries where Saccharum species are native. This includes countries such as Papua New Guinea (the centre of diversity for S. officinarum and S. robustum), India and South Asia (considered the centre of origin for S. spontaneum). In the other countries where P. kuehnii occurs, such as Indonesia and the south Pacific, sugarcane has been present for many centuries and the incidence of the pathogen could be assumed to be for the same length of time, probably having been introduced with Saccharum germplasm. In Australia, where sugarcane was introduced around 150 years ago, there are no known native hosts and the pathogen is also likely to have been introduced. There have been indirect (unconfirmed) reports of a rust disease in sugarcane in Queensland for over 100 years. It is not clear if these reports were of P. kuehnii or were actually misdiagnosed reports of downy mildew or some other disease. It is likely that the pathogen was introduced with some of the early sugarcane introductions from Papua New Guinea.
The major development in recent times in Australia has been an apparent change in strain of the pathogen in, or before, 2000. In that year, the widely grown cultivar Q124, occupying 45% of the cropped area, suddenly became susceptible. Within 12 months, crops of this cultivar were badly diseased right along the coastal cropping areas (over 2100 km from Mossman in northern Queensland to northern New South Wales in the south). Molecular studies are ongoing and will shed more light on the possibility of strain differences.
Risk of IntroductionTop of page There is risk of disease spread to currently uninfested countries and areas. The main risk is in spores blowing from diseased areas and countries to uninfested areas. This was most probably the mechanism for spread throughout the Queensland cropping districts. Another minor means of spread is on the clothes of those who have contact with the crop. A couple of instances of new minor outbreaks were associated with movement of people from diseased to uninfested crops. There have been many reports of agricultural workers travelling through diseased crops and emerging with orange shirts, covered in urediniospores.
Another potential means for spread is in the movement of diseased leaves into disease-free areas.
There has been no effort to specifically quarantine P. kuehnii, though normal sugarcane quarantine protocols are always followed/recommended when sugarcane is moved between regions and countries.
HabitatTop of page The disease may be seen in wild species of Saccharum in South and South-East Asia (including Papua New Guinea) through to the Pacific countries. In the case of the domesticated species Saccharum officinarum and S. edule, this is in the gardens of indigenous peoples. In the species that grow in the wild, the disease occurs along stream banks and roadsides, the natural habitat of Saccharum robustum and S. spontaneum (Berding and Koike, 1980; Ryan and Egan, 1989; Magarey et al., 2002c).
Hosts/Species AffectedTop of page P. kuehnii is largely confined to species of Saccharum or species of closely related genera (Erianthus, Sclerostachya, Narenga) (Ryan and Egan, 1989). The main economic hosts are hybrid commercial cultivars of Saccharum. As the pathogen has not historically caused large economic losses, host range studies have been limited and few other references on hosts have been published.
Growth StagesTop of page Seedling stage, Vegetative growing stage
SymptomsTop of page The disease is characterized by the development of leaf lesions in association with pathogen infection. The lesions begin as small, chlorotic spots (0.5 mm diameter) on the leaf. These soon develop into elongated brown lesions (2-8 mm long x 0.5-2 mm wide). As the lesions grow, fungal mycelium protrudes through the leaf surface, usually on the underside of the leaf, and abundant urediniospores are produced (Ryan and Egan, 1989; Magarey et al., 2001a). The pustules often occur in patches or groups, rather than being evenly distributed across the leaf surface. However, when the disease is severe, much of the leaf surface is covered with pustules. As the disease increases in severity, badly affected leaf tissue becomes necrotic leading to early senescence of the crop canopy. Affected crops appear brown; in severe cases, little green leaf tissue may remain. During the 2000 epiphytotic in central Queensland, Australia, most crops appeared brown from the air. Symptom development on individual leaves may take 3 to 4 weeks depending on weather conditions, which affect both leaf replacement by the plant and pathogen development.
List of Symptoms/SignsTop of page
|Leaves / abnormal colours|
|Leaves / fungal growth|
|Leaves / necrotic areas|
|Leaves / yellowed or dead|
|Whole plant / discoloration|
|Whole plant / dwarfing|
Biology and EcologyTop of page Genetics
Chromosome studies are unknown. Genetic variation is suggested by the sudden susceptibility of a previously resistant commercial sugarcane cultivar (Q124) in 2000. Molecular studies suggest that there are differences between the species of Puccinia affecting sugarcane (Virtudazo et al., 2001a, b) and that D1/D2 region tree phylogeny is more consistent with phylogenetic relationships, and is consistent with morphological differences, as compared to ITS gene tree phylogeny.
Molecular studies in Australia into strains of P. kuehnii are not yet complete but there is evidence of variation in pathogenicity within the pathogen population. A previously moderately susceptible cultivar (Q78) has been relatively unaffected by orange rust after the outbreak of the disease in Q124, even when badly affected crops of Q124 have been growing close to the same plots of Q78. This has made it difficult to collect enough material of the P. kuehnii infecting Q78, and suggests the possibility of two strains of the pathogen. No hybridization studies have been reported.
Physiology and Phenology
Phenological variation has not been noted or documented. The pathogen survives in Australia, where it is presumed not to be indigenous, on sugarcane crops at different growth stages; in commercial sugarcane production areas, sugarcane foliage is always present and the pathogen appears to survive on these structures. Although a new strain of the pathogen may have developed in recent years (this still requires further confirmation), this is the only instance where the pathogen has shown adaptability to an altered cropping environment. The pathogen is known to infect other species of Saccharum in their centre of diversity (Egan, 1981; Suma and Pais, 1996). Survival of the pathogen in these situations is considered to be through mechanisms as described for Australian cropping situations.
The pathogen is primarily spread through wind-blown or water-splashed urediniospores (Ryan and Egan, 1989). These settle on leaves of the sugarcane plant and infect under conducive temperature and moisture conditions. Spore germination experiments suggest that temperatures between 15 and 25°C are favourable for germination whereas germination increases rapidly above 97% RH (Magarey et al., 2003). Hsieh and Fang (1983) suggest the optimum temperature for germination of P. kuehnii urediniospores is 26°C, whereas for P. melanocephala it is 18°C. These authors found that spores were produced between 10 and 34°C. Fang et al. (1986) suggested that the optimum temperature for teliospore germination is also 26°C. No detailed descriptions of leaf infection have been reported for P. kuehnii. Purdy et al. (1983) also reported conditions for spore germination.
Hsieh and Fang (1983) suggested that urediniospores are produced between 10 and 34°C. Optimum temperatures for urediniospore production have been suggested as 15 and 25°C (Magarey et al., 2003) and 26°C (Hsieh and Fang, 1983). Relative humidities above 97% are known to favour urediniospore germination (Magarey et al., 2003). The effect of varying temperatures and humidities, during and after infection, on disease development has been studied, in part, by Hsieh and Fang (1983). They found the total number of urediniospores produced per sorus in the cultivar F176 was 4700. Urediniospore production occurred over a 23-day period. In the field, warm humid conditions appear to favour disease development, which peaks in late summer or during autumn.
Several organisms parasitize P. kuehnii. These include the parasitic fungus Darluca filum [Endarluca caricis] in India (Dube et al., 1978). In the Australian orange rust epiphytotic of 2000-2002, larvae belonging to the Cecidomyiidae were observed feeding on urediniospores on diseased leaves in the field (PR Samson, BSES, personal communication). In the high-rainfall areas on the north-east tropical coast of eastern Australia, parasitism is believed to have significantly reduced disease levels in the susceptible cultivar Q124, especially towards the end of the epiphytotic (late autumn each year).
Natural enemiesTop of page
|Natural enemy||Type||Life stages||Specificity||References||Biological control in||Biological control on|
Means of Movement and DispersalTop of page Natural Dispersal
Natural transmission of P. kuehnii is by wind and wind-blown rain, and this is likely to be the most important means for disease spread. Wind transmission is thought to have led to dispersal of the disease over long distances (over 2000 km).
Vector transmission (insects) of P. kuehnii is unknown.
There are no reports of seedborne transmission of P. kuehnii. In sugarcane, seed is sometimes used in propagation and this seed still has flower structures attached (fuzz). This could provide a mechanism for pathogen attachment to the seed and subsequent spread.
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|
|Leaves||spores||Yes||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|
|Stems (above ground)/Shoots/Trunks/Branches|
Wood PackagingTop of page
|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|
Impact SummaryTop of page
|Fisheries / aquaculture||None|
ImpactTop of page Orange rust is a disease of historically low economic impact. The disease has rarely caused significant economic losses. The only case of severe impact was in Australia in the year 2000, and in subsequent years as the highly susceptible Q124 was replaced in commercial fields. In this instance, it is estimated that over Aus$200 million was lost due to the disease in the 2000 season alone and this constituted the greatest single season loss to a sugarcane disease in the history of the Australian sugar industry (Magarey et al., 2002b; Staier et al., 2003). Losses of up to 40% were estimated in individual crops.
Environmental ImpactTop of page There are no known environmental effects of P. kuehnii.
Impact: BiodiversityTop of page There are no known effects on biodiversity caused by P. kuehnii.
Social ImpactTop of page The scale of the losses caused by the 2000 orange rust epiphytotic was such that the profitability of sugarcane farms and the sugar factories in the worst affected areas was significantly reduced. In some cases, farmers did not have the finance to replant crops to resistant canes and in one instance, the sugar factory supplied finance for the replanting programme. Profit reductions affected the social fabric of the central Queensland cane farming community, already affected by low industry profitability. There was a significant social cost associated with this rust outbreak.
DiagnosisTop of page Diagnosis is by inspection of visual symptoms on affected leaves and the examination of urediniospores under a microscope. There are no commercial molecular diagnostic tests currently available though this technology is being researched.
Detection and InspectionTop of page The disease is detected by examining leaves of the host for the typical rust pustules. Orange rust pustules in fresh condition contrast to pustules of other sugarcane rust diseases in their orange appearance. Confirmation of the disease is by examination of urediniospores at 100x magnification under a microscope. Urediniospores of P. kuehnii are orange, covered unevenly with papillae, have a crescent-shaped thickening at the spore apex and are slightly larger than those of Puccinia melanocephala (see Morphology).
Similarities to Other Species/ConditionsTop of page In commercial sugarcane crops, orange rust may be confused with brown rust, caused by Puccinia melanocephala. There are several ways of distinguishing the two diseases. Brown rust is favoured by cool nights with a dew, followed by warm sunny days and is often seen in spring and early summer. Orange rust is favoured by warmer temperatures and high humidity, but not necessarily free water, and is seen in late summer and autumn. Orange rust is characterized by slightly smaller pustules (not as elongated), with orange urediniospores in contrast with the cinnamon-brown spores of brown rust.
When the urediniospores are examined under a microscope, the spores of P. kuehnii are slightly larger than those of P. melanocephala, have a crescent-shaped apical thickening, an irregular covering of papillae (there is an even coverage in urediniospores of P. melanocephala) and paraphyses are present. Differences in morphology have been investigated by Mordue (1985), Coutinho et al. (1991) and Virtudazo et al. (2001a, b).
Magnesium deficiency in sugarcane causes small brown lesions somewhat similar to orange rust, but lacking in pustule development. At a distance, affected canopies may appear brown but close examination soon reveals the differences between magnesium deficiency and orange rust.
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.Phytosanitary Measures
There have been few phytosanitary measures suggested for control of orange rust. This type of control is not generally useful in areas where the disease is endemic.
Cultural Control and Sanitary Methods
Cultural control is not an effective means for control of orange rust.
Host resistance is the main commercial disease control strategy. In most sugarcane industries, there has been more than adequate resistance in commercial cultivars (Atienza and Quimio, 1982; Magarey et al., 2001a). Only rarely has there been high susceptibility in any commercial cultivars. In Australia in 2000, a change in strain of the pathogen is thought to be the reason for the susceptibility of the widely grown Q124. Testing of the Australian germplasm for resistance suggested that most cultivars are resistant to the pathogen and only a small percentage susceptible (Magarey et al., 2001a, 2002a). There has been no difficulty in maintaining a pool of resistant commercial cultivars. Under these circumstances, the disease has been very adequately controlled with few other measures necessary to maintain high levels of crop production.
Commercial biological control systems have not been adopted, nor are they especially needed. However, some natural biological control mechanisms are thought to operate. The parasitic fungus Darluca filum [Eudarluca caricis] is known to infest P. kuehnii in diseased crops. In the wetter areas of the Australian sugar industry, mycoparasitism is considered to exert a significant influence on disease levels. However, the system has not been extensively studied.
With the large area planted to the susceptible Q124 in the year 2000, the outbreak of orange rust caused large yield losses in the central district of Queensland, Australia (Magarey et al., 2001a; Staier et al., 2003). A programme was established to screen fungicides for commercial control of the disease until such time as Q124 could be replaced by resistant canes. Several fungicides were found to have activity, including tebuconazole and mancozeb (Staier et al., 2003). Spray schedules were explored and recommendations made for commercial applications. These two fungicides were registered with the Australian National Registration Authority and the fungicides used for disease control, the first time fungicides had been used for leaf disease control in the Australian sugar industry. This was only the second time that fungicides have been used commercially for leaf disease control in sugarcane worldwide (Staier et al., 2003). Even though registered fungicides were available, their use was restricted due to the poor economics of the industry at the time.
Early Warning Systems
Research into the conditions favouring spore germination was undertaken particularly in relation to temperature and relative humidity. Using these as a guide to predicting disease incidence, weather conditions were monitored in the central district of Queensland, Australia, and farmers advised via the local media. The information extended included data from disease monitoring and information on the suitability of weather conditions. Farmers then had the option of applying fungicide if desired.
Field Monitoring/Economic Threshold Levels
Only preliminary studies have been conducted into threshold disease levels and little work has been published. However, crop monitoring has occurred and data suggest that a leaf disease area affected as low as 7% is sufficient to reduce yield (Staier et al., 2003).
IPM programmes for control of orange rust have centred on the use of resistance cultivars in association with fungicide control of the disease in the popular cultivar Q124. There has been a strong emphasis on control through cultivar resistance rather than a combination of other treatments in an IPM strategy.
ReferencesTop of page
Braithwaite K, Croft B, Brumbley S, 2004. Genetic diversity within collections of the sugarcane orange rust fungus. In: 2004 Conference of the Australian Society of Sugar Cane Technologists held at Brisbane, Queensland, Australia, 4-7 May 2004 [ed. by Hogarth, D. M.]. Brisbane, Australia: PK Editorial Services Pty Ltd, 82.
Braithwaite KS, Croft BJ, Magarey RC, Scharaschkin T, 2009. Phylogenetic placement of the sugarcane orange rust pathogen Puccinia kuehnii in a historical and regional context. Australasian Plant Pathology [Papers from Keynote Speakers at the 5th Australasian Soilborne Diseases Symposium, New South Wales, Australia, February 2009.], 38(4):380-388. http://www.publish.csiro.au/nid/39.htm
Briggs GC, Nakhid Z, Alleyne AT, Ayats J, Despradel JO, Elibox W, 2014. First report of orange rust disease of sugarcane in the Dominican Republic. Plant Disease, 98(7):1010. http://apsjournals.apsnet.org/loi/pdis
Briggs, G. C., Cummings, M., Elibox, W., 2018. First report of orange rust of sugarcane caused by Puccinia kuehnii in Guyana., 102(4), 825-826. http://apsjournals.apsnet.org/loi/pdis doi: 10.1094/PDIS-06-17-0915-PDN
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.
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