The symptoms of CMD, first described fully by Storey and Nichols (1938), occur as characteristic leaf mosaic patterns that affect discrete areas and are determined at an early stage of leaf development. Leaf chlorosis may be pale yellow or nearly white with only a tinge of green, or just discernibly paler than normal. The chlorotic areas are usually clearly demarcated and vary in size from that of a whole leaflet to small flecks or spots. Leaflets may show a uniform mosaic pattern or the mosaic pattern is localised to a few areas which are often at the bases. Distortion, reduction in leaflet size and general stunting appear to be secondary effects associated with symptom severity.
Symptoms vary from leaf to leaf, shoot to shoot and plant to plant, even of the same variety and virus strain in the same locality. Variation in symptoms may be due to differences in virus strain, the sensitivity of the host genotype, plant age, and environmental factors such as soil fertility, soil moisture availability, radiation and particularly temperature.
Some leaves situated between affected ones may seem normal and give the appearance of recovery. This behaviour is influenced by the ambient temperature and host-plant resistance. However, symptoms may recur on recovered plants when environmental conditions again favour symptom expression (Gibson and Otim-Nape, 1997). The first few leaves produced by an infected cutting are sometimes symptomless and are subsequently followed by severely affected leaves, but there is a tendency for symptom severity to diminish as plants age, especially in resistant varieties. Symptoms tend to reappear on the axillary growth after the shoot tips are removed. De-topping is sometimes adopted to enhance expression in screening clones for resistance (Jennings, 1960).
Physiological and histological examinations reveal that infected leaves have palisade cells that are either short or undifferentiated from those of the spongy mesophyll tissues (Chant and Beck, 1959). Leaves of plants affected by CMD have marked reductions and distortions of the chloroplasts, increased respiration and peroxidase activity, and decreased total carbohydrate and rates of photosynthesis. Changes have also been observed in the peroxidase isoenzyme components of CMD-affected plants (Bates and Chant, 1970; Chant et al., 1971).
Prevention and control
The two main approaches to controlling CMD are through sanitation and the use of virus-resistant varieties (Thresh and Otim-Nape, 1994; Thresh et al., 1998a). Sanitation has received only limited attention, even though its effectiveness in controlling CMD has been demonstrated convincingly in Uganda (Jameson, 1964). The procedure developed there in the 1950s was to release large quantities of CMG-free cuttings of selected varieties, from official propagation sites at experimental stations, prison farms, farm institutes, training colleges and other establishments. This material was used to displace the heavily infected stocks that were being grown and a systematic campaign was organized so that whole districts were treated before starting on the next. Farmers in treated areas were then subject to local government ordinances to enforce the removal of any remaining infected plants. These measures were successful in Uganda for more than a decade, but then lapsed. They are now being revived in a modified form (Otim-Nape et al., 1997b).
The use of resistant or tolerant varieties has obvious advantages in seeking to decrease virus-induced losses and some form of resistance to CMD has long been a high priority in cassava breeding programmes in Africa (Jennings, 1994). Initial studies in Tanzania in the 1930s and 1940s were followed by others in Madagascar, Ghana and Nigeria. The main centre of activity since 1971 has been at the International Institute for Tropical Agriculture (IITA, Ibadan), which has greatly influenced national programmes in providing training, support and germplasm for local selection and evaluation (Mahungu et al., 1994).
Resistance to CMD is but one of many attributes being sought when developing new cassava varieties and only a few of the improved varieties so far released by IITA or national programmes are highly resistant to CMGs. Others are variously described as 'resistant', 'moderately resistant' or 'moderately susceptible' and their resistance is manifest in different ways. Some improved varieties are more difficult to infect than unimproved ones, but when infected they develop conspicuous symptoms that occur throughout the plant. Others develop relatively inconspicuous symptoms that may be restricted to certain shoots during the later stages of crop growth and plants may eventually become symptomless. A marked feature of some resistant varieties is that they do not seem to be invaded systemically and only some of the cuttings taken from infected plants contain CMGs. An important consequence of this 'reversion' or 'recovery' phenomenon is that stocks of such varieties never become totally infected, even when the same material is grown repeatedly at sites where there is much spread by whiteflies and where susceptible varieties soon succumb (Fargette et al., 1994; Fargette and Vié, 1995).
CMD is arguably the most important virus disease of any African food crop (Geddes, 1990), but total losses are extremely difficult to estimate. Yield losses with individual cultivars have been reported from different countries to range from 20 to 95% (Thresh et al., 1994). Losses depend on variety and stage of infection, but are usually substantial. In Côte d'Ivoire, total losses were estimated to be 0.5 million tonnes per year compared with actual production at the time of 0.8 million tonnes (Fargette et al., 1988). This was based on the assumption that all plants were infected and sustained a 37% yield loss average, as estimated experimentally with a moderately susceptible variety. Extended to the whole of Africa, such calculations indicate yield losses of 30 million tonnes per year. In a recent review more realistic assumptions were used to estimate losses in Africa of 15-24%, equivalent to 12-23 million tonnes compared with actual production estimates of 73 million tonnes (Thresh et al., 1997). There have been no comparable estimates of losses in India or Sri Lanka where the overall productivity of cassava is higher than in Africa.
Data on the effects of CMD on the yield of cassava have been obtained in many countries including Cameroon, Congo, Côte d'Ivoire, Kenya, Madagascar, Malawi, Nigeria, Tanzania, Uganda and Zanzibar (Thresh et al., 1994). These studies have been made on naturally infected plants in farmers' fields or experimental plantings and also in special plots established with CMG-infected and uninfected cuttings. The losses reported have been very variable and range from insignificant to almost total. Nevertheless, several generalisations are valid:
-Plants grown from infected cuttings sustain a greater yield loss than those of the same variety infected later by whiteflies, and plants infected at a late stage of crop growth are virtually unaffected;
-There are big varietal differences in response to infection (Fargette et al., 1988);
-Infected plants of varieties designated as resistant may sustain substantial yield losses (Seif, 1982);
-There is a positive relationship between the extent and severity of symptoms and yield loss (Cours, 1951; Thresh et al., 1997);
-Competition and compensation effects are likely to be important and infected plants surrounded by uninfected ones are more seriously affected than those in groups (Otim-Nape et al., 1997c);
-Effects on yield are influenced by crop duration;
-From experience with other virus-host combinations, it is likely that soil fertility, seasonal factors, crop spacing and other cropping practices, virus strain, weed control and other pests/diseases influence the effects of CMD on growth and yield, although they have not yet been studied.