Fargette, Denis

Fauquet, Claude

Thouvenel, Jean-Claude

Name not available

Yield losses induced by African cassava mosaic virus in relation to the mode and the date of infection

Horizon / Pleins textes

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TROPICAL PEST MANAGEMENT, 1988, 34(1) 89-91 ‘5sq 
Yield losses induced by African cassava mosaic virus in relation to the mode and 
the date of infection 
(Keywords: cassava, virusAGMtJ,whitefly, yield loss, Africa) 
I L’ B 
Laboratoire de Virologie, Institut Francais de Recherche Scientifique pour le Développement en Coopération (ORSTOM), 
B. P. V51 Abidjan, Ivory Coast 
Abstract. Yield reduction of cassava infected with African cassava 
mosaic virus (ACMV) was greater when plants were infected from 
the outset as cuttings than later by the whitefly vector Bemisia tabaci. 
Early infection by B. tabacicaused greater losses than late infection. 
When symptoms first appeared, more than four months after 
planting, there was no significant yield reduction. Yield reductions in 
plots where diseased plants were inter-mixed with healthy ones and 
subject to inter-plant competition were much greater than when they 
were assessed using separate healthy and infected plots. Crop 
losses due to ACMV in the cultivar CB were estimated at Ca 40%. 
border rows, infection was recorded weekly (400 plants in 
all). Four infected cuttings were planted in the middle of each 
of four blocks and a plot of 50 diseased cuttings was planted 
in the middle of the field. Harvesting was carried out 15 and 
12 months after planting for fields 1 and 2, respectively. 
Fresh root weight and date of symptom appearance of 
individual plants were recorded. 
Introduction 
African cassava mosaic is a widespread and serious 
disease of cassava (Manihot esculenta Crantz) in Africa. It is 
caused by African cassava mosaic geminivirus (ACMV) 
(Harrison et al., 1977; Bock and Woods, 1983), which is 
perpetuated by cuttings and transmitted by the whitefly 
Bemisia tabaci (Gennadius) (Storey and Nichols, 1938). 
Several authors have estimated losses induced by ACMV 
(Terry and Hahn, 1980; Seif, 1982). However, in many 
African countries, including the Ivory Coast, the disease 
affects virtually all cassava plants and it has not been 
possible to obtain enough healthy material for comparative 
purposes. Only recently at Toumodi (in the savannah region 
of Ivory Coast, 200 km north of Abidjan) has it been possible 
to raise virus-free material after repeated selection for 
several years (Fauquet and Thouvenel, 1981). 
As losses due to plant diseases may be considered the 
raison d’ être for plant pathology (Main, 1977; Nyvall, 1983) 
fields experiments were started to estimate yield reductions 
induced by ACMV in infected cuttings and also by natural 
spread due to B. tabaci at different stages of crop growth. 
Material and methods 
Healthy cassava cuttings, cv. CB from Toumodi Ex- 
perimental Station, were established at the ORSTOM Ex- 
perimental Station of Adiopodoumé (coastal area of the Ivory 
Coast, 20 km west of Abidjan). Variety trials demonstrated 
that ACMV provokes intermediate level responses in cultivar 
CB, as measured by symptom expression and virus multi- 
plication compared to other cultivars (Fauquet et al., 1986). 
Field 1 of 1 -0 ha was planted in October 1983 in 1 O0 blocks 
of 100 plants (10 rows of 1 O plants at a spacing of 1 x 1 m). 
Five plants were selected along one diagonal of each block. 
They were examined each fortnight and labelled when they 
showed the initial symptoms of infection (500 plants in all). 
Field-2 of 0.5 ha was planted in July 1983 in 50 blocks of 1 O0 
plants at a 1 x 1 m spacing. In 9 blocks, excluding the 
Results and discussion 
Root weights were very variable, which is a typical feature 
of cassava (Rafaillac and Nedelec, 1984). Yields ranged 
from 0.1 to 7.4 kg for the individual plants recorded in field 1 
and from 0.1 to 10.9 kg in field 2. Average yield was 2.4 kg 
per plant in field 1 and 5.2 in field 2. The distribution of dates 
of first symptom expression show differences between the 
two trials. Much spread occurred within 100 days of planting 
in field 1, whereas in field 2 it was mainly after 150 days. 
Despite these differences, both trials showed the effect of 
mode of infection (clonal versus vector) and, with infection by 
B. tabaci, the effect of the time from planting when symptoms 
first appeared. 
There was a highly significant relationship between the 
time of first ACMV symptom expression and root weight for 
fields 1 and 2 (one-way variance analysis: field 1, F = 4-49; 
DF = 12,395; P < 0.001 ; field 2, F = 5.1 9; DF = 1 O, 397; 
P < 0.001). Figure 1 illustrates the results. Symptoms that 
first appeared within 40 days of planting are likely to indicate 
infection as cuttings and after 40 days by whitefly. This is 
because the period required for the growth of enough leaves 
for B. tabac; to settle and feed is around two weeks and the 
incubation period, although somewhat variable, is about 
three weeks. In field 2, all plants derived from diseased 
cuttings exhibited clear symptoms within 30 days of planting. 
Average yield reduction in clonally infected cassava was 
55% and 77% for fields 1 and 2, respectively. In both trials, 
infection by vectors even when it occurred early had less 
effect. Yield losses reached 35 and 60% for fields 1 and 2 in 
plants which showed symptoms at day 45. The greater yield 
reduction induced by clonal infection is consistent with 
results from studies on ACMV in other countries with different 
varieties (Briant and Johns, 1940; Terry and Hahn, 1980). 
This may reflect the longer and earlier period over which the 
pathogen affects host metabolism and the subsequent 
impairment of plant growth during the critical establishment 
phase. Moreover, most cassava plants have more than one 
stem and clonal infection affects usually them all immediate- 
ly, whereas vectors initially infect only one shoot and the 
others grow normally at least for a time. The difference in 
I 1 I Fonds Documentaire IRD I 
90 D. Fargette et al. 
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response could also be influenced by the greater virus 
content and greater metabolic disturbance in plants infected 
as cuttings when compared with those infected by whiteflies. 
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O M loo I50 200 250 H 
First symptoms expressed 
(number of days after planting) 
.o.oz t Y = 5.4.1.1 e r - l  I: nn2 
,, I 
0.0 -1 // 
O 50 loo 150 ?O0 250 H 
First symptoms expressed 
(number of  days after planting) 
Figure 1. Average tuber weight (0) of cassava in relation to the date 
of first ACMV symptom appearance expressed as number of days 
after planting in field 1 (a) and field 2 (b). 
Results are average values for batches of plants for 75-day 
periods (field 1) and 30-day periods (field 2). H represents the plants 
which were still symptomless at the last inspection on day 220 (field 
1) and day 277 (field 2). Vertical lines indicate the 95% confidence 
limits. 
When infection is by B. tabaci both experiments indicate 
that the earlier infection occurs, the greater is the yield loss. 
At day 120, yield losses were significant but only 6 and 13% 
for fields 1 and 2, respectively. When symptoms appeared 
later than four months after planting there was no significant 
yield reduction. 
Of the different equations tested to fit the average 
experimental points, one of the type 
Vint = Y,,,, - ae-bt 
e = natural logarithm 
gave the best fit, where Y,,,, is the yield of healthy plants, t 
the time of symptom appearance expressed as days from 
planting, a and b are constants and Yinr the yield of infected 
plants in kg. Such equations are widely encountered in 
biology and reflect that the change of Y is initially fast, but 
gradually declines until it reaches an asymptotic level (Mead 
and Curnow, 1983). Average points closely fit a curve 
expressed by the equations: 
Field 1 : Yinf = 2.8 - 3-8 e-o'Os* (r = 0.97) 
Field 2: Yinf = 5.4 - 7-7 e-o'02t ( r  = 0-93) 
(2) 
(3) 
These relationships between root weight and the mode and 
date of infection are derived from data for naturally infected 
plants distributed amongst healthy ones. However, infected 
plants in clumps differ in growth from single isolated plants 
and encounter decreased competition from healthy neigh- 
bours (Zadoks and Schein, 1979). Table 1 indicates the 
average tuber weight of plants infected as cuttings when 
planted in a group of 50 plants and when surrounded by 
mostly healthy plants. Yield losses in relation to equivalent 
virus-free plants were much less than when the diseased 
plants were grouped. Such differences may arise because 
small or slow-growing diseased plants that are surrounded 
by healthy ones are masked and overgrown by their healthy 
neighbours. These utilize the available space, water, light 
and nutrients more effectively, thus both decreasing the 
potential yields of the diseased plants and increasing those 
of healthy ones. The extent of the differences (37 versus 
69%) reflect the great ability of cassava to make compensa- 
tory growth and this has been corroborated in agronomic 
trials at different plant densities (Rafaillac and Nedelec, 
1984). 
Table 7 .  Average tuber weight (kg) of healthy cassava and of 
ACMV-infected cassava planted either in groups or singly. 
Healthy Diseased Diseased 
(in group) (isolated) 
Average tuber weight (kg) 5.04 a+ 3.1 6b 1 fJ3c 
(Standard error) (1.13) (1.71) (1.13) 
Yield losses (%) 37% 69% 
+Different letters indicate significant differences at the 95% level. 
These results show that in variety trials of response to 
ACMV, healthy and diseased plants should be compared in 
different blocks and not when intermixed. Moreover, because 
of the great variability between plants and between fields, 
trials should be conducted on rather large areas and 
repeated for several years. If 37% is accepted as the 
average crop loss induced by ACMV, the official crop 
statistics (FAO, 1985) can be used to make a rough estimate 
of the total losses in Ivory Coast and also elsewhere in Africa. 
If it is assumed that 100% of all plants are diseased, for a 
current annual production of 800 O00 tonnes, crop losses 
would be around 500000 tonnes in the Ivory Coast. For 
Africa as a whole, with a production of 51 million tonnes, crop 
losses would be around 30 millions. 
Acknowledgments 
Grateful thanks are due to Dr J. M. Thresh for helpful 
discussions and constructive criticism of the manuscript. 
References 
BOCK, K. R. and WOODS, R. D., 1983. Etiology of African cassava 
mosaic disease. Plant disease 67, 994-995. 
Losses from African cassava mosaic virus 91 
BRIANT, A. K. and JOHNS, R., 1940. Cassava investigations in 
Zanzibar. East African Agricultural Journal 6, 404-41 2. Cited in 
Review of applied Mycology 1940, 19, 580. 
F.A.O., 1985. 1984 FAO Production year book statistics. Series no 
31. V 38. 
FAUQUET, C. and THOUVENEL, J. C., 1981. Mosaïque du manioc. 
Toumodi. Expérimentation ORSTOM. Rapport ORSTOM, 6 pp. 
FAUQUET, C., FARGETTE, D., DEJARDIN, J., LEYLAVERGNE, F., 
COLON, L. and THOUVENEL, J-C., 1986. Multicomponent 
resistance of cassava to African cassava mosaic virus. Proceed- 
ings of the 31h workshop on epidemiology of plant virus diseases. 
Orlando, Florida. 6-8 august 1986, VI1 28-30. 
HARRISON, B. R., BARKER, H., BOCK, K. R., GUTHRIE, E. J., 
MEREDITH, G. and ATKINSON, M., 1977. Plant viruses with 
circular single stranded DNA. Nature London, 270, 760-762. 
MAIN, C. E., 1977. Crop destruction. The ’raison d’ être’ for Plant 
Pathology. In : Plant Disease, an advanced treatise pp. 55-78. 
Eds J. G. Horsfall and E. B. Cowlings. Academic Press. 
MEAD, R. and CURNOW, R. N., 1983. Statistical Methods in 
Agriculture and Experimental Biology. Chapman and Hall, 335 
PP. 
NYWALL, R. F., 1983. The reporting of estimated plant disease 
losses. Plant Disease 67, 1303. 
RAFFAILLAC, J. P. and NEDELEC, G., 1984. Comportement du 
manioc (Manihot esculenta Crantz, Variety CB) pour différentes 
densités de plantation. Premiers résultats. ßapport ORSTOM, 
15 PP. 
SEIF, A. A., 1982. Effect of cassava mosaic virus on yield of 
cassava. Plant Disease 66, 661-662. 
STOREY, H. H. and NICHOLS, R. F. W., 1938. Studies of the 
mosaic disease of cassava. Annals of applied Biology 25, 
TERRY, E. R. and HAHN, S. K., 1980. The effect of cassava mosaic 
disease on growth and yield of a local and an improved variety of 
cassava. Tropical Pest Management 26(1), 34-37. 
ZADOKS, J. C. and SCHEIN, R. D., 1979. Epidemiology and Plant 
Disease Management. Oxford University Press. 427 pp. 
790-806. 
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Yield losses induced by African cassava mosaic virus in relation to the mode and the date of infection

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