Fargette, Denis

Fauquet, Claude

Thouvenel, Jean-Claude

Horizon / Pleins textes

TROPICAL PEST MANAGEMENT 1988 34fl I 92-96 
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Some aspects of the epiaemiology of African cassava mosaic virus in Ivory Coast 
l (Keywords: Cassava. vws. whitefly, ACMV, epidemiology. Africa) 0 
ARGETTE, and L. C. HOUVENEL 1 I 
Laboratoire dP Virolope Vegetale. Institut Francars de Recherche Scientifique pour le Developpement en Cooperation 
(ORSTOM) B. P. V51. Abidjan, Ivory Coast 
Abstract. Re-infection of healthy cassava plants by African cassava 
mosaic virus (ACMV) was followed in different varieties and tor 
several years at various locations in two regions of Ivory Coast. 
Whitefly populations on cassava and virus incidence varied widely 
between sites. even amongst those close to one another. However, 
for each location and in every year. the spread of ACMV showed the 
same general trend Little spread occurred at Toumodi ín the 
Savannah region which IS outside the main cassava production area. 
Much greater spread occurred at a nearby site and at all sites in the 
forest region except one alongside the Ocean where there were no 
cassava plantings upwind. Among sites there was no direct relation 
between virus incidence and the total number of adult whitefly, 
whereas there was a relationship between spread and the occuir- 
ence of .nfected cassava upwind although not necessarily close by. 
Introduction 
African cassava mosaic disease is one of the most 
important factors limiting the production of cassava (Manihot 
esculenla Crantz) in Africa. The disease is caused by a 
gentnivirus (ACMV), which aflects nearly all the cassava 
plants grown. I' IS perpetuated by cuttings and transmitted by 
the whitefly Bemisia tabaci (Cennadius), (Storey anc: 
hiichols. 1938). 
Different strategies of disease control have been proposed 
based on the epiaemiological knowleage available. In Kenya, 
Bock and Guthrie (1977. 1982) reported a low rate of ACMV 
spread into initially mosalc-tree plots and concluded that 
movement of intected cuttmgs by man is a more important 
means o: dissemination than whitefly vectors. Hence il was 
Proposed tha: the disease could be controllec: simply by 
reledsrnr: mosaic-free material (Bock. 1983). Elsewhere, in 
Nigeria and in other West African countries, re-infection by 
whitefly is rdDid and attention has tumed to resistant or 
tolerant varieties (Leuschner, 1977). 
Virus disease spread is greatly influenced by vectors, plant 
growth and virus sources (Gibbs and Harrison. 1976). At lhe 
outset of our investigations, little information was available on 
these factors in relation to the epidemiology of ACMV in the 
Ivory Coast. Accordingly, we assessed spread into initially 
mosaic-free piantings for several years at locations in the 
savannah (Toumodi and Tontonou, 200 km north of Abidjan) 
and lowiand rain forest regions (Adiopodoumé, 20 km west of 
Abidjan) (Foure 1). Re-infection was also followed at five 
trials in different parts of the forest region located along a 
south-north transect (Figure 1 ). Our trials considered spread 
in relation to whitefly populations, cassava growth rate and 
the extent and, .dis!ribution of cassava. in the surrounding 
locäliiy. Tney were intended to determine lhe key 
! 
, 
~ l i .. -- .- , -- 
epidemiological features and the overall ecology of ACMV in 
different situations: 
Figure 1. Sketch map showing location of the trrals in the Ivory- 
Coasf wilh en enlargement of the Dabou-Jacqueville area showing 
the direction of the prevailing wind. 
Material and methods 
Sources of cuttings and planting pattern 
All healthy cuttings originated from healthy cassava 
plantings at Toumodi Experimental Farm. The trial areas 
were divided into units of 1 O0 plants (1 O x 1 O) at a 1 x 1 m 
spacing. I 
1 Fonds Documentaire IRD 
Aspects of African cassava mosaic virus 93 
I. Toumodi. Tontonou and Adiopodoumé trials 
Location of the ;rials and cassava background. The 
Adiopodoumé trials were located in the 200 ha Agricultural 
Experimental Farm of the ORSTOM Institute. Mosaic- 
-*f~cted cassava fields were few (1 or 2 ha of 40), although 
'7 cassava (all infected) is grown intensively elsewhere in 
:%y. At Toumodi. plots were planted in a commercial 
4-0 duction farm, where several hundred ha of 
<:;ad cassava are grown. Each year, the virus- 
-+CS were locatea upwind of infected cassava plant- 
,figs. By contrast. at Tontonou (a few kilometres downwind 
from Toumodi). lhe plots were located in the centre of a 
cassava production farm of several hundred ha, all infected. 
Outside these two commercial farms, cassava is seldom 
grown in the Tontonou-Toumodi area. 
Variety trials. Plantinss of virus-free matelrial began in 
1981 at Toumodi and in 1982 at Adiopodoume. In 1981 and 
1982. the areas planted varied from.0.01 to 0.2 ha according 
to the amount of healthy material available. In 1983 the 
varieties were planted in a latin square arrangement both at 
Toumodi and Adiopodoumé. Planting was done in early July 
and varieties from Ivory Coast (BRl , BR2, Ta49), Madagas- 
car (H57. H58) and Zaïre (CBI were tested. Infected plants 
were counted and removed and whitefly populations were 
estimated, weekly at Adiopodoume and monthly at Toumodi 
and Tontonou in :983. 
Date oi planting trials. In 198 1 and 1984 at Adiopodoumé 
and Toumodi. 0.1 ha areas of healthy cassava cv. CB were 
planted at different dates from March to September. Each 
planting was examined monthly for six months and infected 
plants were removea when found. 
Toumodi. Tontonnu and Adiopodoume trials. In June 
1983. 0.5 ha of a susceptible variety H58 and a resistant one 
BR were planted at the three sites: Adiopodoume, Toumodi 
and Tontonou. Disease incidence was recorded monthly. 
II. The Dabou-Jacqueville multilocation trial transect 
Location o/ th8 trmls and cassava background. All areas of 
cassava were of cv. CE3 planted in early July 1984 in farmers' 
fields in different ecological situations in the Dabou- 
Jacqueville area (40 km west of Abidjan). The five trials were 
located along a 15 km south-north transect at increasing 
distances from the Atlantic ocean (Figure 1). Sites 1 and 2 
were in the 10 km wide strip of land between the ocean and 
the lagoon and sites 3. 4. 5 were inland at various distances 
Trial I: Akrou. 0.07 ha. a few metres from the ocean. No 
Jassava plantings between the shore and the field but with 
diseased cassava a few metres away along the east 
boundary. 
Trial 2: Goyeme. 0-09 ha, 8 km from the ocean. Complete- 
ly surrounded by diseased cassava fields. 
Trial 3: Kaka. 0-09 ha, 200 m from the lagoon shore. Partly 
surrounded by diseased cassava fields. 
Trial 4: IRHO 7. 0.1 ha, 4 km inland. Almost completely 
surrounded by diseased cassava fields only about 10 m 
away. 
Trial 5: IRHO 2. 0-1 ha, 7 hm inland. In a palm plantation: 
no cassava field within 3 km. 
Surveys. Re-infection was followed monthly Sy counting 
the number of diseased plants. Each month, for each trial, 
adult whitefly were counted on 25 plants and crop growth 
was recorded by measuring plant height. 
Results 
I. Adio.podoume, Toumodi and Tontonou plantings 
Vanefy trials. Table 1 indicates disease incidence in eac3 
o! seven varieties 10 months after planting. in the savannah 
region at Toumodi and in the forest region at Adiopodoumé. 
Each year and with each variety the incidence of infection 
was mucn greater at Adiopodoume than at Toumodi. 
Table 1.  The incidence of ACMV (as percentage or total stotld) in 
cassava planrings of seven different varieties 7ff months after 
Dlanrrna at Adiooodoume and Toumodi, in different yean. 
Site and year BA1 0R2 H57 CB Ta49 H58 B 0  
Adiopodoume 1982 
Adiopodoum6 1983 
Aciopoaoume 1984 
Toumodi 1981 
Toumodi 1982 
Toumodi 1983 
Toumodi 1984 
32 - 45 82 - 88 81 
i o  11 25 74 67 84 89 _ - -  4 9 - - -  
- - - 4  4 1 0 1 0  
3 -  3 1 -  5 20 
1 2 2 3 1 2 7  
- - - 4 - - -  
- not planted 
Table 2. The rocidence of ACMV (as percentage of !ora/ stand) :n cassava fields cy. CB planled on different dates six months after planting at 
Adiooodoume and Toumodi. 
~~ ~ ~ ~~~~~~ ~ 
Plnnting date 
Site and year March April May June July August September ! 
Adfooodoume 1981 - - 63 - 26 32 47 
Adirwdoume 1984 91 58 49 42 50 
Toumodi 1981 - - 22 8 4 
Toumodi 1984 4 43 11 4 12 - 
- - 
- - 
% - not planted 
Aspects of African cassava mosaic Virus 9s 
Table 3. The incidence of ACMV. whifefly popblaftons. planting. six months after planfating and fhe sttuatron of fhe five DabouJacqueville 
multilocalion fnal sites. 
SITE 
Disease incidence ( % I t  
Whitefly numbers $ 
Cassava height (mi'' 
Cassava fields upwind !j 
Local 
Distant 
~~ ~ 
Akrou (1 ) Goyeme (2) Kaka (3) IRHO1 (4) IRH02 (5) 
14.1a 4*?b 2.7d 2.4d 3.7c 
1.24d 1.61b 1 *47C 1.47C 2.05a 
17.64 ?@4a 296C 252c 46.0b 
- + t c - 
- - - + + 
t Disease incidence 6 months after planting on 250 plants. * Average whitefly numbers over 6 months on 25 plants. 
Cassava height. 6 months after planting on 25 plants. Oifferent letters indicate significant differences at 95% level (disease incidence: 
9 Local +I- indicates the presencelabsence of cassava fields upwind witnin one kilometre while distant +I-  indicates the presencelabsence 
Chi-square test: whitefly numbers: Man-Whitney test: cassava heights: Student test). 
of cassava fields upwind over greater distances. 
upwind. even at site 5 where there were il0 cassava grown 
within 3 km. 
Discussion 
Among the factors which are likely 'to play a maior role in 
the epidemiology of ACMV, Bock and Guthrie (1977) 
emphasized firstly the size of whitefly populations and their 
behaviour, secondly the cassava growth pattern and thirdly 
the efficiency of transmission by vectors. To these must be 
added the potency, prevalence and distribution of sources of 
infection. 
Cassava is a reservoir of both ACMV and its vector 
(Fargette et al., 1987). and there is evidence that in Ivory 
Coast it is :he major source of infection (Fargette, 1985). 
Whiteflies can disperse far and may be swept considerable 
distances downwind (Fargette et al.. 1985). Thus diseased 
cassava upwind poses a serious hazard and can lead to 
much infection. as observed at Adiopodoume. Tontonou and 
at transect sites 2. 3. 4 and 5. By constrast. with no infected 
cassava upwind. fields are invaded by mainly nonviruliferous 
Whiteflies from other plants. thus resulting in a low disease 
incidence. as observed at Toumodi and Site 1. The high 
incidence of infection at isolated site 5 within a large palm 
Plantation and far from any other cassava was particularly 
notable and suggests spread over several kilometres. In 
Kenya. it has also been found that cassava fields constitute 
SoUrCes Of infection. However, the situation apparently differs 
from that in Ivory Coast as only short range dispersal of 
ACMV occurred and long range dispersal was very limited 
(Bock, 1987) 
There was no vegetation upwind of !he costal site 1 
alongside the ocean. Nevertheless. whitefly at this site could 
have been swept into the area from inland vegetation by sea 
breezes during the .'lay or by land breezes at night (Pedgley. 
1982). The immigrants are likely to have originated from 
plants other than cassava because the incidence of ACMV 
was very low in relation to the whitefly populations recorded. 
Semisia rabacr has : very wide host range including many 
crops and weed soecies that are not host Of ACMV. 
From a practical stand point. our experiments show that it 
IS oossrble at Toumodi to grow largely healthy crops by 
planting virus-free cuttings and roguing, as demonstrated in 
Kenya (Bock. 1983). Indeed the Toumodi site has aiready 
been used to produce large quantities of healthy cunings for 
experiments on #ne epidemiology of ACMV (Fargette. 1985). 
Such sites can also be used to produce healthy cuttings for 
distribution on a large scale to farmers elswhere in Ivory 
Coast. However, our experiments suggest that. in many 
areas of Ivory Coast. the overall infection pressure is high 
and leads to rapid re-infection. This senously restricts the 
possibility of improving productivity by planting virus-free 
cuttings, especrally in those areas where cassava is wjdely 
grown and the many small plantings are in very close 
proximity. Thus the results obtained at Toumodi cannot be 
extended directly !o other regions or for the country as a 
whole unless acceptable varieties became available with 
much greater resistance to infection than those currently 
grown. 
Acknowledgments 
Grateful thanks are due to Dr J. M. Thresh for helpful 
discussions and const:uctive criticism of the manuscript. 
References 
BOCK. K. R., 1983. Epidemiology of Casava mosaic disease in 
Kenya. In Plant virus epidemrology. pp. 337-347. Eds R.T. 
Plumb and J.M. Thresh. Blackwell Scientific Publications. 
3 x  ford. 
BOCK. K. R.. :987. Some aspects of African cassava mosaicvirus in 
coastal districts of Kenya. Abstracts of the lntemational Seminar 
on African cassava mosaic disease and its cuntrol. 4-8 may 
i 987. Yamoussoukro, Ivory Coast. 
BOCK. K. R. ana CUTHRIE. E. J., 1977. African mosaic disease in 
Kenya. Proceedings of the cassava Protection Workshop, 
CIAT. Cali. Columbia. pp 41-44 
BOCK. K. R. and GUTHRIE. E. J.. 1982. Control of cassava mosaic 
disease in Kenya. Tropical Pest Management 28. 219-2222. 
FARGETTE. D.. 1985. Epidemiologie de la Mosaïque africaine du 
manioc en CBte d' Ivoire. PHD thesis. Faculte oes Sciences de 
Montpellier. 201 pp. 
FARGETTE, D., FAUQUET. c. and THOUVENEL J .  C., 1985. Field 
studies on the spread Of African cassava mosaic. Annals of 
Applied Biology 106. 285-294. 
FARGETTE. D.. THOUVENEL. J-C. and FAUQUET. C.. 1987. Virus 
content in relation to leaf symptoms in cassava infected by 
African cassava mosaic virus. Annals of Applied Biology 110, 
65-73. 
I 
94 6. Fiuquet et al. 
Planting dates. Final disease inciaence was greatly influ- 
enced by planting dale but it was always much grealer al 
Adiopodoume than at Toumodï (Table 2). There were slight 
annual fluctuations, but for each variety and for most planting 
dates, much spread occurred at Adiopodoum6 and little at 
Toumodi. This suggests that these general trends of ACMV 
incidence, as they changed little between years, are an 
inherent feature of the sites. 
Adiopodoume. Toumodi and Tontonou plantmngs. ACMV 
spread was not uniform in each region and differed even 
between fields in the same region. Figure 2 illustrates very 
different disease progress curves for plantings of a suscepti- 
blle variety, H58 (left) and a resistant one, BR (right) at 
Adiopodoume, Toumodi and Tontonou. On each date spread 
was always greatest at Tontonou and least only a few km 
away at Toumodi. Final disease incidence was for BR 25 
times and for H58 40 times greater at Tontonou than al 
Toumodi. 
II. The Dabou-Jacqueville multilocation transect iria1 
Figure 3 presents disease spread and the cumulative 
number of aduli whiteflies counted in each of the five fields 
along the Dabou-Jacqueville transect over a six month 
period. Table 3 also indicates the cassava growth pattern 
and some features of the cassava environment. 
/ I  
* 
I m a o m m œ a r p m m  
There were significant diflerences between sites in dis- 
ease inciaence (Chi-square =. 198. DF = 4: P. 0.001) 
Inlection was least at site 1 which was nearest to the ocean 
and greatest at sites 2 and 5. Infection was generally 
intermediate at sites 3 and 4. 
There is some evidence that. within a site. whitefly 
populations and subsequent disease irlcidence are associ- 
’ ated, (Leuschner, 1977: Fargetle el al., 1985). Nevertheless. 
in our experiments differences in disease incidence between 
sites were not directly related to whitefly numbers. PoDula- 
tions differed significantly between sites (Kruskall-Wallis 
H = 75.6; OF = 4; Pcr  0.001) yet there was no direct 
relationship between the number of adult whiteflies and 
disease incidence (Table 3). Site 1 supported the greatest 
number of adult whitefly, yet showed the lowest disease 
incidence. Site 2 with the highest virus incidence supported 
comparatively iew. 
Cassava growth, as measured by stem height. differed 
significantly between sites (Fisher F = 33-5; DF = 4. 24: 
P < 0.001) but there was no obvious relationship between 
growth rate and disease progres. By contrast, our results 
suggest relationships between virus incidence and the 
Occurrence af infected cassava plantings upwind. In both 
sets of trials, lowest contamination (Toumodi and Transect 
site 1) was observed at sites where there were no cassava 
fields upwind either nearby or further away. Considerable 
spread occurred at Sites where infected cassava occurred 
f P _:” :1 
il 
Figure 2. The incidence of A’fricac cassava mosaic disease (as percentage of total stand) in a susceptible variety H58 (left) and a resislani 
variety ER lnght) planted at three locations: Tontonou f.), Adiopodoume (o) and Toumodi (*). 
Figure 3. The incidence o! ACMV ,left) and cumulative number of whitefly (righr) at the five different locations of rhe Dabou-Jacqueville trial. 
Akrou ( 1 )  (W. Goyemme 12) D. Kaka (31 (-2). IRHO1 (4) I*). IRH02 (5) (9). 
f 
o 


Some aspects of the epidemiology of African cassava mosaic virus in Ivory Coast

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