One or more of the features that are needed to show you the maps functionality are not available in the web browser that you are using.
Please consider upgrading your browser to the latest version or installing a new browser.
More information about modern web browsers can be found at http://browsehappy.com/
SCMV causes systemic infection of the sugarcane plant: the whole plant, including roots, contains virus. However, the symptoms (mosaic and/or necrosis) are observed on the leaves and sometimes the stems. Sometimes the whole plant is stunted.
In Saccharum spp., Sorghum bicolor, Zea mays and various grasses, systemic mosaic symptoms may be produced. The classical symptoms are contrasting shades of green on a background of paler green to yellow chlorotic areas. Sometimes yellow stripes and/or necrosis occur. The particular symptoms depend on the virus strain, the host cultivar and the environmental conditions, particularly temperature.
Control of SCMV
Attempts to eradicate SCMV by roguing infected plants have rarely been successful (Abbott, 1961; Koike and Gillaspie, 1989). Roguing by digging out or applying herbicides may be useful in maintaining mosaic-free seed plots of cane if the level of infection is lower than 5% (Koike and Gillaspie, 1989). The use of mosaic-free seed cane is an effective control measure where inoculum pressures are not intense. Thermotherapy of planting material can result in some plants that are free of SCMV (Mirza et al., 1986; Benda et al., 1989).
Mosaic in sugarcane has long been controlled by the development and use of resistant clones. Breeding programmes may be designed to produce resistant clones which can be tested against the prevalent virus strains (Koike and Gillaspie, 1989).
Control of Aphid Vectors
A close relationship exists between ants and aphid vectors of SCMV (Charpentier, 1963). Ants can carry the aphids from one sugarcane plant to another, from grass to cane and from cane to grass. Presumably, ants also decrease attacks on aphids by parasitoids and predators, which would otherwise exert better control.
Because aphids which transmit SCMV come from outside as well as inside the sugarcane crop, care should be given to reduce the build up of the vector species in the vicinity. Crops of maize and sorghum are good hosts of vectors such as R. maidis, and should not be grown near infected sugarcane crops. Altering the times of planting and harvesting so that they do not coincide with high aphid vector populations can reduce losses (Bailey and Fox, 1980).
The use of insecticides failed to prevent aphid vectors from spreading SCMV (Charpentier, 1956).
In the past, SCMV has caused alarming losses in various sugarcane-growing regions, including Hawaii, Egypt, Natal (South Africa), Argentina, Puerto Rico, Cuba, Australia and the USA (Koike and Gillaspie, 1989). Epidemics have been followed by replacement of susceptible noble-type canes by hybrid canes with tolerance or, better still, resistance. The evolution of new strains of SCMV has required a continuing breeding programme to prevent heavy losses.
Losses caused by SCMV are mainly (1) a reduced yield of the crop, (2) the need to include mosaic resistance when breeding new cultivars, and (3) the slowing of the interchange of cultivars between countries because of quarantine concerns over the introduction of new strains of SCMV.
Crop losses caused by SCMV depend on many factors, including the susceptibility of the cultivars to the prevailing strains of SCMV, the incidence of infection, the prevailing environmental conditions, the stage of growth when infection occurs, and interaction with other agents affecting the crop. Crop losses can vary from negligible to severe. Some recent instances of heavy losses in sugarcane crops due to mosaic outbreaks are as follows.
In the 1980s, losses on some farms in the Isis district of Queensland, Australia, were estimated to be about 50% (Jones, 1987). In some commercial plantings of cv. Q95 from an infected source, the infected plants had fewer tillers and were less vigorous than apparently healthy plants nearby (Ryan and Jones, 1986).
In Guatemala in 1974-1976, many stunted stools of mosaic-affected cv. Q83 were responsible for lack of uniformity in fields near Santa Lucia. The cane tonnage in these fields was seriously reduced (Fors, 1978).
Estimations of Potential Losses in Experiments
In Natal, South Africa, plots of sugarcane cv. NCo376 (highly susceptible) and N12 (moderately resistant) were established with either infected or healthy cane. The plots were harvested regularly and tested serologically for SCMV to the 6th ratoon. There was a decline in the number of shoots showing mosaic symptoms in both cultivars during the experiment. However, mean yield reductions were 22% for infected NCo376 and 16% for N12 compared with yields of initially healthy cane (Cronje et al., 1994).
In Brazil, plots in two locations were planted with 0, 25, 50 and 100% initial SCMV infection. Virus spread was noticeable for cv. CB46/47, but negligible for cv. IAC50/134. For CB46/47 yield losses between initially healthy and 25% infected plots were 27% and 19% in the two locations; with 100% infection, yield reduction was 71% in both areas. For IAC50/134 the only significant difference in yield was between 0 and 100% infection, an 18% reduction in diseased plots in both areas (Matsuoka and Costa, 1974).
In Java, Indonesia, field trials with 0 and 100% SCMV-infected seed cane gave sugar yield reductions of 9.3% for POJ3016 and 11.1% for POJ3067 associated with the disease (Kuntohartono and Legowo, 1970).
In Spain, when healthy sugarcane was planted between rows infected by SCMV, the cultivars CO62/175 and NA56/79 were sufficiently resistant for commercial production, but losses of 0.4-0.5 t/ha were found for every 1% infection between the 2nd and 4th cutting (Olalla-Mercade et al., 1984a).
In Pakistan, mosaic-free seed cane gave a significantly higher yield of cane (48.5 t/ha) than mosaic-infected seed cane (44.5 t/ha)(Ahmad et al., 1991).
In East Africa, 10 susceptible maize hybrids had yield losses of 18-46% when inoculated with SCMV in the seedling stage (Louie and Darrah, 1980).
In Germany, SCMV was more prevalent than MDMV, but had a similar effect on growth and yield of maize. Early infection reduced plant height by 25%, total weight by 38% and ear weight by 27% (Fuchs et al., 1990).
SCMV and related potyviruses may occur in disease complexes with other plant pathogens; either additive or synergistic effects may occur.
In Louisiana, USA, losses in sugarcane caused by sorghum mosaic virus (formerly called SCMV-H) and ratoon stunting disease (RSD, caused by the bacterium Clavibacter xyli) were additive in cv. CP67-412, but synergistic (greater than the sum of each disease separately) in CP65-357 (Koike, 1982). In Spain, RSD symptoms were associated with the presence of SCMV, and damage by RSD was greatest in fields with clear mosaic symptoms (Olalla-Mercade et al., 1984b).
In Thailand, inoculation of the downy mildew-susceptible maize cv. Guatemala with an SCMV-like virus increased susceptibility to Sclerospora sorghi only slightly, whereas with the resistant Suwan 1 maize cv., the virus increased susceptibility from 27-61% (Sutabutra et al., 1976).