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The symptoms of stripe rust are the same on wheat and barley. Yellow pustules of stripe rust can occur on all aerial parts of the plant, but are most frequently seen on the leaves. Individual pustules (uredia) are roughly circular and about 0.5-1 mm in diameter. The pustules are often arranged into conspicuous stripes and their linear orientation between vascular bundles can progress the length of the leaf blade. On seedlings, pustules appear individually rather than in lines. During the summer, stripe rust infection of wheat spikes may occur, resulting in the formation of masses of spores between the glume and the lemma. At the end of the season, black telia may form in patches of tissue that have been killed by stripe rust uredia.
The most effective, economic and practical means of control of stripe rust on wheat or barley is through the use of varieties that are resistant to P. striiformis. The frequency of severe epidemics of wheat stripe rust has been obviously reduced in West European countries, North America, China and India since the introduction of resistant wheat varieties in the early 1970s. Work on the development of resistant wheat varieties continues throughout the world. To stabilize the pathogen population and decrease epidemic frequency, it is important to use different sources of variety resistance, including major-gene resistance, polygenic resistance, high-temperature resistance, and adult-plant resistance (Mundt and Browning, 1985).
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P. striiformis occurs on wheat crops in the cooler areas in which wheat is cultivated. It can cause severe infections in maritime climates such as Western Europe, and right across Europe to the Middle East and into Asia in a broad area, including northern and western China and the northern Indian subcontinent. It occurs on high land, such as mountains in Ethiopia, Kenya and Uganda. Since 1979 it has spread significantly, into Australia (O'Brien et al., 1980), New Zealand (Beresford, 1982) and also South Africa (Pretorius et al., 1997). In such extensions of its area, there have been severe infections on highly susceptible cultivars that were never selected to be resistant (Wellings and McIntosh, 1990 for Australasia). Yellow (stripe) rust occurs on wheat in cool climates throughout the American continent, both North and South, especially in areas such as the North West Pacific USA, in Mexico on high land and in Chile and other Andean areas. In some of the areas where yellow rust occurs on wheat, it is on crops that are grown over the cool months of the year, such as in Northern India and Australia. More detail is given in Stubbs (1985).
The major method of control is the use of resistant cultivars. The advent of systemic fungicides has led to the use of chemical control, particularly in areas where yields are high, as in Western Europe, where the cost of fungicide application is low in comparison with the value of the crop. The specialisation of the pathogen into different races and the occurrence of previously unknown races have caused many epidemics when such races attacked previously resistant and widely-grown cultivars. Many such epidemics occurred in all the areas in which yellow rust on wheat is a problem during the second half of the 20th Century (Stubbs, 1985). To cite just one example, a high-yielding wheat from the International Maize and Wheat Improvement Centre (CIMMYT), called Seri 82, was grown, under different names, in many countries in the Middle East and North and East Africa. In each country, in turn, virulence for the two resistance genes in Seri 82 (Yr7 and Yr9) emerged, after which the cultivar was very susceptible and in each country there were severe epidemics of yellow rust on it.
Although there is no known sexual stage of reproduction for this pathogen, the pattern of interaction between the races of the pathogen and many of the identified genes for resistance in the host is characteristic of gene-for-gene interactions. However, not all known resistance to this pathogen has been shown to interact as in gene-for-gene systems, and there are numerous examples of cultivars that have remained resistant during widespread and prolonged cultivation, such as Cappelle Desprez in the UK (Johnson, 1978). Such cultivars are described as possessing durable resistance (Johnson and Law, 1975; Johnson, 1983); one of the objectives of major wheat breeding programmes is to achieve such durable resistance in new cultivars. All cultivars so far recognised as possessing durable resistance have resistance that develops after the seedling stage. Unfortunately, however, the gene-for-gene interactions include some genes that only act after the seedling stage, and durably resistant cultivars cannot be recognised simply by their possession of resistance that develops after the seedling stage (Johnson, 1992).
The pathogen spreads by means of airborne urediospores. When they land on wheat plants they germinate in high humidity, usually at temperatures of less than 15°C, and the germ tubes enter the leaves or other parts of the plant via the stomata. Once inside the leaf, haustoria are inserted into the mesophyll cells and the mycelium spreads along the leaf. In mature leaves it spreads longitudinally between the veins of the leaf. Lines of bright yellow new urediospores are produced and give the typical striped appearance on the leaves from which the specific name striiformis and common name stripe rust are derived. In Europe the yellow colour of the spores caused it to be given the common name yellow rust. Both common names are used in this account.
In susceptible cultivars, there is little response to invasion by the pathogen, giving the appearance that the host and pathogen are compatible. However, damage is caused to the plant by extraction of nutrients via the haustoria of the pathogen and by disruption of the epidermis, which reduces the water retention capacity of the leaves. Sporulation is mainly on the adaxial surface of the leaves. Infections also occur on the ears, and spores accumulate inside the glumes. In resistant cultivars there are signs of incompatibility between the host and pathogen and host cells die, thus limiting the growth of the pathogen.
Frequency of Epidemics
Epidemics of yellow rust require appropriate weather conditions and the presence of susceptible cultivars. It can happen that following years when yellow rust incidence is low, a new resistant cultivar can become well established and widely grown before a change in the pathogen population renders it susceptible. This can lead to a sudden upsurge in the pathogen and an epidemic as noted above for Seri 82 wheat. Unless the susceptible cultivar can be removed from cultivation rapidly, it is probable that epidemics will continue to occur in most years, in most of the areas with favourable environments noted at the start of this section. This was demonstrated in Iran in Seri 82 (under the name Falat) wheat grown near the Caspian Sea where there where repeated epidemics from 1993 to 1995. In the UK it is probable that at least 8 years out of 10 have suitable weather for the spread of yellow rust. However, from about 1956 to 1966 there was no major epidemic when the predominant cultivar was Cappelle Desprez with its moderate but durable resistance. Timing and frequency of epidemics is likely, therefore, to be variable depending not only on weather conditions but also on the susceptibility of cultivars being grown. On highly susceptible cultivars, yellow rust can occur in areas where it is not usually a problem, sometimes giving rise to speculation that it has adapted to higher temperatures. Given the long history of this rust species, it is unlikely that a sudden adaptation to higher temperatures will occur and there is no compelling evidence that such adaptations have occurred.
Estimates of Yield Loss
Several authors have provided estimates of the yield losses associated with various levels of infection. The major grain-producing parts of the wheat plant are the flag leaf and the ear, and severe infections on these parts of the plant may cause large reductions in yield. Several methods have been used to obtain estimates of yield loss. These have included infection of plants in glasshouses, comparative data from cultivars in field trials and from genetically segregating material, from field surveys of disease incidence, and by the use of fungicides to obtain comparisons between clean plants and those infected with yellow rust.
Doodson et al. (1964) infected Jufy 1 spring wheat with yellow rust at various growth stages. Maximum yield reductions of 64.5% were recorded when the top two leaves and the ear were severely infected. It was noted that roots were even more affected, with a maximum reduction of 78%. It was also noted that infection at early growth stages reduced the size of the upper parts of the plant and led to yield reductions even when the later growth stages were not infected. The main causes of yield reduction were reduced numbers of grains per ear, perhaps arising from induced sterility, and in some experiments, reduced kernel weight - caused by the presence of shrivelled grain. Similar yield losses in the wheat cultivar Chogat (C.I. 6244) were recorded by Bever (1937), who also noted severe effects on the roots.
Several field trials were reported in which comparison was made between trials in which no yellow rust was observed and those in which certain cultivars were severely or moderately infected, whereas other cultivars remained resistant. These resistant cultivars were used to estimate expected yields for the susceptible cultivars. In such trials the timing of infection affects the results, with early and continuous infection causing more yield reduction than later infection. For example, with infection of the main upper leaves, the yield of Wilma, a susceptible cultivar, was reduced to 78% (22% yield loss) of that of the resistant cultivar Juliana (Batts and Elliot, 1952). They noted that greater reductions occurred with earlier infections. Batts (1957) noted that yields of susceptible cultivars could be reduced by 50% under severe and prolonged infection in field trials.
Stewart and Hehn (1967), in the USA, observed relative yields of cultivars in trials free from yellow rust, and then calculated expected yields of susceptible cultivars to compare with their observed yields. The yield of a resistant cultivar Cheyenne was given as 61.9 bushels/acre in 1963 when there was severe yellow rust in the trial.
Effects of yellow rust infection of wheat in 1963 on grain yields (bushels/acre)
Cultivar Cheyenne Itana Rego Westmount
Expected 61.9 61.3 60.8 64.1
Observed 61.9 54.5 60.2 45.6
Percentage 0 -11.1 -1.0 -28.8
The maximum yield loss was 28.8% on the most susceptible cultivar, Westmount. In similar types of trials in the UK Doling and Doodson (1968) indicated that similar yield losses occurred in both winter and spring habit wheat cultivars. They calculated a regression coefficient for effects of infection on yield of wheat, recorded at growth stage 10.5.3 (flowering complete at the base of the ears), using, as susceptible trials, those in which susceptible cultivars had >10% of their leaf area infected. For untransformed data they gave L = 0.268R + 3.9 and calculated yield loss as 3 times the square root of the percentage of infection at growth stage 10.5.3.
Allan et al. (1963) used F3 families that were from a backcrossing programme of Norin10-Brevor X Burt5. They estimated that the backcrossing had recovered 96% of the Burt genotype, and that the remaining variation was mainly for height and stripe rust resistance. Families were classified into five classes for rust infection and average yields for the numbers of families in each group were recorded and individual grain weight was determined. Yield was reduced by approximately 33% in the most susceptible families, compared with the most resistant. In their first experiment, weight of individual wheat kernels was not affected, and the main yield reduction was in number of grains. In a second experiment they recorded reduced kernel weights. In a similar type of trial Sunderman and Wiese (1964) compared F1 plants from a backcrossing programme to the susceptible cultivar Lemhi 53. There were only two classes, resistant and susceptible and yield of the susceptible plants was reduced by 37.5%. This was divided into 19.9% caused by lower kernel weight and a 17.6% reduction in grain number caused by induced sterility.
King (1976) used individual wheat stems from a crop survey to estimate yield loss caused by yellow rust infection in a crop of the winter cultivar Maris Templar, which had foci of infection in the field. Nine hundred stems collected randomly in traverses across foci were classified for percentage infection of the flag leaf and second leaf at growth stage 75 (Zadoks et al., 1974) 11.1 (Large, 1954) (milky ripe) into 10 groups from 0% infection to 100% infection. They were tagged and then collected for their yields in mg/ear and grain number to be recorded. Linear regressions of yield per ear, grain number per ear, and single grain weight on infection were calculated. There were no significant effects on grain number, but yield and single grain weight were reduced. As a rough guide it was suggested that the formula y = 0.3x was adequate for comparisons of infections from 0% to 30% on yield loss, where y is the predicted yield loss for x percent infection on the flag leaf at growth stage 75.
Use of fungicides to obtain comparative yield estimates
Fungicides were used in the UK, Australia and Mexico to estimate yield losses caused by yellow rust on wheat.
Mundy (1973) controlled yellow rust on a severely infected crop of the winter wheat Joss Cambier in the UK. The yield of the infected crop was 34% less than that of the part of the crop where fungicide was used to protect it from infection. The main disease in the field was yellow rust and this estimate of yield loss is similar to that obtained in other types of field trial. It was suggested that yield was reduced by 0.022 t/ha for each 1% increase in infection on the flag leaf, the formula L = 0.44R + 3.5 (P = 0.001) accounting for 87% of the variation.
In Australia, Brown and Holmes (1983) assessed the economic threshold for using fungicide to control stripe rust on wheat. They estimated expected yield losses for cultivars, depending on apparent infection rates for different cultivars. They suggested a method of measuring when 1% of leaf area was infected and indicated this as the time to spray. The expected loss from stripe rust was required to be greater than the cost of spraying. The calculation included an estimate of yield loss of 5.3% expected from delaying the spray until 1% infection was reached. The estimation of whether to spray was given by YL > [(5.3% CV + FC)/CV] X 100%, where YL is expected yield loss, CV is value of the crop and FC the cost of fungicide application in $. Clearly, the value of the crop per unit area is critical for the calculation, and wheat yields per hectare are relatively low in many parts of Australia, making the use of fungicides to control stripe rust less economical than in areas with higher yields and greater crop values. Also in Australia, Park et al. (1988) noted that losses arising from stripe rust infections were related to the level of adult plant resistance displayed by cultivars. Those with high levels of resistance did not suffer appreciable yield loss, those with intermediate resistance lost 15 to 25% and highly susceptible cultivars lost between 45 and 50%. Comparisons were made between cultivars kept free of rust by fungicide sprays, and those allowed to develop stripe rust, from an applied inoculum to induce the epidemic. In a more northern area of Australia, Ash and Brown (1990) again reported that early stripe rust epidemics caused greater losses in yield than late epidemics. Early and long epidemics reduced yields of susceptible cultivars by up to 50% in comparison with the same cultivars with disease controlled by fungicides. They also noted that most of the currently recommended commercial cultivars were adequately resistant to protect them from losses caused by stripe rust in most years.
One named gene believed to contribute to durable resistance to yellow rust is Yr18, which provides only a moderate level of resistance on its own. Despite the only partial control of yellow rust provided, Ma and Singh (1996) showed highly significant protection of yield, even when the final score for disease was very high. They compared the effects of yellow rust on near isogenic lines Jupateco S, lacking Yr18, and Jupateco R, possessing Yr18, both unsprayed and sprayed with an effective fungicide. An extract of their results is given showing that with severe infection, and with Jupateco R reaching 100% infection later in the experiment, a large increase in yield was obtained in the line with Yr18 (Table 2).
Levels of infection and yields of wheat lines with and without Yr18, sprayed and unsprayed with fungicide. Scored when the unsprayed susceptible line was fully infected.
1993 24 August
Jupateco R (+Yr18) 50% 5.5t/ha 3.4t/ha
Jupateco S (- Yr18) 100% 5.3t/ha 1.4t/ha
Percentage protection in yield of unsprayed plots [Jupateco R (3.3t/ha) - Jupateco S (1.4t/ha)]/Jupateco R (3.4t/ha) x 100 = 58.8%
The yield of the two lines was similar when the rust was controlled by fungicide.
Discussion of estimates of yield loss
The recorded amounts of yield loss in these examples depended on the timing and eventual severity of the infection. Many of the data from field trials of various types indicate yield losses of around 30%. However, trials where infections were very early and continued throughout growth of the plant, including ear infection, could be considerably higher, at fifty percent or more. All authors noted the severe damage to yield from heavy infections with this pathogen, clearly having severe effects on the economics of growing wheat. There are differences between some of the reports on the sources of yield loss, particularly in respect of the effects on grain number and individual kernel weight. Whereas some authors recorded reduced kernel weight, but not grain number, others recorded the reverse of this. This might relate to the timing of infection and the possible susceptibility of the host to induced sterility as a result of infection, which could reduce grain number so drastically that the remaining grains attain normal size, despite the poor supply of nutrients. Where grain number is not reduced in this way, it is to be expected that reduced individual kernel weight (shrivelling) must be a major contributor to yield loss. It could also happen under some circumstances that the process of thrashing and winnowing the chaff from the grain might tend to blow away very shrivelled grains, which could result in reduced grain number but not reduced kernel weight. It is clear that both grain number and grain size can be reduced by severe infections with yellow rust. An important variable in the amount of damage caused by infection with P. striiformis is the inherent resistance of the cultivars. Fully resistant, and even partially resistant cultivars suffer much lower losses than highly susceptible cultivars.
Financial Losses Caused by Yellow Rust on Wheat
Clearly the damage caused by Puccinia striiformis on wheat is of such magnitude that it must have severe implications of financial loss. The financial value of such losses will depend on local currency conditions and the commercial value of the crop. These can readily be inserted into the formulae for calculations of yield losses. There are relatively few actual money values given for losses caused by yellow rust on wheat. Brennan and Murray (1998) calculated that potential annual losses for stripe rust on wheat in Australia were A$181 million, but that control by the use of resistant cultivars at that time was worth A$161 million. This draws attention to the great value provided by breeding cultivars with resistance. Gosal (2000) gave monetary values for the use of effective genes for resistance to stripe rust in the background of a highly susceptible parent Avocet S. The races in the test possessed virulence for Yr6 and Yr7, but not for the other genes. The genes Yr8 and Yr9 performed less well, and might have had lower potential yields than the Avocet S line in the absence of infection, and also suffered some damage by necrotic responses to avirulent inoculum in the tests.
Yields of wheat lines and values of the incorporation of resistance genes in unsprayed plots, compared with the yield of the susceptible cultivar Avocet S.
Yields Value in A$/ha
Gene in line
Yr1 3.28 450.3
Yr5 3.76 541.5
Yr6 1.06 32.3
Yr7 1.09 34.2
Yr8 1.68 146.3
Yr9 1.45 102.6
Yr10 3.91 570.0
Yr15 3.84 556.7
Avocet S 0.91
Yellow Rust on Barley
The special form of Puccinia striiformis that attacks barley attacks very few wheat cultivars, and the form that attacks wheat attacks very few barley cultivars. As a result, epidemics on wheat and barley do not often occur simultaneously. As with the form infecting wheat, the form infecting barley has spread significantly since 1975. Before this date it was present in neither North nor South America. Occasional reports of yellow rust on barley in South America were found to be the wheat attacking form (Stubbs, 1985). However, in 1975 barley cultivars were attacked more severely and the samples were identified as the f.sp. hordei recorded for the first time in the American continent, and was believed to have arrived there from Europe (Dubin and Stubbs, 1986). As this form had not been present previously, there were, again inevitably, susceptible cultivars, that had been resistant to the wheat-attacking form previously present. From its start in Colombia it spread southward to Argentina by 1982 (Dubin and Stubbs, 1986) and travelled northwards to Mexico by 1987 (Chen et al., 1995) and into the USA by 1991 (Marshall and Sutton, 1995). It then spread rather quickly northwards causing some severe epidemics. It reached the Pacific Northwest USA by 1995 (Chen et al., 1995). The accounts of this spread include details of considerable epidemics, arising because the barley cultivars were not selected for resistance to this form of the pathogen. The barley attacking form of P. striiformis does not appear to have arrived yet in Australia, by the year 2000 (Wellings et al., 2000).
The form of P. striiformis that attacks barley has similar environmental requirements to those of the wheat-attacking form, which include high humidity and temperatures below 15°C for germination and cool conditions for development in the host. Its distribution is therefore similar to that of the wheat-attacking form. Epidemics on yellow rust have been much less common on barley than on wheat in Europe, because many European cultivars apparently possess a durable type of adult-plant resistance. Some race-specificity has been recognised in resistance of barley cultivars but even where such genes are present, some cultivars have remained adequately resistant when such race-specific components have been overcome.
Yield Losses in Barley Caused by Puccinia striiformis
There are few data on the effects of yellow rust on the yield of barley. The most extensive study may still be that of Bever (1937) who compared a resistant cultivar, Khanaka, with the susceptible cultivar Pannier. As this study was performed in the USA many years before the barley-attacking form was present, it must be assumed that Pannier was one of the relatively few cultivars that are susceptible to the wheat-attacking form. The same isolate of P. striiformis was used for both the wheat experiments of Bever, referred to above, and for the barley experiments, which were performed in the glasshouse.
Severe reductions in the growth and grain yield of the susceptible cultivar when inoculation was performed early in the development of the plant, and repeated at 13 day intervals throughout the life cycle. Roots were reduced by 75.9%, which is very similar to the reduction found in the susceptible wheat cultivar, and in the experiments of Doodson et al. (1964) on wheat. Yield was reduced by 64.5% in the barley compared with 65.1% in the wheat experiment, again similar to the data of Doodson et al. (1964) for wheat. Bever (1937) noted that development of the susceptible cultivar was delayed, the plants were smaller, there were fewer ears, a lower number of kernels and shrivelled grain. The author drew attention to the great similarity of the results with wheat and with barley. He noted that losses were reduced as inoculation was initiated later in the life cycle, as did many authors commenting on losses in wheat. Thus, it may be concluded that severe infections of barley with yellow rust are as damaging as those of wheat and, depending on the value of the crops, will have similar financial consequences. Bever (1937) noted that there were some negative effects on growth and yield even in the resistant barley, which could be, as with wheat, a consequence of necrosis caused by hypersensitive responses in the resistant cultivar.