A REVIEW OF AFRICAN CASSAVA MOSAIC VIRUS (ACMV) IRDA SAFNI, SP, MCP. FAKULTAS PERTANIAN Jurusan Hama dan Penyakit Tumbuhan UNIVERSITAS SUMATERA UTARA

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1 A REVIEW OF AFRICAN CASSAVA MOSAIC VIRUS (ACMV) IRDA SAFNI, SP, MCP. FAKULTAS PERTANIAN Jurusan Hama dan Penyakit Tumbuhan UNIVERSITAS SUMATERA UTARA 1. INTRODUCTION Cassava (Manihot esculenta Crantz) is a semi-woody perennial plant from family Euphorbiaceae that becomes the only species in its genus cultivated as a food crop. Since the 19 th century, cassava growing has been increasingly important, particularly in Africa, and then spread to other countries. Cassava is mainly cultivated for the tuberous roots, which are used for human food supply in the world and become the third largest source of carbohydrates (Fauquet and Fargette, 1990). The leaves are also consumed in some countries as important sources of protein and vitamins. In most African countries, cassava, which is grown primarily for local food production, is cultivated by small-scale farmers, traditionally in monoculture or intercropped with maize, bananas, peanuts, rice, bean, and other crops (Fauquet and Fargette, 1990). Several problems have appeared in cassava growing and influenced the cassava production. Many plant diseases including virus diseases have infected the crops. The virus pathogen causes the disease known as African Cassava Mosaic Virus (ACMV), which was first reported in Tanzania in 1894, has been the most important disease widely distributed and causes a significant reduction in cassava yield (Jameson, 1964). The virus is spread by planting infected cuttings, as cassava is propagated vegetatively using stem cuttings (Jameson, 1964). Besides that, whitefly (Bemisia tabaci Genn) has a most important role of virus dissemination, and ACMV become the most important vector-borne disease of any crop in Africa recently (Thresh et al., 1994). ACMV can also be transmissible by grafting and by human activity (Fauquet and Fargette, 1990). This following paper will describe the symptomatology, the causal agent, the virus vector, yield losses, epidemiology and control measures that have been applied. 2. SYMPTOMS The young infected plants show more severe disease and more symptoms than the old ones (Fauquet and Fargette, 1990). The symptoms vary from significant reduction of leaf area to stunting of the plant. The disease severity can be assessed quantitatively by disease scoring systems of Cours scale, which have scale 0-4 ( 0 = no symptoms, 1 = slight mosaic covering less than 20% of the leaf area without leaf distortion or size reduction, 2 = mosaic covering less than 50% of the leaf area 2002 digitized by USU digital library 1

2 without obvious size reduction but has some distortion, 3 = mosaic covering most of the leaf surface with leaf distortion and some leaf reduction, and 4 = severe distortion and stunting either all over the leaf or in the basal area ) ( Fargette et al., 1987). The affected leaves are chlorotic, twisted, and stunted to less than 5% of healthy leaf area. Chlorotic areas, which appear as white or yellow colour dependent on the cultivars, show much more on the leaf area rather than mosaic symptoms. The time of infection affects the growth of leaves, where leaves which appeared before infection have no disease symptoms, whereas leaves produced after infection show curved petioles in a downward S-shape (Gibson et al., 1996). Concentration of ACMV in cassava is positively related to symptom intensity, therefore, virus production increases with severe symptoms of disease (Fargette et al., 1987). As the plant grows, the disease severity increases until about 60 days after planting. After that, the symptoms may remain constant or do not develop, dependent on the cultivars, climatic conditions, and seasonal conditions (Fauquet and Fargette, 1990). For example, during summer there is no virus symptoms developed on the leaves (Fargette et al., 1987). 3. THE CAUSAL AGENT ACMV is a geminivirus from family Geminiviridae that affect seven species of Manihot. The first virus particle was detected in the 1970s when sap was successfully inoculated to cassava and to Nicotiana clevendii. With Koch s postulates, the same symptoms of ACMV were showed when returned to cassava (Bock and Woods, 1983). The virus particles are about 30 x 20 nm, and the coat protein has a molecular weight of about 30,000. Each particle consists of one molecule of circular ssdna (Mr is about 0.92 x 10 6 ), and the genome contains two circular molecules of the same size (Stanley and Gay, 1983). Based on serology and DNA hybridisation, there are two cassava mosaic geminiviruses that have been distinguished in some different parts of Africa, which are known as group A and group B strains, and a third virus, group C strain, is from India and Srilanka (Swanson and Harrison, 1994). 4. THE WHITEFLY VECTOR The whitefly (Bemisia tabaci Genn) is the only vector that transmits ACMV, by the adults, the different larva stages and through the egg (Dubern, 1994). B. tabaci is a member of order Homoptera (Aleyrodidae). Before being adult, it grows through four nymphal stages of instars that can be used to determinate of the insect (Fauquet and Fargette, 1990). The life cycle of whitefly is about 21 days, and varies with climatic factors such as temperature digitized by USU digital library 2

3 As a transmission vector, B. tabaci has some abilities, i.e. - single adult insect can transmit - optimal transmission can be achieved by 10 adult insects per plant - the minimum acquisition period is 3-5 hours, and the optimal period is 5 hours after 3 hour of fasting - the minimum latent period is 3-4 hours, and the optimal period is 6 hours - the minimum inoculation period (the time to transmit the virus to healthy plants) is 5-10 minutes, and the optimum period is 30 minutes - whitefly is infective for about 7-9 days (Chant, 1958; Fauquet and Fargette, 1990; Dubern, 1994). The movement of whitefly influences the spread of the disease in time and space. B. tabaci can fly to about 0.2 m/sec, and affected by wind speed (Fauquet and Fargette, 1990). 5. YIELD LOSSES The yield losses are greater as the disease symptoms develop to become more severe. About 50% of yield losses are estimated due to ACMV infection (Fauquet and Fargette, 1990). The yield losses have been variable from the nonsignificant to significant reduction of cassava production. Cassava crops that are cultivated from the infected cuttings have a greater yield loss than those infected later by whitefly (Thresh et al, 1994). It is estimated that the total yield losses due to growing plants from infected cutting is 55-77% and 35-60% losses from the later infection by whiteflies (Fauquet and Fargette, 1990). There are significant differences among cultivars in response to infection. Even infected plants of resistant varieties may sustain serious yield losses (Thresh et al. 1994). About 24-78% losses occur in resistant cultivars and up to 77% of yield losses in the moderately susceptible cultivars, which depend on the mode and time of infection and on environmental factors (Fauquet and Fargette, 1990). Competition effects between healthy and infected plants also influence the yield losses of cassava. The severity symptoms are greater in the infected plant grown away from the healthy crops (70%) compared to infected plants surrounded by uninfected ones (30%) (Fauquet and Fargette, 1990; Thresh et al., 1994). 6. EPIDEMIOLOGY The effectiveness of control of ACMV, it is important to observe various biotic and abiotic factors that influence the dissemination of the virus. Internal sources of inoculum within the host are less important and roguing is not effective as means of control measures (Fauquet and Fargette, 1990). On the contrary, spread of whitefly is low when using the infected cuttings, not to vectors in coastal and western Kenya (Bock, 1983) digitized by USU digital library 3

4 Several factors influence the spread of ACMV infection, namely the inherent susceptibility or resistance of varieties grown, the sensitivity of the varieties grown, inoculum or infection pressure, phytosanitation measures, and the extent to which ACMV is systemic within infected plants (Fargette et al., 1994). The overall incidence of ACMV in a region is affected by factors such as environment, biology, agroecology, and socioeconomy. The outbreaks of ACMV infection within a field are a result of rapid primary spread from outside sources, which the rate of primary spread is affected by seasonal and other factors (Fargette et al., 1990). Infected fields grown with cassava become important as a source of contamination, because a large group of infected cassava crops can cause secondary spread. Therefore, cassava fields are the main sources of virus and vector (Fargette et al., 1990). 7. CONTROL MEASURES Controlling ACMV disease is quite difficult because the lack of information to initiate the effective management practices and only a few researches on ACMV conducted in Africa. In general, there are two main methods to manage ACMV disease, i.e. sanitation and the use of resistant cultivars. The successful management of using sanitation has been conducted by Jameson (1964) in Uganda. Several official places such as prison farms, farm institutes, training colleges and experimental stations released a large number of ACMV-free cuttings of selected varieties. The effectiveness of sanitation methods depends on the rate of recontamination of ACMV-free planting material, the availability of stocks of cuttings, and the ease of the cuttings can be produced. In addition, application of sanitation can be successful if the planting materials are resistant to ACMV (Fauquet and Fargette, 1990). The use of resistant cultivars is the most promising approach to control ACMV disease. There have been many resistant cultivars developed by breeding programmes at the International Institute for Tropical Agriculture (IITA) in Nigeria. Several cultivars are considered to be very highly resistant, and some others are resistant, moderate resistant or moderate susceptible (Thresh et al., 1994). However, the best management of ACMV is by combining several control methods, because no cassava cultivar is immune to ACMV. Even resistant cultivars can also become infected. Because cassava crops are grown in the traditional environment, only combination of research and development can improve the control approach of ACMV (Fauquet and Fargette, 1990) digitized by USU digital library 4

5 REFERENCES Bock, K.R. and Woods, R.D Etiology of African cassava mosaic disease. Plant Disease 67: Chant, S.R Studies on the transmission of cassava mosaic virus by Bemisia tabaci (Aleyrodidae). Annals of Applied Biology 46: Dubern, J Transmission of African cassava mosaic virus geminivirus by the whitefly (Bemisia tabaci). Tropical Science 34: Fauquet, C. and fargette, D African cassava mosaic virus: etiology, epidemiology, and control. Plant Disease 74: Fargette, D., Thouvenel, J.C. and Fauquet, C Virus content of leaves of cassava infected by African cassava mosaic virus. Annals of Applied Biology 110: Fargette, D., Fauquet, C., Grenier, E., and Thresh, J.M The spread of African cassava mosaic virus into and within cassava fields. Journal of Phytopathology 130: Fargette, D., Thresh, J.M., Otim-Nape, G.W The epidemiology of African cassava mosaic geminivirus: reversion and the concept of equilibrium. Tropical Science 34: Gibson, R.W., Legg, J.P., and Otim-Nape, G.W Unusually severe symptoms are a characteristic of the current epidemic of mosaic virus disease of cassava in Uganda. Annals of Applied Biology 128: Jameson, J.D Cassava mosaic disease in Uganda. East African Agricultural and Forestry Journal 29: Stanley, J. and Gay, M.R Nucleotide sequence of cassava latent virus DNA. Nature 301: 260. Swanson, M.M. and Harrison, B.D Properties, relationships, and distribution of cassava mosaic virus geminiviruses. Tropical Science 34: Thresh, J.M., Fishpool, D.C., Otim-Nape, G.W., Fargette, D African cassava mosaic virus disease: an under-estimated and unsolved problem. Tropical Science 34: digitized by USU digital library 5