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Cassava mosaic disease (African cassava mosaic)


  • Last modified
  • 27 July 2017
  • Datasheet Type(s)
  • Invasive Species
  • Pest
  • Preferred Scientific Name
  • Cassava mosaic disease
  • Preferred Common Name
  • African cassava mosaic
  • Taxonomic Tree
  • Domain: Virus
  •   Unknown: "ssDNA viruses"
  •     Unknown: "DNA viruses"
  •       Family: Geminiviridae
  •         Genus: Begomovirus
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Cassava mosaic disease (African cassava mosaic); symptoms on cassava.
CaptionCassava mosaic disease (African cassava mosaic); symptoms on cassava.
Copyright©Pasquale Piccirillo
Cassava mosaic disease (African cassava mosaic); symptoms on cassava.
SymptomsCassava mosaic disease (African cassava mosaic); symptoms on cassava.©Pasquale Piccirillo


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Preferred Scientific Name

  • Cassava mosaic disease

Preferred Common Name

  • African cassava mosaic

Other Scientific Names

  • African cassava mosaic disease
  • cassava African mosaic bigeminivirus
  • Indian cassava mosaic disease

International Common Names

  • Spanish: mosaico africano de la yuca
  • French: mosaïque africaine du manioc

Local Common Names

  • Germany: cassava mosaik

Taxonomic Tree

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  • Domain: Virus
  •     Unknown: "ssDNA viruses"
  •         Unknown: "DNA viruses"
  •             Family: Geminiviridae
  •                 Genus: Begomovirus
  •                     Species: Cassava mosaic disease

Notes on Taxonomy and Nomenclature

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Cassava mosaic disease (CMD)

Cassava mosaic disease in Africa and the Indian subcontinent is caused by one or other of the three cassava mosaic geminiviruses that have been distinguished: African cassava mosaic virus (ACMV), East African cassava mosaic virus (EACMV) and Indian cassava mosaic virus (ICMV). The mosaic disease of cassava in Central and South America is caused by a different virus of the Potexvirus genus and is referred to as Cassava common mosaic virus.

The three cassava mosaic geminiviruses were originally described as strains of ACMV (Bock and Harrison, 1985), but are now regarded as distinct (Hong et al., 1993).

Cassava mosaic geminiviruses (CMG)

In the absence of any visible pathogen, cassava mosaic disease (CMD) was at first assumed to be caused by a virus, but no particles were detected until 1975, when sap inoculations from cassava to Nicotiana clevelandii were successful (Bock, 1975; Bock and Guthrie, 1978). However, there was initial uncertainty as to the role of the geminivirus isolated in this way and it was at first named cassava latent virus. This was because the virus was isolated from CMD-affected plants in western Kenya, western Tanzania and Uganda, but not from similarly diseased plants in coastal Kenya (Bock et al., 1978).

Uncertainty over the aetiology of CMD was resolved when successful inoculations were made to Nicotiana benthamiana from CMD-affected plants in both western and coastal Kenya (Bock and Woods, 1983). The isolates obtained and characterized were related serologically to those from CMD-affected cassava elsewhere in Africa and caused symptoms typical of the disease when returned to cassava, so fulfilling Koch's postulates.

The various isolates from mosaic-affected cassava in different parts of Africa and India were initially regarded as strains of the same virus (Bock and Harrison, 1985). This was referred to as African cassava mosaic, and serological differences were reported in tests with polyclonal antisera using the 'type strain' from western Kenya, the Kenya coast strain and a strain from India. These and other isolates were later ascribed to separate West African ('A'), East African ('B') and Indian ('C') strain groups based on their serological properties in tests with a panel of monoclonal antibodies (Thomas et al., 1986; Harrison and Robinson, 1988). However, based on serological evidence and nucleotide sequencing, the three groups of isolates are now regarded as distinct viruses and referred to as African cassava mosaic virus (ACMV), East African cassava mosaic virus (EACMV) and Indian cassava mosaic virus (ICMV), respectively (Hong et al., 1993). None of these three geminiviruses has been reported in South or Central America, and the mosaic disease of cassava that occurs there is caused by a different virus of the Potexvirus genus.

In the light of current knowledge, it seems likely that previous studies on transmission by vectors, yield loss, epidemiology, and host plant resistance in Madagascar and coastal areas of Kenya and Tanzania were on EACMV, whereas studies in Nigeria, Côte d'Ivoire, western Kenya and Uganda were on ACMV and those in India were on ICMV (Swanson and Harrison, 1994; Harrison et al., 1995). On pragmatic grounds, the lack of evident biological differences in the results obtained with the three viruses in cassava makes it convenient to continue treating them as a single virus, as in earlier studies and publications. This is the convention adopted here where the abbreviation CMGs is used sensu lato for all three cassava mosaic geminiviruses, and the disease they cause is referred to as CMD.

African cassava mosaic virus (ACMV)

One of three similar viruses of the family Geminiviridae, Begomovirus genus known to cause cassava mosaic disease (CMD). The type strain ACMV (T) was isolated from mosaic-affected cassava in western Kenya. From the available evidence, ACMV was until recently the virus usually causing CMD there and in West and Central Africa and Mozambique, but it has not been reported in the coastal areas of East Africa, Malawi, Madagascar or the Indian subcontinent.

East African cassava mosaic virus (EACMV)

One of three similar viruses of the family Geminiviridae, Begomovirus genus known to cause cassava mosaic disease (CMD). The type strain was isolated from mosaic-affected cassava in coastal Kenya and originally regarded as a strain of African cassava mosaic (q.v.). On current evidence EACMV is the virus usually causing CMD in the eastern parts of Kenya and Tanzania and also in Madagascar, Malawi and Zimbabwe. However, it has been detected occasionally in other parts of Africa (Ogbe et al., 1996, 1997) but not in the Indian sub-continent.

Indian cassava mosaic virus (ICMV)

One of the three similar viruses of the family Geminiviridae, Begomovirus genus known to cause cassava mosaic disease (CMD). The type strain was isolated from mosaic-affected cassava in southern India and originally regarded as a strain of African cassava mosaic virus (q.v.). On current evidence ICMV is the usual virus causing CMD in India and Sri Lanka and it has not been detected elsewhere.

Cassava latent virus (CLV)

The name introduced in the 1970s for the virus isolated from mosaic-affected plants in Kenya and elsewhere in Africa, but not at the time considered to cause cassava mosaic disease (Bock et al., 1978, 1981). This view was later shown to be incorrect and the name became redundant when the different strains were ascribed to African cassava mosaic virus or East African cassava mosaic virus (q.v.). However, somewhat misleadingly the name cassava latent was retained in some later publications.


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The geminate particles of CMGs measure ca 30 x 20 nm, and the coat protein has a molecular weight of ca 30 kDa. The particles each contain one molecule of circular single-stranded DNA (Mr ca 0.92 x 10<(sup)6>), and the genome consists of two circular molecules of similar sizes. In leaf tissue, the virus particles accumulate mainly in the nuclei of phloem parenchyma and of cortical and epidermal cells (Bock and Harrison, 1985). The genomes of CMGs contains six genes (open reading frames) that are also found in other whitefly-transmitted geminiviruses and encode proteins of Mr >10 kDa; four in DNA-A and two in DNA-B. The genes of DNA-A include those encoding the virus particle protein and others concerned with DNA replication; those in DNA-B influence virus spread within the plant. The virus coat protein is implicated in vector transmission (Lazarowitz, 1992).


Top of page CMGs occur throughout Africa, in Indian Ocean Islands (Seychelles, Mauritius, Zanzibar, Pemba), India and Sri Lanka.

Survey data are available for Benin, Cameroon, Chad, Ghana, Malawi, Nigeria, Tanzania, Uganda and Zambia (see Thresh et al., 1997).

Information on the identity of the viruses causing CMD in Cameroon, Côte d'Ivoire, Kenya, Madagascar, Malawi, Tanzania, Uganda and Zambia is available in Swanson and Harrison (1994), Ogbe et al. (1996, 1997) and Harrison et al. (1997a). For further details of the disease in Tanzania and Zambia see Legg and Raya (1998) and Muimba-Koukolongo (1997).

The presence of the disease in Indonesia is unconfirmed (Thresh et al., 1997).

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes


IndiaWidespreadCABI and EPPO, 1998
-Andhra PradeshPresentCABI and EPPO, 1998
-KarnatakaPresentCABI and EPPO, 1998
-KeralaPresentCABI and EPPO, 1998
-Tamil NaduPresentCABI and EPPO, 1998
Sri LankaRestricted distributionCABI and EPPO, 1998


AngolaWidespreadCABI and EPPO, 1998
BeninWidespreadThresh et al., 1997; CABI and EPPO, 1998
Burkina FasoWidespreadCABI and EPPO, 1998
BurundiWidespreadCABI and EPPO, 1998
CameroonWidespreadCABI and EPPO, 1998; Akinbade et al., 2010
Cape VerdeWidespreadCABI and EPPO, 1998
Central African RepublicWidespreadCABI and EPPO, 1998
ChadWidespreadThresh et al., 1997; CABI and EPPO, 1998
CongoWidespreadCABI and EPPO, 1998
Congo Democratic RepublicWidespreadCABI and EPPO, 1998
Côte d'IvoireWidespreadCABI and EPPO, 1998
Equatorial GuineaWidespreadCABI and EPPO, 1998
EthiopiaWidespreadCABI and EPPO, 1998
GabonWidespreadCABI and EPPO, 1998
GhanaWidespreadThresh et al., 1997; CABI and EPPO, 1998
GuineaWidespreadCABI and EPPO, 1998
Guinea-BissauWidespreadCABI and EPPO, 1998
KenyaPresentIntroduced1994 Invasive CABI and EPPO, 1998; IPPC-Secretariat, 2005
LesothoWidespreadCABI and EPPO, 1998
LiberiaWidespreadCABI and EPPO, 1998
MadagascarWidespreadCABI and EPPO, 1998
MalawiWidespreadCABI and EPPO, 1998
MauritaniaWidespreadCABI and EPPO, 1998
MauritiusWidespreadCABI and EPPO, 1998
MozambiqueWidespreadCABI and EPPO, 1998
NigeriaWidespreadThresh et al., 1997; CABI and EPPO, 1998
RwandaWidespreadCABI and EPPO, 1998
Sao Tome and PrincipeWidespreadCABI and EPPO, 1998
SenegalWidespreadCABI and EPPO, 1998
SeychellesWidespreadCABI and EPPO, 1998
Sierra LeoneWidespreadCABI and EPPO, 1998
South AfricaWidespreadCABI and EPPO, 1998
SudanWidespreadCABI and EPPO, 1998
TanzaniaWidespreadCABI and EPPO, 1998
TogoWidespreadCABI and EPPO, 1998
UgandaWidespreadCABI and EPPO, 1998
ZambiaWidespreadCABI and EPPO, 1998
ZimbabweWidespreadCABI and EPPO, 1998

Risk of Introduction

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CMGs seem to have spread rapidly in Africa at the beginning of the century as intensification of cassava production occurred in the continent, despite some unsuccessful attempts to restrict spread through early quarantine controls. One or other of the viruses is now present in all cassava growing regions. Much care is now taken in the transfer of virus-free material from Africa or the Indian sub-continent, in order not to introduce the virus to other regions and to South America in particular, where cassava is extensively grown. CMGs are absent from the neotropics but Bemisia species are present, including B. tabaci on crops other than cassava. Within Africa, different viruses predominate in the East and the West of the continent (Swanson and Harrison, 1994; Harrison et al., 1995, 1997a). Recent epidemics in Uganda are associated with a novel strain that appears to be a recombinant between African cassava mosaic and East African mosaic geminiviruses (Harrison et al., 1997a, b). However, it has also been referred to as a distinctive strain of East African cassava mosaic virus (Deng et al., 1997). Care is also required in moving vegetative propagules within Africa, and in vitro cultures only are transferred after testing.

Hosts/Species Affected

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Experimental hosts:

CMGs are mechanically transmissible experimentally to several solanaceous species including Nicotiana benthamiana, N. clevelandii and Datura stramonium.

Host Plants and Other Plants Affected

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Plant nameFamilyContext
EuphorbiaceaeEuphorbiaceaeWild host
Manihot esculenta (cassava)EuphorbiaceaeMain
Ricinus communis (castor bean)EuphorbiaceaeMain

Growth Stages

Top of page Vegetative growing stage


Top of page 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).

List of Symptoms/Signs

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SignLife StagesType
Leaves / abnormal forms
Leaves / necrotic areas
Leaves / yellowed or dead

Biology and Ecology

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CMGs are disseminated in cuttings derived from infected plants and they are transmitted by the whitefly Bemisia tabaci (Chant, 1958; Dubern, 1994). Experimentally, they can also be transmitted mechanically to some solanaceous species. Dissemination through cuttings is an inevitable consequence of the vegetative propagation of cassava and reflects the overall distribution of the virus in the plant, including the stems which provide cuttings. However, the distribution of the virus is not fully systemic in cassava, especially in resistant genotypes, and a proportion of cuttings derived from infected plants may be virus-free. This is the phenomenon of reversion and the epidemiological consequences are discussed by Fargette et al. (1994) and Fargette and Vie (1995).

The insect vector B. tabaci is a member of the Aleyrodidae, order Homoptera, and has four nymphal instars, of which only the first is mobile. The adult is ca 2 mm long and difficult to distinguish from other whitefly species and the characters of the last nymphal instar are used in determinations (Fishpool and Burban, 1994). The life span of B. tabaci is ca 21 days and depends on climatic factors, particularly temperature.

The adult whitefly needs to feed for ca 3 hours to acquire the virus from an infected plant and, after a latent period of at least 8 hours, ca 10 minutes to transmit the virus to healthy plants. Whiteflies remain infective for about 7-9 days, and CMG is not lost during moulting. No transovarial transmission occurs. The percentage of individuals that become infective when allowed access to infected cassava depends on the cultivars tested and the whitefly population, but has been reported to be at most only a few percent (Fargette et al., 1990).

Vector distribution, virus concentration, and leaf susceptibility to virus inoculation are all related to leaf age (Fauquet and Fargette, 1990). Up to 95% of adult whiteflies found on cassava are concentrated on the abaxial surface of the five youngest leaves of each shoot. Even though symptoms may be present, virus particles cannot be detected in leaves older than the seventh from the apex (Fargette et al., 1987) and only the five youngest leaves of each shoot are susceptible to virus inoculation (Storey and Nichols, 1938).

Spread of CMD in time and space is related to the movements of adult whiteflies. The flight speed of B. tabaci has been calculated to be ca 0.2 m/sec, but the insects can control their flight only at low wind speeds, such as those that occur within the plant canopy. At greater wind speeds, the insects cannot control their movement and may be swept away from the source plants.

Whiteflies are not distributed uniformly within cassava fields; their numbers tend to be highest on the upwind borders and lowest within fields, irrespective of field size or whitefly population (Fargette et al., 1985). The size of vector populations is positively correlated with the virus spread that becomes apparent about 1 month later, which corresponds approximately to the time from inoculation to symptom development (Fargette et al., 1990, 1994). The environmental factor that correlates best with fluctuations in whitefly population is temperature, also with a time lag of 1 month which is the approximate generation time of B. tabaci.

Sources of infection

Despite the limitations of the available data, generalisations on CMG ecology are now possible, in particular on the crucial role of cassava as the main source of infection. Such information is consistent, and cassava may also be the main host of the whitefly vectors as there is evidence from Côte d'Ivoire and Uganda that the biotype occurring on cassava is largely restricted to this host (Burban et al., 1992; Legg, 1998). Studies have indicated that other potential virus reservoir plants, around cassava fields, are unimportant epidemiologically. Thus, it can be concluded, that in areas where growing conditions are generally favourable and cassava is cultivated intensively, conditions facilitate spread by whiteflies because infection sources are abundant, vectors are numerous and plants are vulnerable to infection (Fargette and Thresh, 1994). This occurs where mean annual rainfall exceeds 1500 mm and the length of the crop growing period exceeds 270 days, conditions likely to be optimal for cassava growth. In such areas, methods of control by sanitation are unlikely to be successful unless very resistant varieties are used. The situation is completely different in areas where cassava is little grown and growth is curtailed at periods of the year when conditions are too dry or too cold. In such areas, spread by whiteflies is restricted because of limited inoculum (small, scattered and remote virus sources of low potency), small numbers of whiteflies and reduced plant susceptibility during the dry and/or cool seasons. In these circumstances, infection is largely due to the use of infected cuttings and control by sanitation is feasible and achieved readily.

Spatial distribution

Within newly infected cassava fields, the distribution of CMD shows dispersal gradients correlated with the vector distribution (Fargette et al., 1985). Incidence of CMD is greater along the upwind edges than along the downwind edges of the fields, this distribution appearing as a curvilinear gradient of disease along the direction of the prevailing wind. Such gradients occurred in all fields investigated in Côte d'Ivoire, despite greatly differing areas and exposure conditions. Plant density also influences field contamination, i.e., spread is greatest at wide spacing and incidence of disease, as a percentage of the plant population, is lowest with close spacing (Fargette et al., 1990).

Primary spread of CMGs by viruliferous immigrant whiteflies entering and infesting healthy cassava fields has been distinguished from secondary spread from diseased plants within the fields (Fargette et al., 1990). Evidence from Côte d'Ivoire and Uganda is that primary spread predominates. Within a healthy cassava field, the dispersal gradient from a source of contaminated plants, although occurring in all directions, does not extend over a distance exceeding a few metres and probably is related to the relatively limited flight distance of whiteflies within fields.

Cassava is often cultivated with other food crops, and some experiments have shown that mixed cropping influences the spatial and temporal patterns of virus spread (Fargette and Fauquet, 1988), but additional studies are necessary to evaluate precisely their influence and whether intercrops or barrier crops can be used to facilitate control.

Temporal spread of CMD

Temporal spread of CMD depends on numerous factors, some of which interact. Studies in Tanzania and Côte d'Ivoire have shown that spread of disease varied greatly from month to month and showed an annual periodicity with seasonal fluctuations (Storey and Nichols, 1938; Fargette et al., 1994). In the forested part of the southern Côte d'Ivoire for instance, monthly spread was up to 90% of the stand in March, but incidence did not exceed 4% in August. The susceptibility of plants decreases with age, and little infection occurs after 3 months. Disease incidence largely reflects fluctuations in whitefly populations, but also depends partly on variations in climatic factors, including temperature, rainfall and wind. Relationships among disease incidence, vector populations, plant growth and climatic factors are complex. However, temperature is positively related to vector populations, plant growth and susceptibility and disease incidence (Fargette et al., 1994).

Regional spread

Extensive tests of a range of cultivars were conducted at different locations from 1977 to 1984 in coastal areas of Kenya (Bock, 1983, 1994). There was little spread of CMD (1-2%) into plots of initially mosaic-free selected cassava hybrids, irrespective of plot size, location and annual or regional climatic variations. Some local cultivars seemed to become infected no more readily than hybrids selected for CMD resistance. In Kenya, therefore, it was concluded that infection was prevalent because farmers do not discriminate between contaminated and healthy plants when choosing cuttings. There was little spread of CMD to highly susceptible cassava cultivars at sites isolated from other cassava.

In West Africa, trials conducted in several locations in Côte d'Ivoire revealed sites with consistently high or low incidences of CMD, indicating regions of high and low inoculum availability (Fauquet et al., 1988). Although the number of experimental locations was restricted, it seemed that the inoculum pressure at any one site may have been related to the overall density of cassava cultivation in the region.


Seedborne Aspects

Top of page The virus is not seedborne in cassava. However, the virus is disseminated in the stem cuttings used routinely for propagation.


Top of page 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.


Top of page Polyclonal antibodies originally raised by injecting a rabbit with purified particles of what was later described as the type isolate of ACMV from western Kenya have since detected geminivirus infection in CMD-affected cassava from more than 20 countries in Africa and the Indian subcontinent (Swanson and Harrison, 1994; Harrison et al., 1995). The double-antibody sandwich version of enzyme-linked immunosorbent assay (DAS-ELISA), in which the antibodies are conjugated to alkaline phosphatase, has proved to be convenient and successful and is usually able to detect the viral antigen in extracts of young symptom-bearing cassava leaves at a sap dilution of 1:100, and in some instance 1:1000. However, mosaic-affected plants of many cultivars typically produce flushes of symptom-bearing leaves interspersed with symptomless leaves, in which the virus is not detected by DAS-ELISA. This finding, and other evidence, indicates that the virus is unevenly distributed in cassava shoots and emphasise the importance of selecting young symptom-bearing leaves for diagnostic tests (Fargette et al., 1987).

Geminivirus infection of cassava can also be detected by murine monoclonal antibodies (MAbs) raised against CMGs and used in triple-antibody sandwich ELISA (TAS-ELISA). As with DAS-ELISA, TAS-ELISA with one of these MAbs (SCR 20) has detected geminivirus infection in cassava from more than 20 countries. Moreover, TAS-ELISA is somewhat more sensitive than DAS-ELISA, especially when readings are made after overnight incubation with substrate. It also has the advantage that the background reaction given by extracts of CMG-free cassava leaves is negligible.

Detection is also possible by nucleic acid hybridization tests with probes derived from viral DNA. Probes for DNA-A of a group A isolate hybridize with isolates of all groups. Polymerase chain reaction (PCR) amplification of geminiviruses including CMGs is now possible and has been used to study the strains occurring in Uganda and elsewhere (Deng et al., 1997; Harrison et al., 1997a, 1997b; Zhou et al., 1997). The PCR technique is suitable for diagnosing large numbers of samples for the presence of CMGs using generic/degenerate primers for virus identification. This technique has an added advantage because the PCR product can be analyzed further by restriction site analysis or by cloning the product for sequencing.

Detection and Inspection

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The symptoms of CMD in cassava are usually conspicuous, and much of the evidence on the occurrence, incidence and spread of disease is based on visual observations. However, symptoms are sometimes indistinct, especially in dry conditions when vegetative growth is restricted, or when plants develop symptoms of mineral deficiency, or are severely attacked by cassava green mite (Mononychellus tanajoa) or cassava mealybug (Phenacoccus manihoti). This indicates the limitations of relying solely on symptom expression in ecological and epidemiological studies and such evidence should be treated with caution and ideally confirmed by diagnostic tests. However, some of these are of limited sensitivity and they are not widely available.

Similarities to Other Species/Conditions

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CMGs have a genome of circular, single-stranded DNA and a particle morphology typical of other viruses of the Geminiviridae Begomovirus genus. The particles are serologically related to, and have sequence similarities with, those of other whitefly-transmitted members of the Geminiviridae.

Prevention and Control

Top of page 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).


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Akinbade SA; Hanna R; Nguenkam A; Njukwe E; Fotso A; Doumtsop A; Ngeve J; Tenku STN; Kumar PL, 2010. First report of the East African cassava mosaic virus-Uganda (EACMV-UG) infecting cassava (Manihot esculenta) in Cameroon. New Disease Reports, 21:article 22.

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Bates DC; Chant SR, 1970. Alterations in peroxidase activity and peroxidase isoenzymes in virus-infected plants. Annals of Applied Biology, 65:105-110.

Bock KR, 1975. Maize streak, cassava latent and other similar viruses. In: Abstracts of the Third Congress of Virology, Madrid.

Bock KR, 1983. Epidemiology of cassava mosaic disease in Kenya. In: Plumb RT, Thresh JM, ed. Plant Virus Epidemiology. The Spread and Control of Insect-borne Viruses. Oxford, United Kingdom: Blackwell Scientific Publications, 337-347

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