Cassava Mosaic Virus Disease (CMD)
Taxonomy and distribution
Cassava mosaic virus disease (CMD) is caused by cassava mosaic geminiviruses (CMGs), in the family Geminiviridae and genus Begomovirus. Three species are recognised: African cassava mosaic virus (ACMV), East African cassava mosaic virus (EACMV) and South African cassava mosaic virus (SACMV). A number of variants or strains have been described, the most widely reported of which is the Uganda variant form of EACMV (EACMV-Ug), which is a recombinant virus combining parts of the genomes of both ACMV and EACMV. CMGs are sub-microscopic pathogens viewable only with the help of an electron microscope. They comprise wo join‘sister’ particles which together are approximately 20 by 30 nm in size. The genome is made up of a pair of single-stranded closed circular DNA molecules referred to as the ‘A’ and ‘B’ particles. These are enclosed by a protein coat.


Figure 1. Distribution of cassava mosaic geminiviruses in Africa.
ACMV occurs virtually throughout the cassava growing areas of Africa, with the apparent exception of coastal East Africa, where EACMV occurs largely alone (Figure 1). EACMV occurs together with ACMV in the Great Lakes zone of East and Central Africa. In parts of western Central Africa and West Africa, EACMV occurs at low frequency, and is usually found only in mixed infections together with ACMV. EACMV-Ug occurs in Uganda, western Kenya, north-western Tanzania, north-eastern Rwanda and southern Sudan. There are further provisional reports from eastern Democratic Republic of Congo (DRC) and the Republic of Congo. EACMV-Ug is expanding its range at rates varying from 20-100km per year.

Figure 2. Characteristic
chlorotic mosaic
symptoms caused by CMD.

Symptoms and economic importance
CMD symptoms are variable according to season and variety, but always include a chlorotic mosaic on infected leaves (Figure 2). The colour of chlorosis varies from pale green to whitish yellow and the extent of chlorosis varies from almost 100% of the leaf surface to less than 5%.
  In resistant varieties, plants may ‘recover’, a phenomenon in which newly emerging leaves of an infected plant sprout without symptoms.
Figure 3. Whitefly-borne
dual (ACMV+EACMV-Ug) infection in a susceptible cultivar.
In moderate to severe infections, leaves also exhibit crumpling, the laminae are distorted, and the size is reduced. These effects lead to the stunting of the growth of the plant. There are no symptoms on the stem or roots. Whilst symptoms produced by different CMGs or CMG strains may differ in severity, the general characteristics cannot be readily distinguished. Mixed CMG infections occur commonly and typically give rise to the most severe symptoms (Figure 3). Reduced photosynthetic activity resulting from chlorosis caused by CMD leads to reduced tuberization and smaller yields or no yield at all. Africa-wide losses to CMD have been estimated at between 12 and 23 million tonnes, representing 15-24% of total production.

Transmission and epidemiology
CMGs are transmitted either through planting infected stem cuttings or by the whitefly vector Bemisia tabaci (Genn.). In a newly planted cassava crop, CMD is spread from plants infected through the cutting to neighbouring healthy plants by whiteflies. Surrounding CMD diseased cassava fields are usually more important sources of infection for newly planted cassava crops than plants that sprout diseased within the field. Epidemic conditions may result where there is a high incidence of severe CMD coupled with high whitefly populations. These conditions have been characteristic of the pandemic of severe CMD that has spread through East and Central Africa during the 1990s.

The most important control method for CMD is the use of resistant varieties. Host plant resistance was developed through crossing cultivated cassava with wild relatives. Conventional breeding has produced cassava with high levels of resistance to all CMG species and strains. Mechanisms of resistance include resistance to infection, inhibition of virus replication within the plant leading to lower virus concentration and restriction of virus movement. Where CMD spread is not rapid, the disease may also be controlled through the removal of diseased plants shortly after sprouting (roguing), selection of disease-free stems for planting material and the isolation of new plantings from older diseased plots.


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